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Biomedical subjects

J Britton

Publications and source records attributed to J Britton.

At least 91 records · Page 5Linked to original sources
PubMed1999

Moyamoya disease in a 12-year-old Caucasian boy presenting with acute transient psychosis.

This paper reports the case of a 12-year-old boy who presented with an acute transient psychosis. Investigations revealed Moyamoya disease with occlusion of the left middle cerebral artery. There was no previous history of transient ischaemic attacks, no history of psychiatric disease, no family history of psychosis and no history of illicit drug use. Although no previous cases of Moyamoya disease with psychosis as the sole presenting feature have been described, we suggest the possibility of a causal link.

Acute Disease↗
PubMed1999

Association between - 308 tumour necrosis factor promoter polymorphism and bronchial hyperreactivity in asthma.

BACKGROUND: Tumour necrosis factor (TNF) is a pivotal cytokine in the inflammation underlying asthma. The TNF gene is located in the polymorphic HLA class 3 region on chromosome 6p. Several polymorphisms in this region have been described and associated with alteration of TNF secretion in vitro. OBJECTIVE: In this study we tested the hypothesis that two such polymorphisms, lymphotoxin alpha NcoI B*1 and -308 TNF2 may be components of the genetic predisposition to asthma. METHODS: Five hundred and fifty-six random individuals were studied, comprising approximately equal numbers of asthmatic subjects, with or without atopy, and a nonatopic nonasthmatic control group. In addition, 355 subjects (172 asthmatics) from 60 multiplex families were typed at the LTalpha NcoI locus. RESULTS: There was an association between allele two of the -308 TNF polymorphism and bronchial hyperreactivity (OR 2.12, 95% CI 1.04-4.32, P = 0.036). However, there was no association with LTalpha NcoI alleles. To determine whether this was influenced by linkage disequilibrium within the MHC, 91 subjects with bronchial hyperreactivity and 85 control subjects were typed for class 2 and 3 alleles. Following identification of the extended TNF2 haplotype, we found no independent association of these alleles with BHR. CONCLUSIONS: We conclude that the -308 TNF2 promoter polymorphism may form a component of the genetic predisposition to BHR in asthma.

Adolescent↗
PubMed1999

Smoking and blood pressure patterns in normotensive pregnant women.

This paper examines the relationship between smoking levels and blood pressure patterns of normotensive pregnant women in a prospective cohort of 2193 primiparous and 3176 multiparous, normotensive, Caucasian women selected from the Child Health and Development Studies in Oakland, California, 1959-67. Regression lines were fitted to each woman's blood pressure; mean intercept and slope estimates of the individual regressions were used to create summary profile lines for each smoking dose. Multivariable regression analysis controlled for maternal age, number of visits to the doctor after 20 weeks' gestation, body mass index and maternal education level. Overall, smokers had lower average diastolic blood pressure (smokers vs. nonsmokers adjusted mean: primiparas, 66.1 vs. 67.2 mmHg; and multiparas, 64.0 vs. 64.7 mmHg) but higher systolic blood pressure (smokers vs. nonsmokers adjusted mean: primiparas, 117.0 vs. 116.0; and multiparas, 112.5 vs. 110.0) than nonsmokers among primiparous and multiparous pregnant women after adjusting for potential confounders. However, these differences are small and there was no clear dose-response relationship between smoking level and blood pressure.

Adult↗
PubMed1998

Atopic eczema and domestic water hardness.

BACKGROUND: The environment plays an important part in the aetiology of atopic eczema, but specific causes are unknown. Exposure to hard water is thought to be a risk factor for eczema. We undertook an ecological study of the relation between domestic water hardness and the prevalence of eczema among Nottinghamshire schoolchildren. METHODS: Questionnaire details of 1-year period and lifetime prevalence of eczema were obtained from parents of 4141 randomly selected primary-school children and 3499 secondary-school children in southern Nottinghamshire. Geographical information systems (GIS) were used to link the geographical distribution of eczema prevalence with domestic water-hardness data (four categories). Adjustment was made for potential confounding by sex, age, socioeconomic status, and access to health care. FINDINGS: Among the primary-school children there was a significant direct relation between both 1-year period and lifetime prevalence of eczema and water hardness, both before and after adjustment for confounders. The 1-year period prevalence was 17.3% (261/1509) in the highest water-hardness category and 12.0% (94/786) in the lowest (adjusted odds ratio 1.54 [95% CI 1.19-1.99] p for trend <0.001). The corresponding values for lifetime prevalence were 25.4% (384/1509) and 21.2% (167/786; adjusted odds ratio 1.28 [1.04-1.58], p for trend=0.02). Eczema prevalence trends in the secondary-school population were not significant (adjusted odds ratio for highest compared with lowest hardness category for 1-year prevalence 1.03 [0.79-1.33], p for trend=0.46; for lifetime prevalence 0.99 [0.83-1.23], p for trend=0.93). Eczema prevalence in primary-school children increased in relation to chlorine content of water, but the trend across four chlorine-content categories was not independently significant after adjustment for confounders. INTERPRETATION: Exposure to hard water in the home may increase the risk of eczema in children of primary-school age.

