(1/5222) What parents think of fever.
OBJECTIVES: We aimed to assess knowledge, perception and management of fever by parents. METHODS: We conducted a questionnaire survey among 392 parents of children attending locally a paediatric clinic at The Royal Oldham Hospital. The main outcome measures were answers to questions covering a variety of aspects of the knowledge, perception and management of fever by parents. RESULTS: Almost half the parents used a liquid crystal forehead thermometer. Most could not use a glass thermometer. Thirty per cent did not know normal body temperature and would have treated children with a temperature below 38 degrees C. Sixty-four per cent treated fever with both paracetamol and tepid sponging. Most parents awakened children at night for antipyretics. Eighty-one per cent thought that untreated fever was most likely to cause fits or brain damage and 7% thought it could cause death. CONCLUSION: Parents perceive fever as being dangerous. They have a poor knowledge and measure it inaccurately. Needless consultations and hospital admissions could be avoided by a change in perception. (+info)
(2/5222) B cell lymphoproliferative disorders following hematopoietic stem cell transplantation: risk factors, treatment and outcome.
Twenty-six cases of B cell lymphoproliferative disorder (BLPD) were identified among 2395 patients following hematopoietic stem cell transplants (HSCT) for which an overall incidence of BLPD was 1.2%. The true incidence was probably higher, since 9/26 of the diagnoses were made at autopsy. No BLPD was observed following autologous HSCT, so risk factor analyses were confined to the 1542 allogeneic HSCT. Factors assessed were HLA-mismatching (> or = 1 antigen), T cell depletion (TCD), presence of acute GvHD (grades II-IV), donor type (related vs unrelated), age of recipient and donor, and underlying disease. Factors found to be statistically significant included patients transplanted for immune deficiency and CML, donor age > or = 18 years, TCD, and HLA-mismatching, with recipients of combined TCD and HLA-mismatched grafts having the highest incidence. Factors found to be statistically significant in a multiple regression analysis were TCD, donor age and immune deficiency, although 7/8 of the patients with immunodeficiencies and BLPD received a TCD graft from a haploidentical parent. The overall mortality was 92% (24/26). One patient had a spontaneous remission, but subsequently died >1 year later of chronic GVHD. Thirteen patients received therapy for BLPD. Three patients received lymphocyte infusions without response. The only patients with responses and longterm survival received alpha interferon (alphaIFN). Of seven patients treated with alphaIFN there were four responses (one partial and three complete). These data demonstrate that alphaIFN can be an effective agent against BLPD following HSCT, if a timely diagnosis is made. (+info)
(3/5222) Genetic linkage of IgA deficiency to the major histocompatibility complex: evidence for allele segregation distortion, parent-of-origin penetrance differences, and the role of anti-IgA antibodies in disease predisposition.
Immunoglobulin A (IgA) deficiency (IgAD) is characterized by a defect of terminal lymphocyte differentiation, leading to a lack of IgA in serum and mucosal secretions. Familial clustering, variable population prevalence in different ethnic groups, and a predominant inheritance pattern suggest a strong genetic predisposition to IgAD. The genetic susceptibility to IgAD is shared with a less prevalent, but more profound, defect called "common variable immunodeficiency" (CVID). Here we show an increased allele sharing at 6p21 in affected members of 83 multiplex IgAD/CVID pedigrees and demonstrate, using transmission/diseqilibrium tests, family-based associations indicating the presence of a predisposing locus, designated "IGAD1," in the proximal part of the major histocompatibility complex (MHC). The recurrence risk of IgAD was found to depend on the sex of parents transmitting the defect: affected mothers were more likely to produce offspring with IgAD than were affected fathers. Carrier mothers but not carrier fathers transmitted IGAD1 alleles more frequently to the affected offspring than would be expected under random segregation. The differential parent-of-origin penetrance is proposed to reflect a maternal effect mediated by the production of anti-IgA antibodies tentatively linked to IGAD1. This is supported by higher frequency of anti-IgA-positive females transmitting the disorder to children, in comparison with female IgAD nontransmitters, and by linkage data in the former group. Such pathogenic mechanisms may be shared by other MHC-linked complex traits associated with the production of specific autoantibodies, parental effects, and a particular MHC haplotype. (+info)
(4/5222) Allowing for missing parents in genetic studies of case-parent triads.
In earlier work, my colleagues and I described a log-linear model for genetic data from triads composed of affected probands and their parents. This model allows detection of and discrimination between effects of an inherited haplotype versus effects of the maternal haplotype, which presumably would be mediated by prenatal factors. Like the transmission disequilibrium test (TDT), the likelihood-ratio test (LRT) based on this model is not sensitive to associations that are due to genetic admixture. When used as a method for testing for linkage disequilibrium, the LRT can be regarded as an alternative to the TDT. When one or both parents are missing, the resulting incomplete triad must be discarded to ensure validity of the TDT, thereby sacrificing information. By contrast, when the problem is set in a likelihood framework, the expectation-maximization algorithm allows the incomplete triads to contribute their information to the LRT without invalidation of the analysis. Simulations demonstrate that much of the lost statistical power can be recaptured by means of this missing-data technique. In fact, power is reasonably good even when no triad is complete-for example, when a study is designed to include only mothers of cases. Information from siblings also can be incorporated to further improve the statistical power when genetic data from parents or probands are missing. (+info)
(5/5222) Psychosocial and economic problems of parents of children with epilepsy.
