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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although ischemic cholangitis is an important cause of early cholestatic graft failure in hepatic allografts, it rarely leads to biliary tract abnormalities in the late postoperative period. We describe a 54-year-old woman who underwent orthotopic liver transplantation for alcoholic liver cirrhosis in 1988 and presented in April of 1995 with malaise, jaundice, dark urine, clay-colored stools and cholestasis. An endoscopic retrograde cholangiopancreatography demonstrated a rapid progressive sclerosing cholangitis. Liver biopsy findings showed mild portal hepatitis, specimens were non-diagnostic with regard to cholangitis, and no infection was found. Duplex ultrasonography suggested obstruction of hepatic artery blood flow and celiac arteriogram confirmed complete hepatic arterial occlusion. Progressive destruction and irregular stricturing and dilatation of the intra- and extrahepatic biliary tree, complicating ascending infectious cholangitis, progressive cholestatic jaundice and insufficient endoscopic biliary drainage made a hepatic retransplantation in 1995 mandatory. Ischemic cholangitis is an important cause of cholestatic graft failure, but this type of cholangitis is difficult to diagnose because of its misleading biopsy manifestations. We conclude that liver transplant recipients who exhibit nonanastomotic strictures on cholangiography should be evaluated for occlusion of the hepatic artery as a possible cause.
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PMID:Severe ischemic-type biliary strictures due to hepatic artery occlusion seven years after liver transplantation--a rare cause of late cholestatic graft failure. 967 36

Infection with group A beta-hemolytic streptococci (GABHS) is the most common bacterial cause of acute pharyngitis and tonsillitis beyond infancy. We report on two patients with scarlet fever associated with hepatitis. The patients (boys aged 6 and 7 years) both presented with a scarlatiniform rash, dark urine and light-colored stools. Laboratory studies revealed elevated liver transaminases and negative antibody tests against hepatitis viruses A, B and C, cytomegalovirus and Epstein-Barr virus. Both patients were treated with antibiotics and recovered completely within a few days. Although the association between scarlet fever and hepatitis has been known for many decades, the pathogenesis is still unknown. Physicians treating patients with group A beta-hemolytic streptococcal infections should be aware of possible hepatic involvement.
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PMID:Scarlet fever associated with hepatitis--a report of two cases. 1096 36

A 71-year-old man with chronic atrial fibrillation was treated with aspirin because of a right cerebral infarction. Oral anticoagulation was not initiated because of a secondary hemorrhagic transformation. Six years later after a left cerebral transient ischemic attack aspirin was replaced by ticlopidine. Two weeks after starting ticlopidine he experienced abdominal cramps and diarrhea. Also dark urine and gray-colored stools were noticed, so that the patient stopped taking ticlopidine. 40 days after starting ticlopidine he was admitted to our hospital because of cholestatic jaundice. Serum alkaline phosphatase (305 U/l) and gamma GT (143 U/l) were elevated, the total bilirubin was 18.6 mg/dl at peak. GOT and GPT were 2.7 fold increased. After exclusion of a viral infection and autoimmune disease liver biopsy was performed, which showed a centroacinar cholestasis compatible with a drug-induced liver damage. 79 days after discontinuation of the drug laboratory signs of cholestasis had disappeared. In patients in whom long-term therapy with ticlopidine is indicated regularly laboratory tests and clinical examinations should be done to recognize infrequent side effects such as the cholestatic hepatitis in time.
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PMID:[Cholestatic hepatitis as a rare side effect of therapy with ticlopidine]. 1096 56

A 66 year-old obese woman with arthrosis, self-medicated with oral nimesulide, 200 mg daily. After 6 weeks she developed nausea, jaundice and dark urine. Two weeks later she had recurrent hematemesis and was hospitalized. Besides obesity and anemia her physical examination was unremarkable. An upper GI endoscopy revealed 3 acute gastric ulcers and a 4th one in the pyloric channel. Abdominal ultrasonogram showed a slightly enlarged liver with diffuse reduction in ecogenicity; the gallbladder and biliary tract were normal. Blood tests demonstrated a conjugated hyperbilirubinemia (maximal total value: 18.4 mg/dl), ALAT 960 U/l, ASAT 850 U/l, GGT 420 U/l, alkaline phosphatases mildly elevated, pro-time 49% and albumin 2.7 mg/dl. Serum markers for hepatitis A, B and C viruses were negative. ANA, AMA, anti-SmA, were negative. Ceruloplasmin was normal. A liver biopsy showed bridging necrosis and other signs of acute toxic liver damage. Gastric ulcers healed after conventional treatment and hepatitis subsided after 2 months leaving no signs of chronic liver damage. The diagnosis of toxic hepatitis due to nimesulide was supported by the time-course of drug usage, sex, age, absence of other causes of liver disease, a compatible liver biopsy and the improvement after drug withdrawal. Peptic ulcers or toxic hepatitis have been previously described as independent adverse reactions in patients taking nimesulide or other NSAIDs but their simultaneous occurrence in a single patient is a unique event that deserves to be reported.
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PMID:[Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case]. 1122 44

