Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bumetanide is a potent 'loop' diuretic for the treatment of oedema associated with congestive heart failure, hepatic and renal diseases, acute pulmonary congestion and premenstrual syndrome and in forced diuresis during and after surgery. Bumetanide may be given orally, intravenously or intramuscularly and produces a rapid and marked diuresis, and increased urinary excretion of sodium, chloride and other electrolytes (within 30 minutes) which persists for 3 to 6 hours. Its principal site of action is on the ascending limb of the loop of Henle, with a secondary action on the proximal tubule. Pharmacologically, bumetanide is about 40-fold more potent than frusemide (furosemide), with the exception of its effects on urinary potassium excretion where its potency is lower. Studies in patients with oedema due to congestive heart failure, pulmonary oedema or hepatic disease show that oral or intravenous bumetanide 0.5 to 2 mg/day produces results comparable to those with frusemide 20 to 80 mg/day. In acute pulmonary oedema, intravenous bumetanide produces a very rapid diuresis. Higher doses of bumetanide may be required (up to 15 mg/day) in patients with chronic renal failure or nephrotic syndrome. In these patients muscle cramps are not uncommon with bumetanide, but glomerular filtration rates are unaffected. In most studies, diuretic effects were accompanied by decreased bodyweight, abdominal girth and improvements in a variety of haemodynamic parameters. Comparison of bumetanide with frusemide at a dose ratio of 1 : 40 reveals no significant differences in clinical response with the exception of renal disease, where patients with oedema appear to respond better to bumetanide. Combination with thiazide diuretics enhances the clinical response to bumetanide. Potassium supplements and spironolactone may be beneficial additions to bumetanide where patients at risk of hypokalaemia can be identified. Clinically important side effects are infrequent, with audiological impairment occurring to a lesser extent than with frusemide. Bumetanide thus offers an important alternative to frusemide when a 'loop' diuretic is indicated.
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PMID:Bumetanide. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use. 639 89

Toxic oil syndrome is a multisystemic, epidemic disease that appeared in Spain in 1981, related to the intake of rapeseed cooking oil sold in bulk. It affected 19,748 people, of whom 457 died. The toxic substance was never identified. We report the 8-year follow-up of a cohort of 332 patients. The disease was usually severe and disabling during the first 2 years, but the clinical condition of most of the patients improved thereafter. The acute phase lasted 2 months, and was characterized by pulmonary edema, rash, eosinophilia, and myalgia. During the intermediate phase (second to fourth months), severe myalgia, skin tenderness, subcutaneous edema, altered liver function, and pulmonary hypertension developed. Later on, an early chronic phase developed, from the fourth month to the end of the second year. It was marked by scleroderma, sicca syndrome, polyneuropathy, joint contractures, weight loss, and functional limitations. The clinical manifestations improved during the late chronic phase. Its most prominent clinical features were muscle cramps, chronic musculoskeletal pain, chronic lung disease, Raynaud phenomenon, carpal tunnel syndrome, and psychologic disturbances. Only 9% of the patients achieved remission after the acute phase, the rest developing late clinical manifestations of the disease. The severity of the chronic manifestations was rather variable. At the end of the 8-year follow-up, there were 10 TOS-related deaths (3%), 47% of the patients had some kind of complaint, albeit subtle in most cases, and 16% showed organic involvement related to TOS. The most important pathologic features of TOS were widespread interstitial infiltrates, non-necrotizing angiitis, endothelial proliferation, and tissue fibrosis. Toxic oil syndrome is a dramatic example of an induced scleroderma-like syndrome, similar to the eosinophilia-myalgia syndrome. Patients with EMS may develop some of the late clinical features of TOS in the years to come.
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PMID:Toxic oil syndrome. A long-term follow-up of a cohort of 332 patients. 841 42