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)

As measured by whole body retention of isotopic calcium given in milk, absorption of calcium was impaired in 10 patients with chronic parenchymal non-biliary liver disease who were icteric. Mean absorption was normal in 15 patients with parenchymal liver disease who were anicteric although some individual patients absorbed less than any of the controls. Depressed absorption of calcium was seen in 10 patients with primary biliary cirrhosis and seven patients with intra- or extra-hepatic biliary obstructive disease. The most likely cause for this malabsorption is reduced bile salt secretion into the intestinal lumen which impairs vitamin D and fat absorption. The finding that parenteral vitamin D increased calcium absorption to normal levels in five patients with primary biliary cirrhosis suggests that deficiency of this vitamin is a major and correctable factor leading to calcium malabsorption in such patients. Precipitation of calcium salts by excess intraluminal fat appears to be a further possible factor reducing calcium absorption in these patients. These findings emphasize the importance of parenteral vitamin D therapy in patients with chronic obstructive biliary diseases. They also suggest that certain patients with chronic parenchymatous liver disease, particularly those who are icteric, may also occasionally require therapy with vitamin D.
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PMID:47 Calcium abosrption in parenchymatous and biliary liver disease. 517 34

Two siblings of Turkish-Assyrian extraction, whose parents were first cousins, had poor appetite, slow weight gain and retarded psychomotor development. When given milk the galactose concentration in blood increased. An oral galactose load showed a markedly reduced capacity to metabolize galactose. Fanconi syndrome was present as in classical galactosemia. A galactose-free diet reduced the aminoaciduria but did not normalize the renal tubular function nor the children's general condition. Galactokinase and galactose-1-phosphate uridyltransferase activities in red blood cells were normal. The physical appearance of the children (sparse subcutaneous fat, thin extremities and distended abdomen) and the results of vitamin A and xylose absorption tests, were in accordance with a malabsorption condition. Glucose, however, seemed to be absorbed normally from the gut. There was no evidence of primary liver disease. Since the condition did not normalize with a galactose-free diet, an enzyme defect of galactose metabolism is unlikely. Instead, a more general transport defect with autosomal recessive inheritance is proposed.
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PMID:Familial Fanconi syndrome with malabsorption and galactose intolerance, normal kinase and transferase activity. A report on two siblings. 627 35

It would appear from these observations that the morbidly obese human has an abnormal liver at the time of surgical intervention. This abnormality exists whether the operation performed is an intestinal shunt procedure or a gastric restrictive procedure. In the early period after an intestinal shunt, during the phase of most rapid weight loss, there is a selective malabsorption of fats and proteins with an increase in the proportion of calories absorbed in the form of carbohydrate. It would also appear that there is an overgrowth of bacteria, predominantly anaerobes, in the excluded limb of intestine. Although the production of liver dysfunction after an intestinal shunt is almost certainly multifactorial, it would appear from the evidence presented that the excluded limb of intestine plays a significant role in the production of this syndrome. It would seem reasonable to propose that the already compromised liver is insulted further by protein calorie malnutrition. This insult is compounded by the effect of some type of toxin produced within the excluded limb of intestine. The most likely candidate for this latter agent would appear to be an endotoxin. To date, in the human, no antimicrobial has been demonstrated to be effective in protecting the liver from this damage. Many similarities can be drawn between the histologic changes seen in alcoholic liver disease and the liver disease produced by an intestinal bypass. It is possible that these two disease states share, in part, a common pathway. This pathway may involve a state of malnutrition (maldistribution of a caloric source) but may also be associated with a toxin. Although this toxin may be alcohol or a breakdown product affected by alcohol, we should also consider the possibility that alcohol might have an effect on the intestinal mucosa, allowing the absorption of some other type of toxin. If this latter hypothesis has any validity, then a tenuous link between the two disease states could be proposed.
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PMID:Hepatic complications of jejunoileal bypass. 635 95