Neonatal cholestasis must always be considered in a newborn who is jaundiced for more than 14-21 days and a measurement of the serum total and conjugated bilirubin in these infants is mandatory. Conjugated hyperbilirubinaemia, dark urine and pale stools are pathognomic of the neonatal hepatitis syndrome which should be investigated urgently. The neonatal hepatitis syndrome has many causes and should be investigated using a structured protocol. The most important condition in the differential diagnosis is biliary atresia and affected infants require a Kasai portoenterostomy performed by an experienced surgeon, ideally before the infant is 60 days old. A modified evaluation schedule should be used for preterm infants who have required neonatal intensive care. Genetic causes of the neonatal hepatitis syndrome are increasingly recognized and early diagnosis facilitates genetic counselling and, in some situations, specific treatment. The management of cholestasis is largely supportive, consisting of aggressive nutritional support with particular attention to fat-soluble vitamin status. The use of ursodeoxycholic acid is associated with improvement in biochemical measures of cholestasis and may improve the natural history of cholestasis in some circumstances. Outcome is dependent on aetiology. In idiopathic neonatal hepatitis more than 90% make a complete biochemical and d clinical recovery.
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PMID:Neonatal cholestasis. 1220

Chronic hepatitis C virus is a major worldwide cause of hepatitis, cirrhosis, end-stage liver disease, and hepatocellular carcinomas. Combination therapy of ribavirin with short- or long-acting interferon-alpha is now the standard treatment of chronic hepatitis C. This therapy is associated with a wide range of side effects. Although hemolysis is almost an invariable result of ribavirin, black urine due to hemoglobinuria has never been previously reported. We recently encountered two cases of black urine (hemoglobinuria) in patients treated with combination therapy. Based on reports of dark urine in many of our patients, we suggest that this phenomenon may be more common than is currently appreciated. It indicates a marked degree of hemolysis, which prompts immediate measurement of hemoglobin level.
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PMID:Hemoglobinuria with ribavirin treatment. 1264 48

Viral hepatitides are common diseases of modern man in both industrialized and developing countries, with a varying prevalence of particular types and mode of transmission. In current medicine, viral hepatitides are classified in the A-E nomenclature, differentiating viruses that can be etiologically defined with certainty on the basis of serum markers and hepatitides exhibiting all clinical and laboratory characteristics of viral hepatitis but of as yet nondemonstrable causative agents, classified in the non-A, non-E hepatitis group. Two issues are of high relevance in the pathogenesis of viral hepatitides: route of transmission (fecal-oral or parenteral) and basic mechanism of hepatocyte lesion. Although all hepatitis viruses replicate within the hepatocyte, the exact mechanism of hepatocyte necrosis has not yet been fully elucidated, i.e. direct cytotoxicity or hepatoprogressive immune response mediated primarily by the specific cytotoxic CD8 lymphocytes. Depending on the site of entry, the virus replicates in the adjacent lymphatic tissue for some time, followed by primary viremia, virus replication in the lymphoreticular organs (lymph nodes, liver, spleen), and eventual entry in the target cells--hepatocytes, accompanied by a varying grade of necrosis and inflammatory reaction. The clinical and laboratory signs of the disease correspond to the degree of liver necrosis and are not specific for particular types of viral hepatitis. The most frequent symptoms common to all types of viral hepatitis of moderate severity include elevated body temperature persisting for days, fatigue, gradual loss of appetite, nausea, dull pain and discomfort on DRL, vomiting, multiple loose stools, dark urine, jaundice of the skin and mucosa, and light stools. Generally, the ultimate outcome of the disease is elimination of the virus and complete recovery, however, a fulminant course with lethal outcome or transition to chronic disease may also occur, making viral hepatitides a major public health problem worldwide. In classical infectology, four clinical stages of the disease have been described: incubation or preclinical stage characterized by intensive virus replication; prodromal or preicteric stage with pronounced general symptoms of infection; icteric stage; and stage of recovery. The stages may show great interindividual variation in length and severity. The development of molecular technologies over the last decade has greatly contributed to better understanding of the pathogenesis of viral hepatitides and allowed for appropriate monitoring of the effect of antiviral therapy. However, major disadvantage of these tests is their high cost. The basic clinical characteristics of and diagnostic options for particular types of viral hepatitis are described, with special reference to the latest important concepts on the disease pathogenesis.
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PMID:[Clinical aspects and diagnosis of viral hepatitis]. 1458 62

