Diabetes Insipidus (DI) is either due to deficient secretion of arginine vasopressin (central) or to tubular unresponsiveness (nephrogenic). Drug induced DI is a well-known entity with an extensive list of medications. Polyuria is generally defined as urine output exceeding 3 liters per day in adults. It is crucial to identify the cause of diabetes insipidus and to implement therapy as early as possible to prevent the electrolyte disturbances and the associated mortality and morbidity. It is very rare to have an idiosyncratic effect after a short use of a medication, and physicians should be aware of such a complication to avoid volume depletion. The diagnosis of diabetes insipidus is very challenging because it relies on laboratory values, urine output, and the physical examination of the patient. A high clinical suspicion of diabetes insipidus should be enough to initiate treatment. The complications related to DI are mostly related to the electrolyte imbalance that can affect the normal physiology of different organ systems. 1. Background Though it is a rare disorder, diabetes insipidus was first described in the 18th century [1]. Diabetes insipidus (DI) is either due to deficient secretion of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH) by the pituitary gland (central diabetes insipidus) or due to renal tubular unresponsiveness to AVP (nephrogenic DI). This leads to polyuria, polydipsia with hyposthenuria, causing dehydration and hypernatremia if the patient is deprived of water [2]. 2. Etiology Deficiency of AVP secretion is referred to as central DI, pituitary DI, or neurohypophyseal DI. About 50% of central DI cases are idiopathic [3]. It usually appears within 24 hours followed by a 2-3-week period of inappropriate antidiuresis. In a German study, only 8.7% of DI cases persisted for more than 3 months [4]. Close followup of patients diagnosed with idiopathic DI is necessary to detect slowly growing intracranial lesions. Lung and breast cancer are most common malignancies [5]. Leukemias and lymphomas are known to associate with DI [6]. The incidence of acute DI in severe head injury is high [7, 8]. 16% of central DI is secondary to head trauma. There are several autosomal recessive forms and X linked recessive forms were described causing DI. Gestational DI which manifests during pregnancy and usually remits several weeks after delivery is caused by deficiency of plasma AVP. [9]. Other causes of central DI include infiltrative disorders (histiocytosis X, sarcoidosis) anorexia nervosa, infections such as viral meningitis
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