Clinical features and molecular analysis of arginine-vasopressin neurophysin II gene in long-term follow-up patients with idiopathic central diabetes insipidus. (41/69)

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Lymphocytic hypophysitis with a long latent period from onset of central diabetes insipidus to development of pituitary enlargement. (42/69)

A 61-year-old man presented with central lymphocytic hypophysitis. Initial pituitary MRI imaging was normal, except for loss of the "bright spot" of the posterior lobe. A diagnosis of idiopathic diabetes insipidus was made. Two years later, pituitary gland enlargement with panhypopituitarism was detected. Eight months after commencing a replacement dose of corticosteroid, the pituitary enlargement was reduced in size. These findings resulted in a diagnosis of lymphocytic hypophysitis. In patients with idiopathic diabetes insipidus, it is important to suspect lymphocytic hypophysitis and to perform a long follow-up to repeat endocrinological examinations and pituitary imaging.  (+info)

Central diabetes insipidus and hypothalamic hypothyroidism associated with aceruloplasminemia. (43/69)

Aceruloplasminemia is a rare autosomal recessive disease first reported by Miyajima et al. (Neurology 37: 761-767, 1987); it is clinically characterized by diabetes mellitus, retinal degeneration and neurological abnormalities, such as cerebellar ataxia, extrapyramidal signs and dementia. Aceruloplasminemia is caused by mutations in the ceruloplasmin gene, which results in the absence of serum ceruloplasmin and iron overload in the brain, liver, pancreas and other organ tissues. However, little is known about endocrine diseases associated with aceruloplasminemia. We report herein a case of aceruloplasminemia accompanied by central diabetes insipidus and hypothalamic hypothyroidism.  (+info)

Central diabetes insipidus induced by tuberculosis in a rheumatoid arthritis patient. (44/69)

Tuberculosis, a polymorphic disease, is a diagnostic challenge, particularly when arises concomitantly to an autoimmune disease such as rheumatoid arthritis (RA). Herein, the authors describe a 33-year-old woman with nodular RA who was being treated with methotrexate, sulfasalazine and corticosteroids and presented with subcutaneous nodules simultaneously with aseptic meningitis. Mycobacterium tuberculosis was identified in cultures from a biopsy of an axillary nodule. The patient also developed polyuria and polydipsia with normal glycemia; antidiuretic hormone (ADH) treatment before and after a 3% saline infusion test was performed and diabetes insipidus was diagnosed. An encephalic MRI showed sellar and suprasellar masses, suggesting central diabetes insipidus (CDI). The patient received standard tuberculosis (TB) treatment for 6 months and also DDAVP (desmopressin acetate) during this period. Control of CDI was observed. A pre-surgical magnetic resonance imaging (MRI) showed no pituitary mass. It is known that intrasellar tuberculoma occurs in only 1% of TB patients. TB should be considered in the differential diagnosis of CDI, especially in immunosupressed patients and in countries where this infection is a serious public health problem.  (+info)

Central diabetes insipidus after transsphenoidal surgery in dogs with Cushing's disease. (45/69)

Transsphenoidal surgery (TSS) is an effective treatment for canine Cushing's disease, as well as human Cushing's disease. In humans, only the pituitary adenoma tissue is resected by TSS. However, in dogs, the whole pituitary including normal tissue is resected. Hence, central diabetes insipidus (CDI) may complicate the postoperative course in almost all dogs with Cushing's disease treated by TSS. However, it is difficult to assess the duration of the postoperative CDI, and whether it may be transient or permanent. In this study, postoperative CDI in 21 dogs with Cushing's disease and its predicted prognosis by preoperative parameters was investigated. In this study, CDI after TSS was classified as either transient or permanent based on the requirement for desmopressin. Preoperative circulating serum cortisol concentrations and pre- and post-operative plasma AVP concentrations were not significantly different between the transient CDI dogs and permanent CDI dogs. The duration of postoperative CDI was not correlated to the signal intensity ratio (posterior lobe of the pituitary/cerebral cortex), which is obtained from preoperative magnetic resonance imaging (MRI). However, the pituitary height/brain area (P/B) ratio of the permanent CDI dogs was significantly greater than that of the transient CDI dogs. In addition, there was a significant difference between the enlarged-pituitary (P/B ratio > 0.31) transient CDI dogs and the permanent CDI dogs. These results suggest that the incidence of postoperative permanent CDI is strongly influenced by the pituitary size.  (+info)

Transient polyuria related to central diabetes insipidus caused by lymphocytic infundibulo-neurohypophysitis in a patient treated for Graves' disease. (46/69)

A 45-year-old man was hospitalized because of weight loss, finger tremor, thirst, polydipsia and increased urinary frequency. He was diagnosed with Graves' disease (GD) and central diabetes insipidus (CDI). Magnetic resonance imaging revealed the enlarged posterior pituitary with thickened stalk. Histological examination obtained from biopsy of the pituitary revealed lymphocytic infundibulo-neurohypophysitis. He received treatment with thiamazole (MMI) for GD and desmopressin acetate (DDAVP) for CDI. However, DDAVP administration could be discontinued as GD was gradually improved. This course indicates that not only the recovered renal response to arginine-vasopressin but also the immunomodulative effects of MMI might attribute to the improvement of polyuria.  (+info)

Growth retardation in untreated autosomal dominant familial neurohypophyseal diabetes insipidus caused by one recurring and two novel mutations in the vasopressin-neurophysin II gene. (47/69)

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Genoa syndrome and central diabetes insipidus: a case report. (48/69)

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