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

Knowledge of the cellular changes that lead to hepatic neoplasia in humans is limited. Cirrhosis is a common antecedent or accompaniment of liver cell carcinoma and it seems that both its etiology and its time of duration are relevant risk factors. Many cellular changes have been observed in patients and among populations considered to be at risk. Of these, liver cell dysplasia is the most striking, and studies of its prevalence, natural history, and association with particular forms of cirrhosis suggest that it is a precancerous change. Bile duct carcinoma may follow infestation with liver flukes and duct epithelial hyperplasia is present before the development of cancer. Angiosarcoma from several causes is commonly preceded by a peculiar fibrosis, vascular changes, and Kupffer cell hyperplasia.
 ...
PMID:Precancerous changes in the human liver. 22

The large number of chemical agents administered for therapeutic or diagnostic purposes can produce various types of hepatic injury by several mechanism. Acute injury may be cytotoxic, cholestatic or mixed. Cytotoxic injury may consist of necrosis or steatosis. Cholestatic injury may be cholangiolitic (hepatocanalicular) or bland (canalicular). Chronic hepatic lesions caused by medicinal agents include chronic active hepatitis, steatosis, cirrhosis, fibrosis, hepatoportal sclerosis (non-cirrhotic portal hypertension), hepatic vein thrombosis, peliosis hepatis, adenoma, carcinoma, and angiosarcoma. There is a useful relationship between the type of hepatic injury and the chemical setting in which the drugs are employed. Some agents produce the liver damage because they are intrinsic (true, predictable) hepatotoxins. Other (non-predictable "hepatotoxins"), produce hepatic injury only in the rare and unusually susceptible individual (idiosyncratic injury). Hepatotoxic agents can be recognised by their dose-dependent and experimental reproducibility, properties which are not shared by agents which produce hepatic injury only in idiosyncratic hosts. Intrinsic hepatotoxins may be categorised as direct or indirect. Direct hepatotoxins injure the hepatocyte by direct physiochemical alteration and as a consequence produce metabolic defects. Indirect hepatotoxins selectively block metabolic pathways and, by producing a precise biochemical lesion, lead to structural changes. They may lead to hepatic steatosis or necrosis (cytotoxic indirect hepatotoxins) or block bile flow (cholestatic indirect hepatotoxins). Direct hepatotoxins are rarely encountered as drugs. Overdoses of some drugs and antineoplastic agents appear to be indirect cytotoxic hepatotoxins, and the C-17 alkylated anabolic and contraceptive steroids are indirect, cholestatic hepatotoxins. Idiosyncracy of the host is the mechanism for most types of drug-induced hepatic injury. It may reflect allergy to the drug or a metabolic aberration of the host permitting the production of hepatotoxic metabolites.
 ...
PMID:Drug-induced liver disease. 35 64

Four cases of hepatic angiosarcoma are reported with a review of 99 other cases in the English literature. Angiosarcoma of the liver is associated with chronic exposure to thorotrast, vinyl chloride, arsenicals, radium and possibly copper and with chronic idiopathic hemochromatosis. Although 40% of patients have hepatic fibrosis or cirrhosis at autopsy, the nature of the association between chronic liver disease and hepatic angiosarcoma is unknown. The clinical presentation of hepatic angiosarcoma is nonspecific with abdominal pain, weakness and weight loss common complaints and with hepatomegaly, ascites and jaundice common findings. Liver function tests are usually abnormal but there is no one liver function test or set of tests specific for the tumor. The occurrence of thrombocytopenia and disseminated intravascular coagulation is characteristic of hepatic angiosarcoma and may be related to local consumption of clotting factors and formed blood elements in the tumor. Catastrophic intraabdominal bleeding is also characteristic and occurs in one-fourth of all cases. This complication is likely related to the high incidence of clotting abnormalities and the vascular nature of the neoplasm. Selective hepatic arteriogram and open liver biopsy are the foundations of diagnostic evaluation. Percutaneous liver biopsy should be avoided. Failure to appreciate the possibility of hepatic angiosarcoma in the proper clinical setting, leading to blind percutaneous biopsy, may result in failure to make the diagnosis at the cost of significant morbidity and mortality. Survival of patients with hepatic angiosarcoma is brief; only 3% live longer than 2 years. Treatment of the tumor to date is empirical. There are probably a few patients who might benefit from radical surgery with curative intent. For all others chemotherapy is indicated. Adriamycin is active against hepatic angiosarcoma, but optimal dose and mode of administration require further investigation. Further study is also required to delineate the cause of hepatic angiosarcoma in the 60% of cases without definite epidemiologic association.
 ...
PMID:The clinical features of hepatic angiosarcoma: a report of four cases and a review of the English literature. 36 8

