Acute hepatic failure due to Plasmodium falciparum liver injury

Nine patients with acute liver failure due to Plasmodium falciparum liver injury admitted to the Rajgarhia Liver Unit of the All-India Institute of Medical Sciences during 1982-84 are presented. The liver was palpable in all the patients, and eight had splenomegaly. Investigations revealed mild to moderate abnormality in liver function tests. All were negative for the markers of acute infection due to hepatitis A and B viruses. Blood film examination showed P. falciparum alone in seven and along with P. vivax in the remaining two patients. Liver histology, which was identical in all eight patients where liver biopsy was done, showed centrizonal necrosis and hyperplastic Kupffer cells loaded with malarial pigment. All the patients recovered with specific anti-malarial and supportive treatment. Our observations suggest that malaria due to P. falciparum may present as jaundice and encephalopathy which stimulates acute hepatic failure due to fulminant hepatitis.     

Acute lung injury and acute respiratory distress syndrome in malaria

Malaria is an important treatable cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in the tropics and in the returning traveller in the non-endemic areas. ARDS is an important complication in severe, complicated falciparum malaria and has been described in P. vivax and P. ovale malaria also. Malarial ALI/ARDS is more common in adults than in children. Pregnant women and non-immune individuals are more prone to develop this condition. Increased alveolar capillary permeability resulting in intravascular fluid loss into the lungs appears to be the key pathophysiologic mechanism. In malaria, ARDS can develop either at initial presentation or after initiation of treatment when the parasitaemia is falling and the patient is improving. Patients present with acute onset dysnoea that can rapidly progress to respiratory failure. The diagnosis of malaria is confirmed by slide microscopy supported by the use of rapid antigen tests. Patients with malarial ARDS should be managed in an intensive care unit. Careful attention must be paid to haemodynamic stabilisation and optimising fluid balance. Currently, specific treatment choices for malaria include parenteral artemisinins or intravenous quinine along with doxycycline. Respiratory failure requires endotracheal intubation and assisted mechanical ventilation. Co-existent bacterial sepsis is frequently present in patients with malarial ARDS eventhough an obvious focus may not be evident. Appropriate broad spectrum antibiotic therapy must be started when there is a clinical suspicion after procuring the microbiological specimens. ARDS in malaria is a disease with a high mortality. Early diagnosis, institution of specific antimalarial treatment and assisted ventilation can be life-saving.     

The liver in heart failure

Severe congestive heart failure is associated with two distinct forms of liver dysfunction: jaundice that is related to passive congestion and acute hepatocellular necrosis that is caused by impaired perfusion. Cardiac cirrhosis (fibrosis) may result from prolonged recurrent congestive heart failure. Ischemic hepatitis (shock liver) usually manifests as asymptomatic elevation of the serum aminotransferase levels after an episode of hypotension, although the clinical presentation may mimic that of acute viral hepatitis. In most cases, ischemic hepatitis is of little clinical consequence and is self-limited. Acute liver failure may occur in patients with preexisting cirrhosis, severe chronic heart failure, or sustained hepatic ischemia.     

Fulminant Hepatic Failure in an African Setting: Etiology, Clinical Course, and Predictors of Mortality

This is prospective cross-sectional study on 37 patients presenting to different hospitals in Khartoum state, Sudan, sought to determine the etiology, clinical course, and predictors of mortality in patients presenting with fulminant hepatic failure (FHF). Patients were subclassified into hyperacute, acute, and subacute FHF; all sera were tested for hepatitis A, B, C, and E; negative samples were tested for antinuclear antibodies and anti-smooth muscle antibodies. The commonest etiologic factors included seronegative hepatitis (38%), hepatitis B virus (22%), severe Plasmodium falciparum malaria (8%), autoimmune hepatitis (8%), hepatitis E virus (5%), anti-tuberculous drugs (5%), and lymphomatous infiltration of the liver (5%). The mortality rate was high at 84%. Poor prognostic factors included presentation with grade III/IV encephalopathy, evidence of bacterial infection, and a prolonged prothrombin time of >25 seconds over the controls.     

