Acute liver failure due to white phosphorus ingestion

Background: White phosphorus is chemical compound available in military ammunition as well as in explosive powder of recreational use. This latter form is commonly found in Latin America and Asia as a main ingredient of gunpowder used to make street firecrackers. Small firecrackers may be ingested accidentally or used as a toxic agent in suicidal attempts which may cause of acute liver failure and death; however the clinical features, incidence and outcome are poorly described in the literature.Methods: We describe three cases of white phosphorus intoxication with acute liver failure secondary to the consumption of firecrackers. In two cases, ingestion occurred secondary to suicidal attempts and in one, ingestion occurred by accident. In one case, liver injury improved with supportive care, in the other, the patient required liver transplantation and the third case had a fatal outcome.Conclusions: Clinicians providing care of patients with acute hepatitis of unclear etiology should be aware that the ingestion of firecrackers containing white phosphorus might cause acute liver failure that may require liver transplantation.     

Acute liver failure following the use of ecstasy (MDMA)

The use of "ecstasy" (Methylenedioxymethamphetamine) as a recreational drug is increasing in europe since the 1980's. Aside intended psychological effects the use of ecstasy can be followed by symptoms of intoxication; complications include toxic hepatic damage up to acute hepatic failure. This case-report is about a 17-year old female patient who regularly used "ecstasy" over a six-month period. Two days after the last use of "ecstasy", she reported to her general practitioner with nausea, vomiting, abdominal pain and jaundice. Within 10 days the patient developed acute liver failure. With criteria for liver transplantation fulfilled she was listed for orthotopic liver transplantation of high urgency which was carried out only one day later. Histological examination of the explanted liver showed evidence for a toxic fulminant hepatitis. After transplantation the patient made a full recovery and was released from hospital on day 26 after transplantation. At the first control after six months the patient was in good physical and nutritional condition, serological parameters were normal and ultrasound examination of the transplanted liver was unremarkable. The ethiopathology of "ecstasy"-induced hepatotoxicity, which can occur dose-independently with a symptom-free period from days to weeks after ingestion is not yet fully understood. Possible mechanisms of hepatic damage include influence of MDMA on body temperature regulation, harmful effects of the substance or further components of the "ecstasy"-tablets on the liver cell or a genetic vulnerability of some individuals against amphetamines and amphetamine derivates. There are no parameters existing which could predict the course and severity of "ecstasy"-induced hepatopathy. Especially in young patients with symptoms of hepatic damage frequent controls of clinical status and relevant laboratory parameters are of great importance. Patient transfer to a specialised centre should follow as early as possible; at the latest, when coagulopathy occurs.     

Death following ingestion of MDMA (ecstasy) and moclobemide

Four deaths following the ingestion of moclobemide and MDMA ('ecstasy') are described. The probable cause of death in each case was serotonin syndrome as a result of an interaction between the two drugs. As none of the victims had been prescribed moclobemide it seems that each had taken the drug to enhance the effects of MDMA, with fatal consequences. Warnings are needed against misinformed attempts to potentiate the pharmacological effects of illicit drugs.     

Acute arsenic ingestion

A 21-year-old man presented in shock after ingesting 2 g of arsenic trioxide. He died within 37 hours despite intensive treatment that included intramuscular dimercaprol and hemodialysis. Hemodynamic and laboratory data are presented illustrating the multisystem toxicities of inorganic arsenic. Hemodialysis, previously described as an effective therapeutic adjunct, was shown to be ineffective in this case.     

207例急性胰腺炎合并肝功能损害的临床观察

目的研究急性胰腺炎（AP）合并肝功能损害的临床特点、发病机制及对预后的预测。方法对207例合并肝功能损害AP患者按照病因、严重程度、年龄分组。分别比较各组患者肝功能损害的严重程度、预后及转归，分析对AP严重程度预测灵敏度、特异度较显著的肝功能变化指标。结果重症急性胰腺炎（SAP）肝功能损害的严重程度明显高于轻症急性胰腺炎（MAP）（P〈0．05）。胆源性AP肝功能指标中ALT、ALP、LDH比非胆源性AP损害程度重（P〈0．05）；胆源性AP比非胆源性AP符合SAP人数、转手术率、死亡率均较高．住院天数较长。不同年龄AP患者肝功能损害的严重程度无显著差异（P〉0．05）。各肝功能指标中ALT、AST、LDH对AP严重程度预测灵敏度、特异度较显著。结论胆源性AP合并肝功能损害明显。ALT、AST、LDH等肝功能变化指标可作为对AP严重程度预测的参考指标。     

Acute thrombocytopenia following ingestion of indomethacin

A case of acute thrombocytopenia with shortened platelet survival following ingestion of indomethacin is reported. Drug history and absence of infection exclude both the role of other agents and an acute episode of idiopathic thrombocytopenia. The patient exhibited a poor response to immunosuppressive treatment and a slow resolution of the thrombocytopenia.     

