Endocrine Abstracts

Introduction: Polyuro-polydipsia syndrome (PPS) is defined by urine excretion rate more than 3L per day, associated with a parallel increase in oral fluid intake. It poses problems of positive and etiological diagnosis. We discuss in this observation the modalities of exploration of PPS and its main etiologies.

Case report: A 60-year-old patient, diabetic for 10 years, controlled on metformin, admitted for PPS evolving for 37 years. Clinical examination was normal. Considering a decrease in visual acuity, Pituitary-MRI was requested, which was normal. Blood glucose levels were between 0.9-1.5g/l, the calcium and phosphorus levels were normal. The basal Natremia was 137mmol/l and the basal urinary osmolarity was 180mosm/l. Water deprivation test was performed, and showed progressive urine concentration, decrease in hourly diuresis (250ml at H0 => 40ml at H5 and H6) and increase in urine osmolarity (181.7mosm/l =>387.2mosm/l). The test was stopped after H6 due to the patient’s intolerance to thirst, thus the test was not completed by the administration of desmopressin. Copeptin measurement was not performed (unavailable). The diagnosis of primary polydipsia was retained and the patient was referred to the psychiatric department. During his follow-up, after 3 sessions of psychotherapy, we noted a clear clinical improvement (drinks: 7L/24h vs 19L/24h).

Discussion: Antidiuretic hormone (ADH) and thirst are the main determinants of water homeostasis. Disturbances of these regulatory mechanisms lead to PPS, which includes three different entities: central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia. Determining the correct diagnosis is crucial as treatment strategies vary considerably. The first step in the diagnostic approach is to confirm PPS and to demonstrate its hypotonic or osmotic character. Water deprivation test combined with desmopressin administration is the diagnostic gold standard. However, it has several limitations and may not accurately distinguish patients with primary polydipsia from partial forms of central and nephrogenic diabetes insipidus. Direct measurement of ADH during the water deprivation test has not been widely adopted. Copeptin has been evaluated in PPS and appears to be a useful candidate biomarker for differential diagnosis. Pituitary-MRI is helpful to determine the possible etiology of central diabetes insipidus or if the water deprivation test is inconclusive. It is ordered as a first-line examination if the initial clinicobiological context already points to central diabetes insipidus.

Conclusion: Water deprivation test remains the "gold standard" for the etiological diagnosis of PPS. Copeptin could considerably improve the diagnostic accuracy of this test, thus allowing better management.