Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phenomenon of clinical improvement of diabetes mellitus after occurrence of pituitary insufficiency has been reported occasionally in the medical literature, as a human counterpart of Houssay's experiment with hypophysectomized diabetic animals. We report the case of a 76-year-old woman who developed diabetes in 1928, at the age of 14, and was treated with low doses of insulin. At the age of 29, during the 7th month of her second pregnancy, she suddenly developed severe headaches and soon afterwards an intense polyuria which subsided under treatment with posterior pituitary extract. Her pregnancy followed to term but uterine stimulants had to be used at delivery because of lack of contractions. She was unable to nurse her baby and a permanent amenorrhea ensued. She continued using the posterior pituitary powder for several years, after which she discontinued it without adverse effects. The dose of insulin was decreased gradually until its replacement by chloropropamide in 1967 and glibenclamide in 1970. The present dose of glibenclamide is 2.5 mg daily, on which she has occasional mild hypoglycemic reactions. When the medication was discontinued for 5 days glycemia rose to 450 mg/dl but responded immediately to 2.5 mg of the drug with a mild hypoglycemia. She never required thyroid hormone therapy. Glucocorticoid substitution was instituted recently because of evidence of mild adrenocortical insufficiency. Basal hormone levels were normal for thyroxin, thyrotropin, FSH, LH, prolactin, hGH and cortisol; the responses to pituitary stimulation with TRH and LHRH were subnormal or nil. Cortisol stimulation with ACTH was normal. Insulin levels rose moderately after stimulation with glucagon, and with glibenclamide, with simultaneous marked decrease in glycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Houssay's phenomenon in man]. 820 16

A 62-year-old male with small cell lung cancer (SCLC) associated with Cushing's syndrome and diabetes insipidus (DI) is reported. The patient was referred to our hospital for treatment of SCLC. A diagnosis of paraneoplastic Cushing's syndrome was made on the basis of an elevated serum ACTH (623.5 pg/ml) level, elevated excretion of urinary 17-OHCS (18.01 mg/day), obesity, hypertension, hyperglycemia, persistent hypokalemia, alkalosis, and no history of diabetes mellitus. He was also diagnosed as having DI based on polyuria and polydipsia, low specific gravity of the urine (1.007-1.010), low serum ADH (1.4 pg/ml) level, normal plasma osmolarity (29 mOsm/kg H2O), and the results of water deprivation test. DI and a left visual field defect was suggestive of metastasis to the pituitary region, but no lesion was detected by either CT scan or MRI scan. The patient failed to show a good response to intensive chemotherapy, and died of the tumor five months after commencing chemotherapy. Post-mortem examination revealed metastases to the hypothalamic-neurohypophyseal region, lungs, liver, adrenal glands, bone, bone marrow, and hilar and mediastinal lymph nodes.
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PMID:[A case of small cell lung cancer associated with diabetes insipidus and Cushing's syndrome]. 839 May 89

A 43-year-old man was admitted to our hospital in January, 1991 for further examination of polydipsia, polyuria and hypertension. He had had a personal history of hypertension since 1976 and of diabetes mellitus since 1982. Physical examination and routine laboratory studies showed that the patient was characterized by asymptomatic hypertension in the presence of hypokalemia and increased urinary potassium excretion. Plasma aldosterone concentrations (PAC) were elevated and plasma renin activity (PRA) was suppressed, resulting in a considerable increase in the ratio of PAC to PRA. PAC was not normally suppressed by saline infusion (2 1/2h, iv). PRA remained suppressed and PAC did not rise after stimulation with iv injection of furosemide (40 mg) in combination with walking for 60 min. PAC was increased in response to ACTH injection (0.25 mg, iv) but not suppressed by dexamethasone administration (2 and 8 mg/day, po). PAC did not rise after iv infusion of angiotensin II (20 ng/kg/min for 30 min). Venous sampling showed that PAC was considerably elevated in the bilateral adrenal vein. CT and MRI demonstrated tumor mass in the bilateral adrenal gland and the remaining normal portion in the left adrenal gland. Scintigraphic imaging with 133I-aldosterol during dexamethasone suppression provided bilateral uptake in the adrenals. Oral administration of spironolactone (375 mg/day) suppressed blood pressure and elevated PRA and serum potassium. Elevated PCA and PRA levels as well as hypertension were corrected by right-total and left-subtotal adrenalectomy performed in March, 1991. However, impaired glucose tolerance was not changed after surgery, and plasma glucose levels were well controlled with a small dose of insulin (9U/day). Pathological studies revealed adrenocortical adenoma cells of clear cell type with spironolactone bodies in the bilateral adrenal tumors. These findings indicate that this is a very rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas, which is accompanied by diabetes mellitus.
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PMID:[A rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas]. 846 28

