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Swiss Medical Weekly 2017Primary polydipsia (PP) has been defined as excessive intake of fluids. However, the pathogenesis of PP remains unexplored. Different theories include a dysfunction in... (Review)
Review
Primary polydipsia (PP) has been defined as excessive intake of fluids. However, the pathogenesis of PP remains unexplored. Different theories include a dysfunction in the thirst mechanism, involvement of the hippocampus, stress-reducing behaviour and lesion occurrences in specific areas of the brain. Most studies have been performed in the psychiatric setting, indicating that PP coincides with schizophrenia, anxiety disorder and depression. However, an increasing number of case reports emphasise the incidence of PP in non-psychiatric patients. As often recommended by healthcare professions and in life-style programmes, the phenomenon of excessive fluid intake appears to be growing, especially in health-conscious and active people. PP is part of the polyuria-polydipsia syndrome, so the differential diagnosis diabetes insipidus (central or nephrogenic) must be excluded. The gold standard when differentiating between these disorders has been the water deprivation test. However, new options for distinguishing between these entities have been proposed e.g., measurement of copeptin, a reliable surrogate marker of the hormone arginine vasopressin (AVP). The major risk of excessive drinking is the development of hyponatraemia and the ensuing complications. In patients with PP, factors reducing the renal excretory capacity of the kidney such as acute illness, medications or low solute intake may accumulate in hyponatraemia. Treatment options for PP remain scarce. Different medication and behavioural therapy have been investigated, but never on a large scale and rarely in non-psychiatric patients. This review provides an overview of the pathophysiology, characteristics, complications, and outcomes of patients with PP in the medical and psychiatric patient.
Topics: Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Humans; Hyponatremia; Polydipsia, Psychogenic; Schizophrenia
PubMed: 29120013
DOI: 10.4414/smw.2017.14514 -
Clinical Endocrinology Apr 2023Copeptin is secreted in isomolar amounts along with arginine vasopressin peptide (AVP) from the neurohypophysis. Its stability makes it a perfect candidate for the...
OBJECTIVE
Copeptin is secreted in isomolar amounts along with arginine vasopressin peptide (AVP) from the neurohypophysis. Its stability makes it a perfect candidate for the endocrine approach in the diagnosis of AVP deficiency (AVPD; cranial diabetes insipidus; CDI). However, pediatric reference values are lacking.
DESIGN AND PATIENTS
This is a monocentric retrospective analysis of donated residual serum samples from 72 children and adolescents who underwent arginine or growth hormone-releasing hormone-arginine stimulation to test GH secretory capacity from 2018 to 2022.
MEASUREMENTS
Copeptin was measured in baseline, 30-, and 60-min samples by BRAHMS Copeptin proAVP Kryptor immunofluorescence assay.
RESULTS
Of the 72 patients, 4 suffered from complete AVPD (CDI). The baseline level of copeptin in the 68 non-AVPD (non-CDI) patients was highly variable (range: 1.3-44.4 pmol/L). The increase after arginine was moderate (30 min range: 1.6-40.4 pmol/L). The median baseline and peak copeptin levels were 5.6 and 8.0 pmol/L, respectively. The 2.5th percentile of the baseline and peak values of copeptin were 2.1 and 3.3 pmol/L, respectively. The increase and peak value of copeptin were inversely related to age (R = -.405; p = .011, and R = -.335; p = .0072, respectively) but not to gender, body mass index (standard deviation score) or GH secretion. In the four patients with AVPD (CDI), baseline or stimulated copeptin was below the 2.5th percentile of non-AVPD (non-CDI) patients.
CONCLUSIONS
Stimulated copeptin is a promising parameter for the differential diagnosis of polyuria-polydipsia syndrome. However, the low copeptin increase after arginine and the high limit of quantification of the assay are problematic for use in paediatrics.
