Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The National Heart, Lung, and Blood Institute is currently sponsoring a multicenter clinical trial to evaluate the long-term efficacy of partial ileal bypass in the prevention of recurrent myocardial infarction in hypercholesterolemia patients. Thus we felt that a report of our clinical results with this intervention at the Montreal Heart Institute during the last 11 years would be of interest. Twenty patients with type II hyperlipoproteinemia and a mean age of 38 (range 25-54) years underwent partial ileal bypass between March 1971 and April 1978. This intervention was associated with aortocoronary bypass surgery in 11 patients. All patients were followed at regular intervals. The mean survival time was 70.7 (range 1-123) months. Two deaths were observed during follow-up, one from an acute myocardial infarction and the other from ventricular fibrillation, respectively, 1 month and 1 and one-half years after partial ileal bypass. The ileal bypass was undone twice because of gastrointestinal problems including a malabsorption syndrome and repeated episodes of subocclusion. A progressive decrease of the effects of the operation on serum cholesterol was noted, from a 33 per cent reduction at 3 months to 43 per cent at 2 years and 16 per cent at 6 years. Two patients presented an acute myocardial infarction respectively 3 and 4 years after the operation, respectively, and one patient suffered a right-sided hemiplegia at age 30, 12 months after the operation. Of 14 patients with angina pectoris preoperatively (class III in 10), eight remained symptomatic postoperatively (class I and II angina in five).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial ileal bypass in type II familial hypercholesterolemia. Eleven-year experience at the Montreal Heart institute. 636 76

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47