Central diabetes insipidus was diagnosed by vasopressin measurements during hypertonic stimulation in a 9-year-old male giant Schnauzer with polyuria and polydipsia. The impaired release of vasopressin was believed to be caused by a large pituitary tumor, which was visualized by computed tomography. Studies of the function of the anterior lobe and the pars intermedia of the pituitary gland were conducted, and high concentrations of ACTH and alpha-melanotrophic hormone (alpha-MSH) were found without concomitant hyperadrenocorticism. Studies of the molecular size of the immunoreactive ACTH in plasma by gel filtration revealed that most of the circulating immunoreactivity was not ACTH but its precursor pro-opiomelanocortin (POMC) and low-molecular-weight POMC-derived peptides. The pituitary tumor of this dog probably originated from melanotrophic cells of the pars intermedia. The sensitivity of the pituitary-adrenocortical system for the suppressive effect of dexamethasone was unaffected.
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PMID:Central diabetes insipidus in a dog with a pro-opiomelanocortin-producing pituitary tumor not causing hyperadrenocorticism. 853 Nov 85

A 16-year-old, male, Hanoverian horse had a three-month history of weight loss, hirsutism and polyuria/polydypsia. Examinations revealed neutrophilia, lymphopenia, hyper glycaemia and abnormalities in hepatic function. A tentative diagnosis of hyperadrenocorticism was made. The results of thyroid-releasing hormone and combined dexamethasone suppression and ACTH stimulation tests suggested the presence of a pituitary adenoma. The horse was treated with pergolide and beneficial clinical and biochemical responses were observed within one to six months.
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PMID:Pergolide treatment for Cushing's syndrome in a horse. 883 90

