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)

Biliary obstruction is an important complication of chronic calcifying pancreatitis. In this study, liver biopsies were examined to determine the nature and severity of hepatic complications in 23 such cases. The most striking changes were portal tract expansion due to oedema and fibrosis, with proliferation of bile ducts. Although common, these changes were not severe, and no patient had developed secondary biliary cirrhosis. Other features of note were intrahepatic cholestasis, iron overload (56.5%), copper-associated protein stained with the orcein technique (34.7%) and mild fatty change or perivenular sclerosis in 13%. It is concluded that no serious, irreversible pathological changes occurred in the liver despite clinically marked biliary obstruction.
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PMID:The liver in biliary obstruction due to chronic pancreatitis. 405 70

Recently Brewer et al. reported the possibility of an oral zinc therapy in Wilson's Disease. We treated a 19 years old patient with decompensated liver cirrhosis due to Wilson's disease with zinc-sulphate. D-Penicillamine had to be withdrawn since proteinuria occurred under treatment. After the discontinuation of D-Penicillamine an increase of serum copper almost up to normal range was observed; concomitantly urinary copper elimination decreased. Under oral zinc sulphate therapy (145 mg/day) a drop of serum copper level was achieved and liver function improved: serum albumin, gamma globulins and prothrombin time reached normal values. The patient did not complain any side effects during oral zinc sulphate therapy. Oral zinc therapy in Wilson's Disease may be regarded as an alternative to D-Penicillamine treatment when this drug has to be discontinued because of side effects.
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PMID:[Oral zinc in Wilson disease--an alternative to D-penicillamine]. 406 Jul 99

Forty-two patients with autoimmune liver disease have been investigated. Renal tubular acidosis was detected in 60% of the patients with primary biliary cirrhosis, in 30% with active chronic hepatitis, and in one out of seven cases with cryptogenic cirrhosis. The presence of the defect of renal acidification was not related to the level of plasma potassium, copper, or total globulin, nor to the pattern of immunological abnormalities detected in the serum. It is suggested that autoimmune liver disease and renal tubular acidosis may be part of a systemic disorder in the pathogenesis of which immunological mechanisms are involved.
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PMID:Renal tubular acidosis and autoimmune liver disease. 554 62

The presence of large amounts of copper in the liver in primary biliary cirrhosis has been confirmed; a similar increase is not found in cases of long-standing extrahepatic biliary obstruction. The serum caeruloplasmin levels are raised in primary and secondary biliary cirrhosis, but this increase does not appear to be related to the degree of increase of hepatic copper. The manganese content of the liver is slightly raised in both these conditions.The reason for the increased metal content in these circumstances cannot yet be determined, and the effects are not yet understood.
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PMID:Copper and manganese concentrations in biliary cirrhosis of liver. 566 88

Primary sclerosing cholangitis is a progressive, ultimately fatal, chronic hepatobiliary disorder for which no effective medical or surgical therapy now exists. The syndrome occurs most commonly in young men and is characterized by a chronic cholestatic syndrome, frequent association with chronic ulcerative colitis, hepatic copper overload, a paucity of serologic markers, and characteristic abnormalities in some liver-biopsy specimens and most cholangiograms. The natural history of the syndrome is unclear; the disease is likely to progress slowly and relentlessly, over a decade or longer, from an asymptomatic stage to a condition characterized by symptoms of cholestasis and complicated by cirrhosis, portal hypertension, and possibly carcinoma of the bile ducts. Screening techniques based on automated biochemical analyses are likely to lead to a diagnosis of primary sclerosing cholangitis in increasing numbers of patients, perhaps in the early, preicteric stage. An increased level of serum alkaline phosphatase in a young man, particularly if he has chronic ulcerative colitis, should strongly suggest the presence of this syndrome and the need for additional diagnostic studies. Endoscopic retrograde cholangiography and liver biopsy should be considered under these circumstances.
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PMID:Current concepts. Primary sclerosing cholangitis. 636 57

Ultrastructural studies with the transmission (TEM) and scanning (SEM) electron microscopes have added greatly to our knowledge of cellular structure and function in the liver. The normal polyhedral hepatocyte has numerous subcellular organelles, such as mitochondria, peroxisomes, lysosomes and complex rough (rer) and smooth (ser) endoplasmic reticulum. The normal hepatocyte stores glycogen, and sometimes lipid droplets, and secretes bile through the bile canaliculi between adjacent liver cells. It receives nutrients from the sinusoidal lumen across a fenestrated endothelium which is separated by the Space of Disse' from the plasma membrane. The Space of Disse' contains a scant network of reticulin fibers but no basal lamina. Two types of parasinusoidal cells are found in Disse's space: the fat storing cells of Ito, and the Pit cells which may have an endocrine function. The diseased liver has yielded much information in studies with TEM and SEM. The studies with TEM have been most helpful in studying the etiology of infectious diseases such as hepatitis B; have revealed organelle changes such as megamitochondria in cirrhosis and the fibrillar nature of alcoholic hyaline; have led to the identification of specific deposits in metabolic and storage diseases such as hemochromatosis (iron). Wilson's disease (copper), and alpha-1-antitrypsin deficiency (glycoprotein) have proven useful in identifying drug induced liver cell changes such as proliferation of SER and cholestasis, and are useful for identifying specific cell types in inflammatory and neoplastic diseases. In the future, both TEM and SEM coupled with histochemical, cytochemical, immunohistochemical and other analytic techniques will continue to add greatly to our understanding of the liver in health and disease.
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PMID:Ultrastructure of the liver and biliary tract in health and disease. 637 90

