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)

A 69-year-old female was treated for hyperthyroidism and hypertension. In August 1984, she suddenly began suffering from polyuria and polydipsia. In October, she exhibited fever, headache, vertigo, and poor appetite, probably due to pituitary apoplexy. Her endocrine function was normal, except for partial diabetes insipidus. A contrast-enhanced CT brain scan revealed a pituitary adenoma with a ring-enhanced outer edge and a central low-density area. The MRI scan also indicated cystic adenoma. A CT scan examination repeated 6 months later showed an empty sella with a markedly decreased pituitary adenoma. This case report demonstrates that some empty sella are the final result of pituitary adenoma bleeding or infarction.
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PMID:Pituitary adenoma results in the empty sella syndrome. 258 92

A man aged 61 had recurrent attacks of severe shock. The episodes were preceded by symptoms such as a runny nose, epigastric discomfort with nausea, vertigo, orthostatism and sometimes light fever. During the attacks there were marked hypotension, a strong rise of the haematocrit, a decrease of the protein and albumin concentrations in the blood and prerenal kidney failure. In addition, there was a paraprotein, type IgG-kappa. The shock every time responded rapidly to intravenous administration of fluid and was followed by a period of substantial polyuria. The pattern was characteristic of systemic capillary leak syndrome, a rare but frequently fatal disease characterized by episodes of unexplained extravasation of plasma. The aetiology and pathogenesis are unknown. Attacks are suppressed by supportive therapy (administration of fluids, inotropics) and future attacks may be prevented by the intake of terbutaline and theophylline. The systemic capillary leak syndrome should be considered in the differential diagnosis of idiopathic and anaphylactic shock.
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PMID:[Systemic capillary leak syndrome]. 1068 51

Between 1994 and 2006, a total of 280 cases of varying degrees of tetrodotoxin poisoning following ingestion of the toxic eggs of the horseshoe crab, Carcinoscorpius rotundicauda, were admitted to the medical service of Chon Buri Hospital. The severity of the poisoning was classified into four stages based on clinical signs and symptoms of human tetrodotoxication. Of 245 available medical records; 100 were in stage 1, 74 were in stage 2, 3 were in stage 3 and 68 were in stage 4. The frequencies of symptoms and signs included the following : circumoral and lingual numbness (98%), hands and feet numbness (94.7%), weakness (59.6%), dizziness and vertigo (54.3%), nausea and vomiting (52.6%), transient hypertension (39.6%), respiratory paralysis (27.7%), fixed dilated pupils (14.7%), ophthalmoplegia (12.2%), blood pressure lower than 90/60 mmHg (5.7%), and polyuria (0.4%). All patients received symptomatic and supportive treatment. Endotracheal intubation and mechanical ventilation were considered when paralysis was progressing rapidly. The results of treatment are as follows: 239 patients (97.5%) showed complete recovery, 5 patients (2%) died, and 1 patient (0.4%) suffered anoxic brain damage. Horseshoe crab poisoning occurs both sporadically and epidemically in Chon Buri. Seasonal variation in the number of cases of poisoning was observed with a peak from December through March.
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PMID:Tetrodotoxin poisoning following ingestion of the toxic eggs of the horseshoe crab Carcinoscorpius rotundicauda, a case series from 1994 through 2006. 1856 17

Bartter-Gitelman syndromes are rare inherited autosomal recessive salt-losing tubulopathies characterized by severe and chronic hypokalemia associated with metabolic alkalosis and secondary hyperaldosteronism. Bartter syndrome results from a furosemide-like defect in sodium reabsorption in the Henle's loop leading to hypercalciuria and defect in urinary concentration capacity. The antenatal Bartter syndrome is defined by polyhydramnios and an infantile polyuria with severe dehydration whereas classic Bartter syndrome appears during childhood or adulthood. Gitelman syndrome is a thiazide-like salt-losing tubulopathy. It is associated with hypomagnesemia, hypocalciuria without defect in urinary concentration capacity. The diagnosis is most often made in adolescents or adults. Clinical symptoms include tetany, delay in the height-weight growth curves, chronic tiredness, muscle weakness, myalgia and vertigo. Nephrocalcinosis in Bartter syndrome could lead to chronic kidney disease. Antenatal Bartter syndrome requires hospitalization in intensive care unit to manage the severe newborn dehydration. Chondrocalcinosis is the major complication in the Gitelman syndrome. The corner stones of treatment is the fluid and electrolyte management Bartter and Gitelman syndromes need lifelong oral supplementations of potassium, salt (Bartter) and magnesium (Gitelman). Indomethacin is efficient to reduce water and electrolyte loss in Bartter. In Gitelman, potassium-sparing diuretics may be helping for severe hypokaliemia but they will reinforce hypovolemia.
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PMID:[Bartter-Gitelman syndromes]. 3262 51