decompression. On reevaluation with endoscopic retrograde cholangiography after portal decompression, we found the long narrow stricture of the common bile duct to have opened up, with disappearance of the proximal dilatation. Hence we feel that narrowing of the common bile duct might be caused by extrinsic compression due to portal cavernoma (as was clearly evident in our patient) and that true biliary strictures may be diagnosed in this setting only when they persist after portal decompression. It is surprising that 80% of consecutive patients with EHPVO studied by Khuroo et al. had increased serum alkaline phosphatase levels and that 8 of 21 had icterus. This is rather different from the experiences reported from two other north Indian centers, in which abnormalities in liver test results were seen in only 1.47% and 2.46% (3, 4). Therefore one wonders whether the observations of the authors are applicable to the overwhelming majority of patients with EHPVO in this part of the world. If, indeed, biliary obstruction is as common in EHPVO patients in Kashmir (66.6% had jaundice or increased serum bilirubin), probably another cause should be sought. Dr. Khuroo earlier reported on biliary ascariasis as a significant endemic problem in Kashmir (5). Whether repeated invasions and injury of the common bile duct could be due to such an exotic cause may need consideration.
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