Relinquishment of infants with Down syndrome in Israel: trends by time.

To assess factors affecting parental relinquishment of infants with Down syndrome, we conducted a nationwide cohort study of infants with Down syndrome who were born in Israel during 1979-1983 and 1987-1991. Overall relinquishment rate was 25%. Major factors affecting relinquishment were mother's age, birth order, infant's health status, and study periods.

Incidence of leukemia and other cancers in Down syndrome subjects in Israel.

Epidemiologic data have confirmed the high susceptibility of persons with Down syndrome (DS) to leukemia. The question of proneness to other kinds of cancer is still open. In this study we reassessed the incidence rates of leukemia and other malignancies in Israeli DS subjects, based on the total population.

A novel mutation in the HEXA gene specific to Tay-Sachs disease carriers of Jewish Iraqi origin.

An increased frequency of carriers of 1:140, as defined by reduced hexosaminidase A (HexA) activity, was observed among Iraqi Jews participating in the Tay-Sachs disease (TSD) carrier detection program. Prior to this finding, TSD among Jews had been restricted to those of Eastern European (Ashkenazi) and Moroccan descent with carrier frequencies of 1:29 and 1:110 for Jews of Ashkenazi and Moroccan extraction, respectively. A general, pan-ethnic frequency of approximately 1:280 has been observed among other Jewish Israeli populations.

Risk factors for infant mortality in Down's syndrome: a nationwide study.

The aim of this study was to assess risk factors for the excessive infant mortality rates (IMR) of infants with Down's syndrome (DS). The study population included all 847 Jewish DS births in Israel during 1979-83 and 1987-91. Cases were identified through the National DS Registry.

Tay-Sachs disease and HEXA mutations among Moroccan Jews.

Moroccan Jewry (N>750,000) is the only non-Ashkenazi Jewish community in which Tay-Sachs disease (TSD) is not extremely rare. Previous studies among Moroccan Jewish TSD families identified three HEXA mutations. In this study, extended to enzyme-defined and new obilgate TSD carriers, we found four additional mutations.