Diabetes Insipidus: An Update

Affiliations.

  • 1 Division of Endocrinology, Diabetes and Metabolism, Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland; Department of Endocrinology, University Hospital Basel, University of Basel, Petersgraben 4, Basel 4031, Switzerland.
  • 2 Division of Endocrinology, Diabetes and Metabolism, Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland; Department of Endocrinology, University Hospital Basel, University of Basel, Petersgraben 4, Basel 4031, Switzerland. Electronic address: [email protected].
  • PMID: 32741486
  • DOI: 10.1016/j.ecl.2020.05.012

The differential diagnosis of diabetes insipidus involves the distinction between central or nephrogenic diabetes insipidus and primary polydipsia. Differentiation is important because treatment strategies vary; the wrong treatment can be dangerous. Reliable differentiation is difficult especially in patients with primary polydipsia or partial forms of diabetes insipidus. New diagnostic algorithms are based on the measurement of copeptin after osmotic stimulation by hypertonic saline infusion or after nonosmotic stimulation by arginine and have a higher diagnostic accuracy than the water deprivation test. Treatment involves correcting preexisting water deficits, but is different for central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia.

Keywords: Diabetes insipidus; Polyuria polydipsia syndrome; Primary polydipsia.

Copyright © 2020 Elsevier Inc. All rights reserved.

Publication types

  • Diabetes Insipidus / diagnosis*
  • Diabetes Insipidus / etiology
  • Diabetes Insipidus, Nephrogenic / diagnosis
  • Diabetes Mellitus / diagnosis
  • Diagnosis, Differential
  • Diagnostic Techniques, Endocrine* / standards
  • Diagnostic Techniques, Endocrine* / trends

Supplementary concepts

  • Dipsogenic Diabetes Insipidus
  • - Google Chrome

Intended for healthcare professionals

  • Access provided by Google Indexer
  • My email alerts
  • BMA member login
  • Username * Password * Forgot your log in details? Need to activate BMA Member Log In Log in via OpenAthens Log in via your institution

Home

Search form

  • Advanced search
  • Search responses
  • Search blogs

Diabetes insipidus

  • Related content
  • Peer review
  • Miles Levy , consultant endocrinologist 1 ,
  • Malcolm Prentice , consultant endocrinologist 2 ,
  • John Wass , consultant endocrinologist 3
  • 1 Department of Endocrinology, University Hospitals of Leicester, Leicester, UK
  • 2 Department of Endocrinology, Croydon University Hospital, London, UK
  • 3 Department of Endocrinology, Oxford University Hospital NHS Foundation Trust, Oxford, UK
  • Correspondence to M Levy miles.levy{at}uhl-tr.nhs.uk

What you need to know

In patients with polyuria, diabetes insipidus is very unlikely if urine osmolality is >700 mOsmol/kg

Patients with central diabetes insipidus who are admitted to hospital should have specialist input and safeguards in place to ensure that desmopressin is not omitted

Intercurrent illness with hypernatraemia in a patient with diabetes insipidus should be managed as a medical emergency

Diabetes insipidus is a rare but treatable condition that typically presents with extreme thirst (polydipsia) together with the passing of large amounts of dilute urine (polyuria). Distinguishing these symptoms from those of primary polydipsia, diabetes mellitus, and causes of urinary frequency without polyuria can be challenging. Diabetes insipidus is caused by a problem with vasopressin production in the pituitary gland (central diabetes insipidus), or action of vasopressin in the kidneys (nephrogenic diabetes insipidus). Desmopressin, an analogue of vasopressin, is an effective treatment for cranial diabetes insipidus. Between 2009 and 2016 there were four reported deaths in England resulting from omission of desmopressin, and a further 56 reported incidents where dosing errors resulted in harm. 1 This Practice Pointer offers an approach to diagnosing suspected diabetes insipidus, and guidance on managing people with diabetes insipidus who have intercurrent illness or require hospital admission.

What is diabetes insipidus?

Diabetes insipidus is rare, with a prevalence of 1 in 25 000. 2 Central diabetes insipidus usually results from pituitary pathology, 3 either as a result of infiltrative or inflammatory pathology, or following surgery for a pituitary tumour, but may also be due to a congenital defect in the production of arginine vasopressin. 3 Nephrogenic diabetes insipidus is usually caused by electrolyte disturbance, renal disease, or drug toxicity (commonly lithium 2 ).

Arginine vasopressin causes water reabsorption at the collecting ducts of the kidney ( fig 1 ). Deficiency of or resistance to the hormone, as seen in diabetes insipidus, leads to excessive water loss resulting in polyuria. Typically, the compensatory drive for thirst will provide adequate rehydration, but in severe cases where there is not ready access to water, someone with diabetes insipidus can become rapidly dehydrated, which may lead to hyperosmolality, hypernatraemia, and potentially death. 1

Fig 1

Biochemical assessment of polyuria and polydipsia

  • Download figure
  • Open in new tab
  • Download powerpoint

How is diabetes insipidus diagnosed?

Presenting symptoms.

Extreme thirst and passing large quantities of pale urine are typical presenting symptoms of diabetes insipidus. It may be difficult to distinguish diabetes insipidus from differential diagnoses with these symptoms, but there are pointers in the history and investigation that can help ( table 1 ). A particular challenge is primary polydipsia, which refers to a psychologically driven increase in fluid intake rather than impaired vasopressin regulation and is often seen in patients with severe mental illness and/or developmental disability, 4 5 although it may simply be behavioural and occur in healthy individuals in the absence of psychiatric disease. Polyuria should be distinguished from urinary frequency in the history, the latter suggesting a urological problem.

Clues to help distinguish diabetes insipidus from primary polydipsia

  • View inline

In central diabetes insipidus, the history of polyuria and polydipsia is usually abrupt, presenting within weeks or months of onset. 3 In nephrogenic diabetes insipidus, the onset is more insidious and patients have often had symptoms for months or years before the diagnosis is made. 2

Symptoms suggestive of pituitary disease may include fatigue, dizziness, irregular periods, and galactorrhoea in women, or loss of libido and reduced secondary sexual characteristics in men.

Ask about a history of pituitary disease, major head injury, or neurosurgery, which are risk factors for central diabetes insipidus. Several genetic mutations have been identified for the condition, so a family history of central or nephrogenic diabetes insipidus may be highly relevant. 2 3

Look carefully at medication history. Patients taking loop diuretics and nephrotoxic drugs are at risk of developing nephrogenic diabetes insipidus. 7 Nephrogenic diabetes insipidus occurs in approximately 15% of patients taking lithium. 7

Initial investigation

The initial investigation of a patient presenting with polyuria and polydipsia is summarised in figure 2.

Diabetes mellitus —Exclude diabetes mellitus either by urinalysis or point of care testing, confirmed by formal measurement of fasting or random glucose.

Electrolyte disturbance —Take blood to exclude hypercalcaemia and hypokalaemia as these can cause nephrogenic diabetes inspidus. 2

Urine volume —If 24 hour urine volume is less than 2.5 L, diabetes insipidus is highly unlikely and other causes of urinary symptoms should be considered. Urine volume can be measured by the patient themselves (eg, with a measuring jug), or a 24 hour collection bottle can be given and sent to the laboratory for measurement of volume only.

Paired urine and plasma osmolality —If 24 hour urine volume exceeds 2.5 L, paired serum and urine osmolalities can help to distinguish diabetes insipidus from polyuria caused by primary polydipsia. If baseline urine osmolality is >700 mOsmol/kg, diabetes insipidus is very unlikely as the ability to concentrate urine adequately has been demonstrated. Diabetes insipidus is likely if serum osmolality is high (>295 mOsmol/kg) and urine osmolality low (<300 mOsmol/kg). Because patients with diabetes insipidus compensate by drinking according to thirst, it can be difficult to distinguish diabetes insipidus from primary polydipsia on the basis of a one-off paired urine and plasma osmolality measurement. 6 In this situation it may be necessary to perform more complex investigations in the specialist setting.

Referral and specialist management

Patients with suspected diabetes insipidus should be referred for specialist investigation and treatment. The urgency of referral depends upon the severity of symptoms. If thirst and polyuria are extreme and serum osmolality >295 mOsmol/kg, refer patients within days or a few weeks at most. Patients with known diabetes insipidus who have hypernatraemia should be seen as an emergency the same day.

Specialist investigations

Water deprivation test —Currently, in equivocal cases where the diagnosis of diabetes insipidus is not clear cut, the water deprivation test is the most common confirmatory test used in specialist care. 6 In this test, the person is deprived of water for several hours while their urine output, urine osmolality, and serum osmolality are monitored over time. In patients with severe diabetes insipidus, water deprivation can be highly unpleasant and should be supervised by the endocrine team with continued measurement of serum and urine osmolality, urine volume, and weight. The test should be stopped if the patient is distressed or there is clear evidence of continued high output of dilute urine, an excessive rise in serum osmolality, and an excessive loss in weight, during fluid restriction. In people with diabetes insipidus there is continued polyuria and low urine osmolality despite water deprivation. If urine output falls and urine osmolality exceeds 750 mOsmol/kg, diabetes insipidus is excluded. In such cases primary polydipsia is more likely. In the second part of the water deprivation test, desmopressin is given to those with confirmed diabetes insipidus. Patients with central diabetes insipidus respond to desmopressin with a rise in urine osmolality and fall in urine volume. There is no response to desmopressin in patients with nephrogenic diabetes insipidus.

Other specialist investigations —There is an increasing move to measure copeptin, a marker of arginine vasopressin levels, 8 in response to hypertonic saline infusion. In normal individuals, hypertonic fluid leads to an increase in vasopressin release, and therefore an increase in copeptin levels. In central diabetes insipidus, there is a blunted copeptin rise, and this is probably a more sensitive and specific diagnostic test than water deprivation. Detailed pituitary imaging such as magnetic resonance and positron emission tomography may help to differentiate between inflammatory and infiltrative pituitary disorders.

C entral diabetes insipidus —adequate fluid replacement, treatment of the underlying condition, and desmopressin administration are the mainstays of management. Desmopressin can be taken orally or via an intranasal spray. Central diabetes insipidus usually responds to desmopressin immediately, and patients notice a substantial reduction in polyuria and thirst. Symptoms of under-replacement with desmopressin are thirst and polyuria, while symptoms of over-replacement are headache and mild confusion (due to hyponatraemia) and reduced urine output.

Empowering patients to manage their own condition is an important part of management, and the endocrine specialist nurse plays a key role in this regard. An important area of self management is preventing hyponatraemia, which is a common complication of desmopressin treatment because excessive fluid intake in the presence of continued desmopressin may lead to over-dilution of the blood due to excessive reabsorption of water It is good practice for patients to have a regular diuresis by omitting a desmopressin dose once or twice a week, or waiting until they have passed urine before taking their medication. 9 The Pituitary Foundation produces a diabetes insipidus card and booklet for patients to carry, to alert the treating physician to the diagnosis in the event of an emergency. 10 This ensures that if a patient is too unwell to give a history, the clinician first at the scene is aware of the diagnosis of diabetes insipidus and knows the importance of fluid and desmopressin administration. There is current ongoing work to produce patient information leaflets similar to sick-day hydrocortisone rules in patients with hypoadrenalism.

Nephrogenic diabetes insipidus —is managed with fluid replacement and cause specific treatment, under the care of a renal specialist. 2 Other treatments include diets low in salt and protein, diuretics, and non-steroidal anti-inflammatory drugs. 2

Management of diabetes insipidus for the non-specialist

Inpatient care.

The Society for Endocrinology has recently produced guidance for inpatient management of acutely unwell patients with diabetes insipidus. 11 These guidelines suggest that all patients admitted to hospital with central diabetes insipidus are identified on admission and that the endocrinology or alternative appropriate clinical team is alerted. Any patient with central diabetes insipidus who is admitted to hospital needs close monitoring of fluid replacement as well as appropriate administration of desmopressin.

All patients undergoing elective surgery should be highlighted in the pre-assessment process with a clear perioperative plan. They recommend hospitals develop an alert system to highlight all patients requiring ongoing desmopressin therapy to ensure doses are not missed.

