Cases reported "Liver Diseases"

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1/44. Lamotrigine overdose presenting as anticonvulsant hypersensitivity syndrome.

    OBJECTIVE: To describe the laboratory and physical manifestations of lamotrigine toxicity presenting as anticonvulsant hypersensitivity syndrome. CASE SUMMARY: A 49-year-old white man presented to our institution with a two-day history of low-grade fever, erythema, and edema involving the periorbital area. Five days earlier, he had been placed on lamotrigine treatment for bipolar disorder. He inadvertently received four daily doses of lamotrigine 2700 mg each. physical examination was significant for periorbital edema and discrete and confluent blanching red macules and papules involving the face, trunk, and extremities. Laboratory tests revealed leukocytosis, hepatitis, and acute renal failure. With normalization of the laboratory results, the eruptions and edema gradually resolved. DISCUSSION: Lamotrigine toxicity can lead to periorbital edema, rash, and multiorgan system abnormalities. This presentation has clinical and laboratory similarities with anticonvulsant hypersensitivity syndrome, which suggests that at some threshold concentration the amount of lamotrigine may overwhelm the body's ability to metabolize the drug, leading to a similar hypersensitivity reaction. Lamotrigine is a relatively new agent, and this report may provide useful insights on evaluating the clinical toxicology of this agent. CONCLUSIONS: Healthcare providers should be aware that lamotrigine overdose may present with multiorgan involvement, similar to anticonvulsant hypersensitivity syndrome.
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2/44. Successful use of clopidogrel for cerebrovascular accident in a patient with suspected ticlopidine-induced hepatotoxicity.

    OBJECTIVE: To report a case of successful clopidogrel use in a patient who developed suspected ticlopidine-induced hepatotoxicity during therapy for a cerebrovascular accident. CASE REPORT: A 79-year-old white woman with a history of hypertension, type 2 diabetes, alzheimer disease, and coronary artery disease started receiving ticlopidine 250 mg twice daily three days after hospital admission for a cerebrovascular accident. Medications prior to admission included quinapril, furosemide, insulin, atorvastatin, conjugated estrogen, medroxyprogesterone, donepezil, and vitamin e. The estrogen, medroxyprogesterone, and donepezil were discontinued on admission. Laboratory tests on admission revealed that total bilirubin, alkaline phosphatase, and aspartate aminotransferase (AST) were within normal limits. On day 39 of hospitalization, laboratory tests showed marked increases in alkaline phosphatase, AST, alanine aminotransferase, gamma-glutamyl-transferase, and 5' nucleotidase. physical examination revealed no signs of jaundice or hepatomegaly, and laboratory tests for viral hepatitis were negative. A presumptive diagnosis of ticlopidine-induced hepatotoxicity was made and ticlopidine was discontinued. The following day, clopidogrel 75 mg/d was initiated. liver function tests returned to baseline over the following four months with ongoing clopidogrel therapy. DISCUSSION: ticlopidine-induced hepatotoxicity is well documented in the literature. In the present case, clopidogrel, a structurally similar thienopyridine, was substituted for ticlopidine following the development of presumptive ticlopidine-induced hepatotoxicity. serum liver enzyme concentrations returned to baseline with continued clopidogrel therapy, suggesting that clopidogrel is a suitable alternative in patients who develop ticlopidine-induced hepatotoxicity. CONCLUSIONS: Clopidogrel may be a suitable alternative for patients who develop ticlopidine-induced hepatotoxicity.
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3/44. Oxaprozin-induced symptomatic hepatotoxicity.

    OBJECTIVE: To describe a case of symptomatic hepatotoxicity attributed to oxaprozin use. CASE SUMMARY: A 41-year-old white woman was admitted to the hospital with malaise, anorexia, and right upper quadrant pain. The patient was found to have severe jaundice with liver enzyme elevation. Laboratory test results for potential etiologies were negative, except for the use of oxaprozin for the preceding six weeks. diagnosis of drug-induced hepatotoxicity was made by liver biopsy. The patient's symptoms resolved and liver enzymes normalized after oxaprozin was discontinued. DISCUSSION: Symptomatic hepatic effects attributable to most nonsteroidal antiinflammatory drugs (NSAIDs) are rare and usually mild. Oxaprozin has been shown to cause mild elevation of liver enzymes in clinical studies. This is the second reported case of presumed oxaprozin-induced icteric hepatitis. The mechanism of oxaprozin-induced hepatotoxicity is unclear, but is thought to be due to metabolic idiosyncrasy. Most NSAID reactions are hepatocellular and occur because of individual susceptibility (idiosyncrasy). In general, people aged >40 years and women are more predisposed to NSAID-induced liver injury. CONCLUSIONS: Although this toxicity is rare, clinicians should be aware of the potential for oxaprozin to cause hepatotoxicity and use caution when prescribing this medication. This case also stresses the importance of careful inquiry regarding drug or toxin exposure in cases of unexplained hepatitis.
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4/44. peliosis hepatis with intrahepatic hemorrhage: successful embolization of the hepatic artery.

    peliosis hepatis is defined as the appearance of blood filled lakes in the hepatic parenchyma. It has been associated with various pharmacological agents and infections. Treatment has been primarily symptomatic and includes discontinuation of offending medications, partial hepatectomy or occasionally liver transplantation. We report a 58 year old white female on hormone replacement therapy who developed symptomatic peliosis hepatis and underwent successful superselective hepatic artery embolization with control of bleeding.
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5/44. minocycline-induced pericardial effusion.

