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)

Clinical analysis of 293 cases of cirrhosis from two moderate sized hospitals in the city of Dacca has been presented. Maximum number of cases were in the age group over 40 with 150 (51.2%) males and 19 (5.8%) females. Significant past history included viral hepatitis (21.5%), kala-azar (11.6%) and malaria (10.24%). History of alcoholism was present only in 16 (5.5%) cases. Weakness (84.3%), weight loss (72%) and anorexia (39.3%) constituted the most common symptoms. Ascites (45%), haematemesis (11.6%) and melaena (28.7%) were the next common symptoms. Hepatosplenomegaly was found in about one-third of the cases. Testicular atrophy was recorded in 41.63% cases whereas gynaecomastia was relatively less common (5.5%). Scanty body hair and white nails were present in almost equal number of cases (14.7% and 18%). The cases presented here are those with overt manifestation. Nevertheless, the clinical features are not materially different from those reported by other authors. In the absence of alcoholism, viral hepatitis is presumably the most important aetiological factor in our cases and the clinical features compare favourably with non-alcoholic cirrhosis of the western writers. Cryptogenic cirrhosis has been considered to be most common type constituting 43.7% of our cases.
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PMID:Cirrhosis of liver. 734 4

A 52-year-old oligophrenic man hospitalized for esophageal hemorrhage had histologically proven liver cirrhosis and died from massive rehemorrhage. As a neonate he had survived severe jaundice, had had delayed psychomotor development and remained severely retarded. At age 15 years, bilateral cataracts had been excised and from 18 to 25 years he had had occasional grand mal seizures. The triad oligophrenia, liver cirrhosis and cataracts, prompted suspicion of galactosemia. Deficiency of galactose-1-phosphate uridyltransferase was demonstrated in blood and post mortem tissue. At autopsy, liver cirrhosis and esophageal varices were confirmed and unilateral chronic pyelonephritis, bilateral nephrolithiasis and testicular atrophy were found. There was not brain pathology. The patient appeared to be the oldest nondiagnosed galactosemic and the first male patient in whom hypogonadism was documented.
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PMID:[Decompensated liver cirrhosis caused by galactosemia in a 52-year-old man]. 745 52

Testicular atrophy, loss of libido and feminization are observed in patients with nonalcoholic liver cirrhosis, Serum total and free testosterone levels are decreased in patients with advanced liver cirrhosis and is normal in compensated cirrhotic patients. In compensated liver cirrhosis, sex hormone binding globulin is increased, and is related with increasing serum total testosterone. Serum total and free estradiol levels and ratio of estradiol to testosterone are increased in cirrhotic patients. Hyperestrogenization is related with female physical characteristics. Gonadal dysfunctions observed in cirrhotic patients are primary in the gonadal failure, then a concomitant with pituitary defect occurs. These abnormalities in liver cirrhosis are reversible.
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PMID:[Gonadal dysfunctions in liver cirrhosis]. 811 82

Various endocrine disturbances are often observed in the patients with liver cirrhosis. We focused this paper on the sex hormones. Clinical features of male cirrhotic subjects are feminization(gynecomastia etc) and hypogonadism(testicular atrophy, reduced fertility, loss of libido, impotence etc). Chief abnormalities of sex hormones are a decrease in serum testosterone levels and an increase in serum estrogen levels accompanied by an increase in ratio of estrogen to testosterone in the patients with severe liver cirrhosis associated with the severity of hepatic dysfunction. Hyperestrogenization may be related with feminization of male cirrhotic subjects, whereas hypogonadism is the result of alcohol abuse per se, rather than the indirect consequence of liver cirrhosis.
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PMID:[Endocrine disturbances in liver cirrhosis--focused on sex hormones]. 939 3

The pathogenesis of hypogonadism in cirrhosis is not completely understood. The levels of insulin-like growth factor-I (IGF-I), an anabolic factor with trophic actions on testes, are reduced in cirrhosis. This study was undertaken to evaluate whether rats with advanced cirrhosis develop hypogonadism and whether the administration of IGF-I exerts beneficial effects on testicular structure and function. Wistar rats with ascitic cirrhosis induced with CCl(4) were allocated into 2 groups (n = 10, each) to receive recombinant IGF-I (20 microg x kg(-1) x d(-1), subcutaneously) or vehicle for 3 weeks. Healthy rats receiving vehicle were used as the control group (n = 10). At baseline, both cirrhotic groups showed similar deterioration of liver function tests. Compared with controls, nontreated cirrhotic rats showed decreased serum levels of IGF-I (P <.05), reduced testicular size and weight (P <.001), and intense histopathological testicular abnormalities, including reduced tubular diameters (P <.001), loss of the germinal line (P <. 001), and diminutions in cellular proliferation, spermatogenesis (P <.001), and testicular transferrin expression (P <.001). In addition, low serum testosterone (P <.01) and high serum LH (P <.01) were present in untreated cirrhotic animals. Cirrhotic rats that received IGF-I showed full recovery of testicular size and weight and of all histopathological abnormalities (P <.001 to <.01 vs. nontreated cirrhotic rats; P = ns vs. controls). Serum levels of sex hormones tended to normalize. In conclusion, IGF-I deficiency may play a pathogenetic role in hypogonadism of cirrhosis. Low doses of IGF-I for a short period of time revert testicular atrophy and appear to improve hypogonadism in advanced experimental cirrhosis.
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PMID:Insulin-like growth factor-I reverts testicular atrophy in rats with advanced cirrhosis. 1086 24

