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1.
Allergy, Asthma & Immunology Research ; : 538-546, 2015.
Article in English | WPRIM | ID: wpr-89925

ABSTRACT

PURPOSE: It is controversial whether folate status is a risk factor for the development of asthma or other allergic diseases. This study was conducted to investigate whether indirect or direct exposure to folate and impaired folate metabolism, reflected as methylene-tetrahydrofolate reductase (MTHFR) C677T polymorphism, would contribute to the development of asthma and other allergic diseases. METHODS: Electronic databases were searched to identify all studies assessing the association between folate status and asthma or other allergic diseases. Two reviewers independently assessed the eligibility of studies and extracted data. The relative risk (RR) or odds ratio (OR) with 95% confidence intervals (CI) was calculated and pooled. RESULTS: Twenty-six studies (16 cohort, 7 case-control, and 3 cross-sectional studies) were identified. Maternal folic acid supplementation was not associated with the development of asthma, atopic dermatitis (AD), eczema, and sensitization in the offspring, whereas exposure during early pregnancy was related to wheeze occurrence in the offspring (RR=1.06, 95% CI=[1.02-1.09]). The TT genotype of MTHFR C677T polymorphism was at high risk of asthma (OR=1.41, 95% CI=[1.07-1.86]). CONCLUSIONS: It is indicated that maternal folic acid supplementation during early pregnancy may increase the risk of wheeze in early childhood and that the TT genotype of MTHFR C677T polymorphism impairing folic acid metabolism would be at high risk of asthma development. These results might provide additional information for recommendations regarding forced folate consumption or folic acid supplements during pregnancy based on its well-established benefits for the prevention of congenital malformations. However, currently available evidence is of low quality which is needed to further elucidate.


Subject(s)
Pregnancy , Asthma , Case-Control Studies , Cohort Studies , Dermatitis, Atopic , Eczema , Folic Acid , Genotype , Metabolism , Odds Ratio , Oxidoreductases , Risk Factors
2.
Chinese Medical Journal ; (24): 2986-2993, 2012.
Article in English | WPRIM | ID: wpr-316581

ABSTRACT

<p><b>BACKGROUND</b>The performance of asthma control test (ACT) at baseline for predicting future risk of asthma exacerbation has not been previously demonstrated. This study was designed to explore the ability of the baseline ACT score to predict future risk of asthma exacerbation during a 12-month follow-up.</p><p><b>METHODS</b>This post hoc analysis included data from a 12-month prospective cohort study in patients with asthma (n = 290). The time to the first asthma exacerbation was analyzed and the association between baseline ACT scores and future risk of asthma exacerbation was calculated as adjusted odds ratio (OR) using Logistic regression models. Further, sensitivity and specificity were estimated at each cut-point of ACT scores for predicting asthma exacerbations.</p><p><b>RESULTS</b>The subjects were divided into three groups, which were uncontrolled (U, n = 128), partly-controlled (PC, n = 111), and well controlled (C, n = 51) asthma. After adjustment, the decreased ACT scores at baseline in the U and PC groups were associated with an increased probability of asthma exacerbations (OR 3.65 and OR 5.75, respectively), unplanned visits (OR 8.03 and OR 8.21, respectively) and emergency visits (OR 20.00 and OR 22.60, respectively) over a 12-month follow-up period. The time to the first asthma exacerbation was shorter in the groups with U and PC asthma (all P < 0.05). The baseline ACT of 20 identified as the cut-point for screening the patients at high risk of asthma exacerbations had an increased sensitivity of over 90.0% but a lower specificity of about 30.0%.</p><p><b>CONCLUSION</b>Our findings indicate that the baseline ACT score with a high sensitivity could rule out patients at low risk of asthma exacerbations and predict future risk of asthma exacerbations in clinical practice.</p>


Subject(s)
Adult , Female , Humans , Male , Middle Aged , Asthma , Therapeutics , Cohort Studies , Forced Expiratory Volume , Prospective Studies , ROC Curve , Risk Assessment
3.
Chinese Journal of Medical Genetics ; (6): 575-579, 2009.
Article in Chinese | WPRIM | ID: wpr-287371

ABSTRACT

<p><b>OBJECTIVE</b>To explore the molecular genetic mechanism of complicating depression in asthma by detecting two gene polymorphisms of 5-hydroxytryptamine transporter (5-HTTLPR/Stin2) gene.</p><p><b>METHODS</b>One hundred fifty-six adults with asthma were collected, and divided into group of asthma with depression (HAMD score > or = 8) and group of asthma without depression or single asthma (HAMD score <8) according to the score of Hamilton depression scale (HAMD). A total of 508 adults with depression alone and 433 healthy individuals were enrolled as controls. The target gene fragments containing the polymorphic regions of 5-HTTLPR and Stin2 were amplified by polymerase chain reaction (PCR). The amplified fragments were then analyzed using agarose gel electrophoresis (AGE) and motored molecular imaging system.</p><p><b>RESULTS</b>The frequencies of genotype and allele distribution of the Stin2 polymorphism showed that males with genotype Stin2.12/Stin2.10 and allele Stin2.10 had higher risk for asthma than the others (Stin2.12/Stin2.10: OR = 2.291, 95% CI: 1.195 and 4.390; Stin2.10: OR = 1.942, 95% CI: 1.069-3.527). No significant difference was found in the frequencies of genotype and allele distribution of the 5-HTTLPR locus between the asthma and healthy control groups and the two stratified by gender.</p><p><b>CONCLUSION</b>The Stin2 polymorphism may play a role in the onset of male asthma. There might be association between the genetic pathogenesis of asthma and depression.</p>


Subject(s)
Adult , Female , Humans , Male , Alleles , Asthma , Epidemiology , Genetics , Case-Control Studies , Comorbidity , Depression , Epidemiology , Genetics , Genome-Wide Association Study , Genotype , Polymorphism, Genetic , Serotonin Plasma Membrane Transport Proteins , Genetics
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