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)

Six cases are described of veno-occlusive disease (VOD) after medicinal herb ingestion. The herb Heliotropium eichwaldii, taken by three patients, was found to contain the toxic pyrrolizidine alkaloid, heliotrine. Two patients presented with fulminant hepatic failure while the other four patients had a clinical picture suggestive of decompensated cirrhosis. The medical use of this herb may possibly be responsible for a significant proportion of acute and chronic liver disease in India, making it of public health importance.
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PMID:Herbal medicines and veno-occlusive disease in India. 73 81

A large outbreak of veno-occlusive disease occurred in Afghanistan in which approximately 7,800 in a population of 35,000 subjects were estimated to have been affected. It was caused by consumption of wheat flour heavily contaminated with seeds of a plant of the heliotropium species. These were found to contain pyrrolizidine alkaloids, chiefly heliotrine. Fourteen percutaneous liver biopsies, representing different stages of diseases and liver tissue from eight autopsies were studied. Morphological changes in the liver were characteristic. Centrilobular hemorrhagic necrosis was followed by occlusive changes in the hepatic veins, finally resulting in nonportal cirrhosis. The sequence of changes observed suggests primary parenchymal injury and possibly obstructive lesions at the sinusoidal level. Collagenization of the sinusoids and reorganization of the lobular reticulin begin early in disease. Occlusive changes in the efferent veins apparently follow.
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PMID:An epidemic of veno-occlusive disease of the liver in Afghanistan. Pathologic features. 74 12

Twenty-two patients with previous hepatic compromise who underwent allogeneic bone marrow transplant (BMT) for treatment of hematologic malignancy or other hematologic disease between 1984 and 1990 were chosen for the present study. After transplant, 19 (86.4%) of the patients developed hepatitis, including six cases (27.3%) of acute hepatitis, 12 (54.6%) of chronic hepatitis and one uncharacterized hepatitis. Nine chronic hepatitis patients were followed-up for 7-56.5 months (medium 35.5 months) with biochemistry studies and ultrasonography. Throughout the observation period, liver cirrhosis or hepatoma were not detected and no patients developed veno-occlusive disease. Furthermore patients who developed hepatitis after transplant had worse prognoses. Based on serial serological survey of the various hepatitis B virus (HBV) antigens and antibodies, we have found that most of the recurrent viral hepatitis in transplant patients could be attributed to the reactivation of the virus. In addition, the use of immunosuppressive drugs, persisting infection by HCV and the development of graft-versus-host disease may also play a role in modulating the course of viral hepatitis in BMT patients.
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PMID:Liver disease in patients with liver dysfunction prior to bone marrow transplantation. 162 24

We present 3 cases of juvenile chronic granulocytic leukemia in which there are histological changes in the liver of both portal and bridging fibrosis, with fibrosis around central veins, the latter being confirmed by quantitative measurement. We stress the histological differences from cirrhosis, nodular regenerative hyperplasia, and veno-occlusive disease and describe the evidence which favors an etiology from the leukemic infiltration rather than chemotherapy.
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PMID:Hepatic fibrosis in juvenile chronic granulocytic leukemia: an unusual finding in three cases. 234 56

The authors reviewed the liver histopathology and the clinical features of eight patients with liver metastases from colorectal cancer who were treated by hepatic arterial infusion chemotherapy (HAIC) via an implantable pump (Infusaid). Before HAIC, these patients had no evidence of hepatitis, and results of liver biopsies performed on three patients showed only minor morphologic alterations. All the liver tumors responded to HAIC, but all patients developed hepatitis. Clinical findings included nausea, vomiting, abdominal pain and jaundice. Serum transaminases, alkaline phosphatase and bilirubin levels were increased. Clinical observations suggested that 5-fluoro-2'-deoxyuridine (FUDR), the predominant drug given, was the hepatotoxic agent. Toxic effects were hepatocyte necrosis, steatosis, cholestasis, central vein sclerosis, and alterations in the portal triad. In addition, central vein lesions like those in veno-occlusive disease, and micronodular cirrhosis resembling that induced by alcohol, were encountered. Although individual susceptibility to FUDR appeared to vary, portal triad fibrosis was present in all eight cases and, together with central vein sclerosis and cirrhosis, appeared to be related to the dose and duration of HAIC.
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PMID:Liver pathology following hepatic arterial infusion chemotherapy. Hepatic toxicity with FUDR. 294 Nov 40

Portal hypertension, widely recognized as a complication of cirrhosis, may also develop as an intrahepatic consequence of numerous hepatic disorders in the absence of cirrhosis. When gastrointestinal bleeding occurs in such cases, ruptured esophageal varices must be considered. Among chronic liver diseases, some, such as schistosomiasis, are commonly associated with portal hypertension and its complications. In others, including tuberculosis, amyloidosis, and polycystic disease, well-documented portal hypertension has been reported in only a small minority of cases. Nevertheless, because of the ever-present possibility of variceal hemorrhage whenever portal hypertension occurs, clinicians should be aware of these disorders. Acute conditions associated with noncirrhotic intrahepatic portal hypertension include acute (and particularly fulminant) viral or drug-induced hepatitis, acute alcoholic hepatitis, acute veno-occlusive disease, and acute fatty liver of pregnancy. Portal hypertension may be reversible following recovery in these settings. Particular attention is called to the increasing frequency of acute veno-occlusive disease on bone marrow transplant units, presumably as a complication of high-dose chemo- and radiotherapy.
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PMID:Noncirrhotic intrahepatic portal hypertension. 354 26