Burden of cerebral malaria in central India (2004-2007)

A study on the clinicoepidemiology of cerebral malaria (CM) and mild malaria (MM) among adults and children attending NSCB medical college hospital Jabalpur and civil hospital Maihar, Satna, in central India was undertaken. Of 1,633 patients, 401 were Plasmodium falciparum and 18 P. vivax. Of 401, 199 CM patients and 112 MM patients were enrolled. Severe complications among CM patients were jaundice (26%), acute renal failure (22%), respiratory distress (22%), severe malaria anemia (18%), hypotension (17%), hepatic encephalopathy (7.0%), and hematuria (5%). Among CM cases, seizures and severe malaria anemia were significantly higher in children (P < 0.0001) compared with adults, whereas jaundice (P < 0.0025), acute renal failure (P < 0.0001), and hematuria (P 相似文献   

人微小病毒B19感染所致肝损害19例临床分析

目的探讨B19病毒感染所致肝损害的临床表现、实验室检查特点及治疗与转归。方法对人微小病毒B19感染患者19例的临床资料进行回顾性分析。结果在人微小病毒B19感染的19例患者,主要症状有乏力(12例)、黄疸(10例)、脾肿大(10例),伴有发热(10例)、皮疹(6例)及肌肉关节疼痛(6例),有6例伴有如下疾病或并发症:如妊娠(1例)、急性肝功能衰竭(2例)、精神分裂症(1例)、急性骨髓停滞(1例)和肺炎(1例)。以血清天门冬氨酸氨基转移梅(AST)升高为主,黄疸大多数表现为轻到中度,容易出现凝血酶原活动度(PTA)下降,但胆碱脂酶(CHE)下降不明显。经积极对症支持治疗,肝功能等各项指标正常后治愈出院。人微小病毒B19可致肝功能受损,导致急性肝炎或急性重型肝炎。结论对临床上非甲～戊型肝炎病人,应注意检查血清抗B19病毒IgM。该病毒感染是一个急性或亚急性过程,呈良性经过,有自愈倾向。     

Severe acute exacerbation of chronic hepatitis B: A unique presentation of a common disease

Severe acute exacerbation is a unique presentation of chronic hepatitis B characterized by very high alanine aminotransferase level accompanied by jaundice and hepatic decompensation. The underlying pathogenesis is likely related to excessive immune clearance, which may be related to the genotype of hepatitis B virus. The mortality is very high once hepatic encephalopathy develops, but some patients can recover to almost normal liver function in contrast to patients with end-stage liver cirrhosis. This condition should be differentiated from acute hepatitis B and other causes of acute hepatitis must be excluded. Conventional prognostic systems may not be applicable to severe acute exacerbation of chronic hepatitis B. In general, patients who have thrombocytopenia, hyperbilirubinemia and coagulopathy have a higher risk of mortality regardless of the serum alanine aminotransferase levels. There is no evidence that lamivudine treatment can reduce the short-term mortality of severe acute exacerbation. However, patients with severe acute exacerbation tend to have a higher rate of maintained virological response, higher rate of hepatitis B e antigen seroconversion and low rate of drug resistance on extended lamivudine treatment as compared to other chronic hepatitis B patients. Virological relapse and severe hepatitis reactivation is common after treatment cessation and therefore long-term antiviral treatment is recommended. Liver transplantation, particularly living donor liver transplantation, should be considered for patients who develop hepatic failure secondary to severe acute exacerbation.     

Blood Exchance — A Rescue Procedure for Complicated Falciparum Malaria

Falciparum malaria is the most hazardous form of malaria. Its high degree of parasitemia interferes with vital functions of most organs and is directly responsible for its high rate of mortality and morbidity. Quinine and other antimalarial drugs are relatively slow acting and not always effective due to the growing resistance developed by Plasmodium toward these drugs. Another emergency modality, which would remove the parasitic burden quickly and effectively, is thus much needed. We present a case of a 51-year-old sailor, who was admitted to the hospital because of complicated falciparum malaria. His situation deteriorated rapidly into a desparate stage, despite the various intensive treatments and quinine. He soon developed a systemic inflammatory response syndrome manifested as cerebral malaria, renal failure, acute respiratory distress syndrome and disseminated intravascular coagulation. An emergency blood exchange reversed the situation dramatically, and the patient recovered completely. It is recommended that any doctor, both in endemic and in non endemic areas, dealing with blood transfusions or infectious diseases, should be acquainted with this life-saving modality, regardless of the controversy still surrounding this subject.     

