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Disease Frequency (disease + frequency)
Selected AbstractsA propensity score approach to correction for bias due to population stratification using genetic and non-genetic factorsGENETIC EPIDEMIOLOGY, Issue 8 2009Huaqing Zhao Abstract Confounding due to population stratification (PS) arises when differences in both allele and disease frequencies exist in a population of mixed racial/ethnic subpopulations. Genomic control, structured association, principal components analysis (PCA), and multidimensional scaling (MDS) approaches have been proposed to address this bias using genetic markers. However, confounding due to PS can also be due to non-genetic factors. Propensity scores are widely used to address confounding in observational studies but have not been adapted to deal with PS in genetic association studies. We propose a genomic propensity score (GPS) approach to correct for bias due to PS that considers both genetic and non-genetic factors. We compare the GPS method with PCA and MDS using simulation studies. Our results show that GPS can adequately adjust and consistently correct for bias due to PS. Under no/mild, moderate, and severe PS, GPS yielded estimated with bias close to 0 (mean=,0.0044, standard error=0.0087). Under moderate or severe PS, the GPS method consistently outperforms the PCA method in terms of bias, coverage probability (CP), and type I error. Under moderate PS, the GPS method consistently outperforms the MDS method in terms of CP. PCA maintains relatively high power compared to both MDS and GPS methods under the simulated situations. GPS and MDS are comparable in terms of statistical properties such as bias, type I error, and power. The GPS method provides a novel and robust tool for obtaining less-biased estimates of genetic associations that can consider both genetic and non-genetic factors. Genet. Epidemiol. 33:679,690, 2009. © 2009 Wiley-Liss, Inc. [source] Prevalence of celiac disease among school children in Punjab, North IndiaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2006Ajit Sood Abstract Background:, Celiac disease, as of today, is said to exist in almost all parts of the world, although it is rare among people of purely African,Caribbean, Japanese and Chinese background. The disease has also been considered uncommon in India until recently. Hospital records have revealed an increasing trend of the disease in predominantly wheat-eating areas of North India. The aim of the present study was to determine the prevalence of celiac disease among school children in Punjab, North India. Methods:, The study was carried out in the Ludhiana district of Punjab, Northern India. A total of 4347 children aged 3,17 years attending different schools were enrolled. A structured questionnaire was used to collect sociodemographic data and symptoms and signs related to celiac disease and various sociodemographic factors. The screening for celiac disease for the suspected celiacs was done by testing for antitissue transglutaminase (anti-tTG) by indirect solid-phase immunometric assay (ELISA). All children with high anti-tTG whose parents consented underwent upper gastrointestinal endoscopy for small bowel biopsy from the second part of the duodenum. Histopathology was expressed according to the Marsh classification of 1992. Follow up was carried out among children who were put on a gluten-restricted diet, at monthly intervals for 3 months and every 3 months thereafter. The diagnosis of celiac disease was established on the basis of the revised European Society of Paediatric Gastroenterologists and Nutritionists (ESPGAN) criteria (confirmed cases). Results:, A total of 4347 school children (1967 girls, 2380 boys, age range 3,17 years) were screened for celiac disease. Out of these, 198 suspected children were identified for further evaluation. Twenty-one children tested positive for anti-tTG assay (10.6%, 95% confidence interval: 16.91,34.79). Seventeen of these 21 children agreed to undergo biopsy; of these, 14 had histological changes consistent with celiac disease and all these 14 children had clinical response to gluten restriction. Three children with high anti-tTG had normal mucosa on duodenal biopsy and were not labelled as being in the celiac disease group. In the final analysis the disease prevalence was one in 310 children. Conclusions:, This is the first study on celiac disease prevalence among school children from India. Although this disease frequency of one in 310 is thought to be an under-assessment, it clearly shows that celiac disease is not rare in wheat-eating areas of North India. [source] Sarcoidosis in Singapore: Epidemiology, clinical presentation and ethnic differencesRESPIROLOGY, Issue 3 2007Devanand ANANTHAM Background and objectives: The aim of this study is to better understand the epidemiological and clinical features of patients with sarcoidosis in Singapore and to ascertain if ethnic differences exist. Methods: A review of hospital medical records from June 1998 to May 2004 to identify patients with sarcoidosis. Results: There were 59 patients with sarcoidosis identified (19 Chinese, 29 Asian Indian and 11 Malay). The estimated annual incidence of sarcoidosis in Singapore was 0.56 per 100 000. There was a significant difference between the observed and expected disease frequency in Chinese (32.2% vs 78.7%) and Indians (49.2% vs 6.0%, P < 0.005). A bimodal distribution of age at diagnosis was seen with peaks in the 30,39 years and 50,59 years age groups; 38.9% of cases were over the age of 50. Chinese patients were more likely to be asymptomatic (57.9%, P = 0.015) and less likely to have impaired spirometry (P = 0.013). Pulmonary sarcoid presented largely as stage 0 or stage 1 disease (74.4%). Overall mean spirometry was unimpaired and prognosis was good with 79.2% showing no radiological deterioration. There were no significant differences in organ involvement or treatment between ethnic groups. Conclusion: Sarcoidosis in Singapore is rare and the incidence differs between ethnic groups. Chinese appear to have a lower incidence and a less symptomatic presentation; Indians have a higher incidence and poorer clinical course. [source] Etiology of reactive arthritis in Pan paniscus, P. troglodytes troglodytes, and P. troglodytes schweinfurthiiAMERICAN JOURNAL OF PRIMATOLOGY, Issue 3 2005Bruce M. Rothschild Abstract The character of arthritis has not received the same attention in Pan paniscus as it has in P. troglodytes. Reactive arthritis (a form of spondyloarthropathy) in the latter has been considered to be either a sexually transmitted or an infectious-agent diarrhea-related disorder. The unique sexual promiscuity of P. paniscus enables us to distinguish between those hypotheses. The macerated skeletons of 139 adult P. paniscus, P. troglodytes troglodytes, and P. troglodytes schweinfurthii were macroscopically analyzed for osseous and articular pathologies. The sex of the animal was recorded at the time of acquisition. Twenty-one percent of the P. paniscus, 28% of the P. t. troglodytes, and 27% of the P. t. schweinfurthii specimens had peripheral and central joint erosive disease characteristic of spondyloarthropathy. Subchondral pauciarticular distribution and reactive new bone clearly distinguish this disease from rheumatoid arthritis, osteoarthritis, and direct bone/joint infection. The fact that P. paniscus and P. t. troglodytes were similar in terms of disease frequency makes the notion of sexual transmission unlikely. While the frequencies of spondyloarthropathy were indistinguishable among all species/subspecies studied, the patterns of joint involvement were disparate. The Pan paniscus and P. t. troglodytes home ranges are geographically separate. We assessed possible habitat factors (e.g., exposure to specific infectious agents of diarrhea) by comparing P. paniscus and P. t. troglodytes with P. t. schweinfurthii. The latter shared similar patterns and habitats (separated by the Congo River) with P. paniscus. The explanation offered for habitat-specific patterns is differential bacterial exposure,most likely Shigella or Yersinia in P. paniscus and P. t. schweinfurthii. Am. J. Primatol. 66:219,231, 2005. © 2005 Wiley-Liss, Inc. [source] |