A Society for Endocrinology survey of UK based endocrinologists suggests that the problem of delayed administration of desmopressin and fluids when patients are admitted to hospital is widespread. 12 Fifty five per cent of respondents had concerns about management of patients with diabetes insipidus in their hospital, and 47% reported at least one patient coming to harm because of delayed administration of desmopressin or insufficient fluid replacement. An NHS patient safety alert has reported a series of critical incidents occurring in patients with central diabetes insipidus. 1 Between 2009 and 2016, four inpatient deaths caused by desmopressin omission were reported in England. 1 One was a 22 year old man with a benign pituitary tumour who died after a routine orthopaedic procedure. This safety alert identified several themes from these incidents, including a lack of awareness of the critical nature of desmopressin among medical, pharmacy, and nursing staff; poor availability of desmopressin within inpatient clinical areas; and omission due to nil-by-mouth status or acute illness. A small survey of non-specialist nursing staff found that some were not aware that diabetes insipidus was a different condition from diabetes mellitus. 1

Intercurrent illness

Central diabetes insipidus —In those who are unwell with intercurrent illness, it is important to accurately assess fluid status and measure serum electrolytes. Patients with hypernatraemia should be managed as a medical emergency in a high dependency setting. Monitor serum sodium every four hours during fluid resuscitation. In patients who have impaired consciousness, it may be necessary to administer desmopressin by the intravenous, subcutaneous, or intramuscular route.

Nephrogenic diabetes insipidus —Patients are similarly at risk of hypernatraemia and severe dehydration. Seek specialist input ideally from the renal team. Treat the cause of the intercurrent illness, consider withdrawal of drugs which may be causing diabetes insipidus, as well as fluid resuscitation.

Education into practice

Do your patients with diabetes insipidus have alerts on their electronic patient record that highlight the risk of desmopressin omission?

How might you offer training to staff to highlight the difference between diabetes insipidus and diabetes mellitus?

Do you offer safety cards to patients with diabetes insipidus?

How patients were involved in the creation of this article

No patients were directly involved in the writing of this article. A person with diabetes insipidus wrote the Patient perspective.

Patient perspective—The water deprivation test

The test begins with the words “YOU WILL NOT DRINK ANY FLUIDS FOR THE NEXT EIGHT HOURS.” If you do have suspected diabetes insipidus, you’ll now be in a total panic! I would typically have at least five litres in eight hours—often much more. You are then told that all trips to the toilet will be escorted—just in case you find a dripping tap, or (bliss) a can of icy coke on the way. Half hourly blood tests will break the monotony and you’ll carry a measuring jug at all times. After several hours of the test, any hope of a trickle of saliva has long gone—your tongue is firmly welded to the roof of your mouth. Can these doctors and nurses possibly imagine what you are going through? Why do they remark on your grey pallor and shuddering body—this is dehydration! Even with no fluids going in, your bladder will still twinge, like an annoying buzzing wasp urging you to empty it yet again. Where on earth is all this pee coming from? Finally, the doctor approaches with a cheery “the test is now over, you are free to drink.” You’ll gulp any fluid in sight—the entire ward’s water jugs, the domestic’s dirty water bucket! On completion of the test and if diagnosed, you’ll receive an injection of desmopressin—the most wonderful medicine ever produced for a person with diabetes insipidus. That injection gives you back a normal bladder output, and the raging thirst is quelled. Temporarily, of course, but heaven while it lasts.

Competing interests The BMJ has judged that there are no disqualifying financial ties to commercial companies. The authors declare the following other interests: None.

Further details of BMJ policy on financial interests is here: https://www.bmj.com/about-bmj/resources-authors/forms-policies-and-checklists/declaration-competing-interests

Provenance and peer review: commissioned, based on an idea from the author; externally peer reviewed.

Patient consent obtained for Patient perspective .

  • ↵ England Patient Safety Alert NHS. Risk of severe harm or death when desmopressin is omitted or delayed in patients with cranial diabetes insipidus. 2016. https://www.england.nhs.uk/2016/02/psa-desmopressin/
  • Bockenhauer D ,
  • Garrahy A ,
  • Thompson CJ
  • ↵ Psychogenic polydipsia. BMJ Best Practice 2018. https://bestpractice.bmj.com/topics/en-gb/865
  • de Leon J ,
  • Verghese C ,
  • Josiassen RC ,
  • Milles JJ ,
  • Fujimoto M ,
  • Kawashima Y ,
  • Refardt J ,
  • Fleseriu M ,
  • Hashim IA ,
  • Karavitaki N ,
  • ↵ Pituitary Foundation. Diabetes Insipidus Information Booklet. https://www.pituitary.org.uk/media/339898/Diabetes-insipidus
  • Baldeweg SE ,
  • ↵ Gohil S, Reddy NL, Levy MJ. Cranial diabetes insipidus—a national survey of patient safety concerns in secondary care. Society for Endocrinology Annual Meeting, 2018.

diabetes insipidus research paper

  • Open access
  • Published: 16 February 2022

Challenges and improvement needs in the care of patients with central diabetes insipidus

  • H. Teare 1 ,
  • J. Argente 2 , 3 , 4 ,
  • M. Dattani 5 , 6 ,
  • J. Leger 7 ,
  • M. Maghnie 8 , 9 ,
  • M. Sherlock 10 ,
  • G.-C. Ali 1 ,
  • J. Francombe 1 &
  • S. Marjanovic   ORCID: orcid.org/0000-0002-6956-2007 1  

Orphanet Journal of Rare Diseases volume  17 , Article number:  58 ( 2022 ) Cite this article

5101 Accesses

5 Citations

1 Altmetric

Metrics details

Central diabetes insipidus (CDI) is a rare condition, with significant impact on patient health and well-being. It is a chronic condition which usually requires meticulous long-term care. It can affect both children and adults. There is limited literature considering the needs and challenges inherent in providing high quality care to patients with CDI, across the care pathway. This paper seeks to address this gap by providing a unique and well-rounded understanding of clinical and healthcare systems-related challenges. It draws on insights from the literature, from direct clinical experience contributed by five clinicians as co-authors (providing insights from France, Ireland, Italy, Spain and the United Kingdom), and from patient perspectives provided through interviews with patient representatives from three patient organisations. We identify clinical challenges related to the diagnosis of CDI, including differentiating between other similar conditions and determining the underlying aetiology. Treatment is challenging, given the need to tailor medication to each patient’s needs and ongoing management is required to ensure that patients continue to respond adequately to treatment. Ongoing support is required when patients switch between formulations. We also identify healthcare systems challenges related to limited awareness of CDI amongst primary care physicians and general paediatricians, and the need for highly skilled specialist care and appropriate workforce capacity. There is also a significant need for raising awareness and for the education of both healthcare professionals and patients about different aspects of CDI, with the aim of supporting improved care and effective patient engagement with healthcare professionals. We reflect on this information and highlight improvement opportunities. These relate to developing guidance to support patients, carers, primary care physicians and general paediatricians to identify clinical features earlier, and to consider CDI as a possible diagnosis when a patient presents with suggestive symptoms.

Central diabetes insipidus: a rare disease with significant impacts on patient health and well-being and a limited evidence base on how to improve patient care

Central diabetes insipidus (CDI) is a rare disease affecting approximately 1 in 25,000 individuals [ 4 ]. It has significant impact on patient health and well-being and usually requires long term care. The evidence base on how to care for patients with this condition is fragmented. There is a need to advance knowledge on the diversity of challenges to patient care and to identify scope for improvement.

In this paper, we provide an overview of the diagnosis, treatment and management of patients with CDI to consider the diversity of factors that play a role in determining the quality of patient care. We identify challenges and improvement needs in both adult and paediatric populations. We draw on insights from a narrative literature review, complemented with the experiential knowledge of clinical experts and the views of representatives from patient associations.

CDI is characterised by hypotonic polyuria and polydipsia resulting from decreased concentrations of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH) [ 4 , 11 ]. Other symptoms can include fatigue, dizziness, hypotension and tachycardia related to dehydration, and hypernatremia which is a direct consequence of CDI [ 15 , 24 ]. Severe dehydration is a particular challenge in young children, who may not as yet be able to self-regulate thirst. Children can also experience vomiting, constipation, fever, irritability, sleep disturbance, retardation of growth, failure to thrive and potentially developmental disability caused by repeated dehydration and hypernatremia [ 9 , 15 , 18 , 20 ].

The disease is caused by damage to AVP-producing magnocellular neurons in the hypothalamus. The degree of deficiency of AVP is the main factor that determines the severity of CDI symptoms. Damage to this region of the brain can occur either due to traumatic injury [ 3 , 11 ] or non-traumatically, for example in response to a tumour, infiltration, infection or inflammation, or less frequently as a result of genetic mutations [ 1 , 21 ]. Hereditary forms of CDI present early in life, whereas acquired forms can occur at any age. CDI has a similar prevalence in men and women. A patient’s quality of life is often impeded as a result of the condition, for example from sleep being disturbed by nocturia [ 25 ]. There is also a risk of fatality in the most severe cases, which can happen because of chronic or severe dehydration, hypernatremia, fever and cardiovascular failure due to a compromised ability to regulate blood pressure [ 5 , 7 ]. Adipsia can increase risk of death [ 12 ]. In patients with CDI, an intact thirst mechanism is critical for protecting against hypernatremia and dehydration.

CDI is one of four conditions associated with polyuria and polydipsia, along with nephrogenic diabetes insipidus (NDI), primary polydipsia and gestational diabetes insipidus [ 7 ]. Once diagnosed, treatment of CDI is generally effective, with desmopressin (DDAVP, D-amino D-arginine vasopressin- an AVP analogue) used as the mainstream treatment to help regulate fluid in the body. However, it can be challenging to identify and accurately diagnose patients and to get them onto appropriate treatment [ 7 , 8 , 14 , 15 , 20 , 23 , 24 ]. Optimising dosages and treatment formulations and ensuring personalised care is also not straightforward [ 1 , 22 , 23 ]. In addition, it can be challenging to ensure that patients remain stable on treatment over time, including when managing CDI alongside other concurrent conditions, particularly adrenocorticotropic hormone (ACTH) deficiency. Furthermore, the lifelong treatment that patients with CDI often require [ 7 ] places significant demand on healthcare systems for ongoing management and monitoring.

The aim of this review is to expand on the key features of the care pathway and the associated factors and challenges that influence patient care, and to reflect on areas in need of improvement.

The paper combines findings from a narrative literature review, insights based on experiential knowledge from five leading clinical experts from the United Kingdom (UK), Ireland, Italy, Spain and France who are also co-authors of the paper, and the views of patient representatives from three associations active in the CDI area (the Pituitary Foundation, UK; the Pituitary Foundation, Ireland; and the Italian Family Association of Septo-optic Dysplasia and Pituitary Abnormalities, Italy).

Narrative review

The narrative literature review was conducted using a systematic search strategy, with the search conducted in October 2020. It included papers published between October 2015 and October 2020, with specified criteria for prioritising papers which were then subjected to thematic analysis. It focused on understanding the care pathway for patients with CDI, challenges and wider influences on patient care, and improvement needs. A total of 25 papers were included in the review; further detail of their selection is included in the Additional file 1 .

Focused discussion with clinical experts

To refine, nuance and build on insights from the literature, the paper co-authors—representing healthcare services research experts from the not-for-profit research institute RAND Europe (SM, HT, JF, DRR, GCA) and clinicians working with patients with CDI in France (JL), Ireland (MS), Italy (MM), Spain (JA) and UK (MD)—engaged in focused discussion. This included individual discussions between a RAND Europe health services researcher (either SM, HT, DRR, or JF) and each individual clinician, a total of five one-hour discussions. It also included group dialogue through two online workshops bringing together the clinical experts and RAND Europe researchers (workshops were held on 23 and 27 November 2020). The workshops were opportunities for collective discussion about care-related improvement needs. They also served to explore healthcare system related influences on quality of care and access to care in more depth, given that these aspects are under-explored in the literature. Clinical co-authors from four countries also gathered estimations of the costs of care for a patient in their local healthcare setting (i.e. hospital) to provide a high-level indication of the estimated costs related to hospital care that are incurred during the patient pathway. Although these are just estimates, and do not cover primary care costs for example, they provide initial insights on the resource implications of caring for patients with CDI which can be built on in future studies, and that extend beyond medicine costs alone.

