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)

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

The authors report the case of a 32-year old woman admitted for hepatomegaly, weight loss, and moderate diarrhea. Liver function tests showed anicteric cholestasis with slight increase in serum level of transaminases. Liver biopsy demonstrated massive steatosis. Biological and radiological investigations of the small intestine showed a malabsorption pattern. Stool fat excretion was 54 g per day. Duodenal biopsies disclosed total villous atrophy. A ten-day treatment with metronidazole (1,5 g per day), followed by a gluten-free diet, resulted in rapid improvement of hepatic and intestinal symptoms. This case report shows that: 1) adult celiac disease may be the cause of severe steatosis; 2) anicteric cholestasis with or without hepatomegaly during the course of adult celiac disease may be secondary to steatosis, as well as primary biliary cirrhosis or malignant infiltration of the liver; 3) bacterial overgrowth should be searched and eventually treated in the case of massive fatty liver occurring in adult celiac disease.
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PMID:[Massive hepatic steatosis disclosing adult celiac disease. Study of a case and review of the literature]. 685 13

Bone disease and low serum levels of 25-hydroxyvitamin D are prevalent in cholestatic syndromes such as primary biliary cirrhosis and biliary atresia. Defective hydroxylation, along with malabsorption of vitamin D, could be a factor in 25-hydroxyvitamin D depletion. To assess hepatic hydroxylation during experimental cholestasis, we studied vitamin D 25-hydroxylase activity in liver homogenates of rats after 7, 14, and 21 days of bile duct ligation. We have also studied the effects of bile acids on this enzyme in vitro. Hepatic 25-hydroxylation was depressed after 7 days ligation in only 1 of 4 animals, but by 14 days, all animals showed a marked reduction with a mean decrease of 64% in specific activity. Total liver enzyme activity was reduced by 43% at 14 days. In the ligated animals, liver histology showed progressive bile stasis, focal necrosis, bile ductular proliferation, periductular and periportal inflammation, and fibrosis. Addition of bile acids to the in vitro assay in concentrations approximating those found in cholestasis produced marked inhibition of vitamin D 25-hydroxylase activity.
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PMID:Hepatic vitamin D 25-hydroxylase: inhibition by bile duct ligation or bile salts. 697 44

In this review I have discussed out current understanding of the vitamin D endocrine system. Vitamin D is made available to the body both by intestinal absorption and by photosynthesis in the skin. To be active, vitamin D must be hydroxylated to 250HD, principally in the liver, and to 1,25(OH)2D and 24,25(OH)2D, principally in the kidney. The best studied target tissues for the vitamin D metabolites are bone, kidney, and intestine. However, the list of additional potential target tissues is expanding and includes muscle, endocrine pancreas, parathyroid gland, pituitary, and skin. Disorders of the vitamin D endocrine system can be categorized into three groups: decreased bioavailability, abnormal metabolism, and aberrant target tissue response. A number of illustrative examples for each category have been discussed. Primary biliary cirrhosis typifies the problem of vitamin D malabsorption and disrupted enterohepatic circulation; chronic renal failure is the most devastating problem of vitamin D metabolism; and vitamin D dependent rickets type II is the best example of aberrant target tissue response. However, certain disorders overlap these distinct categories. Others, such as the nephrotic syndrome, which leads to urinary losses of the vitamin D metabolites (presumably bound to DBP), are not readily categorized. Nevertheless, an understanding of the level at which the vitamin D endocrine system is perturbed by any given disorder provides a rational basis for therapeutic intervention.
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PMID:The vitamin D endocrine system. 704 49