Hepatobiliary system in sickle cell disease

This paper reviews the literature reports concerning sickle cell disease and the hepatobiliary system. Sickle cell disease can cause progressive injury to the liver with significant fibrosis, often cirrhosis, and decreased liver function by adulthood. Asymptomatic patients commonly have hepatomegaly and elevated liver enzyme levels. The presence of sickle cell disease obscures features otherwise useful in differential diagnosis. Acute episodes of the disease selectively affect the liver in 10% of patients, causing hepatic crisis with abdominal pain, nausea, fever, jaundice, and transaminase elevation. Viral hepatitis is often clinically indistinguishable from hepatic crisis, but in viral hepatitis the abdominal pain is usually less, the jaundice tends to be more severe, and the transaminase elevation more prolonged. The two can be distinguished by serology and liver biopsy. Furthermore, acute cholecystitis or choledocholithiasis may have clinical and laboratory features similar to sickle cell hepatic crisis or viral hepatitis. By adulthood, 50%-70% of sickle cell patients have gallstones. Elective cholecystectomy is indicated for those who are symptomatic, but, because of operative mortality, there is disagreement concerning surgery for asymptomatic patients. The literature contains nine well-documented cases of acute hepatic failure related to sickle cell disease. The mechanism is unclear; however, as the necrosis is often not severe, a metabolic problem is suggested.     

Acute-on-chronic Liver Failure

Acute-on-chronic liver failure (ACLF) is a distinct entity that differs from acute liver failure and decompensated cirrhosis in timing, presence of treatable acute precipitant, and course of disease, with a potential for self-recovery. The core concept is acute deterioration of existing liver function in a patient of chronic liver disease with or without cirrhosis in response to an acute insult. The insult should be a hepatic one and presentation in the form of liver failure (jaundice, encephalopathy, coagulopathy, ascites) with or without extrahepatic organ failure in a defined time frame. ACLF is characterized by a state of deregulated inflammation. Initial cytokine burst presenting as SIRS, progression to CARS and associated immunoparalysis leads to sepsis and multi-organ failure. Early identification of the acute insult and mitigation of the same, use of nucleoside analogue in HBV-ACLF, steroid in severe alcoholic hepatitis, steroid in severe autoimmune hepatitis and/or bridging therapy lead to recovery, with a 90-day transplant-free survival rate of up to 50 %. First-week presentation is crucial concerning SIRS/sepsis, development, multiorgan failure and consideration of transplant. A protocol-based multi-disciplinary approach including critical care hepatology, early liver transplant before multi-organ involvement, or priority for organ allocation may improve the outcome. Presentation with extrahepatic organ involvement or inclusion of sepsis as an acute insult in definition restricts the therapy, i.e., liver transplant or bridging therapy, and needs serious consideration. Augmentation of regeneration, cell-based therapy, immunotherapy, and gut microbiota modulation are the emerging areas and need further research.     

A study on clinical profile of falciparum malaria in a tertiary care hospital in south India

Malaria continues to be a major problem in tropical countries. To study the clinical features and complications of malaria in a tertiary care hospital in south India, records of 183 patients were analysed. Among 86 patients with P. falciparum and mixed infection, 24 (28 per cent) had cerebral malaria and 32 (37 per cent) had hyperbilirubinemia. Twenty-three out of 32 (72 per cent) patients with jaundice had direct hyperbilirubinemia and elevated liver enzymes suggesting hepatocellular damage. Mortality of the order of 10 per cent was seen only in P. falciparum malaria. High incidence of hepatic involvement and hepatorenal failure were the unusual features observed in the study.     

