To investigate the association of glutathione-S-transferase (GST) polymorphisms with the risk of acute myeloid leukemia (AML), a meta-analysis of case-control studies published between 1998 and 2009 was performed. Pooled odds ratios (ORs) were assessed using both fixed- and random-effects models. Heterogeneity across studies was calculated, and funnel plots were constructed to test for publication bias. Overall, the random-effects OR with GSTM1 null genotype, GSTP1 Val105 allele and GSTT1 null genotype were 1.30 (95% confidence intervals (CI) 1.04-1.62, p = 0.018), 1.03 (95% CI 0.80-1.33, p = 0.80) and 1.24 (95% CI 0.98-1.58, p = 0.06), respectively. Statistically, significant increased risk of AML was observed with GSTM1 while borderline significance was seen with GSTT1 null genotypes. However, fixed-effects model showed significant risk of AML in the presence of null genotypes of GSTM1 and GSTT1(p < 0.05). Significant heterogeneity was found between studies relating to GSTP1 (p = 0.162), however, no heterogeneity was seen in studies that evaluated GSTM1 (Q-value = 44; I(2) = 70.9; p-value < 0.01]; and GSTT1 (Q-value = 26.03; I(2) = 57.74; p-value < 0.01] polymorphisms. From the limited studies on the association of GSTP1 with risk of AML, the role of this gene cannot be ascertained fully. Significant association of these three genes with risk of AML must be evaluated further with respect to population, smoking, eating habits, ethnicity, and race.

A meta-analyses of endothelial nitric oxide synthase (eNOS) and angiotensin-converting enzyme (ACE) gene polymorphisms in pre-eclampsia was performed. We shortlisted 33 studies (17 for ACE; 16 for eNOS gene polymorphisms), of which 29 articles (16 for ACE and 15 for eNOS) were analysed. Overall, 1,620 cases with pre-eclampsia and 2,158 controls were analysed for intron 16 insertion-deletion polymorphism in ACE gene. A total of 1,610 subjects with pre-eclampsia and 2,875 controls were analysed for the Glu298Asp in eNOS gene. Overall, the random-effects odds ratio (OR) with Glu298Asp in eNOS gene was 0.958 (95% confidence intervals, CI 0.747-1.228, p > 0.05), and for the insertion-deletion/ACE polymorphism was 0.987 (95% CI 0.698-1.395, p > 0.05). Significant heterogeneity was observed in the studies that evaluated polymorphisms in ACE (Q value = 55.6; I(2) = 73; p value = 0.000); and eNOS (Q value = 37.2; I(2) = 62.4; p value = 0.001) polymorphisms. No significant risk of pre-eclampsia was observed in both eNOS and ACE genes with these polymorphisms.

Vitamin D receptor (VDR) gene polymorphisms were reported to influence blood lead levels (BLL) and the response of subjects to the symptoms of lead toxicity. However, no studies have been conducted in the Saudi Arabian population which has unique ethnicity and socio-demographic features. This study examined the polymorphisms in exon 2 (allele 1) and intron 8 (allele 2 and allele 3) of VDR gene and their relation to BLLs. As per the CDC guidelines, the recruited lead-exposed workers ( N = 130) were categorized to two groups viz., low BLL group (<10 μg/dL) and high BLL group (>10 μg/dL). The low BLL group had a mean BLL of 4.37 μg/dL, while the high BLL group had levels of 18.12 μg/dL ( p < 0.001). Overall, the genetic variants, TC and CC in the VDR FokI were significantly associated with a risk of lead toxicity and the allele “C” was a risk factor ( p = 0.00026). Furthermore, the TT genotype of VDR ApaI significantly increased the risk of developing lead poisoning ( p = 0.0006). The VDR TaqI SNP was not significantly associated with lead toxicity. The highest BLLs for VDR FokI-CC, VDR ApaI-GG, and VDR TaqI-TT genotypes from High BLL group were 18.42, 15.26, and 18.75 μg/dL, respectively. Older age (51–60 years) was found to be a significant confounding factor for BLLs ( p = 0.012). Additional studies in larger sample sizes are needed to firmly establish the role of VDR genotypes and genetic susceptibility to lead poisoning.

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