The intestinal absorption and hepatic metabolism of vitamin D were studied in a woman with icteric primary biliary cirrhosis (PBC) complicated by pronounced bone pain and muscle weakness due to vitamin-D deficiency. The patient had a markedly reduced intestinal absorption of vitamin D, while the 25-hydroxylation of this vitamin was found to be normal despite the presence of longstanding icterus. The malabsorption of fat-soluble compounds secondary to the cholestasis was probably further impaired by several years of cholestyramine treatment. Administration of 1.25-(OH)2D3 increased intestinal calcium absorption, normalized serum calcium and increased bone mineral content of the proximal tibia. Furthermore, drastic improvement of muscle weakness and relief of bone pain were observed. It is recommended that repeated measurements of serum 25-(OH)D should be carried out in patients with PBC, and especially in those treated with cholestyramine. In certain vitamin D deficient patients, studies using radio-labelled vitamin D may provide clinically valuable information as to the exact site of the underlying disturbances.
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PMID:Normal hepatic vitamin-D metabolism in icteric primary biliary cirrhosis associated with pronounced vitamin-D deficiency symptoms. 709 38

Lundh tests of pancreatic exocrine function were performed on twenty unselected patients with systemic sclerosis. Three patients had very low levels of tryptic activity in their intestinal juice and only nine had results which were unequivocally normal. Eight patients had biochemical steatorrhoea, but in six this was associated with intestinal bacterial overgrowth and a seventh had primary biliary cirrhosis. The remaining patient had no cause for steatorrhoea other than the marked pancreatic insufficiency which had been demonstrated. Although pancreatic damage may contribute to malabsorption in systemic sclerosis, it appears to be less important than other factors such as intestinal bacterial overgrowth.
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PMID:Pancreatic exocrine function in systemic sclerosis. 728 47

Duodenal bile salt concentrations were measured throughout one day in six patients with primary biliary cirrhosis while they were eating a normal ward diet. Five of them had lost weight; none had ascites. Each patient had a radiologically normal small bowel and a normal jejunal biopsy. No clear relationship between high faecal fat excretion and abnormally low duodenal bile salt concentration was found. Xylose absorption was abnormal in five patients. If weight loss in primary biliary cirrhosis is due to malabsorption, factors other than a reduced small intestinal bile salt concentration must be important.
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PMID:Weight loss in primary biliary cirrhosis. 742 37

Primary biliary cirrhosis is a chronic, usually progressive, cholestatic liver disease of presumed autoimmune etiology that affects predominantly young and middle-aged women. It is nearly always associated with an antibody directed against a component of the pyruvate dehydrogenase complex located on the inner wall of the mitochondria. The disease is associated with a number of other associated autoimmune disorders. No totally effective medical treatment has been established for the disease, although urosdeoxycholic acid appears promising. Complications of cholestasis such as fat malabsorption and fat-soluble vitamin deficiency should be excluded or corrected when found. Individual patient prognosis varies. Several models for estimating individual patient survival are available. Liver transplantation is recognized as a procedure to extend and improve the quality of life for patients with advanced disease.
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PMID:Primary biliary cirrhosis. 771 16

This article reviews osteoporosis (OP) in adults with chronic liver disease. OP in this setting is characterized in general by low bone turnover. The pathogenesis is unclear but is probably not related to vitamin D abnormalities. Patients at high risk of OP include those with evidence of cirrhosis, hypogonadism, overt calcium malabsorption, steroid therapy and choleostatic liver disease (particularly primary biliary cirrhosis). OP is best managed by adequate calcium intake, regular weight bearing exercise, and the avoidance of alcohol and tobacco smoking. There is probably no reason for vitamin D supplementation. Hormonal replacement therapy when necessary is indicated in males and should be considered in females. Finally, liver transplantation has the potential to improve or stabilize OP in the median term, although it is associated with significant short-term deterioration.
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PMID:Osteoporosis in chronic liver disease: pathogenesis, risk factors, and management. 785 Oct 1

A number of hepatobiliary tract and pancreatic disorders have been documented in patients with celiac disease. Some disorders have shared immunological or genetic factors, including chronic hepatitis, primary biliary cirrhosis and sclerosing cholangitis. Other hepatic or pancreatic pathological changes in celiac disease have been documented with severe malnutrition and malabsorption, including hepatic steatosis and pancreatic insufficiency, sometimes with pancreatic calcification. Finally, celiac disease may be associated with other very rare hepatic complications, such as hepatic T cell lymphoma.
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PMID:Hepatobiliary tract and pancreatic disorders in celiac disease. 911 4


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