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Biomedical subjects

E Blair

Publications and source records attributed to E Blair.

At least 55 records · Page 3Linked to original sources
PubMed1994

Year-long weight loss treatment for obese patients with type II diabetes: does including an intermittent very-low-calorie diet improve outcome?

PURPOSE: To evaluate a year-long behavioral weight control program, used with and without an intermittent very-low-calorie diet (VLCD) in the treatment of type II diabetes mellitus. PATIENTS AND METHODS: Subjects (n = 93) were randomly assigned to 50-week treatment programs that used either a balanced low-calorie diet (LCD) of 1,000 to 1,000 kilocalories (kcal) per day throughout or included 2 12-week periods of a VLCD of 400 to 500 kcal per day alternating with the balanced LCD. Weight, glycemic control, blood pressure, and lipids were assessed at baseline, at the end of the year-long treatment, and at 2-year follow-up. RESULTS: Subjects in the VLCD program lost significantly more weight than did LCD subjects at the end of the 50-week program (14.2 kg versus 10.5 kg; P = 0.057) and remained off diabetes medication longer (P < 0.05). These benefits of the VLCD were due primarily to the first 12 weeks of the diet; the second diet maintained, but did not increase, these effects. Subjects in both groups experienced marked improvements in glycemic control and cardiovascular risk factors over the year-long program, but attendance declined in the latter weeks of treatment and weight was regained. There was also marked recidivism in both groups in the year following treatment. CONCLUSIONS: The intermittent VLCD improved weight loss and glycemic control, but these effects were quite modest and do not appear to justify the clinical use of an intermittent VLCD. Moreover, lengthening treatment to a full year did not prevent relapse. Thus, further research is needed to develop a successful approach to long-term weight control.

Adult↗
PubMed1994

Family patterns of gestational age at delivery and growth in utero in moderate and severe cerebral palsy.

The relation of familial factors to the aetiology of cerebral palsy was assessed in a case-control study of all moderate and severe cases born in Western Australia between 1980 and 1986. The data did not suggest recurrence of cerebral palsy, congenital malformations or reproductive loss in cerebral palsy families. Preterm and small-for-gestational-age birth recurred within both case and control families. Cases and controls did not differ significantly from their siblings in measures of intra-uterine growth, but (with the exception of controls unmatched for both birthweight and gestational age) were born significantly earlier than their siblings. A family history of preterm or small-for-gestational-age birth was found to affect the risk of cerebral palsy by influencing the risk of preterm birth or growth retardation in the index pregnancy.

Adolescent↗
PubMed1994

Why do aboriginal newborns weigh less? Gestational age at delivery: estimation, distribution and determinants.

We reviewed birth records pertaining to 1,301 Western Australian singleton Aboriginal pregnancies dated before 24 weeks by ultrasound fetometry using Caucasian standards. We compared i) ultrasound- and LMP-derived estimates of age at delivery for 323 pregnancies with available last menstrual period (LMP) dates and ii) distributions of ultrasound-estimated age at delivery for full-blood with part-blood Aboriginal neonates and with statutorily collected estimates for Caucasian neonates. We investigated determinants of age at delivery for Aboriginal neonates. Ultrasound-derived estimates of gestational age for Aboriginal pregnancies were statistically but not clinically significantly shorter than estimates derived from LMP dates claimed to be certain: mean difference = 0.4 weeks (95% CI:0.09-0.71). Aboriginal gestations were shorter than Caucasians' by 2 weeks (median) or 1 week (mode). Some shortening of gestation was accounted for by antepartum haemorrhage, congenital anomaly, history of syphilis, diabetes, hypertensive disease and inductions before 40 weeks without recorded medical complication but not by full-blood (relative to part-blood) Aboriginality. We conclude that Caucasian fetometry standards gave gestational estimates acceptably close to those derived from certain menstrual dates for dating scan before 24 weeks. Aboriginal gestations tended to be shorter than Caucasian gestations but since factors recorded in the medical record accounted for little of this difference, socioeconomic factors may be partly responsible.

Australia↗
PubMed1994

A training project for disability prevention in Malawi.

Musculoskeletal disorders affect an estimated 3% of the population in Malawi. The vast majority of them can be treated by orthopaedic clinical officers who are deployed to the district hospitals after 18 months of training. This article describes a project designed to provide the training, and evaluates its impact after seven years in operation.

Allied Health Personnel↗
PubMed1993

Randomised controlled trial of oxytocin alone versus oxytocin and ergometrine in active management of third stage of labour.