    OBJECTIVE: To describe a reversible hypersensitivity reaction characterized by pericardial effusion and acute mixed liver injury in a woman treated with minocycline. CASE SUMMARY: A 39-year-old white woman developed dyspnea and chest pain with pericardial effusion on echocardiography approximately 20 days after starting minocycline treatment. Additional manifestations consisted of eosinophilia and liver injury. No lung, skin, or joint involvement was noted; antinuclear antibody testing was negative. DiSCUSSION: minocycline has been associated with rare but severe hypersensitivity reactions and autoimmune disorders, generally involving the lungs, skin, or joints. We observed a patient with an unusual minocycline-induced reaction with pericardial effusion and acute mixed liver injury. The number of spontaneously reported cases in national and international databases indicates that minocycline-induced pericardial effusion is very rare as a main clinical manifestation. CONCLUSIONS: Clinicians should be aware of the possibility of pericardial effusion without lung, skin, or joint involvement as an adverse effect of minocycline.
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6/44. Cases from the Osler Medical Service at Johns Hopkins University.

    A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen.On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. urinalysis revealed an elevated specific gravity and numerous muddy granular casts. hepatitis a, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm.What is the diagnosis?
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7/44. Inflammatory pseudotumor of the liver: demographics, diagnosis, and the case for nonoperative management.

    BACKGROUND: Inflammatory pseudotumor of the liver (IPL) is an unusual tumor-like condition that is becoming recognized as an important differential diagnosis in the patient presenting with liver masses. This report describes six cases of IPL. STUDY DESIGN: Clinical, diagnostic, pathologic, and followup data were collected prospectively on six patients presenting to a specialist hepatobiliary unit. RESULTS: Six patients with IPL presented over a 2-year period. Median age was 35 years (range 2 to 79 years) and five patients were men. Three patients were Polynesian (Tongan and Samoan) and one was new zealand Maori. Five patients presented with nonspecific symptoms (fever, arthralgia, myalgia) and IPL was an incidental finding in one patient. At presentation, four patients had elevated white cell counts, and five patients had abnormal liver function tests with elevations in alkaline phosphotase and gamma-glutamyl transferase the most commonly seen. Carcinogenic embryonic antigen and alpha fetoprotein were normal in all patients, although one was a known hepatitis b carrier. In all cases of IPL, diagnosis was made on core biopsy of the liver lesions and all patients were managed nonoperatively with complete resolution of the tumors. Two patients had marked reduction in systemic symptoms (fever and pain) from a short course of oral steroids. CONCLUSIONS: IPL appears to be a relatively common problem in Maori and Polynesians. Recognition and differentiation of this condition from malignant liver lesions are important to avoid unnecessary surgery.
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8/44. Infected hepatic cyst.

    We describe an unusual case involving an infected hepatic cyst. An 88-year-old woman presented with acute onset of right upper quadrant abdominal pain, mild left lower abdominal pain, diarrhea, and fever. On admission, computed tomography revealed multiple hepatic cysts including an 8-cm cyst located in the left medial segment of the liver, which demonstrated a thickened wall enhanced with contrast media. ultrasonography showed an 8-cm hypoechoic lesion which differed in appearance from the other, anechoic hepatic cysts. The serum concentration of c-reactive protein was 29.8 mg/dL; white blood cell count, 12,800/microL; CA19-9, 96 U/mL; and CEA, 2.2 ng/mL. diagnosis of infected hepatic cyst was made by percutaneous transhepatic drainage of the cyst. Milky fluid was obtained and the patient's right upper quadrant abdominal pain resolved after drainage. The cyst fluid CA19-9 concentration was 18,000 U/mL. Cytology of the cyst fluid was negative. serum CA19-9 (41 U/mL) and CEA (1.8 ng/mL) concentrations were improved 1 week after drainage. escherichia coli was cultured from the drainage fluid. The patient was discharged 27 days after admission. Percutaneous transhepatic drainage is effective in the treatment of infected hepatic cysts.
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9/44. Infected solitary hepatic cyst.

    An unusual case involving an infected hepatic cyst in which the correct diagnosis was made without operation is reported. A 93-year-old woman presented with acute onset of right upper quadrant abdominal pain, mild left lower quadrant abdominal pain, diarrhea, and fever. On admission, computed tomography revealed a 15 cm solitary hepatic cyst in the anterior-superior segment of the liver with a thickened wall that enhanced with contrast media. ultrasonography demonstrated a 15 cm anechoic lesion with a hypoechoic area in the dependent portion of the cyst and a thickened wall. The serum concentration of c-reactive protein was 24.3 mg/dL, and the white blood cell count was 13,800/microL. A diagnosis of infected hepatic cyst was suspected, and percutaneous transhepatic drainage of the cyst was performed. Milky yellow fluid was obtained and the patient's right upper quadrant abdominal pain resolved after drainage. klebsiella pneumoniae was cultured from the drainage fluid. The patient was discharged 20 days after drainage. infection has not recurred and the hepatic cyst has not enlarged after 18 months.
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10/44. Focal hemorrhagic necrosis of the liver. A rare cause of hemoperitoneum.

    A 44-year-old white female developed hepatic hemorrhage due to focal hepatic necrosis. This is the only reported case of its kind we have found. No other underlying processes were identified except for the chronic use of oral conjugated estrogens. The possible role of steroids and a possible relationship to the pathogenesis of peliosis hepatis is discussed.
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