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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.

Hepatitis-associated aplastic anemia is a well-recognized clinical syndrome in which marrow failure follows the development of hepatitis. Although aplastic anemia is intimately related to paroxysmal nocturnal hemoglobinuria, until now, no cases of PNH-associated hepatitis have been described. We report a case of recurrent acute hepatitis preceding the clinical onset of PNH. Treatment of PNH with the complement inhibitor eculizumab (Soliris®) prevented both recurrences of episodes of intravascular hemolysis and liver enzyme alteration. This is the first known published case of PNH-associated hepatitis.

Objective: To compare Masson's trichrome (MT), Sirius red (SR) and orcein staining in acute hepatitis (AH) and to correlate them with transient elastography (TE), a noninvasive method to assess hepatic fibrosis. Methods: We evaluated liver stiffness by TE in a cohort of 34 consecutive patients and assessed MT-, SR- and orcein-stained biopsies using the METAVIR scoring system and digital image analysis (DIA). Results: MT and SR both showed severe fibrosis (stage III-IV, DIA = 12.7%). Orcein showed absent or mild fibrosis (stage 0-II, DIA = 4.4%; p < 0.05). In 29/34 cases (85%), stiffness values were >12.5 kPa, in keeping with SR/MT but not with orcein results. Conclusions: Even though in AH true elastic fibrosis is typically absent or mild, TE shows elevated stiffness values, in keeping with SR/MT evaluations. If not properly evaluated in the clinical context, these results would lead to an overestimation of fibrosis. Orcein is the only staining able to evidence the absence of true elastic fibrosis, which is a typical feature of AH. This is the first study comparing different staining procedures performed on AH biopsies by DIA versus TE.

It is increasingly clear that a tailored therapeutic approach to patients with hepatitis C virus infection is needed. Success rates in difficult to treat and low-responsive hepatitis C virus patients are not completely satisfactory, and there is the need to optimise treatment duration and intensity in patients with the highest likelihood of response. In addition, the management of special patient categories originally excluded from phase III registration trials needs to be critically re-evaluated. This article reports the recommendations for the treatment of hepatitis C virus infection on an individual basis, drafted by experts of three scientific societies.

BACKGROUND: Acute viral hepatitis due to hepatitis A virus is a self-limited illness that infrequently has a severe clinical course. METHODS: We analyzed the virological characteristics of acute hepatitis A in a patient with a severe clinical presentation (peak total and conjugated bilirubin levels, 65.5 mg/dL and 40.1 mg/dL, respectively) and a course of disease that lasted 7 months. RESULTS: Hepatitis A virus sequencing revealed coinfection with 2 subgenotypes of hepatitis A virus (Ia and Ib) as etiological factors of the illness. CONCLUSIONS: Hepatitis A virus Ia and Ib coinfection may have accounted for the prolonged and severe course of illness.

Background: Despite the availability of effective vaccines, hepatitis B virus (HBV) infection is still frequent worldwide, and accounts for significant morbidity and mortality. However, data of acute HBeAg negative hepatitis still remain limited. Aims and Methods: To understand clinical pictures of acute HBV hepatitis and its natural evolution, a prospective study was conducted in adult patients. Results: Ninety patients were enrolled between March 2004 and April 2005 at Hospital for Tropical Diseases in Ho Chi Minh city. The prevalence of HBeAg negative was 53%. No significant difference was found in clinical characteristics and laboratory findings between HBeAg positive and negative patients. HBV-DNA was detected in 75% and 88% HBe negative and positive patients, respectively, where the frequency of ALT below 400 U/L was significantly higher in HBeAg negative cases (p = 0.01). Six month follow-up was available in 47 patients. HBsAg positivity was found in 16% of HBeAg negative subjects but only in 4.5% of HBeAg positive cases. Thirty two patients had neither HBsAg nor anti-HBs. Conclusions: The clinical and laboratory feature and the outcome at 6 months of HBV acute hepatitis in Vietnam is similar in HBeAg positive and negative patients.

The incidence of acute and chronic liver damage and its relation to hepatitis B virus (HBV) infection was evaluated in 164 consecutive children with acute leukemia seen in ten Italian hemato-pediatric units. Thirteen out of 164 children (7.9%) had acute hepatitis (AH) during treatment, while 8/90 (8.8%) showed an acute exacerbation of liver damage within 6 months after therapy withdrawal. Seven of the 13 children with AH while on therapy were HBsAg positive. In 12/13 cases, liver disease progressed to chronicity. Five of eight children who developed AH after completion of treatment were HBsAg positive. Eighty-nine patients (54.2%) developed biochemical evidence of chronic hepatitis during therapy; 48/89 were followed after cessation of treatment and 33 of them showed persisting evidence of liver cell necrosis. Thirty-three out of 133 children (24.8%) tested for serum HBsAg were found positive: 26 (78.7%) of them developed chronic hepatitis. Sixty-four out of 133 patients were evaluated after cessation of treatment: Chronic hepatitis persisted in 16/22 HBsAg-positive (72.7%) and in 17/42 HBsAg-negative (40.4%) children during follow-up. The outcome of these liver diseases after treatment withdrawal did not differ significantly in relation to HBV serology, suggesting that viral rather than toxic agents were responsible for liver damage also in most HBsAg-negative patients. The high incidence of chronic HBV infection in children with leukemia found in this multicentric study could suggest a need for active immunization with HBV vaccine, but the efficacy of such approach in this clinical setting is still to be validated.

The excretion of urinaryd-glucaric acid (d-GA), one of the final metabolites of glucuronic acid was determined in 49 patients with acute hepatitis. A 3.7-fold increase ofd-GA was found at an early stage of the disease (37.13 μmol/24hr±3.08se vs 9.91 μmol/24hr±1.18se in normal controls), when serum transaminases and bilirubin were very high (SGOT 589 I.U.±41se; SGPT 954 I.U.±61se; serum bilirubin 8.41 mg/100 ml±0.76se). A lower but significantly elevatedd-GA excretion was also found in the recovery phase of hepatitis at a time when both serum transaminases and bilirubin were considerably reduced (SGOT 89 I.U.±14se; SGPT 185 I.U.±30se; serum bilirubin 1.05 mg/100 ml±0.20se). Urinary glucuronides and free glucuronic acid, measured as total glucuronic acid, were also significantly increased in early hepatitis (1164 mg/24hr±54se vs 782 mg/24hr±84se in normal subjects), but no correlation was found withd-GA excretion. A short treatment with phenobarbital which led to a 3-fold increase ofd-glucaric acid in 12 normal subjects did not cause any further change in the patients with early acute hepatitis. While the mechanism of the urinaryd-GA increase in hepatitis still remains underfined, the findings of this study support the conclusion that its increase may not reflect an induction of liver microsomal enzymes.