In 1992, we reported a lymphocytic adenohypophysitis (LIH) (Neurol Med Chir). We considered this case unusual in that the case was that of a menopausal female and that it was accompanied with diabetes insipidus as classical lymphocytic adenohypohysitis (LAH). Subsequently, Ahmed reported two cases which presented a similar pathological manifestation, except for necrosis, as did our case and named them "necrotizing infundibulo-hypophysitis." Recently we encountered another similar case, which is reported hereunder. A female, 34 years of age, had suffered from headache, polyuria, and amenorrhea. CT scan showed a pituitary mass, and pituitary tumor was surgically removed transcranially at a local hospital. The pathological examination revealed the findings of chronic inflammation and necrosis. One month after the operation, however, she was an in-patient again under the suspicion of meningitis for fever and, when antibiotic therapy at the local hospital resulted in no improvement, she was referred to our hospital. Endocrinological studies showed low FSH, LH, ACTH and plasma cortisol level. Antibodies of serum to RNP, Sm, mitochondria, nucleus, AChR, and DNA were all negative. Because of an intrasellar mass with suprasellar extension on MRI, transsphenoidal operation was conducted four months after the initial operation. The pathological examination revealed the infiltration of lymphocytes, plasma cells, and foamy macrophages, and necrosis. After this operation, the headache was cured and the patient was discharged. Two months subsequent to the second operation, headache recurred and temporal upper quadrantic anopsia was noted. An enlarged tumor was found, but prednisolone worked to cure the pain and the visual field defect was found to have been remedied. The patient's diabetes insipidus is presently persisting, and she still relies on the use of desmopressin acetate and is still in need of cortisol replacement therapy. Including our cases, ten cases of lymphocytic hypophysitis, not related to pregnancy or delivery but with diabetes insipidus, have been reported. Several clinical and anatomical features distinguish these 10 cases from classical LAH. The classical LAH was predominantly related to pregnancy or delivery. However 6 of 10 cases were male in LIH. LAH related to pregnancy or delivery does not accompany diabetes insipidus, but all reported cases of LIH had a diabetes insipidus. Visual field and/or ocular movement disturbance are LAH's chief complaints (15 out of 25 cases) but visual field disturbance seldom occurs in LIH (1 out of 10 cases). Hypopituitarism is more serious in LAH, and 4 cases became fatal from an adrenal crisis. Anatomically, inflammatory change of LIH is located anterior and posterior to the pituitary gland and extends to the pituitary stalk and, at times, hypothalamus. On the other hand, LAH relates to pregnancy or delivery, the inflammatory change localizes to the adenohypophysis. Ahmed emphasized necrosis, while necrosis was not a prominent histological finding in LIH. Necrosis was noted only in 3 of 10 cases. To be stressed, rather, are the inflammatory changes seen on the neurohypophysis and the pituitary stalk, together with the characteristic diabetes insipidus. We believe, in view of the above, that what Ahmed named necrotizing infundibulo-hypophysitis should be named "LIH with diabetes insipidus." Whereas differential diagnosis is necessary between this said new disorder and the conventional LAH, we advocate that the latter, which is related to pregnancy or parturition but is free from neurohypophysitis be identified as "LAH related to pregnancy or delivery." With respect to treatment, steroid therapy is essential. If the symptoms do not improve, a transsphenoidal operation for diagnosis (LIH and LAH) and decompression (the case of LAH with visual or external ocular movement disturbance) is advisable. However, extensive surgery is not recommended, because per
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PMID:[Lymphocytic infundibulo-hypophysitis with diabetes insipidus as a new clinical entity: a case report and review of the literature]. 902 95

A dog was presented with a 2 year history of polyuria and polydipsia due to pituitary-dependent hyperadrenocorticism. A low-dose dexamethasone suppression test and measurement of plasma ACTH concentration confirmed the diagnosis. Treatment was instituted with mitotane at 44 mg/kg/day and then 88 mg/kg/d without complete resolution of signs. The dog collapsed with signs consistent with liver disease and was euthanased. Necropsy revealed a phaeochromocytoma of the left adrenal medulla with extensive metastases to the liver. A chromophobe adenoma of the pars intermedia of the pituitary was found.
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PMID:Mitotane (o,p'-DDD) resistance in a dog with pituitary-dependent hyperadrenocorticism and phaeochromocytoma. 957 78

The present case report describes the rare clinical presentation of diabetes insipidus in a patient with an ectopic ACTH syndrome (morning plasma cortisol 1.10 mumol/l, morning plasma ACTH 322 ng/l) due to disseminated small cell lung cancer including a metastasis in the posterior pituitary. The patient was treated by combination chemotherapy and at the same time received octreotide to control hypercortisolism and desmopressin (DDAVP) to control polyuria. Partial tumour remission was achieved resulting in decreased cortisol production and disappearance of the diabetes insipidus. Medical treatment could be discontinued. Several months later tumour regrowth occurred, with recurrence of hypercortisolism (mean morning plasma cortisol 0.74 mumol/l, mean morning plasma ACTH 112 ng/l) but without diabetes insipidus. Early treatment of hypercortisolism in patients with an ectopic ACTH syndrome and disseminated small cell lung cancer may prolong survival and improve the quality of life.
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PMID:Central diabetes insipidus and Cushing's syndrome due to ectopic ACTH production by disseminated small cell lung cancer: a case report. 971 40

