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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Observations on the clinical effects of venesection therapy in 85 treated, as compared with 26 untreated, patients with idiopathic haemochromatosis showed decreased pigmentation and hepatomegaly together with a return to normal tests of liver function in half the patients who had abnormal tests at presentation. Control improved in 28 per cent of those patients with diabetes mellitus, although some patients developed it during the period of observation, despite venesection. Portal hypertension, testicular atrophy and arthropathy were not improved. In only 12 patients was there sufficient reaccumulation of iron after the initial course of venesection to merit further treatment. Rates of iron accumulation in these patients varied between 1-4 mg and 4-8 mg per day and chelatable iron levels were noted to be inappropriately high in relation to body iron stores during the early stages of the reaccumulation period. Life table data shows that the percentage survival five and ten years after diagnosis was 66 and 32 per cent respectively for the treated patients, and 18 and 6 per cent respectively for the untreated patients, both statistically highly significant differences (p less than 0-01). Possible clinical differences such as age of presentation, the presence of diabetes mellitus, cirrhosis, clinical hepatic failure and hepatoma between the treated and untreated groups that might otherwise have weighted survival in favour of the treated group were corrected by the use of covariant analysis. This gave mean log survival values of 4-15 and 2-88 for the treated and untreated patients respectively, equivalent to 63-4 months and 17-8 months, a highly significant difference (p less than 0-01). Ten patients, all of whom had cirrhosis at the time of diagnosis, died of malignant hepatoma between three and 15 years after completing venesection therapy. There was also a high rate of death from neoplasms in a variety of other sites--22 per cent in the venesected group, strikingly higher than that rate predicted for a similarly aged population using national cancer mortality rates.
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PMID:Long term results of venesection therapy in idiopathic haemochromatosis. 18 63

Serum zinc concentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste, and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy, and impaired wound healing) are common in these patients. It remains unresolved whether these disease states are indicative of true symptomatic or asymptomatic zinc deficiency or merely reflect a decrease in available zinc binding proteins. The low serum zinc concentrations and high urinary zinc excretions in patients with nephrotic syndrome do not appear to be due to loss of zinc bound to urinary proteins. Studies in dogs indicate increased serum and urine concentrations of certain amino acids(cysteine, histidine) greatly increase urinary zinc excretions. Studies are now underway to determine if the hyperzincuria and hypozincemia of cirrhosis, nephrotic syndrome and hyperalimentation can be explained by an increase in these urinary amino acids.
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PMID:Zinc metabolism in renal disease and renal control of zinc excretion. 60 38

Serum zinc conentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy and impaired wound healing) are common in these patients. It remains unresolved whether these low serum zinc concentrations in these disease states are indicative of true symptomatic or asymptomatic zinc deficiency, or merely reflect a decrease in available zinc-binding proteins, as well over 90% of serum zinc is bound to protein in normal subjects. The correlation between serum zinc and albumin concentrations, reportedly the major zinc-binding protein, is unimpressive. Studies of serum and urine binding of added radiozinc65 using Sephadex G-200 gel column chromatography and polyacrylamide gel electrophoresis suggest most of the radiozinc is bound to a protein with a molecular weight near albumin (68,000). Polyacrylamide gel electrophoresis suggests this might be a prealbumin. The low serum zinc concentration in the patient with nephrotic syndrome does not appear to be due to loss of zinc bound to urinary protein.
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PMID:Serum concentrations and urinary excretions of zinc in cirrhosis, nephrotic syndrome and renal insufficiency. 66 9