Rats were injected intraperitoneally with copper-lactate daily for over 160 days (total dose of 30 mg copper in each animal). At 120 to 160 days of copper administration, animals developed symptoms similar to those of Wilson's disease, i.e., kidney functional disturbances, proteinuria, aminoaciduria, decreased blood ceruloplasmin oxidase activity and increased urinary copper excretion. Cirrhosis was found in some animals. Tubular necrosis of the kidneys, liver fibrosis and tigrolysis of thalamic nerve cells were also found. Copper depositions were observed in liver parenchymal cells, renal tubular epithels, thalamus glia cells and on the Descemet's membrane of the cornea. The similarities between induced copper- intoxication in rats and Wilson's disease are discussed.
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PMID:Laboratory and histological similarities between Wilson's disease and rats with copper toxicity. 645 May 19

Zinc is essential for many metabolic and enzymatic functions in man. Deficiency of zinc in man has now been recognized to occur not only as a result of nutritional factors, but also in various disease states, including malabsorption syndromes, acrodermatitis enteropathica, Crohn's disease, alcoholism and cirrhosis of the liver. The deficiency state in human subjects exists as a spectrum extending from mild to severe degree. The clinical manifestations of mild zinc deficiency include oligospermia, weight loss and hyperammonaemia. Moderate zinc deficiency is characterized clinically by growth retardation, hypogonadism in males, skin changes, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In severe zinc deficiency states, bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorders, weight loss, intercurrent infections, hypogonadism in males and, if unrecognized, death have been observed. Zinc is needed for the functions of over 100 enzymes. It is essential for DNA, RNA and protein synthesis and, as such, is important for cell division. Zinc is an inducer of mRNA of metallothionein, a protein which may have an important role in the regulation of intestinal zinc absorption. Zinc has a specific effect on testes in animals and man. Recent reports indicate that in human subjects thymopoietin may be zinc dependent and in animal studies somatomedin may be affected adversely due to dietary zinc restriction. Zinc plays an important role in the protection of cell membrane integrity and may be protective against free radical injury. Zinc is known to compete with cadmium, lead, copper, iron and calcium for similar binding sites. In the future, a potential use of zinc may be to alleviate toxic effects of cadmium and lead in human subjects. Recent evidence suggests that thymic-dependent lymphocytes (T cells are zinc dependent. T-helper and suppressor cells, T-effector cells and T-natural killer cells appear to be zinc dependent. Zinc is also essential for some of the neutrophil functions. Thus, it appears that zinc may play an important role in immunity. One may suggest that some of the clinical features of cirrhosis of the liver, such as testicular atrophy, loss of body hair, night blindness, poor wound healing, poor appetite, susceptibility to infections and enhanced sensitivity to drugs, may be related to conditioned deficiency of zinc, future studies are required to determine whether or not zinc supplementation is beneficial to these patients.
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PMID:The role of zinc in gastrointestinal and liver disease. 661 39

Acute hemolytic anemia and the development of liver cirrhosis with ascites 3 month thereafter suggested Wilson's disease in a 12 years old child, which was confirmed by inappropriate copper metabolism. In addition, neurological symptoms and renal tubular insufficiency characterized the early stage of the disease.
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PMID:[Acute hemolysis and liver cirrhosis as leading symptoms of Wilson's disease in childhood]. 663 16

Using atomic absorption spectrophotometry, the authots determined zink levels (in correlation with the time-course of copper elimination) in the blood serum and urine of 28 patients with hepatocerebral dystrophy prior to and during the first year of D-penicillamine treatment and in 55 patients who had been on this therapy for a number of years. The zink concentration in the patients' blood serum prior to treatment tended to decline. Such a decrease was also noted in cirrhosis of other etiologies. Thiol therapy resulted in a gradual increase in the urine zink elimination which followed a pattern of the drug dose increment and could be two to three times higher than normal in cases of prolonged treatment. Nevertheless, these patients exhibited no symptoms of zink insufficiency and the zink concentration in the blood serum had been normal for a number of years, which may be explained by an enhanced absorption of zink from the intestines and by its mobilization from the tissue depots. The pathological manifestations observed in six patients with the asthenoneurotic syndrome regressed following zink administration.
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PMID:[Changes in zinc metabolism during long-term D-penicillamine treatment of patients with Wilson-Konovalov disease]. 672 Jan 76


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