Objectives
To conduct a household and biomarker survey to assess the baseline prevalence of folate deficiency and insufficiency and vitamin B12 deficiency in women of reproductive age prior to the start of a wheat flour fortification program in the Ambala District in Haryana, India.
Methods
A multistage cluster probability household and biomarker survey was conducted. Participants were women of reproductive age (18–49 y) who were not pregnant and resided in rural areas of two subdistricts in Ambala District in Haryana. Venous blood samples were collected among 866 women. Plasma, serum, and red blood cells (RBC) were separated by centrifugation, processed, and stored at <-80ºC until analysis. RBC and serum folate concentrations were measured using microbiologic assay and serum vitamin B12 was measured via chemiluminescence. Serum folate deficiency was defined as serum folate <7 nmol/L and RBC folate deficiency and insufficiency were defined as RBC folate <305 nmol/L and <748 nmol/L, respectively. Vitamin B12 deficiency was defined as vitamin B12 <200 pg/mL and vitamin B12 marginal deficiency was defined as vitamin B12 ≥200 and <300 pg/mL.
Results
The geometric mean concentrations for serum folate, RBC folate, and serum vitamin B12 were 12.3 (95% confidence interval [CI]: 11.8, 12.9) nmol/L, 544 (95% CI: 516, 573) nmol/L, and 190 (95% CI: 176, 206) pg/mL, respectively. The prevalence of folate deficiency was 11.3% (95% CI: 9.2, 13.9) for serum folate and 9.7% (95% CI: 7.8, 12.0) for RBC folate, and the prevalence of RBC folate insufficiency was 78.6% (95% CI: 74.8, 82.5). A total of 58.3% (95% CI: 54.2, 62.5) of women were vitamin B12 deficient (<200 pg/mL) and an additional 22.9% (95% CI: 19.7, 26.1) were marginally deficient for vitamin B12.
Conclusions
The magnitude of folate insufficiency and vitamin B12 deficiency in this Northern Indian population is a substantial public health concern. The findings from the survey help establish the baseline for a planned wheat flour fortification program aimed at reducing these micronutrient deficiencies.
Funding Sources
Centers for Disease Control and Prevention.
Introduction: Inherited Factor VII (FVII) deficiency is commonest among the rare bleeding disorders. A small number of patients present in infancy with severe bleeding, and many may remain asymptomatic but detected before surgery/invasive procedures. Genetic testing may be helpful in predictive testing/prenatal diagnosis in severe cases. Aim: Characterisation of clinical and genotypic spectrum of patients with inherited FVII deficiency. Methods: Retro-prospectively, 35 cases with prolonged prothrombin time and FVII activity (FVII:C) <50 IU/dl were subjected to targeted resequencing. After in-silico analysis, variant/s were validated by Sanger sequencing in index cases and family members. Haplotype analysis was done for F7 polymorphisms. Results: Severe FVII deficiency was found in 50% of patients (FVII:C ≤1 IU/dl), and 42.9% were asymptomatic. Clinical severity assessment revealed 17% severe, 17% moderate and 22.9% patients with mild bleeds. FVII levels ranged from .3 to 38 IU/dl. Molecular analysis revealed variants in 30/35 cases, of which 17 were homozygous, 10 were compound heterozygous and 3 were heterozygous. Twelve genetic variants were identified, one promoter variant c.-30A>C; seven missense (c.215C>G, c.244T>C, c.253G>C, c.904G>A, c.961C>T, c.1109G>T, c.1211G>A), two deletions (c.21delG, c.868_870delATC), and one each of nonsense c.634C>T and splice-site variant c.316+1G>A. Recurrent variants c.1109G>T and c.215C>G were found in 17 and 8 cases, 12 of the former cases were homozygous. They had the same haplotype, indicating the founder effect in North Indians. Conclusion: This is the largest cohort of FVII genotyping from India, confirming heterogeneity in terms of clinical manifestations, FVII activity and zygosity of the variants with a limited genotypic phenotypic correlation.
The association of the fibrinolytic markers with deep vein thrombosis (DVT) is still a matter of debate. The present study aimed to investigate the association between fibrinolytic markers and DVT. This observational study recruited 52 adult cases with lower limb DVT and 52 healthy adult volunteers as controls. The quantitative determination of plasminogen activator inhibitor-1 (PAI-1), plasminogen, thrombin activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA) and a2antiplasmin (a2-AP) was performed by ELISA. TAFI, plasminogen and t-PA were significantly higher in cases than controls and PAI-1 was significantly lower in cases than controls. In addition, TAFI, plasminogen and t-PA levels were significantly increased in unprovoked and idiopathic DVT cases than controls. The present study suggests that the fibrinolytic markers tested in patients with a remote history of DVT are different than in individuals with no history of DVT and, with further study, may prove useful as screening assays for
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