Between July 1986 and April 1989, 334 hospitalized adult Ethiopian patients with chronic liver disease were studied according to a protocol to define their clinical features and to identify risk factors with the aim of preventive intervention. Of these, 14 had chronic hepatitis, 208 cirrhosis and 112 hepatocellular carcinoma (HCC). Both clinical and histological diagnostic criteria were employed. A detailed questionnaire was used to document demographic and clinical data. A common clinical presentation among patients with chronic hepatitis was darkening of the face and hands with or without hypertrichosis of the face and blisters over the dorsi of the hands. This overt or latent form of porphyrea cutanea tarda (PCT) responds to chloroquine. Patients with cirrhosis of the liver commonly present for the first time with ascites, splenomegaly, haematemesis and/or melena from oesophageal varices, and mental changes due to hepatic encephalopathy. Overt or latent forms of PCT are also common features. Peculiar to these cirrhotics is the rarity of spider naevi, gynaecomastia, testicular atrophy, Dupuytren's contracture, parotid gland enlargement and clubbing of the fingers. Exhaustion, loss of appetite, rapid loss of weight, right upper quadrant and/or epigastric pain (all often of less than 6 months' duration, a big, hard, tender and grossly nodular liver with bruit, signs of portal hypertension, and/or hepatic encephalopathy, in a young male with a rapid down hill course characterize the Ethiopian patient with HCC. Serum anti-nuclear factor, anti-mitochondrial anti-bodies and anti-smooth muscle anti-bodies were absent in those with chronic hepatitis and were uncommon in the cirrhotics and HCC cases. One or more hepatitis B virus markers were found in 86% of chronic hepatitis, 88% cirrhosis and 78% HCC and the HBsAg carrier state was found in 36%, 29% and 23%, respectively. Among the HBsAg carriers, HBeAg positivity was less common than anti-HBe but anti-HDV was significantly higher than in the healthy general population. Alphafetoprotein (AFP) levels greater than 500 mg/ml were present in 16 (8%) cirrhotics and 58 (52%) patients with HCC. Histologically, 3 of the chronic hepatitis patients had progressed to cirrhosis, 8 of the cirrhotic patients had chronic active hepatitis and 85% of HCC cases occurred in a background of macronodular cirrhosis. Three cirrhotics developed HCC during follow-up.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic liver disease in Ethiopia: a clinical study with emphasis on identifying common causes. 131

Primary or genetic haemochromatosis is an inherited disease characterized by an inappropriate degree of iron absorption with accumulation of excessive amounts of tissue iron. Parenchymal iron accumulation results in the typical clinical features of the disease including hepatic cirrhosis, diabetes, testicular atrophy and skin pigmentation. The disease is inherited in an autosomal recessive manner. The gene for the disease has not been identified but is tightly linked to the A locus of the histocompatibility complex on chromosome 6. The approximate homozygote frequency in Caucasians is 0.3% with an equal sex ratio. Excessive body iron stores have been described in a number of other conditions, particularly alcoholic liver disease. There is increasing evidence that many of these individuals are in fact also suffering from genetic haemochromatosis. Diagnostic tests including serum iron, transferrin saturation, serum ferritin and liver iron concentration make it possible to detect sufferers of the disease. Screening relatives of affected individuals with these tests allows a diagnosis to be made before permanent tissue damage has occurred. Removal of excess iron stores by repeated phlebotomy is the primary treatment. If iron is removed before significant tissue damage has occurred, the complications and natural course of the disease will be prevented provided reaccumulation of iron does not occur. Excessive iron accumulation with resultant organ damage also occurs in anaemias associated with ineffective erythropoiesis and after excessive parenteral iron administration or repeated blood transfusions. Similar clinical features may be seen. Chelation therapy is the mainstay of treatment in these cases where long-term venesection is not possible.
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PMID:The clinical manifestations of chronic iron overload. 266 Sep 35

The size of the testicle (absolute weight, relative weight as the index X, length, and width was measured in 142 late patients aged 17 to 87 a (mean age = 54 a) serving as controls, in 193 deceased patients aged 20 to 81 a (mean age = 47 a) with a history of alcoholism, and in 136 defunct patients aged 30 to 92 a (mean age = 59 a) with cirrhosis. A significant difference in the mean size of the testicles was demonstrated between the cirrhosis group and both the control and alcoholism groups. No statistically significant differences was observed between the control group and the alcoholism group. The degree of acute alcoholic intoxication has no significant effect on the degree of testicular atrophy. Chronic alcoholism exerted a more significant effect on the degree of testicular atrophy than acute alcoholism. Coexistent cirrhosis increased this difference even more. The type of cirrhosis and the degree of its inflammatory activity had no significant influence on the testicular size. Such effect was demonstrated, however, if diffuse fatty infiltration of the cirrhotic liver was present. In the biomorphosis, the greatest mean testicular size was observed in the 4th and 5th decade of life. From the 6th decade on, the testicular size decreased statistically significantly. The curve of the values of the mean testicular size in alcoholism was more flat than in the control group and was situated below it. No statistically significant differences among the values of the testicular size in this curve were found. The testicular size curve in cirrhosis was below both these curves, and a statistically significant difference was found between the 7th and the 9th decades. The mean weight of the testicules in controls, alcoholics, and patients with cirrhosis was 17.58, 16.49, and 13.25 g, respectively, the mean volume was 16.37, 15.34, and 12.21 ml, respectively, the value of the index X was 2.47, 2.52, and 1.97, respectively, the testicular length was 5.05, 4.08, and 3.61 cm, respectively, the width was 2.93, 2.87, and 2.70 cm, respectively.
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PMID:Studies on the size of human male gonad in biomorphosis, alcohol intoxication, and cirrhosis--a review and own findings. 322 4