OBJECTIVE: To compare intramuscular oxytocin alone and intramuscular oxytocin with ergometrine (Syntometrine) for their effect in reducing the risk of postpartum haemorrhage when both are used as part of the active management of the third stage of labour. DESIGN: Double blind, randomised controlled trial. SETTING: Two metropolitan teaching hospitals in Perth, Western Australia. SUBJECTS: All women who expected a vaginal birth during the period of the trial. Informed consent was obtained. MAIN OUTCOME MEASURES: Postpartum haemorrhage, nausea, vomiting, and increased blood pressure. RESULTS: 3497 women were randomly allocated to receive oxytocin-ergometrine (n = 1730) or oxytocin (n = 1753). Rates of postpartum haemorrhage (> or = 500 ml or > or = 1000 ml) were similar in both arms (odds ratio 0.90 (0.82); 95% confidence interval 0.75 to 1.07 (0.59 to 1.14) at 500 ml (1000 ml) threshold). The use of oxytocin-ergometrine was associated with nausea, vomiting, and increased blood pressure. CONCLUSIONS: There are few advantages but several disadvantages for the routine use of oxytoxinergometrine when prophylactic active management of the third stage of labour is practised. Further investigation of dose-response for oxytocin may be warranted.

Blood Pressure↗
PubMed1993

When can cerebral palsy be prevented? The generation of causal hypotheses by multivariate analysis of a case-control study.

Causal hypotheses for spastic cerebral palsy were sought by comparing a population based sample of 183 cases with 549 matched controls. A time-ordered multivariate analysis was used to distinguish confounders and consequences of disease from possible causes, which could be single factors or sequences of factors. Eighteen factors were identified as having an association with spasticity that did not arise by confounding with other identified factors nor as a consequence of the disease. Nearly half the cases (48.6%) but only 14.4% of controls experienced one or more of these factors, but no one factor was experienced by > 11%, and most by < 5%, of cases. Those factors identified as occurring before labour commenced affected 35% of all cases. The proportion of cases experiencing identified factors and the distribution of those factors between epochs varied with gestation of delivery and with description and severity of impairment. The possible timing of causes in cases without identified factors and the role of preterm birth and poor intrauterine growth are discussed. We conclude that there were many pathways to spastic cerebral palsy many of which could not be identified. Each contributed only a small proportion and many may have been multifactorial. Intrapartum initiation of the aetiological pathway was relatively unimportant, being likely in about 9% of cases, but the majority of pathways commenced predelivery.

Adult↗
PubMed1993

Aetiological pathways to spastic cerebral palsy.

An aetiological pathway is a sequence of interdependent events culminating in disease. Recognition of such pathways can be clinically useful if it suggests more effective methods of disease prevention. Kernicterus arising from feto-maternal Rhesus incompatibility and resulting in choreoathetosis comprises an aetiological pathway to cerebral palsy. The failure to recognise sufficient causes or to intervene effectively when a sufficient cause is suspected in the majority of cerebral palsy cases suggests that there may be other aetiological pathways. Evidence for other pathways was sought in the data from the Western Australian case-control study of 183 children with spastic cerebral palsy. Two or more factors likely to be of aetiological significance were recognised for nearly one-third of cases. As anticipated, the numbers with any specific combination of factors were small, pointing to the need for collaborative studies to obtain larger numbers to confirm their aetiological significance. The implications for the true proportion of cases with multifactorial aetiology and the problems inherent in such an investigation are discussed.

Birth Injuries↗
PubMed1993

Spastic quadriplegia in Western Australia: a genetic epidemiological study. I: Case population and perinatal risk factors.

In a case-control study of all cerebral palsy cases with moderate and severe spastic quadriplegia born between 1976 and 1985, males comprised three-quarters of the cases and tended to have more severe motor impairment than females. The majority of cases had multiple and severe disabilities, and 27 per cent had died by the time of data collection. There was an excess of low-birthweight and preterm births compared with all live births in WA. An intrapartum cause was considered possible in 18 of the 74 children; however, half of these had evidence of compromise before labour.

Australia↗
PubMed1992

Intrauterine growth and spastic cerebral palsy II. The association with morphology at birth.