Liver disease with inclusions of copper was recognized among 30 rural workers with "vineyard sprayer's lung." The pathological findings were varied: focal or diffuse swelling and proliferation of Kupffer cells; histiocytic and sarcoid-like granulomata; fibrosis of variable degree in the perisinusoidal, portal, and subcapsular areas, accompanied by atypical proliferation of the sinusoidal lining cells; micronodular cirrhosis; angiosarcoma of the liver; idiopathic portal hypertension. Abundant deposits of copper were revealed by histochemical techniques within hepatic and pulmonary lesions in these patients. The observations on the human and experimental material suggest an etiological relationship between exposure to copper sulfate and the lesions described. A morphological resemblance was noted between the "liver disease of vineyard sprayers" and the hepatic lesions reported in workers exposed to inorganic arsenic and to vinyl chloride. The identification of the inhaled foreign material within the liver lesions raises important etiological considerations.
 ...
PMID:Liver disease in vineyard sprayers. 55 10

A cross-sectional mortality study of 4,341 deaths occurring among current and former employees of 17 PVC fabricators during 1964-1973 is presented. The objectives are: (1) to identify any angiosarcoma deaths among the employees of these fabricators, and (2) to examine the distribution of deaths by cause. No angiosarcoma deaths were found among the study group. Sex-race-cause-specific Proportionate mortality Ratios (PMR's) were computed, using the corresponding U.S. mortality as the standard. Among white employees, there appears to be an excess in total cancer mortality, particularly that of the digestive system. Observed deaths were found to exceed the expected in cancers of the breast and urinary organs among white females. Deficit mortality was observed in cirrhosis of liver among both male and female white employees.
 ...
PMID:Mortality among employees of PVC fabricators. 56 4

A 39-year-old male with bleeding esophageal varices due to portal hypertension was observed. The patient had taken an arsenical preparation during a period of 12 yr because of psoriasis and subsequently developed keratotic changes of the palms and soles of his feet and an epithelioma of the scrotum. Physical examination was unremarkable except for splenomegaly and skin lesions. Liver function tests were normal; a needle biopsy of the liver (right lobe) showed nonspecific changes. Combined hepatic and umbilicoportal catheterization revealed, on splenography and portography, huge esophageal varices and patent portal vein; dilation, distortion, and cut-off of many intrahepatic portal branches were found. A marked gradient existed between the free portal venous pressure (25 mm Hg) and the wedged hepatic venous pressure (9.5 mm Hg). Hepatic blood flow, portal PO2, cardiac output, cardiac index, and blOOD volume were within normal range. Arteriographies did not reveal arteriovenous shunts in the splanchnic or splenic vessels. A splenorenal shunt were performed and a wedged biopsy of the liver (left lobe) revealed nonspecific changes. Three years later the patient had not experienced any episode of hemorrhage or hepatic encephalopathy but developed an epithelioma of the tongue. No known cause could be incriminated in the pathogenesis of the portal hypertension. However, there was unequivocal chronic arsenic intoxication. Toxic hepatitis, cirrhosis, noncirrhotic portal hypertension, and hemangiosarcoma of the liver have been reported with the intake of arsenicals. Thus, it is suggested that in this patient, presinusoidal portal hypertension was secondary to chronic arsenical intake associated with marked intrahepatic vascular changes seen on portography.
 ...
PMID:Noncirrhotic presinusoidal portal hypertension associated with chronic arsenical intoxication. 112 3

Between April 1986 and August 1990, 151 liver transplantations were performed at our institution, 16 (11%) of them in 14 patients with primary hepatic tumors. There were 12 hepatocellular carcinomas, 1 angiosarcoma, and 1 Klatskin tumor. None of the tumors was resectable, and there was no preoperative evidence of extrahepatic tumoral extension. Exploratory laparotomy was performed prior to transplantation in three patients and selective embolization of the tumor in six patients. There was no difference in the intraoperative requirements for blood or plasma in the patients with hepatic tumors when compared with other transplant recipients (28.6 +/- 23.6 units packed red blood cells [PRBC] versus 20.1 +/- 17.8 units PRBC, and 17.9 +/- 12.2 units plasma versus 17.1 +/- 10.5 units plasma, respectively). Extracorporeal venovenous bypass was used in all but one patient. There was no significant differences in the incidence of acute rejection or in the length of hospitalization in these patients when compared with other transplant recipients. All patients received triple immunosuppressive therapy (corticosteroids, azathioprine, and cyclosporin A). Intraoperative mortality was zero. At a mean of 13.3 months' follow-up (range: 1 to 47 months), 2 of 14 patients had died of sepsis and 1 of terminal cirrhosis (autopsies revealed no evidence of tumor recurrence); 3 patients (21%) had recurrences of the tumor (1 in the central nervous system and liver, and the other 2 in the lung). One of the three patients with a recurrent tumor is still alive after 16 months. The remaining nine patients (64%) are still alive.
 ...
PMID:Liver transplantation in malignant primary hepatic neoplasms. 131 58