Ranitidine may cause liver injuries ranging from transient, subclinical serum transaminases increase every 100-1,000 treated patients to cholestatic hepatitis in less than 1/100,000. Other H2-receptor antagonists are more dangerous: 11 toxic hepatitis cases have been reported as adverse effect after 1 year of marketed ebrotidine. A 75-year-old male with ischemic cardiopathy history was started on an 8 days treatment of oral ranitidine due to pirosis, without any other changes of therapy; 48 h after drug withdrawal, light-coloured stools, dark urine and icteric scleras developed. On hospital admission, 10 days later, physical examination showed slight hepatomegaly and severe jaundice with skin excoriations followed by serum mixed bilirubin further increase and aminotransferases activities mild rise. Total bilirubin peaked at 381.33 mmol/l (5.1-17.1) and progressively returned to normal, after discharge home, in 3 months and now, 1 year later, there is no sign of liver disease. Ultrasonographic biliary anomalies and the most frequent causes of liver damage were excluded. Liver biopsy confirmed ranitidine as the most likely cause of liver toxicity since histological and ultramicroscopical study revealed a drug-induced picture. We report a rare case of intrahepatic cholestasis jaundice related to ranitidine, a widely used drug. Diagnosis would need an ethically unacceptable rechallange test.
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PMID:Intrahepatic cholestatic jaundice related to administration of ranitidine. A case report with histologic and ultramicroscopic study. 1578 90

We report a case of hepatotoxicity induced by methimazole treatment in a patient affected by hyperthyroidism. A 54-year-old man, presented to our observation for palpitations, excessive sweating, weakness, heat intolerance and weight loss. On physical examination, his blood pressure was 140/90 mmHg and heart beat was 100/min regular. He had mild tremors and left exophthalmos. Laboratory test revealed a significant increase in serum thyroid hormone levels with a decrease in thyroid stimulating hormone levels. A diagnosis of hyperthyroidism was made and he began treatment with methimazole (30 mg/day). Fourteen days later, he returned for the development of scleral icterus, followed by dark urine, and abdominal pain in the right upper quadrant. Laboratory examinations and liver biopsy performed a diagnosis of cholestatic hepatitis, secondary to methimazole usage. Methimazole was promptly withdrawn and cholestyramine, ursodeoxycholic acid, and chlorpheniramine were given. After five days, abdominal pain resolved and laboratory parameters returned to normal. Naranjo probability scale indicated a probable relationship between hepatotoxicity and methimazole therapy. In conclusion physicians should be aware the risk of hepatotoxicity related with methimazole.
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PMID:Hepatotoxicity induced by methimazole in a previously healthy patient. 1953 46

Artemisinins are a class of compounds that include artesunate, artemether, and artemisinin and have potent antimalarial activity. In combination with other drugs (artemisinin combination therapy), these compounds are the first-line treatment recommended by the World Health Organization for Plasmodium falciparum infections. Artemisinins have been available in the United States without a prescription as herbal supplements for at least 10 years; these supplements are marketed for general health maintenance and for treatment of parasitic infections and cancers. On August 27, 2008, CDC was notified of a patient who developed hepatitis after a 1-week course of an herbal supplement containing artemisinin. The patient had abdominal pain, dark urine, and laboratory results consistent with hepatitis (e.g., serum alanine aminotransferase of 898 IU/L [normal: 10-55 IU/L]). Samples of the supplement were sent to CDC and the Georgia Institute of Technology for analysis to determine the amount of artemisinin and to identify any contaminants. Analysis indicated that the supplement contained 94%-97% of the 100 mg of artemisinin stated on the packaging and the supplement contained no other common pharmaceutical active ingredients. Given the patient's clinical course and laboratory evaluation, CDC investigators concluded that the hepatitis might have been associated with ingestion of the herbal supplement containing artemisinin. More data are needed to establish any causal connection between artemisinin and hepatitis. Health-care providers should be aware of the possibility of hepatic toxicity in patients taking herbal supplements containing artemisinin.
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PMID:Hepatitis temporally associated with an herbal supplement containing artemisinin - Washington, 2008. 1968 Feb 21


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