Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After reviewing recent data concerning the pathologic physiology of cystic fibrosis the authors present an anatomoclinical study of 30 infants, of which 13 neonates, with a diagnosis of mucoviscidosiss, emphasizing the clinical and pathohistologic polymorphism of this affection, and, particularly involvement of the liver and intestines. Specific hepatic lesions were encountered in only 10% of the group studied (Bodian biliary cirrhosis and mucus stoppers in the bile ducts). Unspecific hepatic lesions were dominant, common with those of neonatal hepatitis, and hepatic steatosis. Stress is laid on the presence of atrophy of the villi in children with hepatic steatosis, proof of a lesional substrate of malabsorption in this disease. The authors note the early onset of hepatic lesions, the gravity of the cases with an early clinical expression and hepatic biopsy puncture as the only method revealing hepatic affection in cystic fibrosis. In the first semester of life there exists purely digestive forms, hepatic steatosis and oedematous dystrophy in infants at this age being highly suspect of the etiology.
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PMID:[Clinical and histopathologic polymorphism in cystic fibrosis]. 250 62

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in the population subsisting mainly on cereal proteins. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE (acrodermatitis enteropathica), and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy, and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances, and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and biochemical manifestations of zinc deficiency in human subjects. 258 Aug 77

The role of the liver as a contributory factor in the vitamin D deficiency of cholestatic liver disease has been studied in vivo in dogs with chronic bile duct ligation, whereas controls underwent diversion of the bile flow through the urinary bladder via a choledococystostomy anastomosis. The hepatic extraction of vitamin D3 was evaluated by the multiple indicator dilution technique, and the formation of 25-hydroxyvitamin D3 was assessed by directly sampling the hepatic effluent for up to 150 min after vitamin D3 administration. The serum and hemodynamic data indicate that dogs with chronic bile duct ligation had severe cholestasis and hepatocellular injury; histologically, macronodular cirrhosis was present. Dogs with choledococystostomy anastomosis had normal livers and normal liver function. The data indicate that the absence of normal bile flow into the intestinal lumen led to a progressive depletion of vitamin D reserve in both animals with choledococystostomy anastomosis and those with chronic bile duct ligation. However, neither the hepatic fractional extraction of vitamin D3, its hepatic clearance nor its transformation into 25-hydroxyvitamin D3 was significantly changed by chronic bile duct ligation. The results of the present studies indicate that the hepatic handling of vitamin D3 including its C-25 hydroxylation, is well preserved in the presence of severe cholestasis. They also suggest that the state of vitamin D depletion which often accompanies chronic cholestatic liver disease can largely be accounted for by factors such as secondary malabsorption of the vitamin due to the absence of adequate amounts of bile salts in the intestinal lumen, or by other factors which seem independent of the hepatic metabolism of vitamin D.
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PMID:Severe cholestasis leads to vitamin D depletion without perturbing its C-25 hydroxylation in the dog. 319 71

Peptide YY has been localized within human ileocolonic endocrine cells and may contribute to the regulation of gastric secretion and gastric emptying in man. Since our previous studies had shown decreased colonic concentrations of peptide YY in the idiopathic inflammatory bowel diseases, a specific radioimmunoassay was used to measure fasting serum concentrations of peptide YY in healthy controls and in patients with adenocarcinoma of the rectum, idiopathic chronic active liver disease and hepatic cirrhosis, ulcerative colitis, and Crohn's disease. In healthy controls and in patients with adenocarcinoma of the rectum, serum concentrations of peptide YY ranged from 50 to 260 pg/ml. Serum concentrations of peptide YY in patients with hepatic cirrhosis ranged from 59 to 717 pg/ml. Serum concentrations of peptide YY in patients with ulcerative colitis were similar to healthy controls. In patients with Crohn's disease, serum concentrations of peptide YY were less than 50 pg/ml in three patients who had had a previous proctocolectomy, and were more than 260 pg/ml in 14 patients who had had previous resection of more than 48 cm of ileum or presently had symptomatic Crohn's disease subsequently requiring surgical resection of a total of more than 75 cm of ileum. These results suggest that most circulating peptide YY is released from the colorectal region. Hepatic cirrhosis, previous ileal resection, and symptomatic Crohn's disease were associated with elevation of fasting serum peptide YY. The mechanism of increased fasting serum peptide YY in patients with Crohn's disease could be the loss of an ileal inhibitory factor or possibly an increased release of colonic peptide YY in response to fat malabsorption. The effect of alteration of serum peptide YY concentrations on the pathophysiology of Crohn's disease is yet unknown.
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PMID:Abnormalities of fasting serum concentrations of peptide YY in the idiopathic inflammatory bowel diseases. 356 36

Two siblings had olivopontocerebellar degeneration, failure to thrive, hepatic fatty change and cirrhosis, and a dyslipoproteinemia characterized by low cholesterol and elevated triglycerides. This condition was distinct from other cerebellar atrophies and ataxias and was not due to malabsorption or malnutrition. Cerebellar degeneration progressed rapidly during the first year of life, and both children died from intercurrent infections and surgical complications at 11 and 17 months. Stereotyped clinical and pathologic findings in the two patients suggest a previously unreported genetic metabolic disorder affecting the liver and the CNS.
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PMID:Lipoprotein disorder, cirrhosis, and olivopontocerebellar degeneration in two siblings. 370 66

