As illustrated in Fig. 1, a range of CCrs12979860 genotype frequencies may evolve in patients with chronic HCV infection; this depends on the frequencies in uninfected subjects and

the rates of spontaneous resolution of infection. However, from this figure, it is obvious that a 67% CC genotype rate at rs12979860 should not develop in an uninfected population Small molecule library with a 45% CC genotype rate, as reported for HCV genotype 2/3 by Montes-Cano et al.,4 unless the clearance rate in patients carrying a non-CC genotype is higher than that in the CC genotype group. An alternative explanation might be that, for epidemiological reasons, HCV genotype 2/3 preferentially spreads in populations with higher frequencies of the CC genotype. We propose that these putative mechanisms should be explored, although, as suggested by Montes-Cano et al., a positive selection on the basis of unknown

virological or biological phenomena might also explain the high frequency of the CC genotype in patients with genotype 2/3. Magnus Lindh M.D.*, Martin Lagging M.D.*, Gunnar Norkrans M.D.*, Kristoffer Hellstrand M.D.*, * Department of Infectious Diseases, University of Gothenburg, Gothenburg, Sweden. “
“A young woman, aged 19, presented to the Emergency Department with abdominal pain and gastrointestinal bleeding. Pain had been present for 4 days and, on the day of admission, she had episodes of nausea and vomiting. Subsequently, selleck kinase inhibitor she Hydroxychloroquine chemical structure began to vomit blood and also developed melena. She had been previously diagnosed with a hypercoagulable state resulting from a JAK-2 mutation and was known to have portal vein thrombosis with extension of the thrombosis into the splenic and superior mesenteric veins. She had also been previously diagnosed with esophageal varices but had not had episodes of gastrointestinal bleeding. She ceased treatment with warfarin 1 month prior to admission but restarted the drug after the onset of abdominal pain. Blood tests revealed a hemoglobin

of 7.6 g/dL (76 g/l) with an international normalized ratio (INR) of 2.1. After fluid resuscitation and the correction of coagulopathy, upper gastrointestinal endoscopy was performed. Esophageal varices of moderate size were present but did not appear to be responsible for bleeding. However, there was a bleeding lesion in the duodenal cap that seemed likely to be related to a duodenal varix (Figure 1). A contrast-enhanced computed tomography scan showed extensive thromboses in the portal venous system with the formation of a portal cavernoma. An endoscopic ultrasound study confirmed the presence of periduodenal varices (Figure 2) and a subsequent angiogram confirmed the presence of extensive portal thromboses with large intra-abdominal collaterals that precluded treatment with a transjugular intrahepatic portosystemic shunt.