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Human T-lymphotropic viruses types I and II (HTLV-I and HTLV-II) cause chronic infections of T lymphocytes that may lead to leukemia and myelopathy. However, their long-term effects on blood counts and hematopoiesis are poorly understood. We followed 151 HTLV-I–seropositive, 387 HTLV-II–seropositive, and 799 HTLV-seronegative former blood donors from 5 U.S. blood centers for a median of 14.0 years. Complete blood counts were performed every 2 years. Multivariable repeated measures analyses were conducted to evaluate the independent effect of HTLV infection and potential confounders on 9 hematologic measurements. Participants with HTLV-II had significant (P < .05) increases in their adjusted lymphocyte counts (+126 cells/mm3; approximately +7%), hemoglobin (+2 g/L [+0.2 g/dL]) and mean corpuscular volume (MCV; 1.0 fL) compared with seronegative participants. Participants with HTLV-I and HTLV-II had higher adjusted platelet counts (+16 544 and +21 657 cells/mm3; P < .05) than seronegatives. Among all participants, time led to decreases in platelet count and lymphocyte counts, and to increases in MCV and monocytes. Sex, race, smoking, and alcohol consumption all had significant effects on blood counts. The HTLV-II effect on lymphocytes is novel and may be related to viral transactivation or immune response. HTLV-I and HTLV-II associations with higher platelet counts suggest viral effects on hematopoietic growth factors or cytokines.

Human T-lymphotropic viruses types I and II (HTLV-I and HTLV-II) cause chronic infections of T lymphocytes that may lead to leukemia and myelopathy. However, their long-term effects on blood counts and hematopoiesis are poorly understood. We followed 151 HTLV-I–seropositive, 387 HTLV-II–seropositive, and 799 HTLV-seronegative former blood donors from 5 U.S. blood centers for a median of 14.0 years. Complete blood counts were performed every 2 years. Multivariable repeated measures analyses were conducted to evaluate the independent effect of HTLV infection and potential confounders on 9 hematologic measurements. Participants with HTLV-II had significant (P< .05) increases in their adjusted lymphocyte counts (+126 cells/mm3; approximately +7%), hemoglobin (+2 g/L [+0.2 g/dL]) and mean corpuscular volume (MCV; 1.0 fL) compared with seronegative participants. Participants with HTLV-I and HTLV-II had higher adjusted platelet counts (+16 544 and +21 657 cells/mm3; P< .05) than seronegatives. Among all participants, time led to decreases in platelet count and lymphocyte counts, and to increases in MCV and monocytes. Sex, race, smoking, and alcohol consumption all had significant effects on blood counts. The HTLV-II effect on lymphocytes is novel and may be related to viral transactivation or immune response. HTLV-I and HTLV-II associations with higher platelet counts suggest viral effects on hematopoietic growth factors or cytokines.

Little is known about the occurrence of specific congenital malformations among offspring of mixed race‐ethnicity.Using data from a population‐based registry, we explored the occurrence of selected malformation phenotypes in offspring to parents who were of different race‐ethnicity. Data were derived from the California Birth Defects Monitoring Program, a population‐based active surveillance system for collecting information on infants and fetuses with congenital malformations using multiple source ascertainment. Approximately 2.6 million live births and stillbirths occurred during 1989–2000. Information on parental race‐ethnicity (non‐Hispanic white, Hispanic, black, and Asian) was obtained from birth certificates and fetal death files. Malformation phenotypes studied were spina bifida, anencephaly, cleft lip, cleft palate, tetralogy of Fallot, d‐transposition of great arteries, hypospadias, small intestinal atresia, preaxial polydactyly, microtia, and hypertrophic pyloric stenosis.A total of 11.2% of births were to parents of mixed race‐ethnicity. Compared to births of parents who were both white, moderately increased risks (risk ratio ≥ 1.7) of anencephaly, polydactyly, and microtia, and decreased risks (risk ratio ≤ 0.6) of hypospadias and hypertrophic pyloric stenosis were observed among births of several mixed race‐ethnicity groups. For anencephaly, polydactyly, and microtia, but not other phenotypes, the risks were different depending on whether maternal versus paternal race‐ethnicity was considered. Risks observed between births of a nonwhite parent and a white parent and births of parents who were both nonwhite were similar for most malformation phenotypes.Some malformation phenotypes appear to vary in their risk based on mixed racial‐ethnic groupings. Birth Defects Research (Part A), 2004. © 2004 Wiley‐Liss, Inc.

There is a paucity of epidemiologic information about the external ear malformations anotia and microtia.Using data from a large population‐based registry, we explored prevalences and maternal/infant characteristics associated with anotia and microtia. Data were derived from the California Birth Defects Monitoring Program, a population‐based active surveillance system for collecting information on infants and fetuses with congenital malformations using multiple source ascertainment. Approximately 2.5 million births (live‐born and stillborn) occurred during the ascertainment period, 1989–1997. Information on maternal and infant/fetal characteristics was obtained from California birth certificate and fetal death files.The prevalence of anotia/microtia was 2.50 per 10,000 live births and stillbirths. Isolated cases, i.e., those live births and stillbirths with no other accompanying anomaly diagnoses, revealed a prevalence of 0.63 per 10,000, whereas among nonisolated cases, the prevalence was 1.53 per 10,000 live births and stillbirths. Prevalences of isolated anotia/microtia were substantially higher among U.S.‐born Hispanics, foreign‐born Hispanics, and Asians compared to non‐Hispanic whites, with relative risks ranging from three‐ to seven‐fold. Similar prevalences for maternal race/ethnicity (except for Asians) were observed for live births and stillbirths with nonisolated cases of anotia/microtia, but the magnitude of risks were lower than those observed for isolated cases. Prevalence of nonisolated anotia/microtia was substantially lower among women whose education was 12 years or more.These data reveal descriptive epidemiologic features of anotia/microtia most notably substantial risks associated with race/ethnic groups and lower maternal education. Additional study for factors associated with these characteristics could reveal clues for the etiology of these ear anomalies. Birth Defects Research (Part A), 2004. © 2004 Wiley‐Liss, Inc.