Topics: Humans; Child; Adolescent; Arginine; Retrospective Studies; Glycopeptides; Diabetes Insipidus, Neurogenic
PubMed: 36710502
DOI: 10.1111/cen.14880 -
Clinical Endocrinology Jan 2019Central diabetes insipidus (CDI) is characterized by hypotonic polyuria due to impairment of AVP secretion from the posterior pituitary. In clinical practice, it needs... (Review)
Review
Central diabetes insipidus (CDI) is characterized by hypotonic polyuria due to impairment of AVP secretion from the posterior pituitary. In clinical practice, it needs to be distinguished from renal resistance to the antidiuretic effects of AVP (nephrogenic DI), and abnormalities of thirst appreciation (primary polydipsia). As nephrogenic diabetes insipidus is rare in adults, unless they are treated with lithium salts, the practical challenge is how to differentiate between CDI and clinical disorders of excess thirst. The differential diagnosis is usually straight forward, but the recommended gold standard test, the water deprivation test, is not without interpretative pitfalls. The addition of the measurement of plasma AVP concentrations improves diagnostic accuracy, but the radioimmunoassay for AVP is technically difficult, and is only available in a few specialized centres. More recently, the measurement of plasma copeptin concentrations has been claimed to provide a reliable alternative to measurement of plasma AVP, without the sampling handling challenges. In addition, the measurement of thirst ratings can help the differentiation between CDI and primary polydipsia. Once the diagnosis of CDI is biochemically certain, investigations to determine the cause of AVP deficiency are needed. In this review, we will outline the diagnostic approach to polyuria, revisit the caveats of the water deprivation test and review recent data on value of adding AVP/copeptin measurement. We will also discuss treatment strategies for CDI, with analysis of potential complications of treatment.
Topics: Adult; Arginine Vasopressin; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Disease Management; Glycopeptides; Humans; Polydipsia, Psychogenic
PubMed: 30269342
DOI: 10.1111/cen.13866 -
Journal of Clinical Nursing Apr 2015This review will (1) explore factors related to thirst in chronic heart failure and (2) describe interventions to alleviate thirst in chronic heart failure patients. (Review)
Review
AIMS AND OBJECTIVES
This review will (1) explore factors related to thirst in chronic heart failure and (2) describe interventions to alleviate thirst in chronic heart failure patients.
BACKGROUND
Thirst is a common and troublesome symptom of chronic heart failure. Despite the burden and prevalence of this symptom, there are limited strategies to assist in its management.
DESIGN
This is a review of literature on the burden of thirst, contributors to thirst and potential management strategies of thirst in patients with chronic heart failure.
METHODS
Medline, Cumulative Index for Nursing and Allied Health, PubMed and Scopus were searched using the key words thirst, chronic heart failure, angiotensin II, fluid restriction and intervention. Of the 165 citations yielded, nine studies (n = 9) were included. The eligibility criteria included participants with confirmed diagnosis of chronic heart failure, randomised controlled studies or any studies with thirst as primary or secondary outcome, in humans and in English. There was no limit to the years searched.
RESULTS
Factors related to thirst in chronic heart failure were condition; prolonged neurohormonal activation, treatment; pharmacological interventions and fluid restriction and emotion. No intervention studies were found in chronic heart failure patients. Interventions such as artificial saliva and chewing gum have been investigated for their effectiveness as a thirst reliever in haemodialysis patients.
CONCLUSION
Thirst is a frequent and troublesome symptom for individuals with chronic heart failure. It is highly likely that this contributes to poor adherence with fluid restrictions. Chewing gum can help alleviate thirst, but investigation in people with heart failure is needed.
RELEVANCE TO CLINICAL PRACTICE
Increasing awareness of thirst and interventions to relieve it in clinical practice is likely to improve the quality of care for people with chronic heart failure.
Topics: Chewing Gum; Chronic Disease; Fluid Therapy; Heart Failure; Humans; Polydipsia; Renal Dialysis; Thirst
PubMed: 25441537
DOI: 10.1111/jocn.12732 -
Best Practice & Research. Clinical... Mar 2016Copeptin is part of the 164 amino acid precursor protein preprovasopressin together with vasopressin and neurophysin II. During precursor processing, copeptin is... (Review)
Review
Copeptin is part of the 164 amino acid precursor protein preprovasopressin together with vasopressin and neurophysin II. During precursor processing, copeptin is released together with vasopressin. Copeptin concentrations respond as rapidly as vasopressin to changes in osmolality, a decrease in blood pressure or stress and there is a close correlation of vasopressin and copeptin concentrations. For these reasons, copeptin is propagated as a surrogate marker for vasopressin in the differential diagnosis of the polyuria-polydipsia syndromes and hyponatremia. Results of prospective studies show that a baseline copeptin level without prior fluid deprivation >20 pmol/L is able to identify patients with nephrogenic diabetes insipidus, whereas osmotically stimulated copeptin levels differentiate between patients with partial central diabetes insipidus and primary polydipsia with a high sensitivity and specificity >94%. In hyponatremia, low copeptin levels point to primary polydipsia and high levels to hypovolemic hyponatremia. The copeptin to urinary sodium ratio differentiates accurately between volume-depleted and normovolemic disorders.
