Djidjik et al. (2008) investigated the role of NOS1 -84 G>A and NOS3 -786 T>C, 894 G>T and 27 base pair (bp) repeat polymorphisms in 125 patients suffering from asthma and/or rhinitis and mono-sensitized against Dermatophagoides pteronyssinus (Dpter) and 111 controls from Algeria. Results indicated a higher frequency of the -786 C NOS3 allele in patients than in controls [corrected P value (Pc) = 0.04], especially in female cases (Pc = 0.02) and that the 'ab' genotype of the 27-bp polymorphism was significantly associated with specific immunoglobulin E production against Dpter (P = 0.006) and demonstrating a possible participation of NOS3 gene polymorphism in the pathogenesis of respiratory allergic disorders.

Alfadhli et al. (2008) investigated evidence for the association of eNOS gene polymorphism with alopecia areata (AA). Genomic DNA was extracted from 176 subjects, 87 Kuwaiti AA patients and 89 matched (for ethnicity, gender and age) healthy controls. A significant association was found between the intron-4 27 bp-VNTR and AA, where 4b was identified as the risk allele had (chi(2) = 4.42, p = 0.035, OR = 2.03). Genotype (4b/4b) was found to have a significant association with susceptibility to AA and had a frequency of 22% higher in AA patients than in healthy controls (71 vs 49%) and a chi(2) = 6.39, (p = 0.011, OR = 2.63). Alfadhli et al. (2008) concluded that a significant association of a polymorphism within the eNOS gene and susceptibility to AA was found.

Ali et al. (2013) partly investigated the association of the eNOS G894T (p.E298D) polymorphism with hypertension in Saudi subjects.  This study involved 250 controls and 120 cases with hypertension, among which 51 were obese and diabetic.  Genotypic and allelic frequencies were obtained through a PCR-based reaction assay using hybridization probes specific to the polymorphic variant.  All cases showed no difference in the carrier frequency of the mutant eNOS p.E298D allele relative to controls.  Hypertensive cases with obesity and diabetes showed a higher carrier frequency of the mutant p.E298D allele than controls, albeit with no significance (p=0.34).  Filtering hypertensive cases with combined genotypes of the ACE insertion/Deletion and eNOS p.E298D alleles, only the mutant ACE D allele showed significant association.  Genotype data was filtered through gender, age, parental consanguinity, and smoking, each of which showed no significant association with susceptibility to hypertension (p>0.05).  Results suggest that the eNOS p.E298D variant does not predispose to hypertension.