Cases reported "Jaundice, Obstructive"

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1/7. metformin-induced cholestatic hepatitis.

    OBJECTIVE: To report a case of metformin-induced cholestatic hepatitis. methods: We present a detailed case report, including laboratory and biopsy findings. In addition, similar cases from the literature are reviewed. RESULTS: In a 68-year-old man with newly diagnosed diabetes mellitus, metformin therapy was begun. The dosage initially was 500 mg twice daily and later was increased to 850 mg twice a day. Four weeks after met-formin treatment was initiated, jaundice, pruritus, and liver enzyme abnormalities were noted. The patient underwent an extensive work-up, including a hepatitis screen, ultrasonography, magnetic resonance imaging, and endoscopic retrograde cholangiopancreatography, all of which showed normal findings. A liver biopsy revealed severe cholestasis and mild portal inflammation. Treatment with metformin was discontinued, and the liver enzymes normalized except for a persistently increased level of alkaline phosphatase, most likely related to a prolonged cholestatic effect of metformin. CONCLUSION: Although rare, metformin can be responsible for inducing liver damage, and patients and physicians should be aware of this side effect.
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2/7. Botryoid rhabdomyosarcoma of common bile duct.

    common bile duct is an unusual site for occurrence of botryoid rhabdomyosarcoma. Clinically it is often misdiagnosed as infectious hepatitis. early diagnosis and treatment has greatly improved the prognosis of this aggressive neoplasm. Here the authors present a case report of Bortroyid rhabdomyosarcoma of CBD in a two and half year old child masquerading as obstructive jaundice.
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keywords = hepatitis
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3/7. Acute myeloid leukaemia presenting as cholestatic hepatitis.

    A 40 year old man presented with abdominal pain, jaundice, weight loss, and hepatosplenomegaly. liver function tests revealed cholestatic jaundice and a computed tomography scan showed an enlarged liver, with a normal biliary tree. Liver biopsy showed diffuse infiltration by neutrophils, monocytoid cells, and blasts. Peripheral blood film and bone marrow were consistent with acute myeloid leukaemia. After treatment with chemotherapy using an acute myeloid leukaemia protocol (UK Medical research Council AML-12), there was complete resolution of jaundice and the patient went into complete molecular remission.
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4/7. An uncommon presentation: chronic meningococcaemia associated with cholestatic hepatitis in a Turkish child.

    Chronic meningococcaemia is a very rare clinical manifestation of invasive infection by neisseria meningitidis. A 9-year-old girl was admitted to our clinic with complaints of fever, headache, arthralgia, and maculopapular rash. The diagnosis was made by the growth of neisseria meningitidis in the blood cultures. Four days after admission, liver function tests were increased and were compatible with cholestatic hepatitis. Thereafter, the patient was successfully treated and symptoms were completely resolved. To our knowledge, there have been no previous reports of neisseria meningitidis causing cholestatic hepatitis. Herein, we present an unusual child patient with chronic meningococcaemia associated with cholestatic hepatitis.
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5/7. Severe cholestatic jaundice in hyperthyroidism after treatment with 131-iodine.

    A 39-year-old white man was referred to our hospital for evaluation of his jaundice and pruritus. The patient was treated with I for diffuse toxic goiter prior to his referral to our hospital. Clinical examination and laboratory investigations excluded viral hepatitis, autoimmune hepatitis, granulomatous disease, primary biliary disease, extrahepatic biliary obstruction, and heart failure. Liver biopsy showed severe intrahepatic and canalicular cholestasis with minimal inflammatory changes. The patient's jaundice promptly resolved with therapy for hyperthyroidism and thyroid storm as bilirubin levels decreased from 35 mg/dL (normal: 0.5-1.2 mg/dL) to 0.4 mg/dL. thyrotoxicosis can be an uncommon cause of profound cholestasis. Our case differs from all other reports in the literature because of the severity of the cholestasis and its prompt resolution with treatment for thyrotoxicosis.
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keywords = hepatitis
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6/7. Intrahepatic cholestatic jaundice related to administration of ranitidine. A case report with histologic and ultramicroscopic study.

    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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keywords = hepatitis
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7/7. Extra-hepatic hepatocellular carcinoma presenting as obstructive jaundice.

    Hepatocellular carcinoma is a neoplasm with a uniformly poor prognosis. risk factors for its development include chronic hepatitis b or C infection, haemochromatosis and alpha-1-antitrypsin deficiency, but individuals with any type of chronic liver disease are predisposed. The incidence is significantly higher in asia and africa although it has been noted to be increasing in the united states. We present a patient with notable atypical clinical features for hepatocellular carcinoma. The patient had neither predisposing risk factors nor a primary liver lesion causing obstructive jaundice. After multiple tissue specimens were obtained, the final pathological diagnosis was established. Hepatocellular carcinoma generally requires a surgical cure, but patients who are icteric often portend poorer prognoses. For those at high risk, screening may be indicated to identify early curative treatment.
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