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Biomedical subjects

C Bower

Publications and source records attributed to C Bower.

At least 91 records · Page 5Linked to original sources
PubMed1993

Trends in neural tube defects 1980-1989.

OBJECTIVES: To determine trends in prevalence of neural tube defects in Australia over the past decade; to investigate the impact of terminations of pregnancy on the birth prevalence of neural tube defects; and to provide a baseline against which to evaluate the potential effects of preventive public health measures. DATA SOURCES: Two population-based registries in Victoria and Western Australia and a statewide survey from Tasmania. DESIGN AND METHOD: A cohort study. Data on the numbers and the prevalence proportions of neural tube defects from three States--Western Australia, Victoria and Tasmania--were compared by Poisson regression. RESULTS: The prevalence proportions for all neural tube defects for all three States remained level over the study period 1980-1989. Terminations of pregnancy for all neural tube defects increased significantly over the decade in all three States. By 1989, 39.9% of all neural tube defects were ascertained as terminations before 20 weeks' gestation, while 10 years previously only 2.9% were. The percentage of cases of anencephaly ascertained as terminations of pregnancy increased from 4.8% in 1980 to 58.6% in 1989. Corresponding figures for spina bifida were 1.4% (1980) and 26.9% (1989), and for encephalocele 0% (1980) and 12.5% (1989). This increase in terminations was associated with a decrease per year in the birth prevalence proportion for anencephaly of 7.0%, for spina bifida of 4%, and for encephalocele of 11.0%, and a reduction in the risk of a birth with a neural tube defect in 1989 of 47% compared with the risk in 1980. CONCLUSION: Complete ascertainment of all terminations for neural tube defects as well as births with neural tube defects is necessary to provide reliable baseline data on the prevalence of neural tube defects. Such data are essential in evaluating primary preventive measures such as the effect of an increase in folic acid intake by women of child-bearing age.

Abortion, Induced↗
PubMed1993

Absorption of pteroylpolyglutamates in mothers of infants with neural tube defects.

The ability to hydrolyse and absorb pteroylpolyglutamates (PteGlun) included in a standard meal in mothers who had given birth to an infant with a neural tube defect was tested by comparing them with mothers who had not had any infants with this defect. When compared with control mothers working in the research unit in which the study was performed, case mothers had significantly lower baseline serum and erythrocyte folate levels, and smaller increases in serum folate following the meal containing PteGlun. However, all estimates of folate were similar when case mothers were compared with a group of mothers who were friends of the case mothers. The results show that the higher the baseline levels of serum and erythrocyte folate the greater the increase in serum folate after the test meal. Fitting a model for the serum folate response curve resulted in coefficients which differed significantly between case mothers and all control mothers. We conclude that intestinal hydrolysis of PteGlun taken orally is not impaired in mothers who have had infants with neural tube defects when compared with control mothers with similar baseline folate levels, although the curves describing the response to the meal for the two groups do differ significantly. Further investigation is required to determine the mechanism underlying this difference.

Adult↗
PubMed1993

Amniotic band syndrome: a population-based study in two Australian states.

A search for cases of amniotic band syndrome was made in two population-based Australian birth defects registries, using defined selection criteria. Over a period of 4 years in Western Australia and 5 years in South Australia, 25 cases of amniotic band syndrome had been identified as such by the two registries, and an additional 15 new cases were identified by the study selection process, giving an annual prevalence of amniotic band syndrome over the study period of 2.03 per 10,000 births. Similar proportions of male and female infants were affected, although the syndrome was more common in mothers younger than 25 years of age, and in first births. Limb defects only (upper and/or lower) were found in 24 cases, limb-body-wall defects in four cases, and complex craniofacial and other malformations in 12 cases. A heightened awareness of the syndrome should enhance the identification of amniotic band syndrome, which has implications for genetic counselling, and our understanding of the aetiology and pathogenesis of this condition.

Amniotic Band Syndrome↗
PubMed1992

Dietary folate and nonneural midline birth defects: no evidence of an association from a case-control study in Western Australia.

In a population-based case-control study of dietary folate and neural tube defects, information was collected by interview and self-administered questionnaires from the mothers of cases with only neural tube defects, from the mothers of matched control infants with defects other than neural tube defects, and from the mothers of matched live-born infants with no birth defects. The association of midline birth defects (excluding neural tube defects) with dietary folate intake in the first 6 weeks of pregnancy was assessed by restricting the analysis to the 59 mothers of infants with midline defects in the first control group and comparing them with their matched control infants in the second control group. The crude and adjusted odds ratios for dietary folate and for folic acid supplementation were close to one, and all confidence intervals embraced unity. These data do not provide evidence of an association between midline birth defects (excluding neural tube defects) and either dietary folate or folic acid supplementation.

Australia↗
PubMed1992

Birth defects in the infants of aboriginal and non-aboriginal mothers with diabetes in Western Australia.

