Cases reported "Liver Failure"

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11/483. amoxicillin/clavulanate-associated hepatic failure with progression to stevens-johnson syndrome.

    OBJECTIVE: To describe a patient who developed hepatic failure, stevens-johnson syndrome (SJS), and died after receiving amoxicillin/clavulanate therapy. CASE SUMMARY: A 37-year-old white man without significant past medical history received a 10-day course of amoxicillin/clavulanate for treatment of pneumonia. Thirty-two days after starting amoxicillin/clavulanate, he developed jaundice, rash, pruritus, and increasing fatigue. On further evaluation, with the exclusion of toxicity from other drugs or diseases, the time course to development of cholestatic jaundice correlated with the use of amoxicillin/clavulanate. The patient consequently died with progressive hepatic failure, renal failure, and SJS. DISCUSSION: Hepatic injury has been reported with amoxicillin/clavulanate. signs and symptoms of jaundice and pruritus may appear up to to six weeks after stopping therapy. Most cases of liver injury have been benign and reversible on discontinuation of the amoxicillin/clavulanate. Reported hepatic reactions have been mainly cholestatic, with some mixed cholestatic/hepatocellular liver function test abnormalities. CONCLUSIONS: Clinicians should be aware of amoxicillin/clavulanate as a drug capable of causing hepatitis with eventual systemic dysfunction. While recovery is usually complete following withdrawal of the drug, in patients with rash associated with hepatic dysfunction, renal insufficiency, or other unusual symptoms, earlier consideration of initiating systemic steroids or liver transplantation referral, in hopes of avoiding progressive systemic response, might be worthwhile.
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ranking = 1
keywords = hepatitis, b
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12/483. Severe multisystemic hypersensitivity reaction to carbamazepine including dyserythropoietic anemia.

    OBJECTIVE: To report a case of multisystemic hypersensitivity reaction to carbamazepine. CASE SUMMARY: An 81-year-old white man was admitted to our hospital because of fever, morbilliform pruritic rash, and jaundice. Fifty days before admission he had taken carbamazepine 200 mg p.o. tid because of seizures. During the first few days following admission, a maculopapular rash progressed to generalized erythroderma with subsequent extensive skin exfoliation. After discontinuing carbamazepine the fever disappeared within 72 hours and hepatic function tests returned to normal within four days. Moreover, after admission the hemoglobin values gradually fell to 6.7 g/100 mL. A bone marrow aspirate showed hypercellularity with marked dyserythropoietic abnormalities, and the bone marrow biopsy showed large and diffused infiltration due to the presence of a low-grade small lymphocytic lymphoma. No specific therapy for the lymphoma was undertaken. The biochemical follow-up showed a total improvement of hemoglobin values. Eight months after drug discontinuation, the patient was asymptomatic; peripheral blood cell count and hemoglobin concentrations were persistently normal. DISCUSSION: To the best of our knowledge, this is the first published case report implicating carbamazepine as the cause of anemia associated with bone marrow hypercellularity and dyserythropoietic changes, instead of hypocellularity and reduction of erythroid precursors. An interesting point raised by our observation is the possible relation between carbamazepine intake and actual lymphoproliferative disease. The development of non-Hodgkin's lymphoma following carbamazepine treatment has been reported, with regression after the drug was discontinued. However, in our case, a bone marrow biopsy repeated eight months after drug discontinuation confirmed the diagnosis of low-grade lymphoma. CONCLUSIONS: This case report describes a severe multisystemic reaction, characterized by generalized erythroderma; and renal, hepatic, and bone marrow failure in a patient who started carbamazepine therapy 50 days beforehand.
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ranking = 0.015276698474685
keywords = b
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13/483. hepatitis a-induced diabetes mellitus, acute renal failure, and liver failure.

    A 38-year-old otherwise healthy man presented with hepatic failure (aspartate aminotransferase of 7212 U/L, alanine aminotransferase of 6629 U/L, total and direct bilirubin of 10.7 mg/dL) and acute renal failure (creatinine of 11.6 mg/dL and blood urea nitrogen of 42 mg/dL), which required hemodialysis when the creatinine increased to 21 mg/dL, with a blood urea nitrogen of 115 mg/dL, and the patient became oliguric. On admission, this patient also had a lipase of 1833 U/L, amylase of 211 U/L, glucose of 210 mg/dL, and reactive IgM antibody for acute hepatitis a. The hepatitis and acute renal failure resolved in 3 months, but this patient continues to have type II diabetes mellitus 7 years after the hepatitis a infection. This case illustrates that hepatitis a infection may be severe with liver failure, acute renal failure, and permanent diabetes mellitus as sequale of this infection.
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ranking = 3.9898155343502
keywords = hepatitis, b
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14/483. Macromastia in a newborn with alagille syndrome.