This study tests the hypothesis that children with spastic cerebral palsy had different birth morphologies, defined in terms of their weight, length, head circumference, ponderal index and length to head circumference ratio, from that of the normal liveborn population. An earlier study showed a highly significant association of spastic cerebral palsy with low birthweight for gestational age in infants over 34 weeks gestation at delivery. This analysis defines morphological measurements as "abnormal" if not within the 10th-90th percentile ranges of appropriate total liveborn populations. The proportions with combinations of such measurements in 104 cases of spastic cerebral palsy from a population register of cerebral palsy are compared with those in a total liveborn population. Categories of 'abnormal' measurements associated with increased risk contained 44.4% of cases in excess of the proportion observed in the total population. More than half these excess cases were short for their gestation (suggesting size deficits originating before the 3rd trimester) and tended to have more severe forms of cerebral palsy. A further excess of 7.4% of cases had a head circumference above their 90th percentile: these generally developed mild cerebral palsy.

Birth Weight↗
PubMed1992

Detection of HIV in haemopoietic progenitors.

Peripheral blood cytopenias present a major problem in the management of patients with HIV infection. Their pathophysiology is likely to be multifactorial, although there is controversy as to whether haemopoietic progenitors are a target for HIV. In order to investigate the haemopoietic defect in HIV infection, we looked at bone marrow culture characteristics of marrow from eight HIV+ patients compared to normal controls. We performed long-term liquid culture (LTC) and colony forming assays for granulocyte-macrophage (CFU-GM) and granulocyte, erythroid, megakaryocyte, macrophage (CFU-GEMM). In LTC we found normal stromal appearance and haemopoietic focus formation. There was no difference in colony assays of CFU-GM and CFU-GEMM between HIV+ and normal controls. Colonies taken from CFU-GM and CFU-GEMM were analysed for HIV DNA sequences, and we were able to detect HIV DNA in colonies from all HIV+ patients. Our results indicate that despite infection of haemopoietic progenitor cells by HIV, bone marrow function is preserved. This suggests that HIV-related cytopenias may be due to alternative mechanisms not present in our in vitro system.

Adult↗
PubMed1991

Why have we failed to reduce the frequency of cerebral palsy?

OBJECTIVE: To review the data on children with cerebral palsy in relation to quality of obstetric care. DATA SOURCES AND STUDY SELECTION: In our Institute, a regular Medline print-out, certain key journals and Current Contents are perused to create an updated computerised file of publications on the epidemiological, aetiological and other aspects of cerebral palsy. For this study we reviewed data from the Western Australian Cerebral Palsy Register, more than 150 publications from which studies were chosen for sound methodology in countries with modern obstetric practices, and recent population data on cerebral palsy. DATA EXTRACTION AND SYNTHESIS: Three major areas were studied to see: (i) if the prevalence of cerebral palsy has fallen with increasing use of obstetric and neonatal interventions aimed at reducing birth asphyxia; (ii) if there is any evidence that cerebral palsy is caused by birth asphyxia; and (iii) if there is any evidence that intrapartum fetal monitoring or caesarean section reduces the prevalence of cerebral palsy. CONCLUSIONS: We concluded that: cerebral palsy proportions are not falling in spite of significant increases in obstetric and neonatal interventions aimed at reducing asphyxia; cerebral palsy proportions in low birthweight infants are rising in most developed countries, coincident with increases in the neonatal survival of low birthweight babies; few cases of cerebral palsy seem to be caused by birth asphyxia and those that are may not have been preventable by obstetric care; and parents will continue to sue if obstetricians keep promising perfection from obstetric care in the face of 2.0-2.5 cases of cerebral palsy per 1000 children born.

Asphyxia Neonatorum↗
PubMed1990

Intrauterine growth and spastic cerebral palsy. I. Association with birth weight for gestational age.

Birth weight, gestational age at delivery, and other factors were collected for 171 white children with spastic cerebral palsy. Their birth weights were compared with the birth weight distribution expected for a population of the same race, gestation, sex, maternal height, and parity, born in the same geographic area, and during the same time period. Birth weights of children with spastic cerebral palsy tended to be significantly lower than the median birth weight of their comparison population. Analysis stratified by gestation at delivery suggested that if the reduced birth weight were causally associated with the spastic cerebral palsy, 22% of cases were attributable to being below the 10th percentile of the comparison population birth weight distribution. The risk of spastic cerebral palsy associated with poor intrauterine growth was dependent on gestation at delivery; poorly grown infants delivered between 34 and 37 weeks' gestation were at highest risk. Some probable pathways by which growth retardation could result in brain damage (intrapartum hypoxia, hypoglycemia, and hypothermia) were investigated. Only intrapartum hypoxia may have played a causal role but probably accounted for less than 2% of all cases. These data suggest that spastic cerebral palsy is associated with poor intrauterine growth in infants of more than 33 weeks' gestation, but no important causal mechanism has yet been identified.

Birth Weight↗