Objective: To assess the role of polymerase chain reaction in defining infectiousness among people infected with hepatitis C virus. Design: Published studies of hepatitis C transmission were examined. Twenty nine studies with identified sources of hepatitis C infection who were tested for presence of hepatitis C RNA by polymerase chain reaction were reviewed, including studies of vertical transmission (n = 21), transmission after transplantation (n = 3), transfusion of blood components (n = 3), and needlestick exposure (n = 2). Subjects: All patients identified in studies. Results: A total of 2022 people who had been exposed to sources positive for antibody to hepatitis C were identified. Among 1148 people exposed to sources positive by polymerase chain reaction 148 cases of transmission occurred compared with no definite case among 874 people exposed to negative sources. Rates of transmission from positive sources were 6.2% for perinatal exposure, 6.1% after needlestick exposure, 78% after solid organ or bone marrow transplantation, and 83% after transfusion of blood components. Other factors influencing risk of vertical transmission were coinfection with HIV and level of hepatitis C viraemia. Conclusions: Negative results by polymerase chain reaction indicate an extremely low probability of transmission of hepatitis C from a person with antibody to hepatitis C.

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The aim of this study was to identify factors predictive of individual final height (FH) in subjects born small for gestational age (SGA). All full-term singleton subjects born SGA (birth weight and/or length <3rd percentile) during the period 1971-1978, matched with appropriate birth weight for gestational age (AGA) subjects (birth weight between 25th and 75th percentile) were followed from birth to FH and evaluated before puberty at a mean age +/- SD of 6.1 +/- 0.7 y and after puberty at a mean age of 20.8 +/- 2.0 y (subjects born SGA, n = 213; born AGA, n = 272). When adjusted for target height, a significant deficit in final height (p < 0.0001) was found in SGA as compared with AGA subjects for both male subjects (-3.99 cm with 95% confidence interval from -5.6 to -2.4) and female subjects (-3.64 cm with 95% confidence interval from -5.0 to -2.3), with 13.6% of subjects in the SGA population presenting short final stature. In a multiple regression analysis, target height and studied group (SGA or AGA) were found to be the strongest predictors of individual FH (p < 0.0001, r2 = 0.35 for male subjects, p < 0.0001, r = 0.40 for female subjects). For SGA subjects and according to a multiple stepwise linear regression model, 31% of the variability of individual FH [SD score (SDS)] and 58% of the variability of individual height gain SDS could be explained at birth from mother's height, father's height, and birth length SDS. No other variables were found to be predictive such as sex, gestational age (from 37 to 42 wk), birth weight SDS, ponderal index at birth, or risk factors during pregnancy associated with intrauterine growth retardation such as pregnancy-induced hypertension, smoking, or a history of SGA in offspring. Although a significant increase of body mass index SDS was documented before and after puberty in SGA subjects, puberty was not found to have any influence on growth outcome.

Objective The aim of this study is to investigate both maternal and paternal contributions in the familial aggregation of small for gestational age. Design Nested case -control study.Setting Metropolitan area of Haguenau, France.Population Data were drawn from a French population-based maternity registry. After selection, 256 cases born either small for gestational age or average for gestational age were included. Methods Controlling for known pregnancy-related risk factors, logistic regression models were used to determine the risk of the child being small for gestational age, given that the mother, father or both were small for gestational age, and to examine interactions between maternal small for gestational age and pregnancy risk factors. Main outcome measures Specifically, we investigate to what extent having either or both parents born small for gestational age increases the risk of small for gestational age in their offspring, after controlling for the established risk factors of small for gestational age and maternal and paternal characteristics. We also explore the extent to which the intergenerational predictors of small for gestational age may modify the effect of current pregnancy-related risk factors. Results The risk of a small for gestational age offspring was 4.7 times greater for mothers and 3.5 times greater for fathers who were small for gestational age, compared with average for gestational age counterparts. Furthermore, the risk of a small for gestational age offspring was 16.3 times greater when both parents were small for gestational age. No significant interactions between maternal small for gestational age and maternal smoking, hypertension or parity were observed. Conclusion These results indicate that small for gestational age in both mother and father significantly influences the risk of their offspring being small for gestational age. While previous research has indicated that the birth outcome of the mother is an important determinant of the birth outcome of her offspring, these data indicate that the birth outcome of the father plays an equally critical role in determining fetal growth, strongly suggesting a genetic component in the familial aggregation of small for gestational age.

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