Proton pump inhibitor therapy does not increase the incidence of spontaneous bacterial peritonitis in cirrhosis: a multicenter prospective study.

BACKGROUND & AIM: Retrospective studies show an association between proton pump inhibitor (PPI) therapy and spontaneous bacterial peritonitis (SBP). We investigate the relationship between PPI and SBP in decompensated cirrhotic patients in a large nationwide prospective study. METHODS: Seven hundred seventy patients with a diagnosis of decompensated cirrhosis were admitted consecutively in 23 hospitals in Argentina from March 2011 to April 2012; the patients were carefully investigated for PPI consumption in the previous 3 months. In total, 251 patients were excluded because of active gastrointestinal hemorrhage, antibiotic use during the preceding weeks, HIV-positive status and immunosuppressive therapy. RESULTS: Two hundred twenty-six out of 519 patients (43.5%) had received PPI therapy within the last 3 months. In 135 patients, PPIs were administered for longer than 2 weeks. A bacterial infection was shown in 255 patients (49.1%). SBP was diagnosed in 95 patients out of 394 patients with ascites (24.7%). There was no significant difference in the rate of PPI consumption between the infected and the non-infected patients (44.3% vs. 42.8%) or between the SBP patients and the patients with ascites without SBP (46% vs. 42%). In the SBP patients, the duration of PPI administration did not influence the rate of SBP occurrence. The type of bacteria and the origin of SBP infection were similar in the patients with and without PPI. CONCLUSION: In the current large, multicenter, prospective study, PPI therapy, specifically evaluated at admission of consecutive cirrhotic patients, was not associated with a higher risk of SBP.

Congenital candidiasis: confirmation of mother-neonate transmission using molecular analysis techniques.

We describe a case of congenital acquired candidiasis in a preterm female delivered through Caesarean section due to the premature rupture of the amniotic membrane. The neonate presented with suspected chorioamnionitis and erythematous desquamative skin. Candida albicans was isolated from the placenta, mouth, groin, and periumbilical lesions. The infant developed candidemia due to Candida albicans and the same yeast was also isolated from a catheter. Culture inoculated with swabs from the mouth and vagina of the mother yielded C. albicans and C. krusei. All C. albicans isolates from the mother and the neonate were visually indistinguishable by molecular typing techniques which included chromosomal karyotyping and restriction endonuclease analysis followed by pulsed-field gel electrophoresis. These findings allowed the clinical condition to be confirmed as congenital acquisition of candidiasis in this case.