Typhoid fever complicated by multiple organ involvement: report of two cases

Typhoid fever complicated by multiple organ involvement has been rarely mentioned in the literature. We reported two cases of typhoid fever with several unusual manifestations, including acute renal failure, acute hepatitis, acute pancreatitis, disseminated intravascular coagulation, and lower gastrointestinal bleeding. A renal biopsy in the first case showed no pathological change. Bone marrow biopsy showed focal necrosis of matrix, which might have been due to severe illness. A liver biopsy in the second case showed a predominantly histiocytic proliferation with occasional neutrophilic infiltration in the portal areas and hepatic sinusoids. Focal necrosis, bile duct injury, and multiple eosinophilic bodies were also noted. After appropriate antimicrobial therapy, both patients recovered without any sequelae. The potential of multiple organ involvement is highlighted in typhoid fever, which, on rare occasions, may occur simultaneously in the same patient.     

Acute liver damage and ecstasy ingestion.

Eight cases of ecstasy related acute liver damage referred to a specialised liver unit are described. Two patients presented after collapse within six hours of ecstasy ingestion with hyperthermia, hypotension, fitting, and subsequently disseminated intravascular coagulation with rhabdomyolysis together with biochemical evidence of severe hepatic damage. One patient recovered and the other with evidence of hyperacute liver failure was transplanted but subsequently died, histological examination showing widespread microvesicular fatty change. Four patients presented with acute liver failure without hyperthermia. All four fulfilled criteria for transplantation, one died before a donor organ became available, and two died within one month post-transplantation of overwhelming sepsis. Histological examination showed submassive lobular collapse. Two patients presented with abdominal pain and jaundice and recovered over a period of three weeks; histological examination showed a lobular hepatitis with cholestasis. Patients developing jaundice or with evidence of hepatic failure particularly encephalopathy and prolongation of the international normalised ratio, or both, whether or not preceded by hyperthermia, should be referred to a specialised liver unit as liver transplantation probably provides the only chance of recovery.     

Acute hepatic failure due to hepatosplenic B-cell non-Hodgkin's lymphoma in a patient infected with hepatitis C virus

We report a 75-year-old Japanese man infected with hepatitis C virus (HCV) who died of acute hepatic failure due to the hepatic infiltration of B-cell non-Hodgkin's lymphoma (NHL) cells. He suddenly developed jaundice, fatigue, fever, and hepatosplenomegaly during the course of chronic infection with HCV. Postmortem liver necropsy revealed extensive infiltration of lymphoma cells into the liver. Although the association between HCV infection and NHL has recently become a matter of concern, we believe this to be the first reported case of acute hepatic failure caused by hepatic involvement of non-Hodgkin's lymphoma in an HCV-infected patient. (Received Jan. 12, 1998; accepted June 26, 1998)     

Abnormal prothrombin in acute hepatic failure: the characterization and clinical evaluation

Abnormal prothrombin was detected by latex agglutination method in the plasma of the patients with acute hepatic failure (AHF) at significantly higher rate (82% of fulminant hepatitis and 100% of subacute hepatitis) than in acute hepatitis (33%). The concentration of abnormal prothrombin was also significantly higher in acute hepatic failure. Since the concentration of abnormal prothrombin reversely correlated with that of hepaplastin test or prothrombin time, the measurement of plasma abnormal prothrombin seemed to be useful in monitoring the severity of acute hepatic injury. Interestingly, enzyme immunoassay which is specific for des-gamma-carboxy prothrombin (PIVKA-II) could not detect abnormal prothrombin in acute hepatic failure. Furthermore, in crossed immune-electrophoresis, the abnormal prothrombin in AHF and that in disseminated intravascular coagulation syndrome showed similar mobility differing from PIVKA-II. These results suggest that abnormal prothrombin can be a useful marker for AHF. Further characterization of the abnormal prothrombin may shed light on the mechanisms of severe coagulopathy in AHF.     