Interviews with patient representatives

Perspectives were gathered from three patient representatives from associations which support patients with CDI in Ireland, Italy and the UK (unfortunately this was not feasible in Spain or France). Their perspectives helped to better understand how patients experience CDI and their views on future priorities to improve the provision of care. Patient representative views are referenced in brackets with PR-INT X, with X being the code number for an individual interviewee. In some instances, where there is a risk of identity disclosure or linkage of information to a country context, or in light of informed consent, we withhold a reference to preserve anonymity.

We have thematically cross-analysed and triangulated insights from these various sources to develop a multifaceted understanding of care pathways, associated challenges and improvement needs.

There are some caveats to consider when interpreting our findings. The literature review covered high income countries and additional insights from low- and middle-income countries would help to enrich these findings. The workshops and one-to-one discussions with clinical experts are limited to the countries they work in and are based on their personal experience—however these are all leading experts in their country contexts. The interviews are with patient representatives of a limited number of patient organisations who could engage with the study, in part related to the small number of existing patient organisations active in CDI. The cost estimations in particular are limited by the availability of data and detail that could be provided, and thus can only provide an initial indication of cost rather than a comprehensive overview. Despite these caveats, the insights from the literature review and complementary views from clinical experts and patient representatives provide a valuable contribution to enriching our understanding of how care for CDI is provided and what the challenges and improvement needs are.

The care pathway and associated challenges related to diagnosis, treatment and ongoing management

Diagnosing cdi.

In children and adults, CDI is diagnosed using a series of tests to confirm polyuria and polydipsia and to try to understand the underlying cause. Investigations tend to follow a logical progression of clinical history and examination followed by biochemical and endocrinological assessment, followed by radiology. The approach to diagnosis is similar across the different healthcare settings considered in this paper [workshop insights]. In countries where primary care is generally the first point of access to healthcare, patients with CDI will usually first present to a primary care physician (or general practitioner) having experienced symptoms such as dehydration, thirst and frequent urination [PR-INT1, PR-INT2, PR-INT3]. Following basic tests by a primary care physician, in most cases patients will be referred to a specialist endocrinologist for further diagnostic testing [PR-INT1, PR-INT2, PR-INT3].

Both adults and children follow a similar diagnostic pathway. A water deprivation test (WDT), during which the patient is not allowed to drink, has been the gold standard for diagnosing CDI [ 20 ]. It involves meticulous and regular measurements of urine production, blood electrolyte concentrations, plasma and urine osmolality and weight for approximately 7 h (and occasionally for shorter durations in children, if cessation of the test is necessary due to weight loss or hypernatremia) [ 20 ]. This usually takes place in a specialist hospital setting supported by an endocrinologist and specialist nurses, as water deprivation requires careful monitoring [ 24 ]. Patients can find the WDT test extremely unpleasant and challenging [PR-INT2, PR-INT3]. The water deprivation test is sometimes done in modified versions and for shorter periods of water deprivation in some paediatric patients and may be avoided in infancy if hypernatremia with low urine osmolality is present. Parents of children with CDI symptoms may also be asked to measure their child’s fluid balance [PR-INT3]. A WDT may not always be necessary for pregnant women, for whom such a test could be overly cumbersome [ 22 ]. There is potential for increased use of alternative diagnostic tests in the future [PR-INT2], for example measurement of copeptin and the use of dynamic tests such as arginine or hypertonic saline infusions. However, the current use of such tests across different countries remains unclear.

Magnetic Resonance Imaging (MRI) is essential to determine potential causes of CDI—for example it can show thickening of the pituitary stalk which might indicate inflammation/autoimmune conditions, tumours or other disorders, or a neoplastic process in the sellar region [ 7 ]. However, there are challenges associated with using MRI to identify etiological markers of CDI [ 20 ]. Absent neurohypophysis can be diagnosed by MRI if the posterior pituitary bright spot is missing.

Differentiating between the various conditions which share symptoms of polyuria and polydipsia can be challenging and can take considerable time [ 7 , 8 , 12 ]. Existing diagnostic tests can risk false diagnoses, both positive and negative, particularly in patients with mild or partial forms of CDI [ 23  PR-INT2]. Understanding the potential cause of symptoms can help in the diagnostic process, as some events, such as traumatic brain injury are associated with increased likelihood of CDI and can, together with other tests, help to confirm whether a patient has CDI or another condition. Therefore, a full patient history is an important part of the diagnostic process [ 11 ].

Timely diagnosis is impeded if symptoms are not noticed promptly [ 10 ], or if other aetiologies for polyuria and polydipsia are investigated first [ 13 ]. A lack of awareness among primary care physicians regarding the symptoms of CDI [PR-INT1, PR-INT2] can also impede timely diagnosis and referral. The time to diagnosis can vary across countries.

Costs associated with diagnosis can vary a great deal depending on the speed of diagnosis and the complexity of the underlying aetiology, and if additional support is needed, for example intensive care support in instances of traumatic brain injury, or genetic testing to confirm cause (see the cost section below).

Treating CDI: treatment initiation and optimisation

Once a diagnosis has been reached, it is necessary to tailor treatment to the individual; given the marked variability in patient response to treatment, each patient needs a personalised protocol [ 2 , 9 , 20 ].

As introduced previously, CDI is most often treated by replacing AVP with a synthetic vasopressin analogue called desmopressin, in both adult and paediatric populations [ 1 , 6 , 8 , 10  PR-INT1, PR-INT2, PR-INT3, workshop insights]. In all patients with chronic CDI, a common starting point for treatment is to first address nocturia, by administering the first dose of desmopressin before bed [ 22 ]. The patient's response and dose will be measured and adjusted over time until their symptoms are effectively controlled. Initial treatment optimisation generally involves starting with a low dose and gradually increasing if needed [ 10 ]. Some adult patients may only need a single dose per day to control their symptoms overnight (although the strength of the single dose can vary significantly between patients), while severe cases might need up to 200 μg twice or three times a day (occasionally up to 1 mg in total) [ 11 ].

Infants and young children will require much lower doses than adults, which will need to be adjusted over time, as the children grow and develop. Young infants are also dependent on fluid such as breast milk or formula for nutrition, and this can present additional challenges to fluid regulation and dose optimisation. This is because the primary therapeutic goals of treating CDI in young children are to reduce polyuria and decrease excessive thirst to support appropriate levels of fluid uptake, and to ensure appropriate growth. Children require adequate fluid intake and various doses of DDAVP ranging from a low dose of 10 µg/day for infants in cases of neonatal DI to 60 µg/day three times a day during later childhood, although higher doses could be necessary for individualised patients. Careful exact dosing by cutting the available oral disintegrating tablet DDAVP formulation should be performed, particularly for young paediatric patients. Starting with low doses and titration of the dose is important.

Given desmopressin’s mode of action, ongoing patient monitoring during treatment dose optimisation is important. This is because of the risk of developing hyponatremia if too little water is excreted or too much fluid ingested [ 13 ], or hypernatremia [ 8 , 12 , 16 , 17 ] if too much water is lost or too little fluid ingested. It is important to allow water offload in this process, to prevent hyponatraemia. Optimisation therefore involves a specialist endocrinology clinic to determine patient response to treatment and whether the dose needs to be further adjusted. It usually takes 2–3 days, or up to a week as an inpatient, but can take longer for infants [workshop insights]. Treatment optimisation occurs during the same admission as the diagnostic stage.

Desmopressin is available in several different formulations. Decisions relating to which formulation is most appropriate depend on the patient being treated. It can be administered orally as a tablet or as an oral disintegrating tablet (ODT), as a buccal preparation, as a nasal spray, or parenterally (usually intramuscularly or intravenously). The latter may be required in patients that are required to fast pre-operatively or for patients needing intensive care [ 1 , 6 , 8 , 10 , 24 , PR-INT1, PR-INT2].

Desmopressin lyophilizate sublingual tablets are a valuable option for treating CDI in infants and young children, with evidence of more stable absorption than intranasal formulations and oral tablets [ 9 , PR-INT1 and PR-INT2]. However, it can be difficult to split these sublingual tablets into small enough doses for infants. Subcutaneous DDAVP administration enables the administration of small doses to infants but this can lead to more variable sodium concentrations than other formulations [ 9 , and the experience of an expert involved with this research suggests that subcutaneous DDAVP should only be administered in intensive care or post-operatively. According to one patient representative and in their country context, paediatric patients are generally initiated on a nasal spray due to ease of administration, but the formulation may be changed depending on the patient’s response [interview reference withheld to preserve anonymity]. In mild cases of CDI in some countries, clinicians may consider not prescribing DDAVP and instead suggest strategies for managing fluid balance and using fluid replacement [interview reference withheld to preserve anonymity]. Different formulations also take different times to act and hence some patients may prefer formulations which provide relief quicker [PR-INT2].

Treating CDI with desmopressin is generally safe and effective and shown to improve patient quality of life [ 11 ], but can come with side effects. Side effects, while rare, vary slightly between formulation. The intranasal spray, for example, may lead to dizziness, eye irritation, headache, flushing, nausea, vomiting, rhinitis or epistaxis and tachycardia. Evidence suggests that oral DDAVP is better tolerated by some patients [ 20 ]. Dose adjustment can help to mitigate side effects [workshop insights].

Although desmopressin is the main treatment for CDI across different types of patient groups at present, some other treatments are used in some countries (even if not specific for use in CDI) with slightly different modes of action and side effects. These include thiazide diuretics, carbamazepine, chlorpropamide, clofibrate and indapamide [ 9 , 10 , 13 , 15 ]. However, desmopressin remains by far the most commonly used form of treatment [ 10 ].

There is a lack of data on the costs associated with treatment optimisation and these costs are likely, at least in part, to depend on the complexity and length of the optimisation process.

Managing patients with CDI over time

Given that CDI is usually a chronic condition, lifelong management and ongoing monitoring are necessary to ensure that patients respond well to their specific treatment over time. Ongoing care is also necessary to ensure that any changes to treatment are carefully managed [ 7 ]. It is difficult to predict how a patient will respond to treatment. Patient response can be influenced by their ability to adhere to treatment regimens, for example to control fluid intake or regularly take medication. It can also be influenced by other factors such as other illnesses—for example a cold which might affect how well a patient absorbs desmopressin nasal spray, or vomiting which will influence the intake of an oral tablet [ 2 , 11 , 15 , 16 ]. Patient response to a specific treatment dose and formulation can also be influenced by lifestyle factors such as foreign travel to a warm country due to changing water intake behaviours or participating in sport which might impact fluid requirements [workshop insights]. Annual or biannual clinic appointments with an endocrinologist are often required to ensure treatment doses and formulations remain effective. Such clinic appointments are the main healthcare service-related cost associated with the longer-term management of CDI, as outlined in the cost section below.

As part of patient management, it is sometimes necessary to not only adapt dosage but also to switch between different formulations of desmopressin. This can happen if patients find a specific formulation easier to administer [ 15 ] or due to potential supply issues, or differences in the effectiveness of a formulation [two interviewees, interview references withheld to preserve anonymity]. Switching between formulations requires dose titration to optimise the dose for each patient, as it is not possible to predict how patients will respond to new formulations based on their previous treatment protocols [ 14 , 15 ]. This is related to the absence of conversion factors between different formulations. Switching between formulations will require further in-clinic support, which can add to the cost of treatment. Establishing conversion factors between different formulations is challenged by the fact that different formulations have different bioavailability and that there is diversity in how individuals respond to any specific formulation and dose. The UK electronic medicines compendium Footnote 1 provides a correlation table for oral tablet and melt formulations for adults, but this is based on bioavailability correlation research which tends to take place in healthy volunteers, rather than patients with CDI. Whereas such information may help orient clinicians, it cannot guide clinical decision-making given the highly personalised nature of dose optimisation for CDI, and the frequent need for starting with lower doses as part of the dose optimisation process.

Specialists—generally endocrinologists—determine which brand (or generic) and formulation to use, depending on what they think is best for the patient or what they are most familiar with [workshop insights]. In the countries included in this research, the use of branded versions appears more common at the point of prescription, possibly because generic versions are not available or because of clinician preference [workshop insights]. Whether there is therapeutic equivalence between branded or generic products for CDI has not been researched. If patients are followed up in primary care, primary care physicians can make decisions to switch between branded or generic versions, if generic versions are available. However, they generally would not change the dose for paediatric patients without discussion with a specialist. In some countries, repeat prescriptions tend to be organised by primary care without specialist involvement, although the specialist centre would still direct dosage and monitor the patient as needed.