OBJECTIVE: Because of the high prevalence of non-insulin-dependent diabetes in Australian Aborigines, and a suggestion that the prevalence of birth defects was high in the infants of Aboriginal mothers with gestational diabetes, this study was undertaken to determine the prevalence of birth defects in infants of Aboriginal and non-Aboriginal mothers with insulin-dependent, non-insulin-dependent, and gestational diabetes mellitus. DESIGN: A retrospective cohort study of all births to diabetic and non-diabetic mothers in Western Australia, 1980-1984. MAIN OUTCOME MEASURE: Birth defects diagnosed at any time up to the age of six years. RESULTS: Compared with infants of non-diabetic, non-Aboriginal mothers, the prevalence ratio for birth defects in infants of non-Aboriginal insulin-dependent mothers was 2.08 (95% confidence interval, 1.2-3.7), and for infants of mothers with non-insulin-dependent diabetes the ratio was 3.64 (95% CI, 1.5-8.6). The corresponding ratios for infants of Aboriginal mothers were 4.85 (95% CI, 0.8-28.2) and 3.64 (95% CI, 1.3-10.4). For birth defects in infants of gestational diabetic mothers, the prevalence ratio was 1.07 (95% CI, 0.6-1.9) for the non-Aboriginal group and 3.65 (95% CI, 2.3-6.0) for the Aboriginal group. Diabetes could have accounted for 0.14% of birth defects in infants of non-Aboriginal mothers and for 4.62% in infants of Aboriginal mothers. CONCLUSIONS: The excess of birth defects in infants of Aboriginal women with gestational diabetes may be due to non-insulin-dependent diabetes that predates the pregnancy but is only diagnosed during pregnancy. For Aboriginal infants, maternal diabetes may be the single most common known cause of birth defects that is amenable to change.

Cohort Studies↗
PubMed1992

Periconceptional vitamin supplementation and neural tube defects; evidence from a case-control study in Western Australia and a review of recent publications.

STUDY OBJECTIVE: The aim was to assess the association of neural tube defects with periconceptional vitamin supplementation. DESIGN: This was a matched, population based case-control study. SETTING: Western Australia, 1982-1984. PARTICIPANTS: Mothers of 77 cases (93% of those eligible) with isolated neural tube defects, mothers of 77 matched control infants with defects other than neural tube defects (control group I), and mothers of 154 liveborn, matched, control infants with no birth defects (control group II) participated in the study. MEASUREMENTS AND MAIN RESULTS: Information was collected by interview and self administered questionnaire. Crude and adjusted odds ratios (and their 95% confidence intervals) showed a small but non-significant protective effect of folate supplementation in comparisons with both control groups. The adjusted ratios for the three months before pregnancy were 0.69 (0.06, 8.53) with control group I, and 0.11 (0.01, 1.33) with control group II. In the first six weeks of pregnancy, the adjusted odds ratios were 0.70 (0.32, 1.52) with control group I and 0.74 (0.29, 1.88) with control group II. The odds ratios for vitamin supplementation of any kind were all very close to or greater than one, and all confidence intervals embraced unity. CONCLUSIONS: These data do not provide evidence of an association between periconceptional vitamin supplementation and neural tube defects, although a protective effect of folate supplementation cannot be excluded with confidence, due to the low power of the study. Of three other observational studies of vitamins and neural tube defects, two have shown an association. While further studies of this kind may be of value, evidence must now be sought from randomised controlled trials.

Case-Control Studies↗
PubMed1991

Congenital toxoplasmosis: a large survey in western Australia.

OBJECTIVE: To determine the birth prevalence of congenital toxoplasmosis in Western Australia. DESIGN: A prospective serological study of randomly selected pregnant women and their newborn infants. Paired sera collected from the mothers at their first antenatal visit and cord blood specimens taken from their infants were tested for toxoplasmosis by the direct agglutination test and Toxoplasma IgM-capture enzyme-linked immunosorbent assay. SETTING: A major Perth metropolitan obstetric teaching hospital where approximately one-quarter of infants born in Western Australia during January 1986 to December 1989 inclusive were delivered. PARTICIPANTS: Sera were obtained from 10,207 pregnant women presenting for routine clinical evaluation at their first antenatal visit. Cord blood specimens were taken from 18,908 infants; 7523 of these could be paired to maternal specimens. MAIN OUTCOME MEASURES: Maternal infection was indicated in cases where Toxoplasma specific IgM antibody was present or where an initial maternal specimen gave negative results for Toxoplasma antibody but the paired cord blood specimen gave positive results. Toxoplasma specific IgM antibody in a cord blood specimen indicated fetal infection. RESULTS: Of the 10,207 women 3544 (35%) were Toxoplasma immune at their first antenatal visit; in 11 Toxoplasma specific IgM antibody was detected. There was no serological or clinical evidence of congenital toxoplasmosis in any of the offspring of these 11 mothers. The rate of maternal infection in susceptible pregnancies was 1.6 per 1000; the maternal-fetal transmission rate was estimated to be no greater than 24%. Three of the 18,908 cord blood specimens tested gave positive results for Toxoplasma specific IgM antibody giving a birth prevalence of congenital infection of 0.23 per 1000 births to non-immune mothers. There were no clinical features of congenital infection in these three infants but they will require long-term follow-up. Thirteen of the 14 mothers infected during pregnancy were interviewed retrospectively and in only three was a known risk factor for infection present. CONCLUSIONS: a toxoplasmosis screening programme for pregnant mothers is not justifiable in Western Australia. A public education programme is also likely to have limitations.

