ABSTRACT
Liver transplantation is currently the only definitive modality for the treatment of end-stage liver disease due to chronic hepatitis C. However, recurrent hepatitis C after liver transplantation is nearly universal. Cirrhosis may develop in 20% of recipients within 5 years, and recurrent hepatitis C may lead to graft failure, retransplantation, and even death. A subset of recipients may develop post-liver transplant cholestatic hepatitis C (PLTCHC), which is characterized by cholestasis, hepatocyte ballooning, and rapid progression to graft failure. We present a systematic review of PLTCHC that is focused on hepatitis C-infected liver transplant recipients. We compare the pathological definitions of PLTCHC, clinical factors, management strategies, and outcomes reported in studies. We found differences among studies in the types of histological criteria used to diagnose PLTCHC during liver biopsy and in the types of clinical information provided. Three of the 12 studies published after 2003 used the definition of PLTCHC published by the first International Liver Transplantation Society expert panel consensus conference on liver transplantation and hepatitis C. We propose that studies on PLTCHC use the consensus criteria for diagnosis and suggest clinical information that should be provided in future studies with the goal of improving our understanding and management of this deadly disease.
Subject(s)
Hepacivirus , Hepatitis C, Chronic , Liver Cirrhosis/surgery , Liver Failure/surgery , Liver Transplantation , Biopsy , Cholestasis/etiology , Cholestasis/pathology , Graft Rejection/physiopathology , Graft Rejection/prevention & control , Graft Rejection/surgery , Hepacivirus/pathogenicity , Hepatitis C, Chronic/etiology , Hepatitis C, Chronic/physiopathology , Hepatitis C, Chronic/virology , Humans , Liver/pathology , Liver/virology , Liver Cirrhosis/etiology , Liver Cirrhosis/pathology , Liver Failure/etiology , Liver Failure/physiopathology , Liver Function Tests , Liver Transplantation/adverse effects , RecurrenceSubject(s)
Duodenal Diseases/etiology , Duodenal Diseases/pathology , Immunoglobulin M/metabolism , Leukemia, Lymphocytic, Chronic, B-Cell/complications , Leukemic Infiltration/pathology , Biopsy, Needle , Budesonide/therapeutic use , Diarrhea/diagnosis , Diarrhea/etiology , Duodenal Diseases/drug therapy , Duodenoscopy/methods , Follow-Up Studies , Humans , Immunohistochemistry , Intestinal Mucosa/immunology , Intestinal Mucosa/pathology , Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis , Leukemic Infiltration/diagnosis , Male , Middle Aged , Rare Diseases , Risk Assessment , Treatment OutcomeABSTRACT
BACKGROUND: Ethnic disparities in colorectal cancer (CRC) mortality are observed in the United States. The authors studied this among minority New Yorkers with CRC. METHODS: In a study of CRC patients in a New York City teaching hospital, 5-year data on demographics and clinical features were reviewed. Adjusted cancer-related deaths and early deaths (within 6 months of diagnosis) were compared among African Americans (AAs) and Hispanics. Descriptive analyses, odds ratios (ORs), and 95% confidence intervals (CIs) are reported. A P value of <.05 was considered significant. RESULTS: Among 202 CRC subjects, we noted the following: Hispanics, 148 (73%); AAs, 54 (27%); women, 107 (53%); mean age, 64.5 years; and screening colonoscopy, 44 (22%). CRC was diagnosed by colonoscopy in 157 (78%) and by surgery in 45 (22%) cases. One hundred twenty-two (60%) had stage 0-II CRC, and 69 (34%) had proximal colonic lesions. Fifty-four of 202 patients died during the study period (median, 27 months), of whom 24 (11.9%) were early deaths. Significantly higher odds of death (OR, 3.98; 95% CI, 2.03-7.81), especially early death (OR, 5.94; 95% CI, 2.42-14.6) was observed among AAs. There was no difference in demographic and other clinical features, or treatment between Hispanics and AAs (P = nonsignificant). CONCLUSIONS: The first to compare inner city minority subjects with CRC, the authors observed increased odds of death in AAs, despite similar clinical features and living environment. Tumor behavior or host response among AAs could explain this difference. Aggressive therapeutic and early detection strategies need to be tested in a large randomized study setting to substantiate our study findings.