Cases reported "Liver Failure, Acute"

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1/5. Case of the month. Hepatic and renal failure in a patient taking troglitazone and metformin.

    Troglitazone is a thiazolidinedione with insulin-sensitizing activities when administered to humans or animals with type 2 diabetes mellitus. It has been shown to have numerous desirable metabolic effects on glucose and lipid metabolism. A major adverse effect of troglitazone is the development of hepatotoxicity. In early clinical trials, elevations of serum aminotransferases (> 3 times upper normal limit) occurred in 48 of 2510 (1.9%) subjects receiving troglitazone. In December 1997 and again in August 1998, the united states food and drug administration issued stronger warnings after getting reports of more than a hundred cases of liver damage, including liver failure requiring transplantation in three patients and death in another patient. Warner-Lambert Company announced on March 21, 2000 that it is voluntarily discontinuing the sale of Rezulin (troglitazone) tablets for the treatment of type 2 diabetes. Media reports sensationalizing the risks, associated with Rezulin therapy had created an environment in which patients and physicians were simply unable to make well-informed decisions regarding the safety and efficacy of Rezulin. Under these circumstances, and after discussions with the FDA, the company decided it was in the best interests of patients to discontinue marketing Rezulin. Concerns about the hepatotoxicity of troglitazone led the medicine Control Agency of the United Kingdom to request voluntary withdrawal of the drug from the UK in December 1997.
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2/5. Inappropriate pemoline therapy leading to acute liver failure and liver transplantation.

    A 36-year-old female, presenting with jaundice, developed acute liver failure requiring orthotopic liver transplantation. On admission, none of the known causative factors for acute hepatitis, including use of drugs, were found to be present. Several days after hospitalization, the patient admitted taking therapy prescribed by a "non-traditional" physician, that she had been using for several years due to overweight and which had recently been modified with the introduction of pemoline. A considerable body of evidence exists in the medical literature showing that pemoline, which is a central nervous system stimulant, has variable hepatotoxic effects, ranging from a mild transient increase of serum transaminases to liver failure, including some lethal cases.
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3/5. Acute hepatic sequestration in sickle cell disease.

    Sickle cell anemia is a disease that affects one out of every 600 african americans. It is often debilitating and can cause many physical restrictions to individuals with the disease. The disease has many complications which can be vexing for patients and their physicians. The hepatic complications attributed to vascular occlusion encompass a variety of clinical syndromes of which the relationship among clinical presentation, biochemical findings, and histologic features remains unclear. The conditions range from the self-limiting hepatic right upper quadrant syndrome (hepatic crisis) to the potentially lethal intrahepatic cholestasis and acute hepatic sequestration syndromes. Few cases have been documented, and there have not been many sizable studies on acute hepatic sequestration in sickle cell disease. This case is useful for clinicians who are not familiar with the intrahepatic vaso-occlusive syndromes in sickle cell disease. It provides insight into the presentation, diagnosis, and management of these syndromes.
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4/5. Living related liver transplantation for acute fulminant hepatitis B: experience from two possible hyper-acute cases.

    Fulminant hepatic failure, which is represented by fulminant hepatitis, is fatal in most cases unless prompt liver transplantation is performed. Even if liver transplantation is performed, irreversible neurological damage is often complicated. In this case report, we describe two cases of fulminant hepatitis induced by acute hepatitis b virus infection, both of which were successfully rescued by living related liver transplantation without significant complications. The case 1 was a 45-year-old Japanese male. He complained general malaise and anorexia. His local physician diagnosed him as acute hepatitis B, and referred to our hospital. Due to severe coagulopathy, plasma exchange was performed 3 times. However, his hepatic coma progressed rapidly along with rapid decrease of both his direct/indirect bilirubin (D/T) ratio and serum blood urea nitrogen (BUN) levels. Living related liver transplantation was performed under the diagnosis of acute fulminant hepatitis B. The case 2 was a 34-year-old Japanese male. His complaints were fever and skin rush. He was referred to our hospital under the diagnosis of acute hepatitis B. On the second day after admission, he developed grade II hepatic coma, which deteriorated into grade III in spite of intensive therapy including plasma exchange. He also demonstrated rapid decrease of both D/T ratio and serum BUN level. Living related liver transplantation was performed on the next day. Both cases recovered without any evidence of neurological sequelae. In general, it is extremely difficult to rescue fulminant hepatitis by conservative treatments, particularly in cases with rapid progression. Although emergency liver transplantation may be an only option to rescue in such a case, living related liver transplantation has an advantage in view of urgent organ donation over cadeveric transplantation.
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5/5. Acute liver failure due to iron overdose in an adult.

    The vast majority of acute iron toxicity cases occur in children less than 5 years of age. Moreover, clinical hepatic injury is uncommon with most symptoms stemming from the intestinal tract (eg, nausea, vomiting, diarrhea). Therefore, physicians, particularly those who do not routinely treat pediatric patients, are often unfamiliar with hepatotoxicity related to iron overdose. Nevertheless, hepatotoxicity caused by acute iron poisoning is associated with a high mortality rate. We report a case of severe hepatic injury in an adult who overdosed on iron tablets with suicidal intent. Tests for other hepatotoxins (eg, acetaminophen), hepatatrophic viruses, and other causes of acute liver injury were negative. Although peak serum iron level (340 microg/dL) was significantly lower than that reported to cause hepatotoxicity (>1,700 microg/dL), rapid and significant elevations in aminotransferases (>4,000 U/L), total bilirubin (5 mg/dL), and prothrombin time (50 seconds) occurred within 48 hours. Treatment with deferoxamine was prompt and followed by empiric N-acetylcysteine once liver injury was apparent. The patient was minimally symptomatic and she eventually had a full recovery.
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