ABSTRACT
Background: Helicobacter pylori [H. pylori], is a common infection in pregnant women accompanied by variations in the levels of the IgM, IgA and IgG antibody isotypes. The variations of anti-H. pylori antibodies during and after pregnancy, and the extent of protection they provide to the mother and the fetus are not completely understood
Objectives: To investigate the changes of the anti-H. pylori IgM, IgA and IgG levels in healthy Omani pregnant women during pregnancy and 3 months after delivery
Methods: Serum samples obtained from 70 Omani healthy pregnant women, with no history of autoimmune diseases, were tested for anti-H. pylori IgM, IgA and IgG in the first trimester of pregnancy and 3 months after delivery. In parallel and as a control group, sera obtained from a group of 70 healthy non-pregnant Omani women were tested. The levels of anti-H. pylori IgM, IgA and IgG were measured using standard Enzyme Linked Immunosorbent Assays [ELISAs]
Results: Anti-H. pylori IgA levels were found to be significantly higher during pregnancy [p=0.046] and after delivery [p=0.02] when compared to the control group. Moreover, a significant increase in the levels of anti-H. pylori IgM, IgA and IgG was detected after delivery [p=0.002] when compared to the levels during pregnancy
Conclusion: Pregnancy is associated with an increase in the levels of anti-H. pylori IgA antibodies. In addition, anti-H. pylori IgM, IgG and IgA antibody levels increase after delivery
ABSTRACT
Spinal muscular atrophy has been classified into four groups based on the age of onset and clinical severity of the disease. Homozygous deletion in SMN1 gene causes the disease but the clinical severity may be modified by copy number of homologous gene SMN2 as well as the extent of deletion at SMN locus. In the view of scarcity of genotype and phenotype correlation data from India, this study has been undertaken to determine that correlation in SMA patients by using the SMN and NAIP genes and two polymorphic markers C212 and C272 located in this region. Two to four alleles of the markers C212 and C272 were observed in normal individuals. However, majority of Type I patients showed only one allele from both markers whereas in Type II and III patients, 2-3 alleles were observed. The SMN2 copy number in our type III patients showed that patients carry 3-5 copies of SMN2 gene. Our results suggest that extent of deletions encompassing H4F5, SMN1, NAIP and copy number of SMN2 gene can modify the SMA phenotype, thus accounting for the different clinical subtypes of the disease.