RESUMO
Background: The Val66Met single nucleotide polymorphism (SNP) of the brain-derived growth factor (BDNF) and deletional mutation of the cytochrome P4502D6 (CYP2D6) have been reported to be linked to the etiology and severity of depressive disorders (DD) in a variable manner among different ethnicities and populations. Aims: The present study was aimed to find the relationship of mutational variations of these two neurotrophins with the severity of DD and their serum cortisol levels as a marker of the stress factor. Methods: In 104 drug-naïve newly diagnosed cases of DD and 106 control subjects, the severity of depression was assessed using the HAM-D score. Val66Met SNP of the BDNF was analyzed in them using restriction digestion of its polymerase chain reaction (PCR) product. CYP2D6 deletional variants were detected by the absence of their PCR products. Serum cortisol levels were measured by the enzyme-linked immunosorbent assay (ELISA) technique. Results: The Chi-square test (Χ2 = 1.42, P = 0.49) did not show any higher prevalence of Val66Met SNP of the BDNF gene in the case group. A correlation coefficient (R) of -0.14 for HAM-D score with a P value of 0.29 signified no direct link of the severity of DD with this SNP. However, a Χ2 of 12.68 with P < 0.001 indicated a significantly higher prevalence of the CYP2D6 deletional mutants in DD cases, whereas an R-value of 0.39 for HAM-D score with P < 0.001 suggested a significantly higher severity of DD having with them. Serum cortisol level showed a significant positive correlation with the deletional variants of CYP2D6 (R = 0.198, P = 0.04) and the HAM-D score (R = 0.22, P = 0.025). Conclusion: We conclude that CYP2D6 deletion significantly contributes to the severity and stress factor in the DD patients in our study population. Early identification of these mutations may provide important molecular and cellular predisposition for the disease and may lay the ground for possible more effective measures of intervention.