A unique presentation of acute liver failure from herpes simplex virus hepatitis

We present the case of a patient, with history of myelodysplastic syndrome and recent bone marrow transplant, who developed fulminant liver failure secondary to herpes simplex virus (HSV) hepatitis. His presentation was unique, as findings of liver microabscesses on computed tomography scan have not been described previously in this patient population. Despite initial treatment with acyclovir, he continued to deteriorate, and later sensitivities found the HSV strain to be resistant to acyclovir. HSV hepatitis with secondary liver failure is rare and, without appropriate treatment, its mortality is >80%. Early suspicion and immediate therapy are the keys to improve patient survival.     

Herpes simplex hepatitis after liver transplantation: case report and literature review

Herpes simplex virus (HSV) hepatitis is an uncommon cause of liver failure, but may have a dramatic outcome. We herein present a case report of a liver graft infection by HSV‐1 associated with liver failure and encephalitis. A complete hospital chart review of the case and a literature search were undertaken. Literature review suggests that herpes simplex acute liver failure is rare and associated with a poor prognosis, even with early treatment. Novel diagnostic and preventive approaches need to be instituted.     

Acute liver failure due to severe Herpes simplex viral hepatitis in an elderly woman: A case of initial infection

The high mortality rate due to severe Herpes simplex viral (HSV) hepatitis is associated with the difficulty of its diagnosis. We describe the extremely rapid disease course of a patient who died of severe HSV hepatitis. A 73‐year‐old woman was admitted for a bronchial asthma attack. Her symptoms improved with steroid treatment, but she developed a sore throat and painful swallowing. On day 12 after admission, she suddenly went into shock. Blood test results showed a significant increase in the liver enzyme levels, with remarkable disseminated intravascular coagulation. She died the same day. The autopsy revealed extensive coagulative necrosis of the liver. Viral inclusion of type A Cowdry bodies was found in the residual hepatocytes in the hepatic lobule. Immunostaining revealed HSV type 1 positivity. We diagnosed the cause of death as severe HSV hepatitis. On examination of a stored serum sample, the patient tested positive for the HSV immunoglobulin (Ig)‐M antibody, and the HSV RNA level was very high (1 × 10⁹ copies/mL). Remarkably, the HSV IgG test result was negative, and we diagnosed her as having had an initial HSV infection. Hepatitis due to HSV is very rare in healthy adults; however, there are many reports of immune‐deficient cases. The presence of HSV IgG is decreasing in the elderly population because of the change in living environments/lifestyles. The increasing use of immunosuppressive drugs, such as steroids, for treating diseases in elderly patients could be linked to the increased prevalence of initial HSV infections, resulting in liver injury.     

A case of acute liver failure due to hepatitis E virus,liver transplantation,and development of de novo autoimmune hepatitis

Acute hepatitis E virus (HEV) infection could lead to acute liver failure (ALF), which requires liver transplantation (LT). HEV infection could progress to chronic infection in an immunosuppressed host. De novo autoimmune hepatitis (AIH) is a rare occurrence of AIH during post‐LT immunosuppressive therapy in patients who underwent LT due to not AIH but some other etiology. Here, we report the first case of ALF due to HEV infection, the recurrence of HEV after LT that responded to ribavirin therapy, and then the development of de novo AIH showing a complete response to glucocorticoid therapy but multiple relapses after steroid withdrawal. This peculiar case suggests that HEV could have a pathogenic role in the development of the de novo AIH; additionally, this case report could help clinicians make therapeutic decisions in the post‐LT condition.     

