Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 7 families with hereditary angioneurotic oedema (HANE) have been found in Finland. Six HANE patients have died from laryngeal oedema, 27 patients with diagnosed HANE are alive and 21 members have a haematological abnormality typical of HANE, i.e. a deficiency of the inhibitor of the activated first component of complement (C1-INH), but no manifest symptoms. The largest family has 363 living members, 303 of whom were investigated for C1-INH, C4 and C3. Fourteen patients had HANE, 18 relatives were symptomless but had C1-INH deficiency, and 3 members of the family had died from laryngeal oedema. In two families only one case of HANE was diagnosed, the parents in both cases being symptomless with normal C1-INH levels. All patients who had died from laryngeal oedema and 10 of the 27 HANE patients still alive had a typical triad of paroxysmal abdominal pain, peripheral oedema and laryngeal oedema. Six patients have had abdominal attacks alone, three peripheral oedema alone and two only laryngeal oedema. The age at onset of symptoms was 1-51 years. Three patients, who have received continuous methyltestosterone therapy, had hardly any symptoms during the treatment. Thirteen patients have received tranexamic acid, either during an attack or continuously, with positive effects in all except two. Cinnarizine treatment was beneficial in three out of four cases, both when given continuously or during an attack.
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PMID:Hereditary angioneurotic oedema in Finland. Clinical, immunological and genealogical studies. 89 63

Drug treatment of patients with hyperlipoproteinaemia is indicated to reduce the risk of atherosclerosis in patients with increased concentrations of atherogenic lipoproteins, and to lower the plasma concentrations of triglyceride-rich lipoproteins in patients with severe hypertriglyceridaemia who are at risk of abdominal pain and pancreatitis. Such therapy should be initiated only after satisfactory exclusion of secondary causes of hyperlipoproteinaemia, and should be regarded as an adjunct to rather than a substitute for appropriate dietary therapy. Drug therapy should be strongly considered in those patients with concentrations of atherogenic lipoproteins which exceed the 90th to 95th percentile for age. In patients with increased plasma concentrations of low density lipoproteins (LDL), agents which enhance the rate of LDL catabolism (cholestyramine and colestipol) or reduce the rate of LDL synthesis [e.g. nicotinic acid (niacin)] are the 'drugs of choice'. For those patients with concurrent hypertriglyceridaemia, nicotinic acid is the preferred initial drug, and in both patient groups combined drug therapy is often necessary to attain optimal reductions in LDL cholesterol concentrations. Clofibrate remains the 'drug of choice' for the rare patient with type III hyperlipoproteinaemia, whereas the newer agent gemfibrozil should be used in patients with plasma triglyceride concentrations above 1000 mg/dl who are at increased risk of abdominal pain and pancreatitis. Although currently limited to investigational use, mevinolin and related compounds, which are specific inhibitors of the rate-limiting enzyme in cholesterol biosynthesis (HMG Co-A reductase), offer considerable promise in the therapy of patients with primary hypercholesterolaemia due to elevated levels of LDL cholesterol.
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PMID:Lipid-lowering drugs. An overview of indications and optimum therapeutic use. 355 97