Complications requiring hospitalizations occur in over 10% of PSC patients undergoing ERCP. Cholangitis occurs more often in PSC patients and correlates with the length of the procedure. Further studies to confirm the role of aggressive prophylactic antibiotics in patients with PSC who undergo prolonged procedures are warranted.

Patients with primary sclerosing cholangitis (PSC) are at increased risk for developing cholangiocarcinoma (CCA). Fluorescence in situ hybridization (FISH) is a cytological test designed to enhance early CCA diagnosis. The long-term outcome of PSC patients with a positive FISH test (polysomy, trisomy/tetrasomy) are unclear. All PSC patients with at least one FISH test were identified and defined to have CCA if they had a positive tissue biopsy, positive cytology, or evidence of cancer in the explant after liver transplantation. A total of 235 PSC patients had at least one FISH test performed, and 56 patients had CCA on histopathology (n ‫؍‬ 35) or cytology (n ‫؍‬ 21). Overall, 120 of 235 (51%) of PSC patients tested for FISH were positive, but only one third of these positive patients had CCA. Sensitivity and specificity for FISH polysomy were 46% and 88%, and for trisomy/tetrasomy they were 25% and 67%, respectively. Survival analysis showed that patients with FISH polysomy had an outcome similar to patients with CCA; whereas FISH trisomy/tetrasomy patients had an outcome similar to patients with negative FISH tests. The FISH polysomy patients without cancer compared with those with CCA had lower serum bilirubin, lower carbohydrate antigen 19-9 (CA 19-9), lower Mayo risk score, and lower occurrence of dominant strictures. Conclusion: In PSC patients, the presence of a dominant stricture plus FISH polysomy has a specificity of 88% for CCA. Patients with FISH showing trisomy or tetrasomy have a similar outcome to patients with negative FISH. FISH testing should be used selectively in patients with other signs indicating CCA and not as a screening tool in all PSC patients undergoing endoscopic retrograde cholangiopancreatography (ERCP).

We read with great interest the article by Azzalini et al., 1 who demonstrated that cigarette smoking worsens the severity of nonalcoholic fatty liver disease (NAFLD) in obese Zucker rats. In a related letter, Xu and coworkers 2 showed that cigarette smoking may act as a cofactor but not as an independent factor for NAFLD in humans. However, currently it is uncertain whether there is a significant association between smoking patterns and the severity of liver histology among patients with NAFLD. Clarification of this aspect may help to explain the underlying mechanisms and may be of clinical importance in planning preventive and therapeutic strategies. We have therefore assessed whether there is a significant association between liver histology and smoking patterns among patients with biopsy-proven NAFLD. A total of 90 consecutive outpatients with NAFLD (43 males and 47 females, mean age, 47 6 8 years) were recruited from our clinics. All patients had chronically elevated liver enzymes and hepatic steatosis detected by ultrasonography. The NAFLD diagnosis was based on liver biopsy and exclusion of other known etiologic factors of chronic liver disease (alcohol abuse or intake !20 g/day, viral hepatitis, autoimmune hepatitis, and use of hepatotoxic drugs). An experienced pathologist blinded to clinical data scored the liver biopsies according to the National Institute of Diabetes and Digestive and Kidney Diseases NASH Clinical Research Network scoring system. 3 Pack-years of smoking were calculated as the product of the duration of smoking (in years) and the average number of cigarettes smoked per day. The protocol was approved by the local ethics committee, and all participants gave written informed consent. In multivariable-adjusted linear logistic regression models, each histological feature of NAFLD (i.e., steatosis grade, necroinflammatory grade, or fibrosis stage analyzed separately) was considered as the dependent variable. Sex, age, body mass index, smoking, low-density lipoprotein cholesterol, homeostasis model assessment of insulin resistance (HOMA-IR) score, and metabolic syndrome (considered as a single clinical entity) were included as covariates. A total of 30 patients had ever smoked, 26 were past smokers, whereas 34 were current smokers. The distribution of nonsmokers, past smokers, and current smokers was not different in NAFLD patients classified according to liver histopathology (steatosis alone, borderline steatohepatitis, definite steatohepatitis). Notably, pack-years of smoking were not associated with degree of hepatic steatosis (P ¼ 0.67), necroinflammation (P ¼ 0.34), and fibrosis among patients with NAFLD (P ¼ 0.41). These results suggest that the severity of liver histopathology among patients with NAFLD is not associated with smoking patterns, after allowance for classical risk factors, insulin resistance, and the presence of the metabolic syndrome. This study has shown for the first time that the histological severity of NAFLD is not independently predicted by smoking patterns after ad...

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