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Hypothesis: Distal splenorenal shunt (DSRS) is a safe and effective treatment for patients with Child-Pugh class A and B cirrhosis with recurrent variceal hemorrhage after failed transjugular intrahepatic portosystemic shunt., Design: Retrospective case review., Setting: Hepatobiliary surgery and liver transplantation department in a tertiary referral medical center., Patients: Between August 1, 1985, and May 1, 2005, 119 patients with Child-Pugh class A and B cirrhosis underwent DSRS for recurrent variceal hemorrhage. Of these, 17 (14.3%) had thrombosed or failing transjugular intrahepatic portosystemic shunt prior to DSRS., Intervention: Distal splenorenal shunt for recurrent variceal hemorrhage after failure of conservative management., Main Outcome Measures: Morbidity, mortality, and subsequent liver transplantation rate., Results: The overall perioperative morbidity rate was 31.5%. Thirteen patients (11.7%) developed encephalopathy and 6 (5.4%) had recurrent variceal hemorrhage. Other complications included portal vein thrombosis, pancreatitis, pancreatic pseudocyst, pneumonia, and wound infection. The 30-day operative mortality rate was 6.4% (n = 7). The 1-year survival rate was 85.9%. The incidence of DSRS for failed transjugular intrahepatic portosystemic shunt during the first 12 years of the study (1985-1997) was 11.1% (9/81). This proportion increased to 26.7% (8/30) during the second half of the study (1997-2005). During the 20-year period, 15 patients (13.5%) underwent liver transplantation a mean of 5.1 years after DSRS without an increase in morbidity or mortality after transplantation., Conclusions: Distal splenorenal shunt may be the preferred treatment for recurrent variceal hemorrhage in the patient with well-compensated cirrhosis. In addition, DSRS does not cause increased morbidity or mortality in subsequent liver transplantation.

We have studied intrachromosomal gene conversion in mouse Ltk- cells with a substrate designed to provide genetic evidence for heteroduplex DNA. Our recombination substrate consists of two defective chicken thymidine kinase genes arranged so as to favor the selection of gene conversion products. The gene intended to serve as the recipient in gene conversion differs from the donor sequence by virtue of a palindromic insertion that creates silent restriction site polymorphisms between the two genes. While selection for gene conversion at a XhoI linker insertion within the recipient gene results in coconversion of the nearby palindromic site in more than half of the convertants, 4% of convertant colonies show both parental and nonparental genotypes at the polymorphic site. We consider these mixed colonies to be the result of genotypic sectoring and interpret this sectoring to be a consequence of unrepaired heteroduplex DNA at the polymorphic palindromic site. DNA replication through the heteroduplex recombination intermediate generates genetically distinct daughter cells that comprise a single colony. We believe that the data provide the first compelling genetic evidence for the presence of heteroduplex DNA during chromosomal gene conversion in mammalian cells.