Cases reported "Liver Failure, Acute"

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1/20. Hemophagocytic syndrome presenting as acute hepatic failure in two infants: clinical overlap with neonatal hemochromatosis.

    Two patients with hemophagocytic lymphohistiocytosis who presented with acute liver failure are reported. Both presented with fever, hepatosplenomegaly, markedly elevated liver function tests, abnormal coagulation profiles, and an increase in serum ferritin. Both infants were diagnosed with neonatal hemochromatosis based on a clinical picture of hepatic insufficiency with hyperferritinemia and were referred for liver transplantation. The first patient died of liver failure and septicemia before transplantation. review of autopsy material revealed a hepatitis-like pattern and extensive infiltration of liver and other organs including bone marrow by histiocytes, some of which were hemophagocytic. The second patient underwent liver transplantation but died 44 days thereafter from progressive hemophagocytic lymphohistiocytosis. Examination of the resected liver demonstrated a hepatitis-like pattern, proliferation of histiocytes, and hemophagocytosis, and the bone marrow revealed hemophagocytic histiocytosis. Hemophagocytosis recurred in the allograft. Hepatic manifestations are common in hemophagocytic lymphohistiocytosis and overt hepatic failure may occur, but initial presentation as fulminant hepatic failure is not well recognized. Elevated serum ferritin can make the distinction from neonatal hemochromatosis and other forms of neonatal liver failure difficult. Hemophagocytic lymphohistiocytosis should be considered in the differential diagnosis of neonatal liver disease, especially when it is accompanied by cytopenias.
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2/20. Potential hepatotoxicity of lamotrigine.

    Lamotrigine is a new antiepileptic drug that is effective for a broad range of seizures in adults and children. Three children with seizures of different causes who were treated with lamotrigine and developed reversible hepatotoxicity are reported. In one child, this therapy led to relatively severe hepatic failure that required and responded to aggressive therapy. Unlike most of the previously reported six patients with similar severe hepatic involvement, this patient's liver function and blood hepatic enzymes became normal. All three patients were on multiple drugs, and two were in epilepsia partialis continua secondary to encephalitis. Two of the patients had relatively rapid medication titration schedules. The close time relationship between the initiation of the lamotrigine therapy and the reversal of the liver abnormalities with lamotrigine discontinuation argues against a cause other than the lamotrigine; however, because of the complexity of the reported cases, the causality remains an assumption. review of the literature revealed six other previously reported patients (five adults and one child) who had hepatotoxicity during lamotrigine therapy, with or without associated multisystem failure, and similar patient profiles. Lamotrigine is generally a safe and effective medication; however, it should be used with caution in patients on polytherapy and in those with complicated acute systemic and central nervous system conditions, such as fever, status epilepticus, epilepsia partialis, and encephalitis.
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3/20. Usefulness of exchange transfusion in acute liver failure due to severe falciparum malaria.

    Acute hepatic failure is a rare and serious complication of severe falciparum malaria. The management of uncomplicated falciparum malaria comprises of specific antimalarial drugs and supportive therapy. In a few patients who are critically ill because of severe falciparum malaria and heavy parasitaemia, exchange transfusion has been used. We describe a young male Saudi patient who presented with a 2-day history of fever, jaundice, and confusion. On examination he was deeply jaundiced, confused, and irritable. There were no signs of chronic liver disease. His laboratory workup revealed a markedly raised direct hyperbilirubinaemia and transaminases with prolonged prothrombin time. His serology was negative for HbsAg, HBc IgM, anti-HCV, HAV IgM, HEV IgM, and IgG. He was initially treated with parenteral quinine and other supportive treatment, without any improvement of his clinical and laboratory parameters. At this stage he was treated with whole blood exchange transfusion. He slowly improved, with complete normalization of his liver function tests and prothrombin time.
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4/20. dengue infection with unusual manifestations: a case report.

    Since 1978, there has been an increasing number of reported cases of dengue infection with unusual manifestations and most of them had dengue shock syndrome. We report here one patient who had dengue hemorrhagic fever grade II with liver failure and hepatic encephalopathy and very high elevation of liver enzymes. She made a complete recovery after conservative therapy. She is the fourth case of reported dengue hemorrhagic fever grade II who had unusual manifestation.
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5/20. Interstitial nephritis, hepatic failure, and systemic eosinophilia after minocycline treatment.

    This report describes a 15-year-old white boy who presented with fever, back pain, a disseminated exanthematous rash, renal failure, and hepatopathy 3 weeks after the initiation of oral minocycline therapy for facial acne. Marked peripheral and urine eosinophilia were noted. A bone marrow aspiration showed more than 50% eosinophils without any evidence of malignancy, and a simultaneous kidney biopsy showed acute interstitial nephritis (AIN). The patient's symptoms and laboratory findings improved after high-dose steroid therapy was initiated, worsened when it was withheld, and improved again after it was reinitiated in view of the biopsy findings. The patient recovered completely, and steroids were tapered to discontinuation over 3 months. Over a year later, the patient's peripheral blood mononuclear cells (PBMCs) were cultured for 2 weeks in the presence or absence of minocycline ex vivo, and minocycline was found to induce the emergence of CD4( ) cells after 1 week in culture. In conclusion, this article shows for the first time several new aspects of minocycline-induced morbidity: renal and hepatic failure can occur together, and AIN and elevated blood eosinophil counts can be accompanied by marked bone marrow eosinophilia, suggesting a systemic allergic response as the underlying pathomechanism. Furthermore, the initial phase of such a response appears to involve CD4( ) T cells detectable ex vivo. Lastly, high-dose treatment with corticosteroids appears to be beneficial in this setting.
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6/20. Tolterodine-associated acute mixed liver injury.