Adolescent↗
PubMed1998

Cerebellitis presenting as acute hydrocephalus.

A 14-year-old boy presented acutely with occipital headache, nausea and vomiting. MRI showed obstructive hydrocephalus and marked bilateral cerebellar swelling with increased signal on T2-weighted imaging. Following treatment with oral corticosteroids, the clinical and radiological signs resolved. The clinical course and radiological appearances were consistent with cerebellitis associated with a significant mass effect and hydrocephalus.

Adolescent↗
PubMed1998

Status epilepticus and venous infarction in Sturge-Weber syndrome.

Sturge-Weber syndrome (SWS) is a neurocutaneous disorder that is typically associated with progressive neurological deterioration. We describe a 12-year-old girl with SWS who suffered a permanent cerebral insult as the result of a period of protracted status epilepticus. The case illustrates the unique susceptibility of patients with SWS to uncontrolled venous hypertension and emphasises the need for optimal seizure control and preservation of venous outflow. We discuss the relevance of our observations to haemodynamic concepts of neurological decline in SWS.

Anticonvulsants↗
PubMed1998

Giant aneurysm of the petrous internal carotid artery: diagnosis and treatment.

We report the case of a giant fusiform aneurysm of the petrous internal carotid artery in a 15-year-old patient who had presented with headache, hearing loss and Horner's syndrome. Definitive radiological diagnosis was made by non-invasive imaging techniques, including magnetic resonance angiography (MRA). The aneurysm was obliterated by endovascular balloon occlusion following successful tolerance of test occlusion of the internal carotid artery.

Adolescent↗
PubMed1998

Association study of asthma and atopy traits and chromosome 5q cytokine cluster markers.

BACKGROUND: Linkage studies have provided evidence for the presence of gene(s) in the 5q cytokine cluster region which control total serum immunoglobulin E (IgE) concentration, and bronchial hyperreactivity (BHR). However, the identification of the gene(s) involved has been confounded by the lack of power of the published linkage studies and the presence of multiple candidate genes mapped to the region. OBJECTIVE: To define the important loci on 5q31-33 which are implicated in the control of total serum IgE and BHR through a case/control study of association. METHODS: We performed an association study between 11 polymorphic markers (spanning the region 5q31.1-33.1) and total serum IgE and BHR traits. A case/control sample of 181 individuals was drawn from a larger set of 2415 adults, sampled at random from a district in Nottingham, UK. Half of the subjects in this case/control sample were hyperreactive to methacholine and asthmatic (cases), while the other half were non-reactive and non-asthmatic (controls). Association analysis was performed using the non-parametric chi-squared and Mann-Whitney U-tests. RESULTS: We observed no evidence of strong allelic association between any of the above markers and the studied traits. Markers D5S404, interferon regulatory factor 1 (IRF-1) and D5S210 showed evidence of borderline association with BHR (P = 0.04, 0.03 and 0.04 respectively), and D5S404 showed borderline significance with IgE levels (P = 0.029). CONCLUSIONS: This study presents evidence against the presence of a strong association between markers mapped to 5q31-33 and either BHR or total serum IgE. The significance of the weaker associations observed with markers D4S404, IRF-1 and D5S210 is not clear. Whether this represents a type I error secondary to multiple hypothesis testing or a true association is uncertain.

Adolescent↗
PubMed1998

Beta2-adrenoceptor polymorphisms are in linkage disequilibrium, but are not associated with asthma in an adult population.