Although many studies have observed variations in the prevalence of specific malformations by sex, there is a lack of population‐based data on potential malformation prevalence differences by sex at birth.Our objective was to explore differences in the prevalence of structural congenital malformation phenotypes between sexes in a California population of 2.5 million live‐ and stillbirths, using data from a population‐based active surveillance system. Ascertainment was performed among offspring of California women who delivered in nonmilitary hospitals during the period of 1989–1997. Malformations were grouped according to the four‐digit malformation codes of the British Pediatric Association.Overall, 32,619 males and 21,835 females were considered to have structural congenital malformations, with prevalences of 2.52% and 1.76%, respectively. Thus, males demonstrated a malformation prevalence that was 22% higher than that in females. Using a criterion of a 40% increase or decrease in the relative risk for males, increased risks for 15 and decreased risks for 17 specific malformation categories were observed. Increased risks were associated with most organ systems, with the notable exception of the nervous system (increased risks for nervous system malformations were observed among female births). Risks were not substantially influenced by adjusting for maternal age, race/ethnicity, parity, or education.Our observations extend the relatively few studies that have investigated differential prevalences of a large number of specific structural malformations between male and female births. Birth Defects Research (Part A) 67:000–000, 2003. © 2003 Wiley‐Liss, Inc.

Human T-lymphotropic viruses types I and II (HTLV-I and HTLV-II) cause chronic infections of T-lymphocytes, leading to adult T-cell lymphoma (HTLV-I) and myelopathy (both types) in a minority of infected humans. However, their long-term effects on blood counts and hematopoiesis are not fully understood. We followed 151 HTLV-I and 387 HTLV-II seropositive former blood donors, and 799 HTLV seronegative donors from five US blood centers prospectively for a median of 14.0 years. Complete blood counts were performed every 2 years on fresh anticoagulated blood at licensed clinical laboratories near each center. Multivariable repeated measures analyses were conducted to evaluate the independent effect of HTLV infection and potential confounders on 9 hematologic measurements. HTLV-II subjects had significant (p<0.05) increases in their adjusted lymphocyte counts (+126 cells/mm3; approx +7%), hemoglobin (+0.2 gm/dL) and mean corpuscular volume (MCV; 1.0 fL) compared to seronegative subjects. Both HTLV-I and -II subjects had higher adjusted platelet counts (+16,544 and +21,657 cells/mm3; p<0.05) than seronegatives. Among all subjects, time led to decreases in platelet count (−6,750 to −6,600 cells) and lymphocyte counts (−67 to −66 cells), and to increases in MCV (+0.4 fL) and monocytes (+19 to +20 cells per uL; all per two-year interval). Women had lower hemoglobin but higher platelet and white blood cell (WBC) counts than men. Blacks had lower hemoglobin, MCV and neutrophil counts, but higher platelet and lymphocyte counts than whites. Heavy drinking was associated with higher MCV but lower WBC counts, whereas cigarette smoking was associated with higher WBC counts of all lineages. These results suggest that HTLV-I and -II infection can produce significant, independent and long term changes in lymphocytes, platelets and red blood cells. The finding of increased lymphocytes in HTLV-II infection is novel and may be related to viral transactivation or immune response. HTLV-I and –II associations with higher platelet counts suggest viral effects on hematopoietic growth factors or cytokines.

Human T-lymphotropic viruses types I and II (HTLV-I and HTLV-II) cause chronic infections of T-lymphocytes, leading to adult T-cell lymphoma (HTLV-I) and myelopathy (both types) in a minority of infected humans. However, their long-term effects on blood counts and hematopoiesis are not fully understood. We followed 151 HTLV-I and 387 HTLV-II seropositive former blood donors, and 799 HTLV seronegative donors from five US blood centers prospectively for a median of 14.0 years. Complete blood counts were performed every 2 years on fresh anticoagulated blood at licensed clinical laboratories near each center. Multivariable repeated measures analyses were conducted to evaluate the independent effect of HTLV infection and potential confounders on 9 hematologic measurements. HTLV-II subjects had significant (p<0.05) increases in their adjusted lymphocyte counts (+126 cells/mm3; approx +7%), hemoglobin (+0.2 gm/dL) and mean corpuscular volume (MCV; 1.0 fL) compared to seronegative subjects. Both HTLV-I and -II subjects had higher adjusted platelet counts (+16,544 and +21,657 cells/mm3; p<0.05) than seronegatives. Among all subjects, time led to decreases in platelet count (−6,750 to −6,600 cells) and lymphocyte counts (−67 to −66 cells), and to increases in MCV (+0.4 fL) and monocytes (+19 to +20 cells per uL; all per two-year interval). Women had lower hemoglobin but higher platelet and white blood cell (WBC) counts than men. Blacks had lower hemoglobin, MCV and neutrophil counts, but higher platelet and lymphocyte counts than whites. Heavy drinking was associated with higher MCV but lower WBC counts, whereas cigarette smoking was associated with higher WBC counts of all lineages. These results suggest that HTLV-I and -II infection can produce significant, independent and long term changes in lymphocytes, platelets and red blood cells. The finding of increased lymphocytes in HTLV-II infection is novel and may be related to viral transactivation or immune response. HTLV-I and –II associations with higher platelet counts suggest viral effects on hematopoietic growth factors or cytokines.