The role of the viral genotype, especially genotype 1b, in the severity of liver injury induced by chronic hepatitis C virus (HCV) infection is unclear, probably because of confounding factors such as the date and mode of contamination. Host genetic or environmental factors such as heterozygous MZ alpha1-antitrypsin deficiency or alcoholism, could also be potential risk factors for the development of cirrhosis. The aim of this study was to compare the prevalence of genotypes, alpha1-antitrypsin phenotype, past hepatitis B virus infection, and alcohol consumption in cirrhotic and noncirrhotic patients with chronic hepatitis C. We conducted a case-control study comparing 84 consecutive cirrhotic patients with chronic hepatitis C (cases) with 84 noncirrhotic patients with chronic hepatitis C (controls) selected from a cohort of 464 patients hospitalized during the same period. Controls were paired with cases according to age, sex, risk factors, and date of infection. HCV genotypes were determined using the InnoLiPA technique (Innogenetics, Zwijnaarde, Belgium) and classified according to the method of Simmonds. Patients were divided in three groups according to alcohol consumption: <30 g/d (light), 30 to 80 g/d (moderate), and >80 g/d (heavy). Cirrhotic and noncirrhotic patients were not significantly different in terms of genotype distribution (1a/1b/2a/3a/others/undetermined: 10/48/7/17/0/2 versus 11/43/10/10/5/5), alpha1-antitrypsin phenotype distribution (MM/MS/MZ: 84%/14%/2% vs. 87%/11%/2%, respectively), and prevalence of antibody to hepatitis B core antigen positivity (29% vs. 23%). Alcohol consumption was significantly different between cases and controls (L/M/H: 58%/27%/16% vs. 76%/15%/9%, respectively; P < .05). Two conclusions regarding patients with chronic hepatitis C virus infection can be drawn from this study: 1) viral genotype, especially 1b, past hepatitis B virus infection, and heterozygous MZ alpha1-antitrypsin deficiency are not risk factors for cirrhosis; and 2) alcohol consumption, even moderate, is a risk factor for cirrhosis.

X-ray powder diffraction experiments are performed to prove the possible crystallization of nitric acid dihydrate (HNO(3).2H(2)O, further denoted NAD) and to determine the best thermal conditions for growing a single crystal. It is shown that the kinetic behaviour of NAD strongly depends on the preliminary thermal treatment. One good single crystal obtained by an in situ adapted Bridgman method procedure enabled determination of the crystal structure. The intensities of diffracted lines with h odd are all very weak. The H atom of nitric acid is delocalized to one water molecule leading to an association of equimolar nitrate (NO(3)(-)) and an H(5)O(2)(+) ionic group. The asymmetric unit contains two such molecules. These two molecules are related by a pseudo a/2 translation (with a 0.3 A mean atomic distance difference), except for one H atom of the water molecules (0.86 A) because of their different orientations in the two molecules. The two molecules, linked by very strong hydrogen bonds, are arranged in layers. Two layers which are linked by weaker hydrogen bonds are approximately oriented along the c axis. The structure may be described by translations of this set of two layers along the c axis without hydrogen bonds leading to a two-dimensional hydrogen-bond network. The structures of the monohydrate (NAM) and trihydrate (NAT) are re-determined for comparisons. These structures may be described by one- and three-dimensional hydrogen-bond networks, respectively.

A new assay (illumigene C. difficile; Meridian Bioscience), based on the original loop-mediated isothermal amplification (LAMP) assay, was evaluated with 472 unformed stools from patients suspected of Clostridium difficile infection. Compared to the toxigenic culture, the sensitivity, specificity, and positive and negative predictive values were 91.8, 99.1, 91.8, and 99.1% for the illumigene C. difficile assay and 69.4, 100, 100, and 96.6% for the cytotoxicity assay, respectively.

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