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It has been thought that neurohypophysial involvement manifesting as central diabetes insipidus in lymphocytic hypophysitis is rare. The radiological and clinicopathological features of two cases represent a variant of lymphocytic adenohypophysitis and/or lymphocytic infundibulo-neurohypophysitis are discussed.
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Vasopressin and aldosterone are essential hormones in the regulation of water and sodium balance. Aldosterone regulates sodium reabsorption, although synergistic effects on collecting duct water permeability have been shown. We investigated the effects of 7-day aldosterone infusion or oral spironolactone treatment on water balance and aquaporin (AQP) 2 expression in rats with 21 days of lithium-induced nephrogenic diabetes insipidus (Li-NDI). In rats with Li-NDI, aldosterone markedly increased (271 +/- 14 ml/24 h), whereas spironolactone decreased (74 +/- 11 ml/24 h) urine production compared with rats treated with lithium only (120 +/- 11 ml/24 h). Aldosterone increased free-water clearance and creatinine clearance, whereas spironolactone caused a decreased creatinine clearance but unchanged free-water clearance. Immunoblotting showed unchanged AQP2 expression in cortex/outer stripe of the outer medulla and inner medulla. In the inner stripe of the outer medulla aldosterone caused a decreased AQP2 expression, whereas spironolactone caused an increase compared with rats treated with lithium only. Semiquantitative confocal immunofluorescence microscopy of AQP2 immunolabeling showed reduced AQP2 expression in the apical plasma membrane domain in connecting tubule (CNT) and initial cortical collecting ducts (iCCD) in response to aldosterone-treated rats compared with rats treated with lithium only. Spironolactone significantly increased apical AQP2 expression in the iCCD compared with rats treated with lithium only. We also tested whether similar changes could be observed in vasopressin-deficient BB rats and found similar changes in urine production and subcellular AQP2 expression in the CNT and iCCD in response to aldosterone and spironolactone. This study shows that aldosterone treatment perturbs diabetes insipidus and is associated with AQP2 redistribution in CNT and iCCD likely mediated by the spironolactone-sensitive mineralocorticoid receptor.
A 22-year old woman in the 37th week of her third pregnancy (twins) developed acute fatty liver complicated with a haemorrhagic syndrome from disseminated intravascular coagulation. Two normal girls were delivered by caesarean section. Persistent surgical bleeding required hysterectomy and a short stay in an intensive care unit. The disseminated intravascular coagulation subsided within 8 days. Three weeks after delivery a pituitary insufficiency (Sheehan's syndrome) was diagnosed. A second liver biopsy showed that the lesions had regressed. One week after delivery, the patient developed polyuria and polydipsia. The diagnosis of diabetes insipidus was confirmed by the lack of increase of plasma antidiuretic hormone level during an 8-hour water deprivation test. The pathophysiology of these different syndromes is discussed. Disseminated intravascular coagulation might be the link between hypopituitarism and diabetes insipidus.
A 38-year-old man presented with headache, fever, and double vision associated with right abducens nerve paresis. He had neither nuchal rigidity nor visual field defect. Laboratory data revealed elevated erythrocyte sedimentation rate (ESR), eosinophilia, and lymphocytic pleocytosis in the cerebrospinal fluid (CSF). Provocation tests of pituitary hormones showed partial hypopituitarism. Magnetic resonance imaging (MRI) revealed swelling of the hypophysis and a mass lesion expanding into the right cavernous sinus. The supplement dose of dexamethasone for hypothalamic hypocortisolism manifested diabetes insipidus. Biopsy, carried out through the transsphenoidal approach, revealed giant cell granuloma. Systemic granulomatous diseases were ruled out, and the lesion was considered to be idiopathic giant cell granulomatous hypophysitis. Right abducens nerve paresis, diabetes insipidus and dysfunction of the anterior lobe were amended by the treatment with prednisolone for 4 months, and findings of the pituitary gland and stalk were normalized. The present case shows that glucocorticoid has an effect on amendment of idiopathic giant cell granulomatous hypophysitis.
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A 40-year-old patient presented with intractable headache, panhypopituitarism and diabetes insipidus 5 months after a severe shock syndrome. The magnetic resonance imaging of the brain confirmed a hemorragic necrosis of the pituitary gland. On follow-up, the patient recovered a normal pituitary function, except for the persistence of a partial ACTH deficiency. The pituitary image also normalized. Pituitary apoplexy is a rare disease of severe prognosis due to its neurological and endocrine consequences. It can now be more easily recognized by the new imaging techniques.
A 35-year-old man with congenital nephrogenic diabetes insipidus (NDI) is reported. Renal biopsy revealed miniaturized and rounded mitochondria of the proximal tubular cells and decreased brush-borders. Trichlormethiazide combined with triamterene resulted in an apparent reduction of daily urine volume and concomitant increment in urine osmolarity. The present case seems rare in that some morphological changes in the renal tissues could be demonstrated in an adult case with congenital NDI.
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A 22 year-old woman with diabetes insipidus on chronic therapy with desmopressin acetate (DDAVP) developed recurrent venous thromboembolism and transient thrombocytopenia temporally related to the administration of DDAVP. Large increases in plasma von Willebrand factor (vWF), vWF-activity, and relative increases in the concentrations of the larger multimeric forms of vWF-antigen were observed, as well as a plasma factor which sensitized normal platelets to undergo spontaneous aggregation in vitro. Additional studies showed that the patient's plasma retained the platelet aggregation inducing activity after selective removal of vWF by immunoabsorption. The nature of the platelet activating factor and the relationship of this factor and the excessively increased and transiently abnormal vWF to the recurrent venous thromboembolism in this patient remain uncertain. Although the findings do not implicate definitively DDAVP in the elevation of vWF in this patient, it is suggested that its use be considered with caution in patients with diabetes mellitus and increased levels of vWF.
We report a pediatric patient who presented with hypogonadism and diabetes insipidus. Further evaluation revealed hypothyroidism. MRI of the brain revealed a suprasellar mass. Following frontal craniotomy for mass biopsy, histological analysis of the mass revealed benign lymphoid hyperplasia. The patient has had no progression of his mass or symptoms at most recent follow-up (10 months). We review this unusual case and other similar conditions. We believe this to be the first reported case of lymphoid hyperplasia without malignant cells of the suprasellar region.
A rare case of acute lymphoblastic leukemia presenting with vasopressin-responsive diabetes insipidus (DI) is reported. The patient presented with polydypsia and polyuria of 9 L/day. Findings from special investigations of the CNS, including brain scan, computerized tomographic scan, EEG, and lumbar puncture were within normal limits. The patient's condition improved substantially after receiving vasopressin injections and later chlorpropamide. The incidence and underlying mechanism of this rare complication of acute leukemia are reviewed, and the response of DI to chlorpropamide is discussed briefly. In this patient it is presumed that the DI was caused by leukemic infiltration of the supraopticohypophyseal tract, posterior pituitary, or hypothalamus.