Long term management decisions other than those related to medication will also be dependent on whether patients are able to regulate thirst themselves, or whether they are adipsic. Patients who are able to experience thirst are generally encouraged to avoid excess fluid intake, and drink to thirst rather than habit. For adipsic patients, it is more difficult to keep track of how much water intake is needed [ 11 ]. Therefore, a routine approach to drinking with a daily fluid regimen based on strictly regulated fluid intake with fixed amounts of water, is important to help mitigate the risk of hyper- or hyponatremia [ 9 ]. This can be particularly challenging if patients contract other illnesses, for example if they are vomiting or eating less or have diminished consciousness [ 11 ]. Fasting for a surgical procedure can also introduce risk, and must be supervised by a specialist, particularly if it requires a change in treatment formulation, for example if the patient usually administers ODT [ 11 ]. According to experts consulted for this research, physicians should be aware of associated, treatable hypothalamic abnormalities such as obesity, sleep apnoea, seizures and thermoregulatory disorders when managing patients with adipsic diabetes insipidus. From a fluid balance perspective, these patients require regular DDAVP to treat their CDI but also need a daily fluid prescription in order to maintain euvolaemia (an appropriate blood fluid volume within the body) and eunatraemia (an appropriate concentration of sodium in blood plasma). Adjusting the desmopressin dosage and fluid intake for adipsic patients is generally done in a hospital setting and regular weighing and checking of serum sodium levels is necessary.

Similarly, patients with CDI diagnosis prior to pregnancy who are already receiving doses of exogenous vasopressin or desmopressin may require increased doses during pregnancy and additional monitoring to ensure that there are no complications due to increased dosages [ 1 ].

Given the impact of CDI on growth and development in infants, more frequent monitoring is also particularly important in this vulnerable patient population. This will include monitoring serum sodium, weight and hydration to allow doses to be modified, and home-monitoring including weighing wet ‘diapers’ [ 25 ]. According to an expert involved with this research, daily weighing of an infant/young child patient should make it possible to detect abnormal weight gain, and plasma sodium concentration should be monitored frequently to reduce the risk of hyponatremia. The challenges associated with dose adjustment mean that it is important to involve the relevant experts early in this process to support any required changes to dose [ 10 ]. In paediatric inpatients who are unable to tolerate oral desmopressin (for example while they are unwell with other conditions such as gastro-intestinal issues) a switch to parenteral therapy may be required, although such cases are rare. This would typically be delivered intramuscularly, but intravenous pitressin infusion (vasopressin injection) can also be used. If this is different from the patient’s usual desmopressin formulation, particularly close monitoring is required as it is not possible to predict how the patient will respond [ 10 ].

Both for adults and children, management of the condition at home is also an important part of the patient and/or carer journey [PR-INT1, PR-INT3]. Although patients will tend to have regular six-monthly or annual follow-up appointments, ensuring appropriate medication adherence and administration at home is key [PR-INT2]. Lifestyle issues also require patients to engage with ongoing management or monitoring through their own behaviours. For example, stress, menstruation or unusual consumption of a lot of salty/sweet foods may require desmopressin to be taken at specific times in the day [PR-INT2].

Influences on patient care and the care pathway within healthcare systems

The diagnosis of patients with CDI, decisions about treatment dosage and formulation, and ongoing patient monitoring and management are strongly influenced by features of the wider healthcare system in which patients are treated, as discussed below [ 4 , 5 , 7 , 8 , 9 , 10 , 11 , 13 , 16 , 20 , 21 , 22 , 23 , 25 ].

Influences related to skills and workforce capacity

Supporting patients with CDI requires specialist skills involving endocrinologists and including paediatricians and nurses to support infants and children. Patient support will also draw on other specialties depending on the cause of CDI and specific patient needs [ 9 ]. For example, patients with CDI as a result of a tumour, or as a result of tumour surgery, will require oncologist and neurosurgeon involvement in care. Patients with CDI as a result of traumatic brain injury may need intensive care teams, and patients with CDI in pregnancy will need additional support, for example from obstetrics [workshop insights]. Appropriate support requires the healthcare system to have sufficient workforce capacity and a cadre of highly skilled staff across specialties [ 2 , 11 , 15 , 16 ].

Several of the healthcare systems included in this paper have specialist centres that support patients across a large geographic region. This allows expertise to be concentrated but can also require patients to travel long distances to seek specialist advice and support [PR-INT1, PR-INT3]. This places significant emphasis on the first stages of patient support, often through primary care or other departments such as emergency medicine or oncology, to recognise specific patient needs [workshop insights]. In some countries, the limited number of hospitals with relevant clinical expertise can also create long waiting times for treatment [PR-INT1] or necessitate remote management.

Healthcare professionals in primary care (both primary care physicians and nurses) can sometimes lack sufficient awareness about the symptoms of CDI which can complicate timely diagnosis and referrals [PR-INT1, PR-INT2, PR-INT3]. This can sometimes lead to inappropriate treatment [PR- INT1, PR-INT2]. Primary care physicians are also sometimes not appropriately trained on the importance of carefully managing and monitoring appropriate treatment dosing and formulations as patient conditions change [workshop insights]. In a hospital care setting, not all physicians always understand how desmopressin acts, which can complicate the inpatient care of patients with CDI who are admitted for other conditions [ 8 , 25 ].

Adjusting treatment formulations and dosages over time also requires significant skills to make appropriate decisions and to support personalised care, given that different formulations have significantly different bioavailability and that patient response differs [ 16 , 19 ]. Any potential changes in relation to bioavailability between branded and generic products require further research (as there are gaps in evidence on this issue), to inform policies on generic substitution and automatic dispensing.

The COVID-19 pandemic has also created specific challenges for patients with CDI. These include limited access to primary care physicians to get a referral to an endocrinologist [interview reference withheld to preserve anonymity], challenges accessing and undertaking diagnostic testing [PR-INT1], and lack of sufficient follow up with clinicians related to ongoing management needs. According to one patient representative, some patient support groups and helplines saw an increase in enquiries as a result [interview reference withheld to preserve anonymity]. There is a need to consider how patients can best be cared for in the context of any future pandemics, both in terms of remote care and any essential face to face contact with clinicians.

Influences related to patient engagement with care related decisions and behaviours

Patients and/or caregivers have an important role to play in the ongoing management of CDI and in engaging with healthcare professionals about optimising treatment [ 17 ]. For example, patients may have preferences for specific formulations [workshop insights] in light of their absorption, the types of complications experienced or how straightforward the formulation is to administer. Patient engagement is also essential in the context of monitoring treatment effectiveness and reporting any changes in effectiveness to healthcare professionals [ 6 , 17 ], as well as in the context of ensuring dose adherence and compliance with treatment [ 8 , 20 ]. For some formulations, patient skills in administering the treatment, such as dexterity in administering intranasal formulations, play a role in treatment effectiveness [ 16 ].

Patient education can help equip patients with knowledge about how to manage their disease, what to look out for and side effects [ 8 , 12 , 23 ], which can in turn support effective communications with primary care physicians about treatment and monitoring needs [workshop insights]. In the UK, the Pituitary Foundation provides resources that patients can share with general practitioners if they suspect they have CDI. There are also efforts in some countries to rename the condition so as to remove the term ‘diabetes’ to avoid confusion with diabetes mellitus [interview reference withheld to preserve anonymity].

While there is a need for information and awareness raising regarding the symptoms of CDI [PR-INT1], there is also a need for more education on how families can support treatment and management. This includes a need for improved access to information about water intake, food, salt levels and measuring water balance [PR-INT3]. Beyond patients, interviewees also highlighted the need for better public understanding of CDI [PR-INT1, PR-INT2], for example to avoid patients being refused access to toilet facilities in some settings like shops [PR-INT2]. Awareness raising amongst other professions such as teachers, university lecturers and air stewards may also be needed so that patients can manage their condition with as much ease as possible [PR-INT2].

Those patients who are on both glucocorticoid (for example in the case of panhypopituitarism) and DDAVP replacements may need educational support about specific sick day management. Glucocorticoids are essential for the excretion of water. Some patients who have central diabetes insipidus also have anterior pituitary dysfunction and as such require glucocorticoid replacement. When a child taking both regular glucocorticoid and DDAVP becomes unwell, the parents may need to ensure that the glucocorticoid is doubled or trebled, and that the child is passing urine before giving further doses of DDAVP. In the event of inadequate glucocorticoid administration, water will not be effectively excreted and the administration of DDAVP can lead to water intoxication and hyponatraemia with related complications such as seizures.

Availability and use of appropriate treatment formulations and medicines management and the role of regulation

The availability of appropriate formulations that are safe and effective as well as convenient to administer plays a role in treatment decisions and their appropriateness for users [ 12 , 16 , 20 , 25 ]. Communication between clinicians and patients in relation to why some formulations may be available and why there may be shortages of others (or lack of availability) matters in terms of patient-centred care and good patient-physician communication [workshop insights]. Patient representatives raised issues regarding treatment availability and supply [interview reference withheld to preserve anonymity]. In one country, an interviewee commented that intranasal solution and nasal spray forms of desmopressin have been unavailable since the autumn of 2020, with patients and support groups not knowing when the supply will return [interview reference withheld to preserve anonymity]. Many patients using nasal formulations have subsequently transferred to sheets/melts, which created further supply issues.

Regulation plays an important role in ensuring the availability of appropriate treatments and in promoting good practice. For example, the intranasal spray formulation of desmopressin is no longer approved by the United States Food and Drug Administration, and this has led to a switch to the tablet or melt formulation in many countries [ 15 ]. Similarly, it is important that regulatory officials understand reasons for certain decisions, for example in relation to medicine switching and reasons for product recalls, to support national decisions and guidance that can impact patients directly [ 15 ].

While there is literature discussing good practice for specific patient groups (e.g. children and infants) [ 9 ], and guidance on inpatient management of CDI [ 4 ], we did not identify national level guidelines in the sample of papers reviewed relating to the countries of interest, namely: France, Ireland, Italy, Spain or the UK.

Costs and effective resourcing to ensure appropriate capacity

Economic considerations will vary across healthcare systems, and economic burden may play a role for some patients [ 3 , 25 ]. For example, a US-based study reported a one-month supply of intranasal DDAVP to cost USD 245.80 (based on 2016 data, equivalent to 179.43 euros in 2016), while a one-month supply of subcutaneous DDAVP cost USD 565.25 for treating infants in the USA (based on 2016 data, equivalent to 412.63 euros in 2016 Footnote 2 ) [ 25 ]. This can have significant cost implications over a patient’s lifetime. Data from the UK Footnote 3 provides costs for desmopressin acetate, with 90 oral tablets of 100 μg individual doses reported to cost £44 (based on 2016 data, equivalent to 46.62 euros in 2016) and a pack of 100 sublingual disintegrating tables of 60 μg individual doses reported to cost £51 (based on 2016 data, equivalent to 54.03 euros in 2016). A pharmacoeconomic analysis of vazomirin spray (a treatment used in Russia with desmopressin as the active ingredient) compared with other forms of administration concluded that the cost of vazomirin spray, compared to vazomirin tablets is reduced by 45–48% in patients after resection of chiasmo-sellar region (CSR) tumours [ 3 ]. In general, cost considerations are an important factor in making treatment decisions. Although this research study did not focus on gathering specific medicines cost data in individual countries as part of its scope, the costs of CDI treatment are likely to vary across different geographies, as is the case with many medicines. Therefore, costs in a US context cannot be used to make inferences about costs of medicines in different European countries.

Clinical experts from four countries shared cost estimations for their own hospital settings (see Table 1 ). In all four countries, the costs of healthcare service provision (i.e. consultations and diagnostic tests) are covered by the public healthcare system. However, the clinical experts also noted that given the personalised nature of CDI treatment and management, costs per patient can vary substantially within any one given context [workshop insights]. This means that healthcare services costs are not directly comparable between countries as well as between different hospital settings. In terms of medicine costs, in health systems with a mixture of public and private funding, desmopressin is usually covered as part of a long-term illness scheme, and therefore publicly funded [workshop insights].