A 15-month-old girl from Coimbra (Portugal) had a history of numerous hemorrhagic episodes with multiple bruises, hematomas but not hemarthroses. On serial testing she showed deficiency of factors II, VII, IX, X and protein C. Malabsorption-induced vitamin K deficiency, liver disease or ingestion of a coumarin compound were excluded. An absence of detectable abnormalities was found among her relatives. Consanguinity was not present. The immunologic assay, immunoelectrophoresis or antibody neutralization, revealed much higher levels of these factors than the clotting assay. The non-physiological activator (Echis carinatus venom) produced higher levels of prothrombin activation than those detected by physiological activation. Two-dimensional immunoelectrophoresis of the patient's plasma in calcium showed that prothrombin had the same mobility as acarboxyprothrombin. No significant response to large doses of intravenous vitamin K3 (6 mg) was observed. Transfusion of 120 ml of frozen fresh plasma led to an immediate increase in the procoagulant activities of vitamin K dependent protein, similar to that found after perfusion of plasma plus vitamin K3. The results obtained from this patient suggest a defect in the gammacarboxylation mechanism inside the hepatocyte.
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PMID:Congenital deficiency of vitamin K-dependent coagulation factors and protein C. 654 83

All patients at Children's Hospital Medical Center who had ultrasonic evidence of cholelithiasis during the period from June 1979 to June 1982 were identified. Their charts and radiographs were reviewed, as were the surgical and pathologic reports of those who had cholecystectomy. Cholelithiasis was found to be less rare than expected. Sixty-five patients were identified during the three-year period. Exclusion of 13 patients more than 21 years old left 52 patients, 29 of whom were female and 23 male, ranging in age from 3 months to 21 years. Predisposing diseases or circumstances were present in 83 per cent of the cases. These included hemolytic anemia (15), cystic fibrosis (4), metabolic disease (3), liver disease (4), postpartum state (4), prior bowel resection or malabsorption (4), cardiac disease (4), prior orthopedic surgery (2), other (3). There were only nine cases in which no identifiable predisposition to cholelithiasis could be found. Although the gallstones were not subjected to chemical analysis, at least 53 per cent of them were visible on the 34 available abdominal radiographs, indicating the presence of calcium and thus stones of a mixed type.
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PMID:Cholelithiasis in children: recent observations. 664 68

Metabolic bone disease is common in patients with cholestatic liver disease. The importance of vitamin D status and calcium malabsorption in the pathogenesis of bone disease in these patients remains undefined. We have measured intestinal calcium absorption in relation to vitamin D status in 14 patients with chronic cholestatic liver disease including 11 with primary biliary cirrhosis. Fractional calcium absorption was determined from radioactive counts in the right forearm after separate oral and intravenous doses of 47CaCl2 in the fasting state. Eight of 14 patients (57%) had a decreased calcium absorption compared to controls. A significant correlation was observed between serum 25-hydroxyvitamin D levels and fractional calcium absorption (r = 0.623, p less than 0.02). Treatment with oral 25-hydroxyvitamin D3 in three patients with low serum 25-hydroxyvitamin D levels resulted in correction of serum 25-hydroxyvitamin D levels and improvement in fractional calcium absorption. No correlation was found between serum 1,25-dihydroxyvitamin D levels and fractional calcium absorption (r = 0.221). Calcium malabsorption was common in this series of patients, and serum 25-hydroxyvitamin D levels were useful in predicting fractional calcium absorption. Treatment with oral 25-hydroxyvitamin D3 was accompanied by improved calcium absorption.
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PMID:Intestinal calcium absorption and vitamin D status in chronic cholestatic liver disease. 670

