Naidu, Priscilla Iswari Vythilingum2021-12-182021-12-182021https://hdl.handle.net/10539/32458A research report submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in partial fulfilment of the requirements for the degree of Master of Medicine in Psychiatry, 2021A consistent finding in psychiatry is Hypothalamic-Pituitary-Adrenal (HPA) axis activation in major depression. These findings would usually be expressed as hypercortisolism at baseline (Alheira,2005; Mackin, 2004; Manthey, 2011; Young, 2004). However, there are contradicting studies illustrating hypocortisolism secondary to chronic stress or depression as a result of fatiguing of the HPA axis (Yehuda, 1995; Oldehinkel, 2001). Major depressive disorder is a significant burden in South Africa, with a lifetime prevalence of 9.7 % (Tomlinson, 2009). Thus, it is important to understand the pathophysiology exhibited in a South African population group, in order to better the management provided. AIM: This study aimed to assess the severity of depression using salivary cortisol levels, as well as the Hamilton Depression Rating Scale (HAMD), both pre and post antidepressant therapy. METHOD: This was a prospective and quantitative study, looking at the change in cortisol levels using salivary cortisol samples and Hamilton Depression Rating Scale (HAMD) scores, before and after one month of antidepressant therapy, in a South African group of treatment naïve participants. RESULTS: Forty-three participants were initially recruited for this study, of which only 28 had complete data sets at the end of the study. The majority of the sample population consisted of black (89.3%), unmarried (85.7%) and unemployed (61.7%) females (92.9%), primarily in the 18-34 year old age group (60.7%) who had attained a secondary school level of education(85.7%). Prior to antidepressant therapy, majority of the participants exhibited elevated HAMD scores (median HAMD score of 27.5; range: 16-38) and morning hypocortisolism (median cortisol level of 0.80 nmol/L; range: 0.03-5.21); with a significant negative correlation between HAMD scores and cortisol levels at baseline. After administration of antidepressant therapy for one month, it was found that there was no significant change in cortisol concentration (median cortisol level of 0.80 nmol/L; range: 0.10-7.59). However, there was a significant decrease in HAMD score (median HAMD score of 18.5; range: 8-37). The reduction in HAMD score was <50%, thus implying considerable residual depressive symptoms. Cortisol findings were found to not be significant. There were no statistically significant difference between the change in HAMD from baseline to after one month of treatment (∆) HAMD scores and demographical data. There were also no statistically significant difference between ∆cortisol levels and demographical data. CONCLUSION: This study did not find high circulating cortisol due to HPA axis dysregulation amongst depressed participants, but rather hypocortisolaemia. It is postulated that, similar to other studies which reported these findings, the low cortisol levels may 105be attributed to chronic stress experienced by the participants as a result of their lower socioeconomic and disadvantaged backgrounds. Treatment with an antidepressant had no impact on the cortisol levels. Hence, cortisol levels in this population is not always useful as a predictor of the severity of depression or as a measure of the response to treatment as there was some improvement in the HAMD but none in the cortisol levelsenThesis