The parents of children with epilepsy (PCE) face multiple psychosocial and economic problems that are often neglected. We undertook this study to ascertain these problems among the patients attending a tertiary referral center for epilepsy in India. A structured questionnaire was administrated to parents of 50 children aged between 5-10 years and having epilepsy for more than 1 year's duration. Some 52% of the children had partial epilepsy whilst the remaining had generalized epilepsy. The median seizure frequency was one per 6 months. The majority of the patients (86%) were living in villages. The family income was less than 1000 Rs per month (1 USD = 42 INR) for 66% of the patients. A decline in social activities, after the onset of epilepsy in their children, was reported by 80% of the parents. Daily routines were significantly affected in over 75% of the parents. Parents had been experiencing frustration (52%) and hopelessness (76%), whilst 60% were in financial difficulties. The most important item of expenditure was cost of drugs or cost of travel to hospital for 54% and 36% parents respectively. Impaired emotional status and poor social adaptation were co-related with the severity of epilepsy (frequent seizures/generalized seizures/attention disorder) and low economic status of the parents. These observations need to be borne in mind while organizing rehabilitation programs for epilepsy. (+info)
(6/5222) Health effects of passive smoking-10: Summary of effects of parental smoking on the respiratory health of children and implications for research.
BACKGROUND: Two recent reviews have assessed the effect of parental smoking on respiratory disease in children. METHODS: The results of the systematic quantitative review published as a series in Thorax are summarised and brought up to date by considering papers appearing on Embase or Medline up to June 1998. The findings are compared with those of the review published recently by the Californian Environmental Protection Agency (EPA). Areas requiring further research are identified. RESULTS: Overall there is a very consistent picture with odds ratios for respiratory illnesses and symptoms and middle ear disease of between 1.2 and 1.6 for either parent smoking, the odds usually being higher in pre-school than in school aged children. For sudden infant death syndrome the odds ratio for maternal smoking is about 2. Significant effects from paternal smoking suggest a role for postnatal exposure to environmental tobacco smoke. Recent publications do not lead us to alter the conclusions of our earlier reviews. While essentially narrative rather than systematic and quantitative, the findings of the Californian EPA review are broadly similar. In addition they have reviewed studies of the effects of environmental tobacco smoke on children with cystic fibrosis and conclude from the limited evidence that there is a strong case for a relationship between parental smoking and admissions to hospital. They also review data from adults of the effects of acute exposure to environmental tobacco smoke under laboratory conditions which suggest acute effects on spirometric parameters rather than on bronchial hyperresponsiveness. It seems likely that such effects are also present in children. CONCLUSIONS: Substantial benefits to children would arise if parents stopped smoking after birth, even if the mother smoked during pregnancy. Policies need to be developed which reduce smoking amongst parents and protect infants and young children from exposure to environmental tobacco smoke. The weight of evidence is such that new prevalence studies are no longer justified. What are needed are studies which allow comparison of the effects of critical periods of exposure to cigarette smoke, particularly in utero, early infancy, and later childhood. Where longitudinal studies are carried out they should be analysed to look at the way in which changes in exposure are related to changes in outcome. Better still would be studies demonstrating reversibility of adverse effects, especially in asthmatic subjects or children with cystic fibrosis. (+info)
(7/5222) Diabetic nephropathy is associated with an increased familial risk of stroke.
OBJECTIVE: To test the hypothesis that genetic susceptibility to diabetic nephropathy is associated with an increased familial risk of vascular disease, we have examined the causes and rates of death of parents of individuals with type 1 diabetes complicated by diabetic nephropathy compared with the causes and rates of death of parents of control subjects with diabetes uncomplicated by nephropathy. RESEARCH DESIGN AND METHODS: Individuals with at least a 14-year duration of type 1 diabetes complicated by diabetic nephropathy were identified and matched for age, sex, and duration of diabetes to control subjects. A total of 118 patients and 118 matched control subjects were identified and approached to obtain information on parental age and cause of death. For parents who had died, the cause of death was ascertained from the death certificate. RESULTS: Kaplan-Meier curves showed that parents of subjects with nephropathy (PN) had reduced survival compared with parents of diabetic subjects without nephropathy (PC) (log rank test P < 0.05). There was an excess of all vascular deaths and, in particular, strokes in the parents of subjects with nephropathy (PN: 20 of 103 deaths, 19% vs. PC: 3 of 66 deaths, 4%; Fisher's exact test P < 0.01). CONCLUSIONS: Parents of diabetic patients with nephropathy have reduced survival. This seems to be largely explained by an increase in vascular deaths and, in particular, a four-fold increase in the number of strokes. This supports the hypothesis that a common hereditary risk factor predisposes to both vascular death and diabetic renal disease. (+info)
(8/5222) Urinary cotinine and exposure to parental smoking in a population of children with asthma.
BACKGROUND: Studies of the effects of tobacco smoke often rely on reported exposure to cigarette smoke, a measure that is subject to bias. We describe here the relationship between parental smoking exposure as assessed by urinary cotinine excretion and lung function in children with asthma. METHODS: We studied 90 children 4-14 years of age, who reported a confirmed diagnosis or symptoms of asthma. In each child, we assessed baseline pulmonary function (spirometry) and bronchial responsiveness to carbachol stimulation. Urinary cotinine was measured by HPLC with ultraviolet detection. RESULTS: Urinary cotinine concentrations in the children were significantly correlated (P <0.001) with the number of cigarettes the parents, especially the mothers, smoked. Bronchial responsiveness to carbachol (but not spirometry test results) was correlated (P <0.03) with urinary cotinine in the children. CONCLUSION: Passive smoke exposure increases the bronchial responsiveness to carbachol in asthmatic children. (+info)