Topics: Biomarkers; Glycopeptides; Humans; Hyponatremia; Polydipsia; Polyuria
PubMed: 27156761
DOI: 10.1016/j.beem.2016.02.003 -
Nutrients Jul 2019The detrimental effects of dehydration, to both mental and physical health, are well-described. The potential adverse consequences of overhydration, however, are less... (Review)
Review
The detrimental effects of dehydration, to both mental and physical health, are well-described. The potential adverse consequences of overhydration, however, are less understood. The difficulty for most humans to routinely ingest ≥2 liters (L)-or "eight glasses"-of water per day highlights the likely presence of an inhibitory neural circuit which limits the deleterious consequences of overdrinking in mammals but can be consciously overridden in humans. This review summarizes the existing data obtained from both animal (mostly rodent) and human studies regarding the physiology, psychology, and pathology of overhydration. The physiology section will highlight the molecular strength and significance of aquaporin-2 (AQP2) water channel downregulation, in response to chronic anti-diuretic hormone suppression. Absence of the anti-diuretic hormone, arginine vasopressin (AVP), facilitates copious free water urinary excretion (polyuria) in equal volumes to polydipsia to maintain plasma tonicity within normal physiological limits. The psychology section will highlight reasons why humans and rodents may volitionally overdrink, likely in response to anxiety or social isolation whereas polydipsia triggers mesolimbic reward pathways. Lastly, the potential acute (water intoxication) and chronic (urinary bladder distension, ureter dilation and hydronephrosis) pathologies associated with overhydration will be examined largely from the perspective of human case reports and early animal trials.
Topics: Animals; Aquaporin 2; Arginine Vasopressin; Brain; Cognition; Disease Models, Animal; Drinking; Female; Humans; Male; Mice; Organism Hydration Status; Polydipsia; Signal Transduction; Urination; Volition; Water Intoxication; Water-Electrolyte Balance
PubMed: 31284689
DOI: 10.3390/nu11071539 -
Endocrinology, Diabetes & Metabolism... Oct 2021Hyponatraemia is the most common electrolyte disturbance in hospitalised patients and is associated with numerous adverse outcomes. Patients with schizophrenia are...
SUMMARY
Hyponatraemia is the most common electrolyte disturbance in hospitalised patients and is associated with numerous adverse outcomes. Patients with schizophrenia are particularly susceptible to hyponatraemia, in part due to the close association between this condition and primary polydipsia. We report the case of a 57-year-old woman with schizophrenia and primary polydipsia who was receiving inpatient psychiatric care. She became increasingly confused, had multiple episodes of vomiting, and collapsed 1 week after being commenced on quetiapine 300 mg. On examination, she was hypertensive and her Glasgow coma scale was nine. She had a fixed gaze palsy and a rigid, flexed posture. Investigations revealed extreme hyponatraemia with a serum sodium of 97 mmol/L. A CT brain demonstrated diffused cerebral oedema with sulcal and ventricular effacement. A urine sodium and serum osmolality were consistent with SIAD, which was stimulated by the introduction of quetiapine. The antidiuretic effect of vasopressin limited the kidney's ability to excrete free water in response to the patients' excessive water intake, resulting in extreme, dilutional hyponatraemia. The patient was treated with two 100 mL boluses of hypertonic 3% saline but deteriorated further and required intubation. She had a complicated ICU course but went on to make a full neurological recovery. This is one of the lowest sodium levels attributed to primary polydipsia or second-generation antipsychotics reported in the literature.