A 25-yr-old black man with cystic fibrosis and cirrhosis developed symptoms of osteomalacia and hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and low circulating 25-hydroxyvitamin D (25-OHD). Serum 1,25-dihydroxyvitamin D (1,25-[OH]2D) was within the normal range. Iliac crest bone biopsy confirmed the diagnosis of osteomalacia. Oral administration of 50,000 IU of vitamin D2 failed to relieve symptoms or raise serum 25-OHD levels to normal. Intramuscular vitamin D2, 10,000 IU every 8-12 week, improved symptoms, raised serum 25-OHD to normal, and increased circulating 1,25-[OH]2D to values five times normal. Over the next 10 mo circulating 1,25-[OH]2D remained elevated despite normalization of serum calcium, phosphorus, and parathyroid hormone. Repeat bone biopsy 1 yr after parenteral vitamin D showed healing of the osteomalacia. Malabsorption of vitamin D appears secondary to profound steatorrhea due to pancreatic insufficiency and secondary biliary cirrhosis. Although extensive hepatocellular disease was present, hepatic conversion of vitamin D to 25-OHD was intact. Both high and low circulating 1,25-[OH]2D levels during active osteomalacia have been reported; initially, the level was in the normal range and higher values in this patient occurred with repletion of 25-OHD substrate. This study shows that symptomatic osteomalacia may be a major manifestation of cystic fibrosis in those patients surviving into adulthood. Measurements of serum 25-OHD in cystic fibrosis patients may identify those who should receive supplemental vitamin D.
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PMID:Vitamin D metabolism and osteomalacia in cystic fibrosis. 387 14

To determine if malabsorption of zinc contributes to the zinc deficiency found in cirrhosis, the absorption of an oral dose of ZnCl2, labeled with 65Zn and a nonabsorbed marker 51CrCl3, was determined from the ratio of these isotopes in a stool specimen. Average 65Zn absorption in 25 alcoholic cirrhotics, 37 +/- 17% (SD), was low compared to 55 +/- 16% in 31 healthy volunteer controls (P less than 0.01). In contrast, mean 65Zn absorption, 47 +/- 11%, in 11 nonalcoholic cirrhotics was not significantly different from the average result in healthy controls. Low 65Zn absorption was accompanied by low leukocyte zinc in a subgroup of alcoholic cirrhotics with ascites and/or ascites and encephalopathy, but not in the subgroup in which these clinical features were absent. Thus, low zinc absorption contributes to zinc deficiency in decompensated alcoholic cirrhosis. The failure to find similar abnormalities in nonalcoholic cirrhosis suggests that the long-standing consumption of alcoholic beverages contributes to the malabsorption of zinc.
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PMID:Zinc absorption and leukocyte zinc in alcoholic and nonalcoholic cirrhosis. 397 39

Low serum, cerebrospinal fluid, erythrocyte, muscle and bone Mg concentrations have been found in liver cirrhosis, indicating a Mg deficiency. Decreased intake, fat malabsorption, renal tubular acidosis and increased serum levels of aldosterone, growth hormone and glucagon could be the causative factors.
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PMID:Magnesium and liver cirrhosis: a hypothesis. 403 1

Plasma and urinary zinc have been measured in 19 patients with malabsorption and 21 patients with hepatic cirrhosis. The results have been compared with those of 20 control subjects and 23 patients with a variety of other diseases. The diurnal variation in plasma zinc levels has been confirmed and is of such magnitude that this must be taken into account in comparing results in groups of subjects. Plasma zinc levels, both fasting and after a meal, are significantly lower in patients with cirrhosis (71 and 60 mug/100 ml) and malabsorption (76 and 64 mug/100 ml) than in controls (97 and 81 mug/100 ml). In the patients with cirrhosis or malabsorption similar correlations exist between plasma zinc and plasma albumin, suggesting that the low plasma zinc levels may be, at least in part, dependent on the plasma albumin level. Urinary zinc excretion is increased in cirrhosis, but not in malabsorption, indicating that increased urinary loss is unlikely to explain the low plasma levels.
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PMID:Plasma and urinary zinc in patients with malabsorption syndromes or hepatic cirrhosis. 478 84

The oral administration of short (C(6)) and medium (C(8) and (C(10)) chain triglycerides produced no clinical or electroencephalographic changes in patients with cirrhosis of the liver. Arterial ammonia levels were also monitored in these patients and showed no significant change after medium chain triglycerides. It was concluded that medium chain triglycerides, known to be of potential value in the treatment of malabsorption in patients with cirrhosis, are not clinically contraindicated, even in patients with evidence of hepatic encephalopathy.
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PMID:Medium chain triglycerides and hepatic encephalopathy. 484 Dec 75


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