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)

Patients with cystic fibrosis have fat malabsorption, providing an experimental model for evaluation of the hypothesis that a low-fat intake may prevent atherosclerosis. We studied the frequency and extent of aortic precursor lesions (fatty streaks, early fibromusculoelastic lesions, late fibromusculoelastic lesions) found at autopsy in this disease as well as in other patients with debilitating disorders but with no apparent impairment of fat absorption. Fatty streaks were less common in the cystic fibrosis group, as were the late fibromusculoelastic lesions. There was no significant difference in the frequency, length, or thickness of the early fibromusculoelastic lesions. The findings suggest that fat may be responsible for progression but not initiation of the fibromusculoelastic precursor lesions, and support the concept that early restriction of dietary fat may prevent, delay, or otherwise modify atherosclerosis in the adult.
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PMID:Preatherosclerotic aortic lesions in cystic fibrosis. 75 18

A balanced intake of alimentary lipids is necessary for calcium and phosphorus absorption, as for growth and calcification of bone. In lipid deprivation or excess, important disorders of phospho-calcic metabolism appear particularly in young growing subjects. The qualitative content of ingested fats has, too, a great influence : lipids containing short and medium-chain fatty acids, essential fatty acids and oleic acid stimulate calcium absorption. An excess of long chain and saturated lipids, or intake of erucic acid depress calcium absorption and retention. These facts are possible pathophysiological mechanisms in human disorders: The so-called humanized milks are close to human milk regarding their capacity of stimulation of phospho-calcic absorption and growth. In these milks, oleic and linoleic triglyceride level must be increased. In adult pathology, lipidic deficiency of steatorrhea is partially responsible for calcium and vitamin D malabsorption. Conversely, lipid-calcium interactions are not one-way, and an elevated dietary calcium depresses saturated lipid absorption, and has a hypolipemic action interesting in prevention of atherosclerosis of aged patients.
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PMID:[Lipid calcium interactions in experimental and human nutrition (author's transl)]. 77 52

Results related to long term treatment with Colestipol (a new resin sequestering bile acids) in 23 subjects with familial hypercholesterolaemia, 12 with Type IIA, 8 with Type IIB and 3 homozygotes are reported. Patients were given 15 g/day active drug for a period of 12 months and a double dose (30 g/day) for a successive period of 4 months along with a low cholesterol, low saturated fat, polyunsaturated fat-rich diet. Mean cholesterol decrease was --42 +/- 18 mg/dl (P less than 0.05) after 12 months of 15 g/day Colestipol and --69 +/- 17 mg/dl (P less than 0.01) after the following 4 months of 30 g/day Colestipol. The difference between the two periods of treatment (15 g and 30 g/day was not statistically significant. A slight but not significant increase in triglyceride levels was observed. Serum uric acid showed a significant increase throughout the entire period of treatment. No malabsorption syndrome or signs of toxicity were seen. Most frequent side effects were constipation, nausea, and metheorism which, with the exception of 4 cases which were withdrawn from the study, were reported as being transitory and mild.
Atherosclerosis
PMID:Long-term effects of colestipol (U-26,597 A) on plasma lipids in familial type II hyperbetalipoproteinaemia. 120 Nov 45

We analyzed our surgical experience in 20 patients who underwent revascularization procedures for symptomatic chronic intestinal ischemia caused by atherosclerosis. The group comprised 17 women and 3 men, with an age range of 25 to 71 years (mean 58.6 years). Sixteen patients had postprandial abdominal pain, and 4 had pain not related to eating. The average weight loss was 23.8 lb. Malabsorption and diarrhea were present in 8 patients. The duration of the symptoms was from 4 to 46 months (mean 13.4 months). One patient presented with acute intestinal ischemia following balloon angioplasty reocclusion of a stenotic celiac artery, and 3 underwent surgery for stenosis of a previously placed graft. Five patients had single mesenteric artery involvement, 10 had double-artery involvement, and 5 had significant occlusion in all 3 mesenteric arteries. The major arteries were revascularized whenever technically possible; therefore, 36 arteries were revascularized in 20 patients. Bypass grafts were done in 27 vessels, reimplantation in 7, and endarterectomy with patch angioplasty in 2. The saphenous vein was used in 12 vessels, polytetrafluoroethylene grafts in 8, dacron in 6, and inferior mesenteric vein in 1. The type of revascularization or graft utilized did not affect long-term patency. Two patients had early graft thrombosis and required intestinal resection. All patients survived the operation. At a mean follow-up of 36 months, all 20 patients were alive and asymptomatic with regard to their abdominal complaint. Ten patients (50%) underwent postoperative abdominal angiography; all the grafts were patent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term results of the surgical management of symptomatic chronic intestinal ischemia. 128 11

