Development Of Adverse Sequelae Research Articles

The influence of hepatitis B virus genotype and subgenotype on the natural history of chronic hepatitis B

Chronic infection with hepatitis B virus (HBV) is associated with a high lifetime risk of developing hepatocellular carcinoma (HCC) and cirrhosis of the liver. To review the studies published to date regarding the association of HBV genotypes and subgenotypes in the development of adverse sequelae from HBV. Review of the literature for articles describing studies of HBV genotype/subgenotypes and development of HCC, cirrhosis, and liver-related death. Eight genotypes of HBV (A through H), which differ from each other in viral genome sequence by more than 8%, and multiple subgenotypes, which differ from each other by 4-8% have been identified. Recently, studies investigating the association between the risks of developing HCC and cirrhosis by specific HBV genotypes and subgenotypes have reported marked differences in outcome. Certain HBV genotypes and subgenotypes, including genotype C, B2-5, and F1, appear to be associated with a higher risk of developing HCC, and others, including genotypes B1, B6, and A2, appear to be associated with a lower risk of complications of HBV. Our understanding of the role of HBV genotypes and subgenotypes on the outcome of HBV infection is limited, as few population-based prospective studies have been performed and most studies compare only the outcome in areas where two genotypes predominate whereas others have not examined subgenotypes. Studies to date suggest that HBV genotypes/subgenotypes have important influences on the outcome of chronic HBV infection, but more population-based prospective studies examining multiple genotypes are needed.

The Systemic Inflammatory Response Syndrome

To the Editor. —I congratulate Dr Rangel-Frausto and colleagues 1 on their recent study that describes the course and natural history of the systemic inflammatory response syndrome (SIRS). The authors provide us with an extensive patient population that was prospectively followed for the duration of their hospital stay, and they provide insight into the development of adverse sequelae and other significant events along the continuum of SIRS. However, I would like to comment on two potential areas of confusion related to this study. First, the authors imply that SIRS can develop into sepsis as part of the natural progression of SIRS. In actuality, according to the proposed terminology of the American College of Chest Physicians—Society of Critical Care Medicine Consensus Conference on sepsis, 2 SIRS encompasses sepsis when its response is secondary to a documented infection. Therefore, sepsis is a form of SIRS and not an initial stage of SIRS

Development of Adverse Sequelae in Children Born with Subclinical Congenital Toxoplasma Infection

Department of Medicine, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California; Division of Allergy, Immunology, and Infectious Diseases, Palo Alto Medical Research Foundation, Palo Alto, California; and Department of Pediatrics, University of Alabama School of Medicine, Birmingham, Alabama

Development of Adverse Sequelae in Children Born with Subclinical Congenital Toxoplasma Infection

Most infants born with congenital Toxoplasma infection are asymptomatic in the newborn period, and therefore their infection is not recognized. We performed follow-up evaluations on 24 such children. The mean age of these children at least examination was 8.5 years. In group I (13 children), the diagnosis was made prospectively. In group II (11 children), no symptoms or signs were noted in the newborn period and the diagnosis was made only after the first sign developed. Eighty-five percent of the children in group I and all of the children in group II have developed chorioretinitis. In group I, three children (23%) have unilateral blindness; in group II, three children (27%) and five children (45%) have unilateral and bilateral blindness, respectively. One child (8%) in group I and two children (18%) in group II developed severe, permanent neurologic sequelae after they initially presented with eye disease. Two of the children in each group are now retarded (IQ score range, 36 to 62). Six of the children in group I who were tested sequentially have had lower IQ scores (mean change from 97 to 74) on repeat tests performed an average of 5.5 years later. Less severe neurologic, intellectual, and audiologic deficits were observed in other children in each group. Treatment of some children may have had a beneficial effect on their outcome.