1/3. Familial central diabetes insipidus detected by nocturnal enuresis.A 10-year-old male referred to our clinic with the chief complaint of nocturnal enuresis also complained of daytime polyuria, frequency, and polydipsia. The clinical diagnosis was central diabetes insipidus. Since the patient's father had complained of similar symptoms, the arginine vasopressin-neurophysin II gene was examined. This revealed a single base substitution in one of two alleles in the patient, his father, and his grandfather (a C to T transition at nucleotide position 280 at codon 19 in the first exon). In conclusion, a history of polyuria or polydipsia should be carefully noted and the urinary volume and urine gravity or osmolarity examined in cases of nocturnal enuresis.- - - - - - - - - - ranking = 1keywords = volume (Clic here for more details about this article) |
2/3. A rare case of central post-gravid diabetes insipidus.Central diabetes insipidus (CDI) arising in the puerperal period has been attributed mainly to Sheehan's syndrome or to lymphocytic infundibulo-neurohypophysitis. We report the case of a 24-year-old woman who came to our observation for the appearance, 3 weeks after a normal delivery, of a polyuric-polydipsic syndrome. Measurements of urinary volumes, plasma osmolality and urinary osmolality, in conditions of free water intake, water deprivation and a water deprivation-vasopressin administration test, demonstrated CDI. brain magnetic resonance imaging showed a normal morphology of the adenohypophysis and total absence of the neurohypophysis. Assays of the pituitary hormones were found to be within normal limits. These results, incompatible with a diagnosis of Sheehan's syndrome and lymphocytic infundibulo-neurohypophysis, excluded all the other known causes of acquired CDI. Our diagnosis was therefore of post-gravid idiopathic CDI. Thus, it is possible that in the puerperal period other diseases of the posterior hypophysis may develop, of unknown etiopathogenesis but equally responsible for CDI.- - - - - - - - - - ranking = 1keywords = volume (Clic here for more details about this article) |
3/3. Pituitary infarction resulting from intranasal cocaine abuse.OBJECTIVE: To report a case of pituitary infarction attributable to long-term intranasal cocaine use. methods: We present the clinical findings, laboratory results, and imaging studies in a woman with hypopituitarism, diabetes insipidus, and a palsy of cranial nerve VI, associated with cocaine-induced destruction of her nasal and paranasal structures and the anterior base of her skull. RESULTS: A 55-year-old woman, a long-term cocaine abuser, presented with delirium, nausea, vomiting, hypoglycemia, hypercalcemia, and hypotension as manifestations of adrenal insufficiency (cortisol levels <1 mg/dL before and after administration of cosyntropin). She was found to have a deficiency of adrenocorticotropic hormone (<1 pg/mL), gonadotropin deficiency (estradiol <20 pg/mL, luteinizing hormone 1.7 mIU/mL, and follicle-stimulating hormone 4.9 mIU/mL), and diabetes insipidus. She also had a palsy of right cranial nerve VI. Computed tomography and magnetic resonance imaging of the head demonstrated extensive destruction of the paranasal sinuses, extending into the base of the skull. Serial magnetic resonance images showed reduction of pituitary volume. Nasal biopsy specimens disclosed findings consistent with cocaine-induced ischemic necrosis. CONCLUSION: To our knowledge, this is the first case of hypopituitarism and diabetes insipidus due to prolonged intranasal cocaine abuse.- - - - - - - - - - ranking = 1keywords = volume (Clic here for more details about this article) |