Virusencephalitis is characterised by clinical symptoms of a parenchymatous inflammation. In addition, early mental status changes often occur as a result of virusencephalitis, beside focal neurological deficiencies, epileptic seizures, cerebral compression, even coma. Other pathological manifestations of virusencephalitis are disturbances of the neurohumoral and the endocrine system, which are often recognised and treated too late. This case report describes symptoms, treatment, and complications of a 76 year old female in-patient, who was diagnosed with virusencephalitis. The number of lymphocytes in the cerebrospinal fluid was increased to 30 cells per microliter, liquor albumin was 1705 mg/l, liquor sugar was 53 mg/dl and liquor lactat was 1.9 mmol/l. IgM antibodies against herpes viruses were found in the cerebrospinal fluid and distinct contrasting foci were found near the mammillary bodies, hypothalamus, tractus opticus, hypophyseal stalk and right parahippocampal in the magnetic resonance imaging of the head, indicating a focal herpes simplex encephalitis. Within seven days, the following symptoms developed: akinetic parkinsonian syndrome, central diabetes insipidus with hypernatremia and polyuria (6 l/die), hypothyreosis, adrenal insufficiency with adynamia, sopor, hypotension and even hypophyseal coma. Panhypopituitarism was diagnosed after measuring the basal hormone levels (ACTH, TSH, FT3, FT4, Cortisol, Prolactin, LH, FSH, ADH) and conducting the pituitary stimulation test. The severeness of all symptoms was slightly improved after substitution with antidiuretic hormone at 0.4 microgram/die and administration of hydrocortisone at 50 mg/die. Administration of amantadine sulphate at 0.6 g/die and L-dopa at 187.5 mg/die for 14 days resulted in a complete regression of the parkinsonism. After administration of aciclovir at 2.25 g/die for 21 days a complete regression of the clinical symptoms could be reached in connection with a decrease of 90% in number and size of cerebral contrasting foci in the magnetic resonance imaging of the head. Three month after therapy, clinical examination and blood serum analysis revealed persistent panhypopituitarism. The present case report is the first description of a viral infection on of the central nervous system (CNS) in combination with parkinsonism, diabetes insipidus, persistent panhypopituitarism and hyperprolactinemia. Early treatment of viral infections of the brain can improve a patient's prognosis dramatically. Early determination and early treatment of a patient's neurohumoral parameters is therefore critical to prevent or reverse early mental status changes like attention disturbances, alterations of personality and behavior, apathy, and slowed cognition.
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PMID:[Virus encephalitis with symptomatic Parkinson syndrome, diabetes insipidus and panhypopituitarism]. 1059 69

A 15-year-old girl developed acute lymphoblastic leukemia (ALL). The patient was treated according to the 13th protocol of the Tokyo Children's Cancer Study Group, and thereafter remained free of disease. However, at the age of 20, she complained of polyuria, polydipsia and amenorrhea. Hematological or meningeal relapse was ruled out on the basis of clinical and laboratory findings. The plasma concentrations of GH, TSH, LH, FSH, ACTH and ADH were low or below the detectable limits. There was no increase in urine osmolarity after water deprivation. Arginine, LH-RH, TRH and CRH tolerance tests revealed no or low responses of GH, LH/FSH, TSH, and ACTH/cortisol, respectively. Magnetic resonance imaging demonstrated thickening of the pituitary stalk, which was homogeneously enhanced by gadolinium administration. A biopsy specimen showed fibrosis and infiltration of CD8-positive T lymphocytes in a portion of the pituitary stalk, whereas the adenohypophysis was normal. In addition, no leukemic cells were observed in the samples. Thus, a diagnosis of lymphocytic infundibuloneurohyophysitis (LIN) was established. All the symptoms were improved by treatment with hydrocortisone, L-thyroxine, desamino-8-d-arginine vasopressin, estrogen and gestagen. This is the first reported case of ALL complicated by LIN.
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PMID:[Lymphocytic infundibuloneurohypophysitis during the first remission in acute lymphoblastic leukemia]. 1119 41


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