Given the limitations set out above, the information in the table below is shared purely for illustrative purposes and cannot be used to infer costs for an entire system nor for other settings. It seeks only to provide some initial information on what healthcare costs are like in some settings, given the paucity of any such insights in the existing literature. The data in the table can also not be aggregated into higher level categories to make inferences about overall diagnosis and care costs, given that different settings collect different types of cost-related information. However, the table begins to shed light on the potential cost items implied in the care of patients with CDI and indicates that the healthcare service costs are not negligible.

The data provided for each country refer to a specific patient population (paediatric or adult CDI patients), with particular mechanisms for data collection and provision based on information clinicians could gather. Other caveats to bear in mind are that the figures provided could be broken down by initial diagnosis, long term care and estimates of total costs for a 10-year timeframe and indicate highly variable ranges, in part dependent on patient complexity. For example, cost can be influenced by whether additional complex testing is needed beyond standard tests for CDI, such as additional cerebrospinal fluid analysis or biopsy to determine the cause of CDI, and by whether patients with CDI caused by traumatic brain injury need to be supported by neurosurgery. It can also be influenced by how long a patient needs to stay in hospital and whether they then need intensive care. If other hormonal treatment is required in addition to desmopressin, such as growth hormone treatment, there will be an additional cost. Therefore, costs of care are highly individualised depending on the specific circumstances of a patient. However, despite these figures being only indicative and context-specific and illustrating diverse cost-ranges across contexts, they indicate that the costs of caring for patients with CDI are not negligible and reinforce key insights we have gained about the complexity of the process.

It is worth noting that there can also be additional out of pocket costs for patients, such as the cost of items necessary for coping with the condition, for example ice cold water, nappies and toilet rolls [PR-INT2].

Discussion and conclusion: towards improved care pathways

Within this paper we have considered current practice in the diagnosis, treatment and management of CDI, and discussed the associated challenges relating to differential diagnosis and highly personalised treatment and management.

We have shown that CDI requires complex patient support. This means care delivery needs to be flexible to meet individual patient needs. The fact that patient response to the mainstream treatment desmopressin can change over time makes long term management needs difficult to predict. This highlights the need for patients to be well-informed in order to effectively engage with healthcare professionals in primary and specialist care. It also highlights the need for highly skilled healthcare professionals to identify symptoms, determine optimal treatment approaches and to effectively manage changes in treatment needs over time.

The cost data drawn from four hospital settings, despite the caveats associated with the data, provides an indication of the impact that time-consuming and challenging diagnostic testing and personalisation of treatment can have on healthcare system resource demands, with costs concentrated in the early stages of the patient pathway. Further research is needed to understand healthcare service-related costs across a broader range of settings.

We have also identified key areas for future exploration, as part of a commitment to improving the diagnosis, treatment and management of patients with CDI and supporting patient quality of life and outcomes. Our research suggests a need to focus efforts on some key areas. We acknowledge that the extent to which these apply more widely—i.e. beyond the countries represented by the clinical co-authors (France, Ireland, Italy, Spain, and the UK)—merits further research. However, these insights are also supported by the challenges highlighted in the wider global literature.

More specifically, in reflecting on the challenges we have identified in this paper, there is scope to consider actions which could lead to improved guidance for primary care physicians on how to identify symptoms and manage patients with CDI. There is also a need for more information, education and awareness raising for patients, carers and families on how to better manage the condition, including in light of comorbidities and changes in patient circumstances. Working with patient associations may be important in this regard. Developing education and outreach for patients may also help patients engage with primary care and with specialists in secondary care.

Given the complexities of managing patients with CDI, further research is needed to understand whether there is potential for greater international consensus or guidance on best practice in the treatment and management of specific types of patients, not dismissing the importance of personalised care. This may require research that would gather retrospective and real-world data to identify how specific practices differ across a broad range of contexts and how they relate to patient outcomes for patients with specific clinical and behavioural parameters.

Finally, the COVID-19 pandemic introduced further challenges for patients with CDI, given high needs for inpatient care during diagnosis and treatment optimisation and there is scope for the clinical community to jointly consider how to approach patient care in the context of future pandemic preparedness.

We hope that the insights and reflections we have shared in this research help to raise awareness of the complexity of managing patients with CDI and support future efforts of clinicians, patient associations, policymakers and the community of patients and carers committed to improving the care of patients with this rare but life-impacting condition.

Availability of data and materials

The data generated or analysed during this study are included in this published article and its Additional file 1 . In line with informed consent, an exception is individual transcripts of interviews and workshop discussions due to risks of disclosing linkage of individual statements to individuals even when data is de-identified and a commitment to preserve anonymity. Further information outlining the methods used in this study is provided in the supporting information.

Electronic Medicines Compendium. 2012. ‘DDVAP Melt 60mcg oral lyophilisate’. Emc. As of 22 December 2021: https://www.medicines.org.uk/emc/product/170/smpc#gref

OECD Data. 2021. ‘Purchasing power parities (PPP)’. OECD. As of 22 December 2021: https://data.oecd.org/conversion/purchasing-power-parities-ppp.htm#indicator-chart

Horizon Scanning Research & Intelligence Centre. 2016. ‘Low dose desmopressin lyophilisate (Noqdirna) for nocturia in adults. NIHR Innovation Observatory. As of 22 December 2021: https://www.io.nihr.ac.uk/wp-content/uploads/migrated/Low-dose-desmopressin-lyophilisate-Noqdirna-June16.pdf

Ananthakrishnan S. Diabetes insipidus during pregnancy. Best Pract Res Clin Endocrinol Metab. 2016;30(2):305–15.

Article   CAS   Google Scholar  

Arima H, Oiso Y, Juul KV, Nørgaard JP. Efficacy and safety of desmopressin orally disintegrating tablet in patients with central diabetes insipidus: results of a multicenter open-label dose-titration study. Endocr J. 2013;60(9):1085–94.

Astaf’eva LI. The efficacy of desmopressin in the treatment of central diabetes insipidus after resection of chiasmo-sellar region tumors. Zh Vopr Neirokhir Im N Burdenko. 2017;81(4):61–9.

Baldeweg SE, Ball S, Brooke A, Gleeson HK, Levy MJ, Prentice M, et al. Society for endocrinology clinical guidance: Inpatient management of cranial diabetes insipidus. Endocr Connect. 2018;7(7):G8-g11.

Barbot M, Ceccato F, Zilio M, Albiger N, Sigon R, Rolma G, et al. Cardiovascular autonomic dysfunction in patients with idiopathic diabetes insipidus. Pituitary. 2018;21(1):50–5.

Chanson P, Salenave S. Diabetes insipidus and pregnancy. Ann Endocrinol (Paris). 2016;77(2):135–8.

Article   Google Scholar  

Christ-Crain M, Bichet DG, Fenske WK, Goldman MB, Rittig S, Verbalis JG, et al. Diabetes insipidus. Nat Rev Dis Primers. 2019;5(1):54.

Christ-Crain M, Hoorn EJ, Sherlock M, Thompson CJ, Wass JAH. Endocrinology in the time of COVID-19: management of diabetes insipidus and hyponatremia. Eur J Endocrinol. 2020;183(1):G9-g15.

Dabrowski E, Kadakia R, Zimmerman D. Diabetes insipidus in infants and children. Best Pract Res Clin Endocrinol Metab. 2016;30(2):317–28.

Elder C, Dimitri P. Diabetes insipidus and the use of desmopressin in hospitalised children. Arch Dis Childh Educ Pract Ed 2017;102:edpract-2016.

Garrahy A, Moran C, Thompson CJ. Diagnosis and management of central diabetes insipidus in adults. Clin Endocrinol (Oxf). 2019;90(1):23–30.

Garrahy A, Thompson CJ. Management of central diabetes insipidus. Best Pract Res Clin Endocrinol Metab. 2020:101385.

Hunter JD, Calikoglu AS. Etiological and clinical characteristics of central diabetes insipidus in children: a single center experience. Int J Pediatr Endocrinol. 2016;2016:3.

Ito A, Nozaki A, Horie I, Ando T, Kawakami A. Relation between change in treatment for central diabetes insipidus and body weight loss. Minerva Endocrinol. 2019;44(1):85–90.

PubMed   Google Scholar  

Kalra S, Zargar AH, Jain SM, Sethi B, Chowdhury S, Singh AK, et al. Diabetes insipidus: the other diabetes. Indian J Endocrinol Metab. 2016;20(1):9–21.

Kataoka Y, Nishida S, Hirakawa A, Oiso Y, Arima H. Comparison of incidence of hyponatremia between intranasal and oral desmopressin in patients with central diabetes insipidus. Endocr J. 2015;62(2):195–200.

Masri-Iraqi H, Hirsch D, Herzberg D, Lifshitz A, Tsvetov G, Benbassat C, et al. Central diabetes insipidus: clinical characteristics and long-term course in a large cohort of adults. Endocr Pract. 2017;23(5):600–4.

Mavinkurve M, McGrath N, Johnston N, Moloney S, Murphy NP, Hawkes CP. Oral administration of diluted nasal desmopressin in managing neonatal central diabetes insipidus. J Pediatr Endocrinol Metab. 2017;30(6):623–8.

Nozaki A, Ando T, Akazawa S, Satoh T, Sagara I, Horie I, et al. Quality of life in the patients with central diabetes insipidus assessed by Nagasaki Diabetes Insipidus Questionnaire. Endocrine. 2016;51(1):140–7.

Patti G, Ibba A, Morana G, Napoli F, Fava D, di Iorgi N, et al. Central diabetes insipidus in children: Diagnosis and management. Best Pract Res Clin Endocrinol Metab. 2020:101440.

Patti G, Scianguetta S, Roberti D, Di Mascio A, Balsamo A, Brugnara M, et al. Familial neurohypophyseal diabetes insipidus in 13 kindreds and 2 novel mutations in the vasopressin gene. Eur J Endocrinol. 2019;181(3):233–44.

Refardt J, Christ-Crain M. Diabetes insipidus in pregnancy: how to advice the patient? Minerva Endocrinol. 2018;43(4):458–64.

Refardt J, Winzeler B, Christ-Crain M. Diabetes Insipidus: An Update. Endocrinol Metab Clin North Am. 2020;49(3):517–31.

Sbardella E, Pozza C, Isidori AM, Grossman AB. Endocrinology and adolescence: dealing with transition in young patients with pituitary disorders. Eur J Endocrinol. 2019;181(4):R155–71.

Smego AR, Backeljauw P, Gutmark-Little I. Buccally administered intranasal desmopressin acetate for the treatment of neurogenic diabetes insipidus in infancy. J Clin Endocrinol Metab. 2016;101(5):2084–8.

Download references

Acknowledgements

We would like to thank Pat MacBride from the Pituitary Foundation, UK, Robert Brady from the Pituitary Foundation, Ireland, and Diana Vitali from the Italian Family Association of Septo-optic Dysplasia and Pituitary Abnormalities, Italy, for their insightful contributions to this study, providing an overview of the patient experience across different health systems. We would also like to thank Dr. Camilla D’Angelo and Giulia Maistrello, analysts at RAND Europe, for their help in translation, as part of the recruitment of patient representatives, and Dr. Daniela Rodriguez Rincon for her involvement in early stages of the research. This research study was funded by Ferring Pharmaceuticals, and we thank Teodor Burtea, MD and Lena Maislisch, M.Sc., both from Global Medical Affairs at Ferring, for their contributions to the concept for this study at ideation stages. The research was conducted and data analysed entirely independently, in line with RAND Europe’s role as an impartial, not-for-profit research organisation.

This research was funded by Ferring Pharmaceuticals.

Author information

Authors and affiliations.

RAND Europe, Westbrook Centre Milton Road, Cambridge, CB4 1YG, UK

H. Teare, G.-C. Ali, J. Francombe & S. Marjanovic

Department of Pediatrics and Pediatric Endocrinology, Hospital Infantil Universitario Niño Jesús, Instituto de Investigación La Princesa, Universidad Autónoma de Madrid, Madrid, Spain

Centro de Investigación Biomédica en Red (CIBER) de Fisiopatología de la Obesidad y Nutriciόn (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain

IMDEA, Food Institute, CEIUAM+CSI, Madrid, Spain

UCL Great Ormond Street (GOS) Institute of Child Health, University College London, London, UK

Great Ormond Street Hospital for Children, London, UK

Assistance Publique-Hôptaux de Paris, Pediatric Endocrinology-Diabetology Department, Reference Center for Growth and Development Endocrine Diseases, Robert Debré University Hospital, Université de Paris, NeuroDiderot INSERM UMR 1141, 75019, Paris, France

Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genoa, Italy

Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy

Department of Endocrinology, Beaumont Hospital and Royal College of Surgeons in Ireland, Dublin, Ireland

M. Sherlock

You can also search for this author in PubMed   Google Scholar

Contributions

G-CA and JF were responsible for conducting interviews with patient representatives, all authors were involved in the workshop discussions. SM and HT contributed to the design of the study. All authors (HT, JA, MD, JL, MM, MS, G-CA, JF, SM) contributed to drafting and developing the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to S. Marjanovic .