The pathomorphologic characteristics of 102 autopsy cases of Thorotrast (Th)-related hepatic malignancies were described and compared to the features of non-Th-related cases. Among the 102 Th-related hepatic malignancies, 44 (43.1%) were cholangiocarcinoma (CHC), 39 (38.3%) were angiosarcoma (AGS), 16 (15.7%) were hepatocellular carcinoma (HCC), and 3 (2.9%) were double cancer. In the non-Th-related cases approximately 90% were HCC, and AGS was very rare. Grossly, the majority (91.7%) of Th-related CHC was located in the middle-peripheral portion of the liver. In contrast, 77.8% of the non-Th-related cases were located in the hilar portion. Th-related AGS was classified into four types: diffuse micronodular, multi-nodular, massive, and mixed multi-nodular and massive. Histologically, AGS was characterized by two cell types (spindle-shaped cells and polyhedral cells) and three growth patterns (sinusoidal, cavernous, and solid). In noncancerous areas foci of varying degrees of sinusoidal dilatation with hyperplastic changes of sinusoidal lining cells were observed in all AGS cases and in some of the cases of Th-related CHC and HCC cases. In many (80%) of the non-Th-related HCC, mixed macronodular and micronodular cirrhosis was associated. By contrast, in Th-related HCC cases cirrhosis was superimposed on varying degrees of hepatic fibrosis related to Th deposition in only four cases (21.1%). Taken together, these findings suggest that Th influences are more carcinogenic to epithelial cells of the bile duct and sinusoidal lining cells than hepatocytes.
 ...
PMID:Pathomorphologic characteristics of 102 cases of thorotrast-related hepatocellular carcinoma, cholangiocarcinoma, and hepatic angiosarcoma. 245 26

To evaluate the effects of continuous low-level ionizing radiation on humans, the follow-up data (1980-85) on Japanese thorotrast-exposed patients were analyzed. The patients were 241 war-wounded military personnel registered with and cared for by the Ministry of Health and Welfare since 1979. During this period, a total of 1144 person-years, 94 patients died. Compared with the expected number of deaths calculated from age- and cause-specific death rates in Japan during the same period, the thorotrast-exposed patients were at three times greater risk of death from all causes (P less than 0.001), had 47 times the risk of liver cancer (P less than 0.001), 12 times the risk of leukemia (P less than 0.05), and 20 times the risk of liver cirrhosis (P less than 0.001). Age at time of thorotrast injection, drinking and smoking habits had little effect on these statistics. Analyses of 30 autopsied patients with liver cancer showed statistically significantly increases in hemangiosarcoma and cholangiocarcinoma. The thorotrast-exposed patients' estimated risk of liver cancer by histological type was 21 times that of the general population for hepatocellular carcinoma, 303 times that for cholangiocarcinoma and 3129 times that for hemangiosarcoma.
 ...
PMID:Increased risk of death in thorotrast-exposed patients during the late follow-up period. 282 75

Among 200 deaths from liver cirrhosis the clinical and autopsy records of 30 histologically confirmed cases of primary liver carcinoma (PLC) were reviewed. Male to female ratio was 5:1. Biopsy-proven liver lesions reflected chronic liver disease, mainly cirrhosis. Autopsy-PLC detected was classified as hepatocellular carcinoma (21 cases) with trabecular and pseudoglandular histological pattern, cholangiocarcinoma (two cases), and hemangiosarcoma. This retrospective analysis pointed to the relationship between PLC and liver cirrhosis, the latter being the primary risk factor for the incidence of PLC in Slovenia (Yugoslavia).
 ...
PMID:Clinicomorphological manifestations of primary liver carcinoma (PLC) in liver cirrhosis. 302 28


1 2 3 4 5 Next >>