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

Portocaval anastomosis (PCA) in the normal male rat causes profound alterations in testicular morphology and function and in plasma levels of sex steroids as well as of gonadotropins. Testicular atrophy is accompanied by a significant decrease of plasma testosterone (0.03 ng/ml versus 0.99 ng/ml) and an increase of estradiol (76.2 pg/ml versus 39.7 pg/ml) and estrone (68. pg/ml versus 45.5 pg/ml). Plasma levels of gonadotropins (LH, FSH) and prolactin are lowered too (LH: 15 ng/ml versus 28.5 ng/ml, FSH:119 versus 182 ng/ml, prolactin:53 versus 109 ng/ml). The altered sex hormone metabolism is reflected in marked changes of the morphology and nucleic acid content of the metabolizing organs i.e. liver, gonades and kidney. The results of this study are consistent with the hypothesis that portosystemic shunt per se plays an important role in the pathogenesis of the disturbed metabolism of sex hormones observed in patients with liver cirrhosis and portal hypertension.
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PMID:[Sex hormones and fertility following portacaval anastomosis in rats]. 670 37

Portacaval anastomosis (PCA) in the rat may be a useful experimental model for examining endocrine changes that occur during cirrhosis of the liver. A marked reduction in diet intake and body weight occurs in rats after establishing the shunt and studies were undertaken to determine the relationship of these effects to the testicular atrophy that also follows PCA. Control, sham-operated animals, experiencing a reduction in food intake similar to that of the animals with a PCA, showed reduced plasma levels of LH and testosterone but also exhibited a marked testicular response to LH. This was consistent with increased sensitivity of the hypothalamic-pituitary axis to the negative feedback of gonadal steroids in chronically underfed animals. Male rats with a PCA exhibited similarly reduced levels of LH and testosterone, but showed poor secretory responses of the pituitary gland to LH releasing hormone (LH-RH) and of the testis to LH. Testicular atrophy and cessation of spermatogenesis occurred in the animals with a PCA. These results suggested that the effects of PCA on the pituitary-gonadal axis cannot simply be explained as a consequence of the restricted intake of diet. This was confirmed by the responses to castration. In both fed and underfed sham-operated rats, castration resulted in a rapid and sustained increase in plasma LH and both groups showed a marked LH secretory response to LH-RH. In contrast, in animals with a PCA castration had little effect on plasma LH and the pituitary response to LH-RH was still poor. The effects of PCA cannot be simply explained by impeded metabolism of gonadal steroids causing increased negative feedback on the hypothalamic-pituitary axis.
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PMID:Effect of portacaval anastomosis and chronic underfeeding on the hypothalamic-pituitary-gonadal axis in the rat. 700 52

The yield of severe cirrhosis of the liver (defined as a shrunken finely nodular liver with micronodular histology, ascites greater than 30 ml, plasma albumin less than 2.2 g/dl, splenomegaly 2-3 times normal, and testicular atrophy approximately half normal weight) after 12 doses of carbon tetrachloride given intragastrically in the phenobarbitone-primed rat was increased from 25% to 56% by giving the initial "calibrating" dose of carbon tetrachloride at the peak of the phenobarbitone-induced enlargement of the liver. At this point it was assumed that the cytochrome P450/CCl4 toxic state was both maximal and stable. The optimal rat size to begin phenobarbitone was determined as 100 g, and this size as a group had a mean maximum relative liver weight increase 47% greater than normal rats of the same body weight. The optimal time for the initial dose of carbon tetrachloride was after 14 days on phenobarbitone.
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PMID:Phenobarbitone-induced enlargement of the liver in the rat: its relationship to carbon tetrachloride-induced cirrhosis. 724 70


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