Chemical hepatic injury may result from accidental or suicidal exposure to toxic agents in the home or at work or from adverse reactions to medicinal agents. Chemical hepatic injury can lead to acute or chronic syndromes. Acute injury may be cytotoxic, cholestatic, or mixed. Cytotoxic injury is characterized by necrosis, steatosis, or both. Cholestatic injury is characterized by arrested bile flow and may be associated with portal inflammation or may occur in a setting in which there is no evidence of inflammation. Chronic hepatic injury includes chronic active hepatitis, steatosis, phospholipidosis, veno-occlusive disease, several forms of cirrhosis, peliosis hepatis, and hepatic neoplasms. The mechanism for injury may be intrinsic toxicity of the agent, reaction of an unusually susceptible host, or a combination of the two factors. Unusual susceptibility may be the result of immunologic idiosyncrasy (hypersensitivity reaction) or injury from a toxic metabolite (metabolic idiosyncrasy) of the drug.
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PMID:Hepatotoxicity. 822 92

Pyrrolizidine alkaloids are the leading plant toxins associated with disease in humans and animals. Upon ingestion, metabolic activation in liver converts the parent compounds into highly reactive electrophiles capable of reacting with cellular macromolecules forming adducts which may initiate acute or chronic toxicity. The pyrrolizidine alkaloids present a serious health risk to human populations that may be exposed to them through contamination of foodstuffs or when plants containing them are consumed as medicinal herbs. Some pyrrolizidine alkaloids (PA) adducts are persistent in animal tissue and the metabolites may be re-released and cause damage long after the initial period of ingestion. PAs are also known to act as teratogens and abortifacients. Chronic ingestion of plants containing PAs has also led to cancer in experimental animals and metabolites of several PAs have been shown to be mutagenic in the Salmonella typhimurium/mammalian microsome system. However, no clinical association has yet been found between human cancer and exposure to PAs. Based on the extensive reports on the outcome of human exposure available in the literature, we conclude that while humans face the risk of veno-occlusive disease and childhood cirrhosis PAs are not carcinogenic to humans.
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PMID:Pyrrolizidine alkaloids in human diet. 1041 31

In a study carried out in two hospitals in South Africa the authors identified 20 children suffering from hepatic veno-occlusive disease thought to be caused by the administration of traditional remedies. The predominant clinical presentation was ascites of various degrees and hepatomegaly. There was a high morbidity and mortality in the young infants, and in those cases who survived and were followed up the clinical pattern was one of progression to cirrhosis and portal hypertension. Pyrrolizidine alkaloid poisoning is one of the causes of the veno-occlusive disease. Therefore there is a need for objective confirmation of this. In four of our cases an on-admission urine specimen was available and in all of these a simple colorimetric screening test confirmed the presence of pyrrolizidine alkaloids. The other cases were admitted from peripheral hospitals and clinics and urine was not obtained until after 72 h, a time at which the levels of pyrrolizidines in urine were below the limit of sensitivity of the screening test. The screening method is helpful for the detection of acute ingestion of pyrrolizidines in large amounts, but is not sufficiently sensitive for the detection of chronic ingestion of smaller amounts. Nevertheless, in those patients who have hepatomegaly and ascites a positive finding of pyrrolizidines is important and may remove the necessity for expensive and invasive investigative measures.
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PMID:Clinical and analytical aspects of pyrrolizidine poisoning caused by South African traditional medicines. 1085 Mar 97

Herbal medication has gathered increasing recognition in recent years with regard to both treatment options and health hazards. Pyrrolizidine alkaloids have been associated with substantial toxicity after their ingestion as tea and in the setting of contaminated cereals have led to endemic outbreaks in Jamaica, India and Afghanistan. In Western Europe, comfrey has been applied for inflammatory disorders such as arthritis, thrombophlebitis and gout and as a treatment for diarrhoea. Only recently was the use of comfrey leaves recognized as a substantial health hazard with hepatic toxicity in humans and carcinogenic potential in rodents. These effects are most likely due to various hepatotoxic pyrrolizidine alkaloids such as lasiocarpine and symphytine, and their related N-oxides. The mechanisms by which toxicity and mutagenicity are conveyed are still not fully understood, but seem to be mediated through a toxic mechanism related to the biotransformation of alkaloids by hepatic microsomal enzymes. This produces highly reactive pyrroles which act as powerful alkylating agents. The main liver injury caused by comfrey (Symphytum officinale) is veno-occlusive disease, a non-thrombotic obliteration of small hepatic veins leading to cirrhosis and eventually liver failure. Patients may present with either acute or chronic clinical signs with portal hypertension, hepatomegaly and abdominal pain as the main features. Therapeutic approaches include avoiding intake and, if hepatic failure is imminent, liver transplantation. In view of the known serious hazards and the ban on distributing comfrey in Germany and Canada, it is difficult to understand why comfrey is still freely available in the United States.
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PMID:The efficacy and safety of comfrey. 1127 98


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