Quantification of viral DNA and liver enzymes in plasma improves early diagnosis and management of herpes simplex virus hepatitis

Summary. Herpes simplex virus (HSV) hepatitis is a rare and potential life‐threatening disease. The diagnosis of HSV hepatitis is hampered by its indifferent clinical presentation, which necessitates confirmatory laboratory data to identify HSV in the affected liver. However, liver biopsies are often contraindicated in the context of coagulopathy, are prone to sampling errors and have low sensitivity in mild HSV hepatitis cases. There is an unmet need for less invasive diagnostic tools. The diagnostic and therapeutic value of HSV DNA load and liver enzyme level kinetics was determined in five patients with HSV hepatitis and twenty disease controls with HSV‐DNAemia without hepatitis. At time of hospitalization, patients with HSV hepatitis had a higher median (± interquartile range) HSV DNA load (6.0 × 10⁶ ±1.2 × 10⁹) compared to disease controls (171 ± 2845). Viral DNA load correlated with liver transaminase levels and disease severity. Antiviral treatment led to rapid decline of HSV DNA load and improvement of liver function of patients with HSV hepatitis. The data advocate the prompt and consecutive quantification of the HSV DNA load and liver enzyme levels in plasma of patients suspected of HSV hepatitis as well as those under antiviral treatment.     

Fatal herpes simplex virus type 2 hepatitis in a heart transplant recipient: a case report and review of the literature

Herpes simplex virus (HSV) hepatitis is often unrecognized clinically with most untreated cases diagnosed postmortem. HSV hepatitis has been reported in solid organ transplant (SOT) recipients, mostly in kidney and liver transplants, and rarely in heart transplant recipients. We describe a fatal case of community‐acquired HSV‐2 hepatitis in a 24‐year‐old heart transplant recipient occurring 3 years after transplant. We also review the literature summarizing HSV hepatitis and the potential role of quantitative HSV polymerase chain reaction monitoring in the SOT population.     

Donor-derived fulminant herpes simplex virus hepatitis after liver transplantation: Two cases and review of literature

Background

Fulminant herpetic hepatitis due to herpes simplex virus (HSV), serotype 1 or 2, is a rare but often fatal complication after solid organ transplantation (SOT). HSV hepatitis in SOT recipients can occur either due to primary infection acquired post transplantation, viral reactivation in a seropositive patient, or as donor-derived infection. Cases of fatal hepatitis have been reported in the liver as well as in other SOT recipients. The fatal outcome is mostly due to delayed diagnosis and treatment, which is explained by the lack of clinical specificity of HSV hepatitis.

Methods

We report two cases of fatal donor-derived HSV hepatitis in liver-transplanted recipients. We reviewed all published cases of donor-derived HSV infections after SOT with an evaluation of the presence of prophylaxis and outcome.

Results

In both liver recipients, the retrospective determination of HSV serostatus was negative, and both cases occurred in the absence of cytomegalovirus or HSV prophylaxis. A review of the literature showed a significant series of cases of severe hepatitis, mostly fatal, as well as the absence of specific preventive therapy guidelines in cases of HSV serology mismatch.

Conclusions

The occurrence of two fatal donor-derived hepatitis made the Swiss Transplant Infectious Diseases working group modify its national recommendations regarding pretransplant serostatus determination and HSV prophylaxis after liver transplantation. Further studies are needed to assess this approach.

     

Human genomics of acute liver failure due to hepatitis B virus infection: An exome sequencing study in liver transplant recipients

Acute liver failure (ALF) or fulminant hepatitis is a rare, yet severe outcome of infection with hepatitis B virus (HBV) that carries a high mortality rate. The occurrence of a life‐threatening condition upon infection with a prevalent virus in individuals without known risk factors is suggestive of pathogen‐specific immune dysregulation. In the absence of established differences in HBV virulence, we hypothesized that ALF upon primary infection with HBV could be due to rare deleterious variants in the human genome. To search for such variants, we performed exome sequencing in 21 previously healthy adults who required liver transplantation upon fulminant HBV infection and 172 controls that were positive for anti‐HBc and anti‐HBs but had no clinical history of jaundice or liver disease. After a series of hypothesis‐driven filtering steps, we searched for putatively pathogenic variants that were significantly associated with case‐control status. We did not find any causal variant or gene, a result that does not support the hypothesis of a shared monogenic basis for human susceptibility to HBV‐related ALF in adults. This study represents a first attempt at deciphering the human genetic contribution to the most severe clinical presentation of acute HBV infection in previously healthy individuals.     

