6 research outputs found

    Candidate gene study of genetic thrombophilic polymorphisms in pre-eclampsia and recurrent pregnancy loss in Sinhalese women

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    Aim: Genetic thrombophilias are known to contribute to adverse pregnancy outcomes. Studies in Western populations show that 5, 10-methylenetetrahydrofolate reductase (MTHFR) 677C>T and Factor V (F5) 1691G>A (Leiden) polymorphisms are commonly associated with pre-eclampsia and recurrent spontaneous pregnancy loss. The objective of this study was to investigate the association of MTHFR 677C>T (rs1801133); 1298A>C (rs1801131) and F5 1691G>A (rs6025); 4070A>G (rs1800595) polymorphisms with pre-eclampsia and recurrent pregnancy loss among Sinhalese women in Sri Lanka. Material and Methods: Genotype and allele frequencies at each polymorphic site in the MTHFR and F5 genes and the haplotypes defined by them were determined in 175 Sinhalese women with pre-eclampsia, 171 normotensive controls, 200 Sinhalese women with two or more recurrent pregnancy losses and 200 controls with two or more living children and no pregnancy losses. Genotyping was done by polymerase chain reaction/restriction fragment length polymorphism. Odds ratios and X²-testing were performed to compare genotype/haplotype frequencies at each polymorphic site for both cases and controls. Results: The genotype frequencies at each polymorphic site in the MTHFR 677C>T; 1298A>C; F5 1691G>A and 4070A>G genes and the haplotypes defined by them were not significantly associated with either preeclampsia or recurrent pregnancy loss. There was no significant association of genetic thrombophilia with either early or late pregnancy losses. Conclusions: The MTHFR and F5 polymorphisms and the haplotypes defined by them were not significantly associated with either pre-eclampsia or recurrent pregnancy loss in this group of Sinhalese women.9 page(s

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    Don’t just do it, do it right: evidence for better health in low and middle income countries Evidence for better health outcomes involves a two-step process: getting the right sort of evidence and getting this evidence used [1]

    Assistant Editors

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    Continued overleaf Management of pain in chronic pancreatitis. New solutions to an old problem Management of pain in chronic pancreatitis is a challenging clinical problem. Lack of proper understanding of the mechanisms responsible for pain, high morbidity and mortality rates historically associated with pancreatic surgery, and the long held view that pain will eventually subside when the pancreas "burns itself out " as a result of progressive fibrosis have all contributed to a non-surgical therapeutic approach for decades [1]. Many recent studies have challenged this view, and at present there is a shift from the "wait and see " approach to a more pro-active type of therapeutic approach in the management of pancreatic pain [2]. It is accepted that, at least in a majority of cases, the pain results from pressure increase within the pancreatic duct system from obstruction to the main pancreatic duct by stones or from post-inflammatory strictures [3]
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