Between August 1980 and October 1990 we treated 36 patients with home total parenteral nutrition (HTPN) with a cumulative treatment duration of 92 years. They included 14 females and 22 males ranging in age from newborn to 75 years, with a mean of 38 +/- 21. The 4 commonest indications for HTPN were short bowel syndrome (mainly due to mesenteric occlusion (50%), inflammatory bowel disease 14%), motility disorders (14%) and malabsorption (11%). All-in-one nutritional mixtures utilizing the big-bag technique were used for all patients. Broviac or Hickman catheters were implanted in 35 patients and an infusion port in 2. Infusions were administered during the night for 8-12 hours with a volumetric pump. 14 patients are still receiving HTPN (39%) while in 8 it was discontinued as they can maintain their nutritional status by the gastrointestinal route (22%). 14 patients have died (39%), 3 from HTPN-related causes (2 of sepsis and 1 of liver failure). Catheter-related sepsis was 0.42/year of HTPN. Other common complications were metabolic bone disease, deranged liver function and cholecystolithiasis. 80% were able to return to work, school, or housekeeping activities, or at least to take care of themselves and cope with HTPN unaided. Social rehabilitation was full or partial in 72% and only 29% were house-bound and needed major assistance. Patients with a poor life quality tended to be older and suffer from intestinal diseases as a manifestation of a systemic disorder, such as atherosclerosis or malignancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A decade of experience with home total parenteral nutrition]. 180 Feb 76

We examined the relationship between cholesterol synthesis and high affinity low density lipoprotein (LDL) catabolism in freshly isolated mononuclear leukocytes and plasma sterols and apolipoprotein concentrations in three homozygous and one heterozygous subject with sitosterolemia with xanthomatosis and in 12 control subjects. Observations in untreated subjects were compared during therapy with lovastatin or interruption of the enterohepatic circulation of bile acids. Plasma cholesterol, plant sterol, and apolipoprotein B concentrations declined more than 50% in the two homozygous sitosterolemic subjects after ileal bypass surgery. In contrast, plasma cholesterol, plant sterol, and apolipoprotein B concentrations remained constant in a homozygous sitosterolemic subject and declined only 7% in a heterozygous sitosterolemic subject during 20 weeks of lovastatin (40 mg/day) treatment compared to a 28% decrease in similarly treated control subjects. Lovastatin treatment decreased cholesterol synthesis more than 60% but did not increase high affinity catabolism of LDL further in the sitosterolemic cells, compared to a more than 20% rise in control mononuclear leukocytes. Conversely, bile acid malabsorption increased cholesterol synthesis 59%, total hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase activity 13%, and receptor-mediated LDL degradation 41% in control cells, but did not stimulate cholesterol synthesis or microsomal HMG-CoA reductase activity in sitosterolemic mononuclear leukocytes although receptor-mediated LDL catabolism rose an additional 26%. These results demonstrate a greater than expected decrease in plasma sterols and apolipoprotein B concentrations in sitosterolemic subjects after stimulation of bile acid synthesis because of the inability to up-regulate cholesterol production. We suggest that bile acid-sequestering drugs or ileal exclusion surgery may be more effective treatments to mobilize accumulated sterol deposits and prevent atherosclerosis in this disease.
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PMID:Unexpected failure of bile acid malabsorption to stimulate cholesterol synthesis in sitosterolemia with xanthomatosis. Comparison with lovastatin. 231 63

The small intestine plays a key role in lipid metabolism by absorbing fat and synthesising apoproteins. Fat malabsorption secondary to intestinal disease results in abnormalities of lipoprotein concentration and composition and can lead to deficiency of essential fatty acids and fat-soluble vitamins. Malabsorption of fat can be induced by administration of neomycin and malabsorption of bile acids by administration of anion-exchange resins or by creating a partial ileal bypass. These induced forms of malabsorption are useful in the treatment of hyperlipidaemic patients liable to atherosclerosis.
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PMID:Lipid related consequences of intestinal malabsorption. 269 46

The histochemical demonstration of the activities of proteases, based in the majority of cases on the use of discriminating synthetic substrates (aminoacyl or peptidyl derivatives of 4-methoxy-2-naphthylamine [MNA]), has proved very valuable in pathology. Its importance is illustrated by three topics investigated in our laboratory, namely lymphocytes, malabsorption syndrome and atherosclerosis.
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PMID:The importance of protease histochemistry in pathology. 286 67

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Magnesium deficiency may play a role in the pathogenesis of atherosclerosis, cardiac arrhythmias, and coronary spasm. Because less than 1% of magnesium (Mg) is extracellular, the serum magnesium (sMg) does not always accurately reflect intracellular Mg stores. To determine the frequency of Mg deficiency in patients with cardiovascular disease, we measured blood mononuclear cell Mg content (mMg) and sMg concentrations in 104 unselected patients admitted to our intensive cardiac care unit (CCU). Twenty-seven normal healthy controls and 33 hypomagnesemic patients with chronic alcoholism and/or malabsorption syndrome served as reference groups. The sMg concentration in the CCU patients was 2.05 +/- 0.03 mg/dl (mean +/- SEM), and did not differ from normal controls (mean 2.01 +/- 0.03 mg/dl). Only 8 of 104 CCU patients were hypomagnesemic (7.7%). mMg in the CCU patients, however, was significantly lower than in the normal controls (1.15 +/- 0.02 micrograms/mg protein and 1.34 +/- 0.02 micrograms/mg protein respectively, p less than 0.001). Fifty-three percent (55 of 104) of CCU patients had mMg contents less than 1.119 micrograms/mg protein, i.e., below that of the lowest normal control. mMg was significantly lower in those patients with congestive heart failure (mMg = 1.08 +/- 0.03 micrograms/mg protein) when compared to those patients without congestive heart failure (1.23 +/- 0.02 micrograms/mg protein, p less than 0.001). We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the sMg would lead one to suspect, and may contribute to clinical cardiovascular morbidity.
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PMID:Low blood mononuclear cell magnesium in intensive cardiac care unit patients. 395 55


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