Given the expanding appreciation of MYH9 function in different cell types,6 it may therefore be of interest to examine the role of MYH9 genetic variation in individuals with abnormal liver-enzyme results

but without other known etiologies. Rémi Favier U0126 chemical structure M.D.*, Analisa DiFeo Ph.D.†, Nathalie Hezard M.D., Ph.D.‡, Monique Fabre M.D.§, Pierre Bedossa M.D., Ph.D.¶, John A. Martignetti M.D., Ph.D.**, * Assistance Publique Hopitaux de Paris, Armand Trousseau Children’s Hospital, French Reference Center for Inherited Platelet, Disorders and Inserm U1009, Villejuif, France, † Case Comprehensive Cancer Center, Case Western Reserve University 2103 Cornell Road, Wolstein Research Building, 2-127 Cleveland OH, USA, ‡ Laboratoire d’Hematologie, Hopital Robert Debre, CHU Reims, France, § Service d’anatomo Pathologie, Institut Gustave Roussy, 94805 Villejuif, France, ¶ Assistance Publique-Hopitaux de Paris, Departement de Pathologie, Hopital Beaujon, 92118 CLICHY, France, ** Departments of Genetics and Genomic Sciences and Pediatrics, Belnacasan Mount Sinai School of Medicine, 1425 Madison Ave., Box 1498, New York, NY 10029, USA. “
“Use of proton pump

inhibitors (PPI) after endoscopic hemostatic treatment of bleeding peptic ulcers is a standard therapy for preventing early re-bleeding.1 However, controversy continues regarding the optimal dose and route of administration of PPI.2 While both i.v. and oral PPI are effective in preventing early re-bleeding, meta-analysis of randomized trials found that i.v. infusion of high-dose PPI is superior to low-dose (i.e. oral or repeated i.v. injections) PPI in terms of the need for surgery.1 Oral PPI have

two major limitations: a slow onset of action and failure to maintain a stably high intragastric pH. One attempt to overcome see more the limitations of conventional oral PPI is the development of immediate-release (IR) formulations. In this issue, Banerjee et al.3 shows that healthy volunteers who received buffered IR esomeprazole 40 mg p.o. had superior intragastric pH profile compared to those who received i.v. pantoprazole 40 mg every 12 h for 24 h. After the first dose of buffered IR esomeprazole, the intragastric pH was rapidly raised to 6 in a median time of 2 min whereas it took 80 min for i.v. pantoprazole to achieve this level of intragastric pH. Furthermore, the mean percentage time to an intragastric pH of more than 6.0 was 91% in the buffered IR esomeprazole group compared to 20% in the i.v. pantoprazole group in a 24-h period. While many readers would agree that the intragastric pH profile achieved by buffered IR esomeprazole was close to perfection, was the result too good to be true? The rapid rise in intragastric pH with buffered IR esomeprazole was not unexpected because the bicarbonate content of the formulation would neutralize gastric acid.