Ethics declarations

Ethics approval and consent to participate.

This research took the form of a literature review, supplemented with a small number of interviews and workshops with clinical experts and representatives from patient organisations. It was judged to pose minimal risks to participants and ethical approval was not sought. The research was conducted in accordance with the Declaration of Helsinki. All participants gave informed consent and were provided with participant information sheets as part of this process.

Consent for publication

All authors have consented to the publication of this manuscript.

Competing interests

The authors have no competing interests to declare.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Additional file 1:.

Methodology supplement.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Teare, H., Argente, J., Dattani, M. et al. Challenges and improvement needs in the care of patients with central diabetes insipidus. Orphanet J Rare Dis 17 , 58 (2022). https://doi.org/10.1186/s13023-022-02191-2

Download citation

Received : 26 October 2021

Accepted : 30 January 2022

Published : 16 February 2022

DOI : https://doi.org/10.1186/s13023-022-02191-2

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Central diabetes insipidus
  • Disease burden
  • Healthcare improvement
  • Healthcare systems
  • Rare disease

Orphanet Journal of Rare Diseases

ISSN: 1750-1172

  • Submission enquiries: Access here and click Contact Us
  • General enquiries: [email protected]

diabetes insipidus research paper

Diabetes Insipidus

  • First Online: 25 February 2021

Cite this chapter

diabetes insipidus research paper

  • Eleonora Seelig 2 &
  • Jonas Rutishauser 2  

1002 Accesses

This chapter will discuss basic aspects of fluid homeostasis, focusing on the clinical features and differential diagnosis of diabetes insipidus.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
  • Available as EPUB and PDF
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
  • Durable hardcover edition

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Suggested Reading

Adams NC, Farrell TP, O’Shea A, O’Hare A, Thornton J, Power S, Brennan P, Looby S. Neuroimaging of central diabetes insipidus—when, how and findings. Neuroradiol. 2018;60:995–1012. https://doi.org/10.1007/s00234-018-2072-7 .

Article   CAS   Google Scholar  

Bichet DG, Bockenhauer D. Genetic forms of nephrogenic diabetes insipidus (NDI): vasopressin receptor defect (X-linked) and aquaporin defect (autosomal recessive and dominant). Best Pract Res Clin Endocrinol Metab. 2016;30:263–76. https://doi.org/10.1016/j.beem.2016.02.010 .

Article   CAS   PubMed   Google Scholar  

Bockenhauer D, Bichet DG. Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus. Nat Rev Nephrol. 2015;11:576–88. https://doi.org/10.1038/nrneph.2015.89 .

Christ-Crain M, Bichet DG, Fenske WK, Goldman MB, Rittig S, Verbalis JG, Verkman AS. Diabetes insipidus. Nat Rev Dis Primers. 2019;5(1):54. https://doi.org/10.1038/s41572-019-0103-2 .

Article   PubMed   Google Scholar  

Christensen JH, Rittig S., Weiss RE, Refetoff S. Chapter 5 Diabetes insipidus (2016) In: Weiss RE, Refetoff S. Genetic diagnosis of endocrine disorders, 2nd edition, Elsevier. Saint Louis, 93–101. doi: https://doi.org/10.1016/B978-0-12-800892-8.00005-1

Chapter   Google Scholar  

Fenske W, Refardt J, Chifu I, Schnyder I, Winzeler B, Drummond J, Ribeiro-Oliveria A Jr, Drescher T, Bilz S, Vogt DR, Malzahn U, Kroiss M, Christ E, Henzen C, Fischli S, Tönjes A, Mueller B, Schopohl J, Flitsch J, Brabant G, Fassnacht M, Christ-Crain M. A copeptin-based approach in the diagnosis of diabetes insipidus. N Engl J Med. 2018;379:428–39. https://doi.org/10.1056/NEJMoa1803760 .

Robertson GL. Diabetes insipidus: differential diagnosis and management. Best Pract Res Clin Endocrinol Metab. 2016;30:205–18. https://doi.org/10.1016/j.beem.2016.02.007 .

Sailer CO, Winzeler B, Christ-Crain M. Primary polydipsia in the medical and psychiatric patient: characteristics, complications and therapy. Swiss Med Wkly. 2017;147:w14514. https://doi.org/10.4414/smw.2017.14514 .

Spiess M, Beuret N, Rutishauser J. Genetic forms of neurohypophyseal diabetes insipidus. Best Pract Res Clin Endocrinol Metab. 2020. in press.

Google Scholar  

Timper K, Fenske W, Kühn F, Frech N, Arici B, Rutishauser J, Kopp P, Allolio B, Stettler C, Müller B, Katan M, Christ-Crain M. Diagnostic accuracy of copeptin in the differential diagnosis of the polyuria-polydipsia syndrome: a prospective multicenter study. J Clin Endocrinol Metab. 2015;100:2268–74. https://doi.org/10.1210/jc.2014-4507 .

Winzeler B, Cesana-Nigro N, Refardt J, Vogt DR, Imber C, Morin B, Popovic M, Steinmetz M, Sailer CO, Szinnai G, Chifu I, Fassnacht M, Christ-Crain M. Arginine-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: a prospective diagnostic study. Lancet. 2019;394:587–95. https://doi.org/10.1016/S0140-6736(19)31255-3 .

Download references

Author information

Authors and affiliations.

Division of Endocrinology, Diabetes and Metabolism, University Hospital, Basel, Switzerland

Eleonora Seelig & Jonas Rutishauser

You can also search for this author in PubMed   Google Scholar

Corresponding author

Correspondence to Jonas Rutishauser .

Editor information

Editors and affiliations.

2nd Department of Internal Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary

Rights and permissions

Reprints and permissions

Copyright information

© 2021 Springer Nature Switzerland AG

About this chapter

Seelig, E., Rutishauser, J. (2021). Diabetes Insipidus. In: Igaz, P. (eds) Practical Clinical Endocrinology. Springer, Cham. https://doi.org/10.1007/978-3-030-62011-0_9

Download citation

DOI : https://doi.org/10.1007/978-3-030-62011-0_9

Published : 25 February 2021

Publisher Name : Springer, Cham

Print ISBN : 978-3-030-62010-3

Online ISBN : 978-3-030-62011-0

eBook Packages : Medicine Medicine (R0)

Share this chapter

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Publish with us

Policies and ethics

  • Find a journal
  • Track your research
  • Open access
  • Published: 30 April 2024

The effect of preoperative TSH levels on perioperative complications in patients undergoing pituitary surgery

  • Gizem Kirbas   ORCID: orcid.org/0000-0003-1178-5723 1 ,
  • Murat Yasar Ozkalkanli   ORCID: orcid.org/0000-0002-9082-7233 1 &
  • Ahmet Salih Tuzen   ORCID: orcid.org/0000-0001-9040-2262 1  

European Journal of Medical Research volume  29 , Article number:  259 ( 2024 ) Cite this article

112 Accesses

Metrics details

Introduction

Pituitary surgery involves special conditions for the anaesthetist due to the anatomical localisation and the role of the pituitary gland in hormonal balance. The aim of this study was to retrospectively investigate the effect of TSH levels on perioperative complication rates in patients undergoing pituitary surgery.

In this study, patients who underwent pituitary surgery at Izmir Katip Celebi University Ataturk Training and Research Hospital between January 2017 and November 2022 were retrospectively screened. Two patients out of the 137 were excluded from the study as they underwent simultaneous aneurysm surgery along with pituitary tumor surgery. A total of 135 patients meeting the criteria were analyzed. Patients were divided into three groups according to TSH levels. Perioperative complication rates and mortality rates were compared between the three groups.

The study included a total of 135 patients, with an age range of 16–76 years. Among the groups with low–normal–high TSH levels, there were no statistically significant difference observed, in postoperative complications, such as epistaxis, rhinorrhea, postoperative nausea/vomiting, seizures, hypertension, and hypotension. When looking at the incidence of postoperative diabetes insipidus, a significant difference was found between the groups. When examining the mortality rates on the 28th day, a significant difference was found between the groups, with a mortality rate of 25% in the high TSH group ( p  < 0.5).

Conclusions

The risk of perioperative mortality is higher in patients with TSH levels above normal.

While medical treatment options are possible for many types of tumors today, surgery remains the primary treatment option for pituitary tumors [ 1 ]. The multidisciplinary evaluation of patients who will undergo pituitary tumor surgery by endocrinologists, neurosurgeons, ear–nose–throat surgeons, neuroradiologists, neuro-ophthalmologists, endocrine pathologists, and anesthesiologists is crucial for ensuring optimal treatment conditions [ 2 ]. Patients with endocrine disorders related to pituitary tumors can present unique challenges for the anesthesiologist [ 3 ].

Considering the anatomical location of the pituitary gland and its role in hormonal balance, complication rates after pituitary surgery are high. The rates of complications are influenced by many factors, including the size and pathological subtype of the tumor, the type of surgery, the patient's comorbidities, the patient's endocrine abnormalities, and various factors related to the surgeon–anesthetist relationship [ 4 ].

In the preoperative period, complications related to anesthesia increase in non-euthyroid patients. Changes in cardiovascular functional status and hemodynamic responses to anesthetic drugs are observed in non-euthyroid patients [ 5 ]. Therefore, changes in thyroid hormone levels of patients with surgical plans should be known in advance by the anesthesiologist, and preoperative and perioperative planning should be made in advance. Endocrinology consultations should be repeated if necessary.

This study aims to shed light on the association between thyroid-stimulating hormone (TSH) levels and postoperative complications in patients undergoing pituitary surgery. By systematically comparing outcomes between individuals with normal TSH levels and those outside the normal range, we seek to contribute valuable insights into the role of thyroid function in the postoperative period. Understanding this relationship has the potential to inform clinical practices, enhance patient care, and pave the way for targeted interventions. As we delve into the methodology and results sections, the significance of TSH levels in influencing postoperative outcomes will become clearer, providing a foundation for evidence-based decision-making in surgical management.

Materials and methods

This study was done in Izmir Katip Celebi University Ataturk Training and Research Hospital with the approval of the ethics committee dated 24.11.2022 (GOKAEK-0515). In this study, patients who underwent pituitary surgery at Izmir Katip Celebi University Ataturk Training and Research Hospital between January 2017 and November 2022 were retrospectively screened. Complete data for 137 patients were obtained from archive files and computer systems.

Demographic characteristics of the patients (age, gender, height, weight), ASA (American Society of Anesthesiologist) class scores, accompanying diseases, preoperatively measured thyroid hormone levels, anesthesia duration, surgical duration, Mallampati score, presence of difficult airway, bleeding status, perioperative complications (rhinorrhea, epistaxis, hypo-hypertension, bradycardia/tachycardia, history of seizures), and the need for postoperative intensive care were recorded by examining computer records and anesthesia monitoring forms, along with the pathological type of the tumor. Two patients out of the 137 were excluded from the study as they underwent simultaneous aneurysm surgery along with pituitary tumor surgery. A total of 135 patients meeting the criteria were analyzed.

Among the 135 patients, three separate groups were formed based on TSH levels. The standardized normal TSH range in our hospital was 0.35–5.35 mU/ml. Patients with preoperative TSH levels < 0.35 mU/ml were included in the first group. There were a total of 24 patients in this group. The second group consisted of patients with TSH levels within the normal range (between 0.35 and 5.35 mU/ml). There were 107 patients in this group. The third group included patients with TSH levels above the normal range, specifically TSH > 5.35 mU/ml. There were four patients in this group. Although the T3/T4 hormone levels of the patients were analyzed, they were not included in the comparison. In this study, based on all the obtained data, patients were classified according to preoperatively measured TSH hormone levels and compared in terms of postoperative complications.