LEARNING POINTS
The combination of primary polydipsia and SIAD can lead to a life-threatening, extreme hyponatraemia. SIAD is an uncommon side effect of second-generation anti-psychotics. Serum sodium should be monitored in patients with primary polydipsia when commencing or adjusting psychotropic medications. Symptomatic hyponatraemia is a medical emergency that requires treatment with boluses of hypertonic 3% saline. A serum sodium of less than 105 mmol/L is associated with an increased risk of osmotic demyelination syndrome, therefore the correction should not exceed 8 mmol/L over 24 h.
PubMed: 34653996
DOI: 10.1530/EDM-21-0028 -
Acta Endocrinologica (Bucharest,... 2023Patients with chronic schizophrenia and psychosis are more prone to develop hyponatremia. Hyponatremia could be due to medications e.g. antidepressants/antipsychotics or...
Patients with chronic schizophrenia and psychosis are more prone to develop hyponatremia. Hyponatremia could be due to medications e.g. antidepressants/antipsychotics or secondary to psychogenic polydipsia. They often present with altered consciousness, seizures and falls. Rapid correction of hyponatremia in patients with psychogenic polydipsia has been associated to cause rhabdomyolysis, an under-recognized yet serious condition which if left untreated can result in various complications e.g. acute kidney injury, electrolyte abnormalities. We report a case of young patient who had background illness of schizophrenia and presented to department with severe hyponatremia secondary to psychogenic polydipsia and was eventually diagnosed as case of rhabdomyolysis due to rapid correction of hyponatremia. Objective of case report is to highlight the correct diagnosis of underlying cause of hyponatremia and challenges associated with managing rhabdomyolysis with IV fluids that can result in worsening of hyponatremia, hence emphasizing the importance of close monitoring of sodium levels and measurement of creatine kinase in any patient who presents with severe hyponatremia, particularly in the presence of other risk factors for rhabdomyolysis and consideration of careful fluid administration strategies in relation to the relative onset and risk of over-correcting hyponatremia.
PubMed: 38356977
DOI: 10.4183/aeb.2023.345 -
Cureus Aug 2021Globally, the prevalence of chronic, non-communicable diseases is increasing at an alarming rate. Amongst it, Type 2 diabetes mellitus (DM) is becoming more prevalent...
Globally, the prevalence of chronic, non-communicable diseases is increasing at an alarming rate. Amongst it, Type 2 diabetes mellitus (DM) is becoming more prevalent among young individuals due to obesity and sedentary habits. With the advent of COVID-19, there has been an increasing trend for diabetes and its complications. Here we describe a 13-year-old female girl with polyuria, polydipsia for two months with further assessment leading to a diagnosis of Type 2 DM who is now closely monitored by a pediatric endocrinologist. She remains euglycemic with insulin and lifestyle changes. Early-onset DM is complex and requires multidisciplinary care for preventing complications and comorbidities. Hence, early recognition and management are crucial.
PubMed: 34513530
DOI: 10.7759/cureus.17578 -
Neuropeptides Oct 2021Traumatic neuroendocrine dysfunction may present with diabetes insipidus (DI) or with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Both these... (Review)
Review
Traumatic neuroendocrine dysfunction may present with diabetes insipidus (DI) or with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Both these pathologies involve a disturbance in the antidiuretic hormone (ADH) secretion, causing dysnatremias. Diagnosis of posttraumatic ADH dysfunction is hampered by technical difficulties in ADH assessment, and relies mostly on non-specific serum sodium, serum and urine osmolality and diuresis, often leading to misdiagnosis in the acute care setting. Research now focuses on the diagnostic role of copeptin, a peptide secreted together with ADH in an equimolar fashion, and which can be accurately evaluated. Recent studies identified cut-off values of 2.6 pmol/L for baseline copeptin and of 4.9 and 3.8 pmol/L for hypertonic saline infusion and arginine infusion stimulated copeptin, respectively, for the diagnosis of DI in patients with polyuria-polydipsia syndrome. Although SIADH is more difficult to be explored due to its heterogeneity, a ratio of copeptin to urinary sodium below 30 pmol/mmol identifies euvolemic hyponatremia. Exploring the role of copeptin assessment in patients with traumatic brain injury (TBI) in the acute phase may improve their diagnosis accuracy, management and outcome.
Topics: Brain Injuries, Traumatic; Diabetes Insipidus; Glycopeptides; Humans; Polydipsia; Polyuria
PubMed: 34175655
DOI: 10.1016/j.npep.2021.102167