Mechanisms of liver cell damage and repair.

Acute liver failure arises from an imbalance between liver cell death and regeneration. The severity of the insult determines whether liver cells die by apoptosis or necrosis, and this in turn affects the magnitude of the inflammatory reaction. Liver cell death occurs through complex cellular interactions and is mediated by immunological, inflammatory and chemical components. Regeneration of the liver cell mass also depends on cellular interactions, often involving those same mediators implicated in the injury itself. A greater understanding of these processes will lead ultimately to targeted rational therapy in acute liver failure.     

Acute fatty liver of pregnancy.

Acute fatty liver of pregnancy (AFLP) is a rare, potentially fatal complication that occurs in the third trimester or early postpartum period. Although the exact pathogenesis is unknown, this disease has been linked to an abnormality in fetal fatty acid metabolism. Early diagnosis of AFLP sometimes can be difficult because it shares features with other common conditions such as pre-eclampsia, viral hepatitis and cholestasis of pregnancy. However, a careful history and physical examination, in conjunction with compatible laboratory and imaging results, are often sufficient to make the diagnosis, and liver biopsy is rarely indicated. Supportive care and expeditious delivery are essential to optimal maternal-fetal outcomes and remain as the mainstay treatment for AFLP.     

Autoimmunity to a liver membrane lipoprotein and liver damage in alcoholic liver disease.

Antibodies reacting with a liver membrane lipoprotein (LSP) have been detected by radioimmunoassay in the sera of 15 (27%) of 55 patients with alcohol-related liver lesions. There was a close association between the presence of the anti-LSP antibody and the findings on liver biopsy of a lymphocytic infiltrate in the portal tracts together with piecemeal necrosis of periportal hepatocytes. These histological features are characteristically found in the autoimmune disorder of chronic active hepatitis, in which anti-LSP antibodies are almost invariably present. It is suggested that in these cases of alcoholic liver disease there is loss of tolerance, and continued production of anti-LSP could promote periportal inflammation and accelerate the progression to cirrhosis. In the cases of acute alcoholic hepatitis without periportal inflammation studied, anti-LSP was not detected demonstrating that production of this autoantibody is not simply secondary to liver damage.     

Acute tyrosine depletion and alcohol ingestion in healthy women

BACKGROUND: Recently we reported that, in vervet monkeys, ingestion of an amino acid mixture deficient in the catecholamine precursors, phenylalanine and tyrosine, produced a decrease in alcohol self-administration. We now report the results of a similar study in humans. METHODS: Three groups of healthy female social drinkers were administered a nutritionally balanced amino acid mixture (B, n = 13), a mixture deficient in the serotonin precursor, tryptophan (Trp-free, n = 14), or a phenylalanine/tyrosine deficient mixture (Phe/Tyr-free, n = 12). Six hours after administration of the amino acid mixture, alcohol ingestion was measured during a free-choice "Taste Test." RESULTS: Compared to the B mixture, Phe/Tyr-free, but not Trp-free, significantly decreased the ingestion of alcohol [p < 0.02]. Neither Phe/Tyr-free nor Trp-free significantly decreased orange juice ingestion or the self-reported "Liking" of either substance. Some subjects experienced transient nausea and/or regurgitated the amino acid mixtures, but excluding these subjects did not change the results. CONCLUSIONS: The results suggest that (a) Phe/Tyr-free may be a suitable method for investigating the role of catecholamines in the self-administration and subjective effects of alcohol, (b) acutely decreased catecholamine neurotransmission might disrupt mechanisms mediating alcohol self-administration, and (c) acutely decreased serotonin neurotransmission seems not to alter alcohol self-administration.     

Anicteric liver damage during nitrofurantoin medication.

Four patients are described in whom anicteric hepatitis appeared to be related to the use of nitrofurantoin. All the patients had increased serum transaminase levels, hypergammaglobulinaemia, and liver biopsies suggestive of chronic active hepatitis. Three patients showed cirrhotic features in the biopsy and two had circulating albumin-IgG-complexes ('tailing-albumin'). The serum transaminases became normal within weeks after withdrawal of the drug whereas the hypergammaglobulinaemia and the liver biopsy findings persisted essentially unchanged during two to six months of observation. One patient was re-challenged with nitrofurantoin, which resulted in recurrence of elevated serum transaminases after nine weeks medication.