Statistical analysis

The statistical analysis of the data obtained in the study was conducted using IBM SPSS Statistics version 22 (IBM Corp., Armonk, NY, USA) software. Descriptive statistics, including mean and standard deviation for continuous variables, frequency and percentage for categorical variables, were reported.

Prior to all analyses, it was evaluated whether if the data confirmed to normal distribution using skewness–kurtosis values, normality tests, and histogram plots. To determine differences in mean values between groups, independent samples t test was used for variables with a normal distribution, and Mann–Whitney U test or Wilcoxon test and Kruskal–Wallis test was used for variables without a normal distribution. In addition, Pearson Chi-square test or Fisher’s exact test was employed to determine differences in categorical variables between groups.

Power analysis

The primary objective of the study is to assess the impaact of TSH levels on the duration oh hospitalization in the respective groups formed. In a reference study, significant differences were observed between the two groups in terms of duration of hospitalization days. The mean ± standard deviation values for the groups were 12.5 and 16, also standart deviation 6 days, with a p value of 0.001. To determine the sample size for the current study, a power analysis was conducted assuming a type 1 error of 0.05 and a study power of 0.85. Based on these calculations, it was determined that a total of 110 patients in each group would be sufficient. Taking into account a potential dropout rate of 10%, a sample size of 125 subjects was planned for the study.

A total of 135 patients ranging from 16 to 76 years were included in the study. The mean age of the cases was 49.19 ± 13.71. among them, 67 were female (49.6%) and 68 were male (50.4%). In the group with low TSH levels (Group 1) and the group with normal TSH levels (Group 2), the majority of patients were in ASA2 risk class (79.2%/63.9%). In the group with high TSH levels, half of the patients were in ASA1 risk class, while the other half were in ASA2 risk class. 19 out of 135 patients (14%) underwent surgery via craniotomy. Upon retrospective examination of patients operated with craniotomy, it was observed that trans-sphenoidal method was not preferred due to reoperation/macroadenoma/accompanying intracranial pathology. In cases, where trans-sphenoidal approach was initially attempted, there was no transition to craniotomy. When examined for all three groups, trans-sphenoidal surgery rates were predominant (83.3%/86.9%/75%). Among all patients, hypertension were the most common accompanying comorbidity (31.9%). The second most common accompanying comorbidity was diabetes mellitus (26.6%). Among the patients in the high TSH group, only one person had coronary artery disease. Visual impairment was the most common presenting complaint among all patients. This was followed by headache and nausea/vomiting. When comparing patients complaints based on TSH values, no statistically significant difference was found between the groups (Table  1 ).

The anesthesia durations and surgical durations were similar among the groups. The length of stay in the postoperative care unit was also comparable for all patients. There were no statistically significant differences between the three groups in terms of hospital stay and the postoperative intensive care (Table  2 ).

Among the groups with low–normal–high TSH levels, there were no statistically significant difference observed, in postoperative complications, such as epistaxis, rhinorrhea, postoperative nausea/vomiting, seizures, hypertension, and hypotension. When looking at the incidence of postoperative diabetes insipidus, a significant difference were found between the groups, with a rate of 43.4% in the low TSH group compared to 17.5% in the normal TSH group and 25% in the high TSH group ( p  < 0.05). Examining the mortality rates on the 7th day, no significant difference was found between the groups. When looking at the need for revision surgery among the patients, no significant difference was observed between the groups. However, when examining the mortality rates on the 28th day, a significant difference was found between the groups, with a mortality rate of 25% in the high TSH group ( p  < 0.5) (Table  3 ).

The findings of this study illuminate crucial insights into the impact of TSH levels on postoperative complications, providing a comprehensive understanding of the role of thyroid function in the context of pituitary surgery. Our analysis has revealed noteworthy distinctions in the occurrence and severity of postoperative complications between patients with normal and abnormal TSH levels. As we reflect on these outcomes, it becomes evident that thyroid function plays a significant role in influencing the recovery process following surgery. The implications of these findings extend beyond the confines of the study population, offering implications for clinical practice, patient management, and avenues for further research. The results of this study have shown that in patients undergoing pituitary surgery, those with elevated TSH levels (Group 3) had higher 28-day mortality rates, and patients with TSH levels below normal (Group 1) had a higher risk of developing diabetes insipidus in the postoperative period. However, no significant differences were observed in other postoperative complications (nausea/vomiting, seizures, rhinorrhea, epistaxis, infectious complications) when comparing patients based on TSH levels.

The trans-sphenoidal approach in pituitary surgery, developed as an alternative to craniotomy, is considered the gold standard due to being a minimally invasive method, providing rapid recovery in the postoperative period, enabling early mobilization, and shortening the hospital stay [ 6 ]. It has been the preferred first option for pituitary tumor surgery in our hospital for approximately 20 years. After a systematic preoperative assessment (pre-anesthetic evaluation, hormonal changes, medical treatment options, determination of surgical type, etc.), patients undergo surgery. Neuroanesthesia is one of the areas that require close collaboration with the surgeon, necessitating close monitoring of the patient in the perioperative and postoperative periods [ 3 ].

Currently, randomized controlled studies comparing mortality and morbidity rates between trans-sphenoidal and transcranial methods are limited, as trans-sphenoidal surgery gives way to craniotomy in cases of macroadenoma presence, invasion of surrounding structures, or the presence of other intracranial pathologies. However, many studies in the literature have associated transcranial methods with increased mortality and morbidity rates [ 7 ]. In this study, it was also found that the risk of mortality was higher in patients operated with the transcranial method. In a study by Agam et al. that investigated the most common complications in the postoperative period following pituitary tumor surgery, which included 1153 patients, the most common endocrine complication reported was transient diabetes insipidus (4.3%). Other commonly encountered endocrine complications included hyponatremia (4.2%), hypopituitarism (3.6%), and permanent diabetes insipidus (0.2%) [ 8 ]. Diabetes insipidus is one of the commonly encountered endocrine complications following pituitary surgery. In this study, transient diabetes insipidus was observed in 30 patients (22.2%) in the postoperative period. Among these patients, it was observed that 41% of the patients in the low TSH group developed diabetes insipidus. In the normal TSH group, the rate of developing diabetes insipidus was 17%, while in the high TSH group, it was 25%. No cases of permanent diabetes insipidus were observed. There was a significant difference in the development of transient diabetes insipidus between the groups ( p  < 0.05). It is known that diabetes insipidus develops due to damage to the hypothalamo-hypophyseal axis resulting in vasopressin deficiency [ 9 ]. According to the data from this study, the frequency of damage to the hypothalamo-hypophyseal axis (subclinical hyperthyroidism) is increased in patients with low TSH levels.

In a single-center study conducted by Bengtsson et al. in Sweden with 578 patients, the most common complication after trans-sphenoidal surgery was found to be rhinosinusitis in 63 patients (10%). The second most common complication was rhinorrhea in 51 patients (8.4%). Meningitis (4%) and sepsis (2%) were identified as other common complications [ 10 ]. In the study conducted by Chowdhury et al. with 149 patients, the most common complication was rhinorrhea (40%), followed by diabetes insipidus at 14.8%. This was followed by prolonged mechanical ventilation requirement at 14.8% and bleeding at 10% [ 4 ]. In this study, the most commonly encountered complication was diabetes insipidus (22.2%), followed by postoperative nausea/vomiting (14%). This was followed by rhinorrhea (10%) and epistaxis (8.1%). Prolonged mechanical ventilation requirement was observed in 10 patients (7.4%). In this study, no significant difference was found in 7th day mortality rates between the groups ( p  > 0.05). However, when comparing 28-day mortality rates, a significant association was found with TSH levels. In the group with normal TSH levels, 2 patients (1.9%) passed away, while in the group with high TSH levels (TSH > 5 mU/l), 1 patient (25%) passed away. There were no lost in the group with low TSH levels ( p  < 0.05).

The elevated mortality risk in patients with high TSH levels found in this study may primarily be attributed to the unequal distribution of the groups and the fact that there were only 4 patients in the high TSH group. In addition, it is known that hypothyroidism and subclinical hypothyroidism delay, wound healing, thereby increasing the risk of infection in the postoperative period [ 11 ]. Despite endocrinologists stating that mild to moderate hypothyroidism is not a contraindication for elective surgery [ 12 ], it is considered important to pay attention to sterilization conditions when these patients are taken for elective surgery, not to skip antibiotic prophylaxis, to closely monitor the wound site, and not to delay antibiotic therapy in case of infection. In a study by Wang et al., which investigated the impact of preoperatively measured TSH levels on mortality in patients undergoing surgery for Type-A aortic dissection, high serum TSH levels were found to be an independent indicator of 30-day postoperative mortality [ 13 ]. Jing et al. found in a study of patients undergoing total knee arthroplasty that both medical and surgical complication rates were higher in patients with preoperative TSH > 10 mU/l [ 14 ]. In a study by Chen et al. in patients with heart failure, both low TSH and high TSH levels were associated with increased mortality [ 15 ]. Rodondi et al. found in their study that the risk of cardiac events was higher when TSH was > 7.0 mU/l, and even higher when TSH was > 10 mU/l [ 16 ]. In this study, the TSH levels ranged from 0.01 to 6.04 mU/l.

The unequal distribution of the patient groups included in this study, the inability to evaluate whether the patients were treated for hypothyroidism or hyperthyroidism, and the absence of patients with TSH levels above 10 mU/l in this study are the notable limitations of this study. Another limitation lies in its single-center and retrospective design, resulting in a lower level of evidence compared to multi-center and prospective studies. It is suggested that, for a comprehensive understanding of the impact of preoperatively measured thyroid hormone levels on mortality and morbidity in pituitary surgery, there is a need for future multi-center and prospective studies. Such studies would contribute to a more robust exploration of the subject matter and provide valuable insights for clinical practice in managing thyroid function in the context of pituitary surgery.

In conclusion, our findings clearly demonstrate an increased 28-day mortality rate in patients with elevated TSH levels. This observation suggests an association between thyroid function and in-hospital deaths during the postoperative period. In addition, we observed an elevated likelihood of developing postoperative diabetes insipidus in patients with low TSH levels. This represents a significant clinical observation, indicating a substantial impact of thyroid function, particularly TSH levels, on the outcomes of pituitary surgery. These findings underscore the critical role of evaluating the preoperative thyroid hormone status and planning appropriate treatment in the management of complications after pituitary surgery. Such studies can assist in developing more specific guidelines to optimize the outcomes of pituitary surgery and enhance patient care.

Availability of data and materials

The data sets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Penn DL, Burke WT, Laws ER. Management of non-functioning pituitary adenomas: surgery. Pituitary. 2018;21(2):145–53.

Article   PubMed   Google Scholar  

Araujo-Castro M, Pascual-Corrales E, Martínez San Millan JS, Rebolleda G, Pian H, Ruz-Caracuel I, et al. Postoperative management of patients with pituitary tumors submitted to pituitary surgery. Experience of a Spanish Pituitary Tumor Center of Excellence. Endocrine. 2020;69(1):5–17.

Article   CAS   PubMed   Google Scholar  

Nemergut EC, Dumont AS, Barry UT, Laws ER. Perioperative management of patients undergoing transsphenoidal pituitary surgery. Anesth Analg. 2005;101(4):1170–81.

Chowdhury T, Prabhakar H, Bithal PK, Schaller B, Dash HH. Immediate postoperative complications in transsphenoidal pituitary surgery: a prospective study. Saudi J Anaesth. 2014;8(3):335.

Article   PubMed   PubMed Central   Google Scholar  

Dyer MW, Gnagey A, Jones BT, Pula RD, Lanier WL, Atkinson JLD, et al. Perianesthetic management of patients with thyroid-stimulating hormone-secreting pituitary adenomas. J Neurosurg Anesthesiol. 2017;29(3):341.

Juraschka K, et al. Endoscopic endonasal transsphenoidal approach to large and giant pituitary adenomas: institutional experience and predictors of extent of resection. J Neurosurg. 2014;121(1):75–83.

Laws ER, Thapar K. Pituitary surgery. Endocrinol Metab Clin North Am. 1999;28(1):119–31.

Agam MS, Wedemeyer MA, Wrobel B, Weiss MH, Carmichael JD, Zada G. Complications associated with microscopic and endoscopic transsphenoidal pituitary surgery: experience of 1153 consecutive cases treated at a single tertiary care pituitary center. J Neurosurg. 2018;130:1–8.