Twenty-nine patients with chronic liver disease, nine of whom had symptoms suggesting bone disease, were studied by bone histology. Nine had osteomalacia; six associated with cholestatic liver disease and three with primarily hepatocellular disease. Two of these had clinical and biochemical features of cholestasis for at least a year and the other had alcoholic cirrhosis associated with severe malnutrition. Excluding the latter patient, histological osteomalacia was significantly associated with presence and duration of cholestasis. Plasma 25-hydroxyvitamin D was low and fasting urine hydroxyproline/creatinine ratio was high in all patients with osteomalacia but were abnormal also in some patients who did not have histological osteomalacia. Serum calcium, phosphate, alkaline phosphatase, vitamin D-binding protein and radiology were unhelpful in many patients with osteomalacia. Vitamin D-deficiency correlated significantly with deficiency of other fat-soluble vitamins and those patients with rachitic levels of plasma 25-hydroxyvitamin D showed no seasonal variation, suggesting a combination of malabsorption of vitamin D and reduced sunlight exposure. We suggest that patients with chronic liver disease with cholestasis for at least a year are at risk from osteomalacia and that those likely to have this complication may be identified by plasma 25-hydroxyvitamin D and/or fasting urine hydroxyproline/creatinine ratio measurements. The diagnosis can only be made with certainty by bone biopsy.
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PMID:Osteomalacia, vitamin D deficiency and cholestasis in chronic liver disease. 698 Nov 20

A toxic effect of alcohol is the principal cause of the development of liver disease in alcoholism. Fatty infiltration of the liver is a consequence of ethanol metabolism due mainly to an increased synthesis and decreased degradation of fatty acids. Mechanisms that have been suggested for ethanol-induced hepatocellular necrosis include centrolobular hypoxia due to an increased oxygen requirement and intracellular accumulation of protein, fat, and water which results in increased cell size. Hepatocellular necrosis, however, may not be a necessary stage in the development of cirrhosis. Chronic ethanol administration increases hepatic collagen deposition, and acute and chronic ethanol administration inhibit liver cell regeneration. Increased humoral and cellular immunological activity to liver tissue and its components may contribute to the persistence of liver disease in the alcoholic. However, only a small proportion of alcoholics and baboons fed alcohol develop cirrhosis, suggesting that other factors, either genetic, environmental, or nutritional, play a role. Malnutrition is common in alcoholics. Liver disease is more common in some malnourished populations, and has been produced by nutrient deficiencies. Decreased dietary intake, as well as malabsorption and alterations in the metabolism of nutrients, are causes of nutrient deficiencies in alcoholism. Some of the effects of alcohol on the liver may be mediated by its actions on nutrient absorption and metabolism.
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PMID:Alcoholic liver disease: roles of alcohol and malnutrition. 700 89

Several recent studies suggest that jejunoileal bypass-induced liver disease results from malabsorption of essential nutrients. However, in experimental animals, resection of the defunctionalized bowel substantially reduces bypass-induced liver injury. Such models are often used to support the theory that bacteria in the defunctionalized bowel produce toxic substances which result in liver damage. We used a rat model to first explore the effects of intestinal bypass vs resection on various parameters of liver injury, and subsequently compared these findings to the effect of both bypass and resection on mucosal adaptation in the remaining intact bowel after each procedure. Bypassed animals had lower levels of hepatic cytochrome P-450, glucose-6-phosphatase, pentobarbital hydroxylase, and serum triglycerides than did animals undergoing resection of defunctionalized bowel. Concurrently, resected animals had much greater increases in mucosal weight, DNA content, and protein content in the intact bowel than did bypassed animals. We speculate that the beneficial effects of resection of bypassed bowel on liver function may be a result of increased mucosal hyperplasia in resected animals, rather than elimination of production of toxic substances in the defunctionalized bowel.
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PMID:Etiology of jejunoileal bypass-induced liver dysfunction in rats. 723 61

Hypocholesterolemia (less than 120 mg/dl) was found in 200 out of 3,700 patients admitted consecutively to a University Department of Internal Medicine. In 91, hypocholesterolemia as defined above could be confirmed in a second serum sample on the following day. Mortality during hospitalization in this group was 32%. When diagnoses were grouped into 5 categories, prognosis was particularly poor in heart (36%) and liver disease (31%) and in malignancies (33%), while patients with malabsorption syndromes had a considerably better prognosis (10% mortality). Hypocholesterolemia was associated with a low cholesterol/phospholipid ratio and may be among the first signs of further deterioration of disease.
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PMID:The prognostic significance of hypocholesterolemia in hospitalized patients. 726 18


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