    We present a case of macromastia in a newborn with alagille syndrome. A review of the literature failed to find any prior reports of this findings in alagille syndrome patients. We propose that this patient's macromastia may be related to her liver failure and abnormal estrogen metabolism.
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ranking = 0.0031336817383969
keywords = b
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15/483. peliosis hepatis with initial presentation as acute hepatic failure and intraperitoneal hemorrhage in children.

    peliosis hepatis, a condition characterized by the presence of blood-filled lacunar spaces in the liver, usually has a chronic presentation pattern and is mainly reported in adult patients in association with chronic wasting disorders and after administration of various drugs. The present report concerns two previously healthy young children in whom peliosis hepatis initially presented as acute hepatic failure and who had escherichia coli pyelonephritis. Both patients had active intraperitoneal hemorrhage from the peliotic liver lesions, and liver ultrasonography showed multiple hypoechoic areas of different sizes, which in this context should suggest the diagnosis. One child died from hypovolemic shock and the other recovered. This study indicates that acute peliosis hepatis can be a serious life-threatening disease in children.
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ranking = 0.0011751306518988
keywords = b
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16/483. cocaine-associated rhabdomyolysis and excited delirium: different stages of the same syndrome.

    Previous case reports indicate that cocaine-associated rhabdomyolysis and excited delirium share many similar features, suggesting that they may be different stages of the same syndrome. We tested this hypothesis by comparing data from 150 cases of cocaine-associated rhabdomyolysis reported in the medical literature with data from an autopsy registry for 58 victims of fatal excited delirium and 125 victims of fatal acute cocaine toxicity. patients with rhabdomyolysis are similar to victims of fatal excited delirium with regard to age; gender; race; route of cocaine administration; the experiencing of excitement, delirium, and hyperthermia; and the absence of seizures. Compared with victims of fatal acute cocaine toxicity, patients with rhabdomyolysis are different with regard to each of these variables. Compared with victims of fatal acute cocaine toxicity, both victims of rhabdomyolysis and fatal excited delirium are more likely to be black, male, and younger; to have administered cocaine by smoking or injection; and to have experienced excitement, delirium, and hyperthermia; they are also less likely to have had seizures. Because cocaine-associated rhabdomyolysis and excited delirium have similar clinical features and risk factors, occur in similar populations of drug users, and can be explained by the same pathophysiologic processes, we conclude that they are different stages of the same syndrome. It appears that this syndrome is caused by changes in dopamine processing induced by chronic and intense use of cocaine rather than by the acute toxic effects of the drug.
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ranking = 0.0090093349978911
keywords = b
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17/483. Erythropoietic protoporphyria with fatal liver failure.

    A 33-year-old woman with a history of photosensitivity, persistent abdominal pain, and liver dysfunction was admitted to our department because of abdominal pain and progression of liver dysfunction. On admission, levels of protoporphyrin and coproporphyrin within erythrocytes were markedly increased. Autofluorescent erythrocytes were also detected, leading to a diagnosis of erythropoietic protoporphyria. A liver biopsy specimen revealed cirrhosis with dark brown granules filling hepatocytes, bile canaliculi, and bile ductules. Transfusion of washed erythrocytes, hemodialysis, and administration of cholestyramine and beta-carotene transiently improved levels of porphyrins and liver function. The patient died of rupture of esophageal varices followed by multiple organ failure. However, the treatments were believed to have extended survival.
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ranking = 0.0039171021729961
keywords = b
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18/483. Bromfenac (Duract)-associated hepatic failure requiring liver transplantation.

    Bromfenac sodium (Duract) is a phenylacetic acid-derived nonsteroidal anti-inflammatory agent introduced in the united states in 1997 and withdrawn in 1998. We describe the first case of fulminant hepatic failure associated with this agent treated successfully with liver transplantation. Similarities to hepatotoxicity with related agents is discussed.
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ranking = 0.00039171021729961
keywords = b
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19/483. Toxic epidermal necrolysis and graft vs. host disease: a clinical spectrum but a diagnostic dilemma.

    We describe a 53-year-old man who developed partial and full thickness skin loss associated with pyrexia, diarrhoea, liver, renal and bone marrow failure, during treatment for an aggressive B cell lymphoblastic lymphoma. The clinical features and histology were compatible with both toxic epidermal necrolysis and graft vs. host disease, causing a diagnostic and therapeutic dilemma. We discuss the possibility that methotrexate was the causative drug, with review of its cutaneous side-effects. Histologically our patient demonstrated the sparse dermal infiltrate with full thickness epidermal necrosis typical of toxic epidermal necrolysis and graft vs. host disease. We discuss this finding with respect to the pathogenesis of toxic epidermal necrolysis.
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ranking = 0.0039171021729961
keywords = b
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20/483. poisoning by amanita phalloides ("deathcap") mushrooms in the Australian Capital Territory.

    amanita phalloides ("deathcap") mushrooms are widespread in south-eastern Australia. Seven patients presented to hospital in the australian capital territory with poisoning by this mushroom between 1988 and 1998. Three developed hepatoxicity and one died. Because A. phalloides is becoming more widespread, increased community and medical awareness is needed to reduce the frequency and morbidity of poisoning.
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ranking = 0.0031336817383969
keywords = b
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