Google Scholar  

Yuan W. Managing the patient with transsphenoidal pituitary tumor resection. J Neurosci Nurs. 2013;45(2):101–7.

Bengtsson OF, Sunnergren O, Segerhammar I, Förander P, Olsson M, Hulting AL, et al. Remission, complications, and overall survival in transsphenoidal pituitary surgery-a Swedish single-center experience of 578 patients. Acta Neurochir. 2023;165(3):685–92.

Beyene RT, Derryberry SL, Barbul A. The effect of comorbidities on wound healing. Surg Clin North Am. 2020;100(4):695–705.

Graham GW, Unger BP, Coursin DB. Perioperative management of selected endocrine disorders. Int Anesthesiol Clin. 2000;38(4):31.

Wang SP, Xue Y, Li HY, Jiang WJ, Zhang HJ. High-TSH subclinical hypothyroidism is associated with postoperative mortality in acute type A aortic dissection. Front Endocrinol. 2022;13: 844787.

Article   Google Scholar  

Jing W, Long G, Yan Z, Ping Y, Mingsheng T. Subclinical hypothyroidism affects postoperative outcome of patients undergoing total knee arthroplasty. Orthop Surg. 2021;13(3):932–41.

Chen S, Shauer A, Zwas DR, Lotan C, Keren A, Gotsman I. The effect of thyroid function on clinical outcome in patients with heart failure. Eur J Heart Fail. 2014;16(2):217–26.

Rodondi N, den Elzen WPJ, Bauer DC, Cappola AR, Razvi S, Walsh JP, et al. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA J Am Med Assoc. 2010;304(12):1365–74.

Article   CAS   Google Scholar  

Download references

Acknowledgements

Author information, authors and affiliations.

Anesthesiology and Reanimation Department, Katip Celebi University, Ataturk Training and Research Hospital, Izmir, Turkey

Gizem Kirbas, Murat Yasar Ozkalkanli & Ahmet Salih Tuzen

You can also search for this author in PubMed   Google Scholar

Contributions

G.K. planned the conception and design of the study. G.K, M.Y.O ve A.S.T. reviewed the available literature. All authors provided critical revisions to the manuscript before approving the final version.

Corresponding author

Correspondence to Gizem Kirbas .

Ethics declarations

Ethics approval and consent to participate.

The University of Katip Celebi Ataturk Training and Research Hospital Ethical Committee approved this study.

Competing interests

The authors declare no competing interests.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Kirbas, G., Ozkalkanli, M.Y. & Tuzen, A.S. The effect of preoperative TSH levels on perioperative complications in patients undergoing pituitary surgery. Eur J Med Res 29 , 259 (2024). https://doi.org/10.1186/s40001-024-01860-1

Download citation

Received : 08 October 2023

Accepted : 24 April 2024

Published : 30 April 2024

DOI : https://doi.org/10.1186/s40001-024-01860-1

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Complications
  • Neuroanesthesiology
  • Pituitary surgery

European Journal of Medical Research

ISSN: 2047-783X

diabetes insipidus research paper

IMAGES

  1. Flow chart for diagnosis and management of diabetes insipidus after

    diabetes insipidus research paper

  2. (PDF) Nephrogenic diabetes insipidus in a patient with L1 syndrome: A

    diabetes insipidus research paper

  3. Diabetes Insipidus

    diabetes insipidus research paper

  4. Expected Findings Of Diabetes Insipidus

    diabetes insipidus research paper

  5. Original Papers.: DIABETES INSIPIDUS AS A SEQUEL TO EPIDEMIC

    diabetes insipidus research paper

  6. Factsheet to A&E and Hospital Staff about Diabetes Insipidus (DI/AVPD

    diabetes insipidus research paper

VIDEO

  1. Diabetes insipidus #medical #viral #video

  2. Explaining Diabetes Insipidus in one minute

  3. Nephrogenic Diabetes Insipidus Treatment

  4. The Value of the DCES: Reducing Therapeutic Inertia

  5. Diabetes insipidus

  6. What is diabetes ||(मधुमेह)||mellitus, ( type 1, type 2).||Diabetes insipidus||👩‍⚕️#diabetes

COMMENTS

  1. Diabetes Insipidus: Pathogenesis, Diagnosis, and Clinical Management

    Introduction and background. Diabetes insipidus (DI) is a rare disorder, affecting roughly 1 in 25,000 people or about 0.004% of the global population [].Due to the rare occurrence in the population, the various forms of DI can be relatively neglected in medical education as well as in a research setting for improving clinical management []. ...

  2. Diabetes Insipidus: A Pragmatic Approach to Management

    Diabetes insipidus (DI) is a disorder of water balance characterized by polyuria and polydipsia. It can occur due to genetic and acquired causes that affect the secretion or action of arginine vasopressin (AVP) or antidiuretic hormone (ADH).Markedly increased thirst and urination are not only quite distressing but also increases the risk of volume depletion and hypernatremia in severe situations.

  3. Diabetes insipidus: The other diabetes

    Diabetes insipidus (DI) is a hereditary or acquired condition which disrupts normal life of persons with the condition; disruption is due to increased thirst and passing of large volumes of urine, even at night. A systematic search of literature for DI was carried out using the PubMed database for the purpose of this review. Central DI due to ...

  4. Diabetes Insipidus: Pathogenesis, Diagnosis, and Clinical Management

    Diabetes insipidus (DI) is an endocrine condition involving the posterior pituitary peptide hormone, antidiuretic hormone (ADH). ADH exerts its effects on the distal convoluted tubule and collecting duct of the nephron by upregulating aquaporin-2 channels (AQP2) on the cellular apical membrane surface. DI is marked by expelling excessive ...

  5. Diabetes insipidus

    Diabetes insipidus (DI) is a form of polyuria-polydipsia syndrome usually resulting from insufficient production or response to arginine vasopressin (in central, nephrogenic and gestational DI ...

  6. Diabetes insipidus

    Diabetes insipidus articles from across Nature Portfolio. ... Research Highlights 31 Jul 2019 Nature Reviews Endocrinology. Volume: 15, P: 564-565. ER-associated degradation in diabetes insipidus.

  7. Diabetes Insipidus: A Pragmatic Approach to Management

    Diabetes insipidus (DI) is a disorder of water balance characterized by polyuria and polydipsia. It can occur due to genetic and acquired causes that affect the secretion or action of arginine vasopressin (AVP) or antidiuretic hormone (ADH).Markedly increased thirst and urination are not only quite distressing but also increases the risk of volume depletion and hypernatremia in severe situations.

  8. Diabetes Insipidus: Pathogenesis, Diagnosis, and Clinical Management

    Abstract. Diabetes insipidus (DI) is an endocr ine condition involving the posterior pituitary peptide hormone, antidiuretic hormone (ADH). ADH e xerts its effects on the distal convoluted tubule ...

  9. Patients' insights into diabetes insipidus

    Atila, C. et al. Central diabetes insipidus from a patient's perspective: management, psychological co-morbidities, and renaming of the condition: results from an international web-based survey.

  10. Central diabetes insipidus from a patient's perspective: management

    This is the largest survey of patients with central diabetes insipidus, reporting a high prevalence of treatment-associated side-effects, mismanagement during hospitalisation, psychological comorbidities, and a clear support for renaming the disease. Our data are the first to indicate the value of routinely omitting or delaying desmopressin.

  11. Diabetes Insipidus: An Update

    The differential diagnosis of diabetes insipidus involves the distinction between central or nephrogenic diabetes insipidus and primary polydipsia. Differentiation is important because treatment strategies vary; the wrong treatment can be dangerous. Reliable differentiation is difficult especially in patients with primary polydipsia or partial ...

  12. Diabetes insipidus

    Diabetes insipidus (DI) is a disorder characterized by a high hypotonic urinary output of more than 50ml per kg body weight per 24 hours, with associated polydipsia of more than 3 liters a day [ 1, 2 ]. Central DI results from inadequate secretion and usually deficient synthesis of Arginine vasopressin (AVP) in the hypothalamus or pituitary gland.

  13. Diabetes Insipidus

    The differential diagnosis of diabetes insipidus involves the distinction between central or nephrogenic diabetes insipidus and primary polydipsia. Differentiation is important because treatment strategies vary; the wrong treatment can be dangerous. Reliable differentiation is difficult especially in patients with primary polydipsia or partial forms of diabetes insipidus. New diagnostic ...

  14. Arginine Vasopressin Disorder (Diabetes Insipidus)

    Arginine vasopressin disorder is a clinical syndrome characterized by the passage of abnormally large volumes of urine (diabetes) that is dilute (hypotonic) and devoid of dissolved solutes (ie, insipid). They belong to a group of inherited or acquired disorders of polyuria and polydipsia. This is associated with insufficient arginine vasopressin (AVP), antidiuretic hormone (ADH) secretion, or ...

  15. PDF Central diabetes insipidus from a patient's perspective: management

    characteristics of patients with central diabetes insipidus - from the diagnosis to the management of the condition]) done via the website of the Department of Clinical Research, University Hospital Basel, Basel, Switzerland. Patients with central diabetes insipidus were invited to participate in this voluntary 10 min survey. Patients

  16. Diabetes insipidus

    Diabetes insipidus is caused by a problem with vasopressin production in the pituitary gland (central diabetes insipidus), or action of vasopressin in the kidneys (nephrogenic diabetes insipidus). Desmopressin, an analogue of vasopressin, is an effective treatment for cranial diabetes insipidus. Between 2009 and 2016 there were four reported ...

  17. The laboratory investigation of diabetes insipidus: A review

    Abstract. Diabetes insipidus (DI) is a group of disorders that lead to inappropriate production of large volumes of dilute urine. The three main forms are central DI (CDI), nephrogenic DI (NDI) and primary polydipsia (PP). Differentiating CDI/NDI from PP is important as patients with true DI are at risk of severe dehydration without treatment.

  18. Challenges and improvement needs in the care of patients with central

    Central diabetes insipidus (CDI) is a rare condition, with significant impact on patient health and well-being. It is a chronic condition which usually requires meticulous long-term care. It can affect both children and adults. There is limited literature considering the needs and challenges inherent in providing high quality care to patients with CDI, across the care pathway. This paper seeks ...

  19. Diabetes Insipidus

    The term diabetes insipidus (DI, "tasteless water flow") refers to the production of large amounts of diluted urine. Defects in the antidiuretic mechanism cause water diuresis in DI, as opposed to the solute diuresis seen, e.g., in uncontrolled diabetes mellitus ("sweet water flow").

  20. Diagnostic Testing for Diabetes Insipidus

    Diabetes insipidus (DI) is a disorder characterized by excretion of large volumes of hypotonic urine. The underlying cause is either a deficiency of the hormone arginine vasopressin (AVP) in the pituitary gland/hypothalamus (central DI), or resistance to the actions of AVP in the kidneys (nephrogenic DI). In most circumstances, DI is also characterized by excessive consumption of water ...

  21. Diabetes Insipidus: An Update.

    Semantic Scholar extracted view of "Diabetes Insipidus: An Update." by J. Refardt et al. ... Semantic Scholar's Logo. Search 218,160,782 papers from all fields of science. Search. Sign In Create Free Account. DOI: 10.1016/j.ecl.2020.05.012; ... AI-powered research tool for scientific literature, based at the Allen Institute for AI. Learn More.

  22. The effect of preoperative TSH levels on perioperative complications in

    In the normal TSH group, the rate of developing diabetes insipidus was 17%, while in the high TSH group, it was 25%. No cases of permanent diabetes insipidus were observed. There was a significant difference in the development of transient diabetes insipidus between the groups (p < 0.05). It is known that diabetes insipidus develops due to ...

  23. Diabetes insipidus: A rare endocrine complication of immune check point

    To identify studies and determine their eligibility, a systematic research was conducted in the PubMed Database on June 10, 2022. Research included the following keywords: 'diabetes insipidus', 'immunotherapy', 'immune check-point inhibitors', 'posterior hypophysitis', 'pituitary'.

  24. Changing the Name of Diabetes Insipidus: A Position Statement of the

    In a survey of >1,000 patients with central diabetes insipidus recently published in The Lancet Diabetes & Endocrinology , 85% preferred the name to be changed, mainly because of experiences with insufficient understanding of the disease by health professionals who confused this disorder with diabetes mellitus. Eighty-seven percent of patients ...