OBJECTIVE: To determine the association between the beta2-adrenoceptor polymorphisms at amino acids 16 and 27 and markers of allergic disease and asthma per se in a random adult population, and to determine the degree of linkage disequilibrium existing between polymorphisms at amino acid positions 16, 27, 164 and nucleic acid residue 523. METHODS: We measured serum IgE, skin-prick test positivity, atopy, bronchial hyperreactivity, wheeze and asthma (self-reported and doctor-diagnosed), and determined beta2-adrenoceptor genotype by allele specific oligonucleotide hybridization, in 630 adults aged between 18 and 70, selected from the electoral role in a local health authority in Nottingham. RESULTS: Homozygotes for the Glycine 16 polymorphism had a significantly higher incidence of atopy (chi2=6.44 (Pearson's), P=0.04). We also observed a significant association between the Glycine 16 allele and atopy (chi2=4.13 (Pearson's), P=0.04), when we assumed the Glycine 16 allele to operate in a dominant mode. No other significant associations between beta2-adrenoceptor polymorphisms and markers of allergic disease and asthma per se were observed. Marked linkage disequilibrium exists between the beta2-adrenoceptor polymorphisms at amino acid 16 and 27 (D=0.38, chi2 P<0.0001), and between the beta2-adrenoceptor polymorphisms at amino acid 27 and nucleic acid residue 523 (C-A) (D=0.36, chi2 P<0.0001). CONCLUSION: There is no consistent association between beta2-adrenoceptor polymorphisms and the risk of developing allergic disease or asthma per se in this adult sample. Marked linkage disequilibrium exists between the amino acid 16 and 27 polymorphisms, and also between the amino acid 27 polymorphism and the nucleic acid residue 523 (C-A) polymorphism. This polymorphism accounts for the Ban 1 RFLP previously described at the beta2-adrenoceptor locus on chromosome 5q 31.

Adolescent↗
PubMed1998

Prenatal diagnosis of a large fetal arachnoid cyst.

A case of prenatal diagnosis and management of a giant fetal arachnoid cyst is presented. The importance of an accurate diagnosis is highlighted and the use of three-dimensional ultrasound is discussed. The recent literature is reviewed.

Adult↗
PubMed1998

Exposure to commonly prescribed drugs and the etiology of cryptogenic fibrosing alveolitis: a case-control study.

Cryptogenic fibrosing alveolitis is an interstitial lung disease of unknown etiology. Since pulmonary fibrosis is a recognized, if rare, complication of certain drug exposures, including antidepressants, betablockers, antibiotics, anticonvulsants, and nonsteroidal antiinflammatory drugs (NSAIDs), we tested the hypothesis that exposure to these drugs might contribute to the etiology of cryptogenic fibrosing alveolitis. Lifetime drug exposure data were collected from general practitioner records for 141 cases of cryptogenic fibrosing alveolitis and 246 age-, sex-, and community-matched control subjects from the Trent region of England. Additional data on lifetime smoking habits were obtained by postal questionnaire. The odds of disease in relation to ever exposure to antidepressants, betablockers, antibiotics, anticonvulsants, and NSAIDs were calculated by conditional logistic regression. For drug groups significantly associated with cryptogenic fibrosing alveolitis, subset analyses were performed to investigate the effects of individual drugs. Cryptogenic fibrosing alveolitis was associated with exposure to antidepressants (odds ratio [OR] 1.79 [95% CI 1.09-2.95], p = 0.022) and specifically to imipramine (OR 4.79 [1.50-15.3], p = 0.01), dothiepin (OR 2.37 [0.99-5.69], p = 0.05), and mianserin (OR 3.27 [1.11-9.61], p = 0.03). The magnitude of the overall effect of antidepressants was not changed by excluding all drug exposures within the 5 yr preceding the diagnosis of cryptogenic fibrosing alveolitis (OR 1.62 [0.94-2.77], p = 0.081), nor were the strong individual effects of imipramine (OR 5.72 [1.54-21.2], p = 0.009) and dothiepin (OR 5.58 [1.12-27.8], p = 0.036). These estimates were not appreciably affected by controlling for smoking history. The attributable risk for antidepressant exposure was in the region of 9-14%. No significant association was noted between cryptogenic fibrosing alveolitis and the four other drug groups in the primary hypothesis. The results of this study suggest that some antidepressant drugs can cause cryptogenic fibrosing alveolitis.

Adrenergic beta-Antagonists↗
PubMed1998

Increasing prevalence of wheeze and asthma in Nottingham primary schoolchildren 1988-1995.

The prevalence of asthma in children has increased substantially in many countries in recent decades, but it is not clear how much this trend has continued into the 1990s. This study aimed to estimate the current prevalence of asthma and wheeze in British primary schoolchildren and to determine whether there has been any increase in the prevalence of these conditions since 1988. The prevalence of self-reported wheeze and asthma was measured by parental questionnaire in 22,968 children aged 4-11 yrs attending primary schools in the Nottingham area of England in 1995, and these estimates were compared with data from a subsample of the same schools in 1988. In 1995, wheezing ever was reported in 24.0% of children, wheezing in the past year in 15.1% and diagnosed asthma symptomatic in the past year in 8.8%. All measures have increased in prevalence since 1988, in absolute terms by 7.7% for wheeze ever, by 2.6% for wheeze in the past year and by 2.7% for asthma. The increases were greater in females than males, but did not vary with age. In conclusion, the prevalence of asthma has continued to rise in British schoolchildren since the late 1980s, particularly in females, and across all ages.

Asthma↗