Hypoxic hepatitis

Hypoxic hepatitis (HH), an acute liver injury also known as 'ischaemic hepatitis' or 'shock liver', is frequently observed in intensive care units. HH is heralded by a massive but transient rise in serum aminotransferase activities caused by anoxic necrosis of centrilobular liver cells. Cardiac failure, respiratory failure and toxic-septic shock are the main underlying conditions accounting for more than 90% of cases, but HH may also occur in other circumstances. Until recently, liver ischaemia, i.e. a drop in hepatic blood flow, was considered the leading, and even the sole, hemodynamic mechanism responsible for HH, and it was generally held that a shock state was required. In reality, other hemodynamic mechanisms of hypoxia, such as passive congestion of the liver, arterial hypoxaemia and dysoxia, play an important role while a shock state is observed in only 50% of cases. Accordingly, 'ischaemic hepatitis' and 'shock liver' are misnomers. Therapy of HH depends primarily on the nature of the underlying condition. The prognosis is poor, with more than half of patients dying during the hospital stay.     

Manifestaciones atípicas de la infección por el virus de la hepatitis A

Acute hepatitis due to the hepatitis A virus usually has a short, benign and self-limited course, without causing chronic hepatitis. However, some cases have an atypical presentation, such as relapsing hepatitis, prolonged or persistent cholestasis, fulminant hepatic failure, or liver failure associated with autoimmune hepatitis. The typical clinical course of acute hepatitis A virus infection is spontaneous remission in 90% of the cases, but atypical cases have a prevalence that varies from less than 1 to 20%, depending on the manifestation (overall prevalence ～7%). There is little information on the atypical clinical courses of hepatitis A virus infection and the lack of recognizing those presentations in clinical practice often results in carrying out numerous studies and treatments that not only are unnecessary, but can also be harmful. The aim of the present article was to describe 3 clinical cases of atypical hepatitis A infection and provide a literature review of such cases.     

Hepatobiliary dysfunction as the initial manifestation of disseminated cryptococcosis

A case of hepatobiliary dysfunction as the initial manifestation of disseminated cryptococcosis is described. The patient was admitted with symptoms of hepatitis with cholestatic jaundice. Antibody tests for hepatitis B and C and human immunodeficiency virus were negative. The patient continued to deteriorate clinically. Eventually, the patient succumbed to hepatic failure. Autopsy disclosed systemic cryptococcosis that caused extensive necrosis of the liver. In review of the literature, only nine cases of cryptococcal infection presenting as hepatitis, cholangitis, and cholecystitis as initial manifestation were reported. Four of these patients had been subjected to exploratory laparotomy for clinical suspicion of acute abdomen. One patient developed cirrhosis as a result of cryptococcal hepatitis. Two patients succumbed to hepatic failure. Cryptococcosis is known to occur commonly in immunocompromised patients, yet only two reported cases presenting as hepatitis were associated with immunocompromised status.     

Pediatric acute viral hepatitis with atypical variants: Clinical dilemmas and natural history

Classical acute viral hepatitis (AVH) has an uncomplicated outcome. Acute liver failure has a grave prognosis. Atypical manifestations of AVH are a group of disorders that causes significant morbidity and dilemmas in children. These include prolonged cholestasis, relapsing hepatitis, ascitic form of AVH, late-onset hepatic failure (LOHF), intravascular hemolysis, and provoking an autoimmune trigger leading to autoimmune hepatitis. These entities cause significant liver dysfunction or worsening and are often difficult to differentiate from chronic liver disease (CLD). Ascitic form of AVH, LOHF, decompensated CLD and acute-on-chronic liver failure have significant overlapping features that need to be carefully dissected out. In many cases, only on long-term follow-up, these clinical entities can be separately identified. Intravascular hemolysis is usually caused by associated glucose-6-phosphate dehydrogenase deficiency. Rarely CLD such as Wilson disease and autoimmune hepatitis can also present with hemolysis in the initial presentation, which can mimic AVH with hemolysis. Identifying deviations from typical manifestations aid in avoiding unnecessary investigations, allowing focused therapy and alleviating anxiety.