Herpes simplex virus hepatitis after pediatric liver transplantation

T. Hori, Y. Ogura, S. Okamoto, A. Nakajima, K. Kami, J. Iwasaki, Y. Yonekawa, K. Ogawa, F. Oike, Y. Takada, H. Egawa, J.H. Nguyen, S. Uemoto. Herpes simplex virus hepatitis after pediatric liver transplantation
Transpl Infect Dis 2010: 12: 353–357. All rights reserved Abstract: Herpes simplex virus (HSV) hepatitis has a fatal impact on the outcome of organ transplanted recipients. Here, we present a thought‐provoking case of HSV hepatitis in a high‐risk recipient after living‐related liver transplantation (LRLT). A 1‐month‐old female newborn infant was affected by HSV encephalitis. Fulminant hepatic failure (FHF) of unknown etiology occurred suddenly at 4.4 years of age. Viral infections were ruled out as the cause of FHF. Intensive care including plasma exchange (PE) was started, and the preoperative treatments for ABO incompatibility were performed. Thereafter, LRLT was performed emergently. Although strong immunosuppression for ABO incompatibility was continued after LRLT, antibody‐mediated rejection (AMR) occurred on postoperative day (POD) 4. PE was repeated and improvements were obtained. However, liver dysfunction appeared on POD 8. Histopathological findings of liver needle biopsy clearly revealed HSV hepatitis, although the results of HSV DNA and antibody titer in blood sample did not clearly indicate HSV infection. On POD 21, thrombotic microangiopathy (TMA) occurred and the plasma and immunoglobulin were replenished. Our pediatric recipient recovered successfully from AMR, HSV hepatitis, TMA, and repeated sepsis. We conclude that well considered therapy based on the real‐time detection of HSV hepatitis is indispensable for the further improvements of outcome in HSV hepatitis after LRLT.     

慢性丙型肝炎并发甲状腺功能亢进导致肝衰竭1例报告

正1病例资料患者女性,50岁,因抗-HCV阳性11个月,尿黄7 d于2015年6月3日入院。既往23年前行剖宫产手术,有输血史。患者2014年7月体检发现抗-HCV阳性,HCV RNA 5.2×106IU/ml,肝功能正常,甲状腺功能四项示促甲状腺激素(thyroid stimulating hormone,TSH)稍低,余正常。给予聚乙二醇干扰素(PEG-IFN)α-2b 80μg/周联合利巴韦林900 mg/d抗     

Metronidazole-induced hepatotoxicity in a patient with xeroderma pigmentosum: A case report

Rationale:Whereas metronidazole-induced hepatotoxicity is quite rare in the general population, in individuals carrying a nucleotide excision repair disorder, namely Cockayne syndrome, there is a high risk of developing this complication.Patient concerns:We report the case of a 44-year-old man, affected by xeroderma pigmentosum, who was admitted to the hospital presenting aspiration pneumoniae caused by worsening dysphagia and with severe hepatotoxicity during the hospitalization.Diagnoses:Acute hepatitis, which was leading to acute liver failure, occurred during antibiotic treatment with metronidazole and ceftazidime with an elevation of liver enzymes consistent with hepatocellular damage pattern.Interventions:Hydration with glucose 5% solution, pantoprazole and vitamin K were administered, meanwhile other causes of hepatitis were ruled out and the ongoing antibiotic treatment was stopped suspecting a drug-induced liver injury.Outcomes:Liver function nearly completely recovered 1 month later with a first rapid improvement, within few days, of aminotransferases and coagulation studies, and slower of cholestatic enzymes.Lessons:We describe the first case available in the literature of hepatotoxicity associated with metronidazole treatment in a xeroderma pigmentosum patient. Clinicians therefore, based on this report and according to the possible underlying mechanism shared by other genetic diseases characterized by alterations in the pathway of DNA-repair, should consider such adverse event also in patients affected by this rare disease.     