Agglutination Tests↗
PubMed1990

Validation studies from the Western Australian Congenital Malformations Registry.

A series of studies was undertaken in 1989 to validate the data held by the Western Australian Congenital Malformations Registry. Comparison with hospital discharge data identified 1585 children six years of age or younger with malformations discharged from hospitals in Western Australia in 1986, 226 of whom were not already recorded on the Congenital Malformations Register. When the records of a special register for cleft lip and palate were examined, all cases of facial cleft known to the special register were also recorded on the Malformations Register. Comparison of the Western Australian data for major groups of malformations with data from the South Australian Birth Defects Register raised the possibility of under ascertainment in Western Australia of cases of congenital heart disease. Multiple sources of ascertainment and evaluation of the ways in which such sources are tapped are important factors in striving for complete and accurate information on congenital malformations for research and public health purposes.

Child, Preschool↗
PubMed1989

The Western Australian Familial Polyposis Registry.

The Western Australian Familial Polyposis Registry was established in 1985 by the Cancer Foundation of Western Australia in conjunction with the Health Department of Western Australia. The primary aim of the Registry is the prevention of colorectal cancer in a group of persons at high risk of the disease. Families are notified to the Registry by medical practitioners throughout the State and, at the request of family members and medical practitioners, the project officer for the Registry will arrange for the collection of data, counselling and reminders for follow-up examinations for both cases and family members who are at risk of developing the disease. A total of 44 families with familial adenomatous polyposis is known to the Registry. The crude incidence of polyposis in Western Australia was 0.24 cases per 100,000 persons over the three-year period 1986-1988. The prevalence of the condition in 1988 was 2.59 cases per 100,000 persons. There are 188 family members in Western Australia who are at a 50% risk of developing familial adenomatous polyposis. Registry data indicate that regular follow-up and early treatment reduce the risk of the development of bowel cancer.

Adenomatous Polyposis Coli↗
PubMed1989

Congenital malformations in aborigines and non-aborigines in Western Australia, 1980-1987.

A comparison of congenital malformations in Aboriginal and non-Aboriginal children in Western Australia has been made by means of data from the WA Congenital Malformations Registry, for births from 1980 to 1987 inclusive. Although the birth prevalence of all malformations was 3.5% for both Aboriginal and non-Aboriginal infants, significant differences were found in the birth prevalence of some individual malformations. Nervous-system and cardiovascular defects, and cleft lip and palate were significantly more prevalent in Aborigines, and pyloric stenosis and urogenital defects were significantly less prevalent. While some of the observed differences may have been a result of biases in ascertainment, others are likely to represent true differences. A discussion of Aboriginal beliefs concerning conception and birth is included, in order that the quantitative findings from the study might be considered in an appropriate cultural setting.

Congenital Abnormalities↗
PubMed1989

Dietary folate as a risk factor for neural-tube defects: evidence from a case-control study in Western Australia.

A population-based case-control study was conducted to test the hypothesis that the risk of the occurrence of neural-tube defects in infants with no other birth defects (isolated neural-tube defects) is associated inversely with the maternal dietary intake of free and/or total folate in early pregnancy. Information was collected from the mothers of 77 case subjects with isolated neural-tube defects who were born in Western Australia from 1982 to 1984, from the mothers of 77 control subjects with birth defects other than neural-tube defects (control group 1) and from the mothers of 154 control subjects with no birth defects (control group 2). The case and control subjects were matched individually by the date of the mother's last menstrual period. Odds ratios were adjusted for a number of potentially-confounding variables, such as the country of birth of the parents, paternal social class, previous pregnancy outcome, interval between index and previous pregnancy and pregnancy order. Crude and adjusted odds ratios showed a protective effect of an increasing intake of free folate in the first six weeks of pregnancy. Adjusted odds ratios, with reference to the lowest quartile of intake, (and their 95% confidence intervals) were 0.72 (0.25-2.08), 0.37 (0.11-1.23) and 0.31 (0.10-0.97) for quartiles 2-4 when control group 1 was used, and 0.44 (0.17-1.13), 0.34 (0.13-0.90) and 0.16 (0.06-0.49) when control group 2 was used. Similar, but weaker, trends were seen when total folate intake was the exposure variable. These findings support the hypothesis that the dietary intake of folate in early pregnancy protects against the occurrence of isolated neural-tube defects in infants. Measures of postpartum dietary folate and of postpartum serum and red-cell folate levels showed no association with the occurrence of neural-tube defects in infants.

Diet↗