    OBJECTIVE: To report a patient with an acute mixed liver injury associated with tolterodine therapy. CASE SUMMARY: An 81-year-old white woman with urge incontinence experienced malaise, fever, and gastrointestinal disturbances 18 days after starting tolterodine 2 mg twice daily. The patient's concurrent medications included flunitrazepam, diclofenac, and dorzolamide/timolol eye drops. Laboratory examination was consistent with the presentation of an acute mixed liver injury with increased transaminase enzymes, alkaline phosphatase, gamma-glutamyltransferase, and bilirubin. Additionally, she had mild leukocytosis with eosinophilia. After tolterodine was discontinued, the abnormal liver and hematologic parameters returned to normal within 4 weeks. DISCUSSION: Tolterodine, a muscarinic receptor antagonist, has predominantly anticholinergic effects. To our knowledge, this is the first case published describing tolterodine-associated acute mixed liver injury. However, some of the patient's additional symptoms can also be considered part of a drug-induced hypersensitivity syndrome. This is usually defined by the triad of fever, cutaneous reaction, and involvement of internal organs, mainly affecting the liver. The close temporal relationship between the start of tolterodine therapy and the first symptoms and the reversibility after dechallenge led us to conclude that the adverse reaction was possibly related to tolterodine exposure. CONCLUSIONS: Our case illustrates that tolterodine may rarely be associated with liver injury. This may have been an organ manifestation of tolterodine-induced hypersensitivity syndrome.
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7/20. liver failure in adult Still's disease during corticosteroid treatment.

    adult Still's disease is a well-characterized rheumatic disorder of unknown origin, which may affect multiple organs and may have a fatal course. However, liver failure has rarely been described in adult Still's disease. We present the case of a 25-year-old woman who was admitted with acute liver failure 2 years after the start of symptoms (arthritis, fever, sore throat) of a yet undefined rheumatic disease. She had been treated with prednisolone for 2 months before admission. The diagnosis of adult Still's disease was made in accordance with well-established criteria. Other causes of liver failure were excluded. Withdrawal of prednisolone did not affect the course of liver disease. ursodeoxycholic acid therapy was started when the patient slowly began to recover. To the best of our knowledge, this is the first case of adult Still's disease reported in which hepatic failure developed when other symptoms were well controlled by corticosteroid treatment.
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8/20. Case report of the first severe acute respiratory syndrome patient in china: successful application of extracorporeal liver support mars therapy in multiorgan failure possibly induced by severe acute respiratory syndrome.

    A previously healthy patient was transferred to our infectious department with a 9-day-history of continued fever. The patient was placed on assisted respiration support in addition to anti-viral medication. The diagnosis of SARS (severe acute respiratory syndrome) was made in view of the severe hypoxemia and the characteristic symptoms exhibited by the patient. Despite the best intensive therapy, he clinically deteriorated into multiorgan dysfunction syndrome (MODS) including additional dysfunction of kidney, liver, and heart. We initiated mars therapy (extracorporeal liver support utilizing albumin dialysis) with intention to positively influence the organ functions in his MODS on the basis of recently published studies which suggested a positive impact of mars in multiorgan failure secondary to respiratory illnesses and the possible influence on inflammatory mediators and cytokines. The application of 4 intermittent mars treatments (8 h each, mean blood flow rate 180 ml/min) on 4 consecutive days resulted in an immediate improvement of clinical conditions within the treatment days. The further improvement of organ functions allowed withdrawing the patient from ventilatory support 13 days after start of mars, and 44 days after admission he was discharged home with completely resolved organ functions and laboratory abnormalities. SARS is a severe form of the epidemic outbreak of atypical pneumonia which remains poorly defined regarding etiology and special therapy recommendations. However, the development and aggravation of this ARDS-like severe acute respiratory syndrome is pathologically associated with the systemic inflammatory response syndrome (SIRS) which may then mediate or cause MODS. To our knowledge, this is the first report of an application of mars therapy in MODS which was probably induced by SARS in a patient in china which improved the clinical condition of the patient in multi-organ failure secondary to respiratory failure indicating that mars might be an additional therapeutic option in multiorgan failure induced by SARS.
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9/20. Hepatic lymphoma metastasis presenting with severe acute liver failure: a rare case.

    Hepatic lymphoma metastasis is rare, and should always be considered in the differential diagnosis of hepatic malignancy. A 52-year-old man presented with a four-day history of fever, fatigue, yellowish skin and nausea. His past medical history was unremarkable. There was no history of alcohol intake or medications. His physical examination revealed generalized jaundice and hepatomegaly. His blood tests showed liver failure and coagulopathy. Abdominal ultrasonography illustrated hepatomegaly. A further work-up included bone marrow and liver biopsy. The pathology report was B-cell lymphoma. He was treated with chemotherapy, and his laboratory findings during follow-up showed steady improvement. In conclusion, lymphoma metastasis to liver can be a cause of liver dysfunction. A high index of suspicion is required for the diagnosis. We emphasize the importance of obtaining tissue sample in all patients with suspicious lesion in any organ to avoid missing the rare but curable pathologies.
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10/20. 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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