Recurrence of autoimmune liver disease in allografts has long been a topic of debate. We conducted a systematic review of the literature to examine the reported incidence of recurrence after liver transplantation of primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH). The MEDLINE, EMBASE, and Cochrane electronic databases were used to identify articles. The inclusion criteria used were articles on patients with at least 90 days of posttransplantation follow-up, histologic criteria for diagnosis of PBC and AIH recurrence, radiologic or histologic criteria or both for diagnosis of PSC recurrence, and exclusion of other causes of liver disease causing similar histologic findings. Incidence in individual studies was combined to calculate the overall recurrence. Risk factors were analyzed whenever crude data were available. Funnel plots were used to assess publication bias. Out of 90 articles identified, 43 met criteria for systematic review (PBC, 16; PSC, 14; AIH, 13). The calculated weighted recurrence rate was 18% for PBC, 11% for PSC, and 22% for AIH. No difference was found in PBC and AIH recurrence by type of primary immunosuppression. There were not enough data to assess this issue in PSC studies. There was evidence of publication bias among PSC and AIH studies but not among PBC studies. In conclusion, recurrence of autoimmune liver disease after liver transplantation appears to be a real concern. As these patients are followed long-term, recurrence of disease may become the primary cause of morbidity.
Infections in patients with end-stage liver disease (ESLD) are an important cause of morbidity and mortality in these patients. Abnormalities in their natural defense mechanisms, alterations in the enteric flora and the growing utilization of invasive procedures increase the risk of infections in these patients. Common bacterial infections in ESLD patients include spontaneous bacterial peritonitis, urinary tract infections, community-acquired pneumonia, dermatologic infections, and bacteremia. Viral infections such as influenza can have a devastating course in ESLD patients. Hepatitis B and C are now among the most common causes of ESLD. They also present an important therapeutic challenge. As patients with human immunodeficiency virus are surviving longer, ESLD due to hepatitis C is now emerging as a leading cause of morbidity in these patients. Prompt detection of infections, use of appropriate antibiotics for treatment and prophylactic measures such as vaccinations can help improve survival in these patients.
Foregut duplication cysts are rare congenital anomalies of enteric origin that arise during early embryonic development. They are usually incidentally found on routine imaging studies. The diagnosis can usually be made by computed tomography (CT) and endoscopic ultrasound (EUS) appearance. On CT, cyst attenuation values usually measure 0+/-20 Hounsfield units (HU). Higher HU is possible with hemorrhage, proteinaceous material or septations. At EUS, characteristic location and anechoic as well as hypoechoic but not necessarily anechoic appearance may be suggestive of a foregut duplication cyst. EUS-guided fine needle aspiration (FNA) has been thought to provide a safe, minimally invasive approach to establish the diagnosis. The purpose of this report is to highlight the potential for infectious risk of EUS-FNA for these cysts, and to suggest CT and EUS features that can suggest this diagnosis without FNA. Three patients who underwent EUS-FNA for diagnosis of incidental mediastinal lesions developed cyst infection despite accepted techniques including prophylactic antibiotics. Combined CT and EUS appearance may be sufficient in making this diagnosis without FNA. IV antibiotics may not be completely protective against infectious complications of FNA of mediastinal duplication cysts.
Currently, there are limited therapeutic options available for chronic hepatitis C (HCV) patients who fail treatment with peginterferon alpha (PEG IFN) + ribavirin (RBV). An option is retreatment with a second course PEG-IFN + RBV. However, the virologic clearance with this option is unknown. Thus, we evaluated the outcome of our cohort of patients with chronic HCV who achieved a sustained viral response when retreated with PEG IFN plus RBV after having no response to an initial course of PEG IFN plus RBV. Nonresponse to treatment was defined as failure to achieve an early virologic response by week 12 or presence of detectable HCV RNA at week 24 or after completion of PEG-IFN + RBV therapy. Twenty patients (12 [60%] men; 8 [40%] women) were treated with PEG IFN alpha-2b plus RBV and PEG IFN alpha-2a plus RBV. The mean age of the patients was 50 years, 85% were white, 95% had genotype 1, and 35% had cirrhosis. Prior to the first course of PEG IFN plus RBV, 12 (60%) of 20 patients had no prior treatment for Hepatitis C. After the second course of PEG IFN plus RBV, 2 (10%) of 20 patients achieved a sustained virologic response. These results suggest marginal benefit of retreatment of patients with chronic HCV with another course of PEG IFN plus RBV after they have not responded to an initial course of PEG IFN plus RBV.
Vitamin A toxicity has been reported to cause severe liver disease and, occasionally, liver failure. Herein we present the case of a 60-year-old male with symptoms of muscle soreness, alopecia, nail dystrophy, and ascites. He continued to deteriorate with the development of refractory ascites, renal insufficiency, encephalopathy, and failure to thrive. In this era of natural supplements, medication toxicity remains a major cause of concern. Biotransformation of drugs is a major function of the liver. Drug-induced liver injury can be serious enough to cause fulminant hepatic failure resulting in death or liver transplantation. We report a case of liver injury from subacute vitamin A toxicity leading to liver transplantation. To our knowledge, there is no prior published report of liver transplantation for vitamin A toxicity in the United States. CASE REPORTThe case was that a 60-year-old gentleman whose initial complaint was muscle soreness of 1-month duration. He also noticed increased shedding of his scalp hair (Fig. 1). He developed cold intolerance, chapped lips, dystrophy of his fingernails, and a skin rash with pruritus within 2 months (Figs. 2 and 3) His past medical history was significant for dyslipidemia, hypertension, and possibly celiac sprue, which was untreated. A comprehensive metabolic profile showed liver injury with aminotransferases elevated to 2 times the upper limit of normal, with alkaline phosphatase slightly above normal. Total bilirubin was normal. The patient was on atorvastatin at that time, and it was discontinued. His alcohol intake was minimal, and he stopped soon after the development of symptoms. When the liver injury tests remained persistently abnormal, he underwent an evaluation for chronic liver disease. This evaluation was essentially normal with a ferritin 26 g/mL, iron serum 43 g/dL, iron binding capacity 348 g/dL, iron saturation 12%, and lactate dehydrogenase 177 U/L. His serologies for hepatitis A, B, and C were negative. Antinuclear antibody and antimitochondrial antibody were negative, and ceruloplasmin and alpha-1 antitrypsin levels and phenotype were normal as well. In the meantime, the patient developed ascites. He was afebrile and anicteric with an erythematous skin rash on the abdomen and extremities. He also had nonscarring alopecia, decreased pubic and axillary hair, and dystrophic nail changes.An abdominal Doppler ultrasound showed ascites and normal Doppler waveforms of the hepatic artery and portal veins. The echogenicity and appearance of the liver were within normal limits. The spleen was normal in size. The patient's laboratory values at this time were as follows: hemoglobin, 11.6 mg/dL; white
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