Herpes simplex virus 2 hepatitis in a lung transplant recipient: a diagnostic challenge

Herpes simplex virus (HSV) hepatitis is a rare and serious complication in immunocompromised patients. We report the case of an HSV hepatitis occurring 4 years after lung transplantation in a cystic fibrosis patient. The presentation was nonspecific, mimicking acute cholecystitis; orogenital signs were absent. The diagnosis was made based on viral cultures performed during cholecystectomy and confirmed by blood quantitative polymerase chain reaction. Although the diagnosis and treatment were delayed, the patient fully recovered with acyclovir, reduced immunosuppression, and intravenous immunoglobulins. The diagnostic difficulties, prognostic factors, and treatments of this infection are discussed.     

严重慢性活动性EB病毒感染1例报告

正1病例资料患者男性,23岁,13年来肝功能反复异常,转氨酶轻度到中度升高,间断予以保肝治疗,转氨酶可降至正常,但仍反复,B超示肝肿大、巨脾,先后行两次肝穿刺活组织病理检查(图1a、b),病理报告慢性肝炎病因未明,予保肝治疗。2012年2月出现发作性意识不清,持续15 min至数小时,无口吐白沫、     

慢加急性肝衰竭合并呼吸道病毒感染伴咯血1例报告

正1病例资料患者男性,43岁,因"腹胀、乏力、厌油10 d"于2015年7月10日转入兰州大学第一医院。患者入院前无明显诱因出现腹胀、乏力、厌油,伴有尿黄,就诊于当地医院查肝功能示:HBsA g阳性、TBil 240.1μmol/L、DBil 170.9μmol/L、IBil 69.2μmol/L、ALT 1364 U/L、AST 860 U/L,给予复方甘草酸苷、腺苷     

Acute liver failure secondary to acute antibody mediated rejection after compatible liver transplant: A case report

BACKGROUNDThe liver has traditionally been regarded as resistant to antibody-mediated rejection (AMR). AMR in liver transplants is a field in its infancy compared to kidney and lung transplants. In our case we present a patient with alpha-1-antitrypsin disease who underwent ABO compatible liver transplant complicated by acute liver failure (ALF) with evidence of antibody mediated rejection on allograft biopsy and elevated serum donor-specific antibodies (DSA). This case highlights the need for further investigations and heightened awareness for timely diagnosis.CASE SUMMARYA 56 year-old woman with alpha-1-antitrypsin disease underwent ABO compatible liver transplant from a deceased donor. The recipient MELD at the time of transplant was 28. The flow cytometric crossmatches were noted to be positive for T and B lymphocytes. The patient had an uneventful recovery postoperatively. Starting on postoperative day 5 the patient developed fevers, elevated liver function tests, distributive shock, renal failure, and hepatic encephalopathy. She went into ALF with evidence of antibody mediated rejection with portal inflammation, bile duct injury, endothelitis, and extensive centrizonal necrosis, and C4d staining on allograft biopsy and elevated DSA. Despite various interventions including plasmapheresis and immunomodulating therapy, she continued to deteriorate. She was relisted and successfully underwent liver retransplantation.CONCLUSIONThis very rare case highlights AMR as the cause of ALF following liver transplant requiring retransplantation.     

Activation and evasion of innate antiviral immunity by herpes simplex virus

Herpes simplex virus (HSV), a human pathogenic virus, has evolved several strategies to evade the production and function of interferons (IFNs) and cytokines generated by the innate immune system to restrict the virus. Equilibrium exists between the virus and the immune response, and a shift in this delicate balance either restricts the virus or enhances virus spread and tissue damage. Therefore, understanding of the cytokine response generated after HSV infection and the underlying virus-cell interactions is essential to improve our understanding of viral pathogenesis. This review summarizes the current knowledge on induction and evasion of the innate immune response by HSV.