Alcohol-induced diseases of the liver, such as fatty liver, hepatitis and cirrhosis with the potential development of hepato-cellular carcinoma can cause many effects on the skin. Even though they are not caused by excessive alcohol alone, but also by other diseases of the liver or other diseases of internal organs, an experienced person will be able to carry out specific diagnostic procedures. Skin symptoms due to liver diseases include 1. Vascular changes, such as spider nevi, teleangiectasias and palmar erythema. 2. Nail changes, particularly white nails. 3. Changes of the mucous membranes, i.e. glossy tongue. 4. Changes due to altered hormones, particularly gyneco-mastia, female distribution of hair and testicular atrophy and 5. Changes in the color of the skin like icterus and melanosis cutis. Rarely pruritus and other diseases of the skin are seen, such as porphyria cutanea tarda, which is often caused by an altered liver function. In the final stages of alcoholism, the neglect of personal hygiene particularly of the skin is evident (cutis vagantium). Since the exact mechanism of the skin symptoms remains obscure, it is difficult to evaluate the significance. Most often they do not correlate with the severity of the liver disease.
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PMID:[Skin manifestations of alcoholic liver damage]. 1080 82

Systemic administration of recombinant IGF1 at low levels has been shown to improve hepatic function, nutritional status and testicular atrophy in rats with CCl4-induced cirrhosis. We have developed a recombinant adeno-associated (rAAV) viral vector containing the cDNA for rat IGF1 and confirmed the expression of IGF1 after intramuscular injection of this vector in a rat model of liver cirrhosis. Although weight of injected muscles was significantly increased in rats with mild cirrhosis, this was not the case in rats with advanced, de-compensated cirrhosis. Furthermore, we found no significant amelioration of liver damage in treated rats at any stage of liver cirrhosis. Our results suggest that IGF1 gene transfer into muscle results in a local effect, at least at the vector dose employed here.
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PMID:IGF1 gene transfer into skeletal muscle using recombinant adeno-associated virus in a rat model of liver cirrhosis. 1260 11

The estrogenic compound diethylstilbestrol (DES) has been widely studied to understand its potential involvement in endocrine function and carcinogenesis. This study examined the influence of DES on adult mice by histopathological analysis and studied the gene expression changes using mRNA differential display. Pathological changes in the mice following DES exposure included testicular atrophy, ovarian and hepatic fibrosis, and reduced numbers of mature oocytes and spermatogenic cells. Other pathological changes, such as cirrhosis of the liver, were also found. To elucidate the molecular mechanism underlying these effects, we used mRNA differential display to analyze changes in gene expression following DES exposure. In total, 20 genes were differentially expressed in liver, kidney, ovary, uterus, and testis. All putative target genes were validated by QRT-PCR. The study provides evidence that DES has an acute effect on gene expression. The results may facilitate the discovery of the genotoxic mechanism of DES and allow one to discover new DES-responsive genes.
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PMID:Histopathological and gene expression analysis of mice exposed to diethylstilbestrol. 2016 89

Hemochromatosis is a genetic disorder of iron metabolism that results in elevated iron absorption in the intestines, which leads to progressive iron accumulation in a variety of organs. Studies have shown that excessive iron deposits in the liver due to hereditary hemochromatosis leads to cirrhosis, which can put an individual at increased risk for developing hepatocellular carcinoma. Testicular atrophy, sometimes caused by excessive iron deposition in the testes, is a risk factor for testicular cancer. Therefore, the possible role of hereditary hemochromatosis in testicular cancer is explored.
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PMID:The possible role of hemochromatosis in testicular cancer. 2154 11

Ethanol is the most abused psychoactive substance. Accordingly to World Health Organization ethanol ranks among the top five risk factors for disease, disability and death (3.3 million/year) throughout the world. This manuscript highlights and critically analyses clinical and forensic signs related to hepatoxicity of ethanol that may lead to suspected of abuse. Namely, steatosis, jaundice, cirrhosis, hemorrhoids, esophageal varices caput medusae, ascites, petechiae, ecchymoses, splenomegaly, hemochromatosis, xanthelasma, nutritional deficiency, testicular atrophy, gynecomastia and dilated congestive cardiomyopathy are discussed and related to the toxic mechanism of ethanol.
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PMID:Signs and Related Mechanisms of Ethanol Hepatotoxicity. 2645 50


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