Objective: Depression is one of the most common mood disorders. Patients with major depressive disorder (MDD) usually present alterations in various cognitive functions. Several cost-effective interventions have shown favorable recovery and positive outcomes in the care and management of depression. The objective of the study was to compare the effect of fluoxetine (selective serotonin reuptake inhibitors), and venlafaxine (serotonin-norepinephrine reuptake inhibitors) on cognitive functioning in patients with MDD. Methods: This prospective, single-blinded, randomized, and comparative interventional clinical study was conducted in a tertiary care hospital in Haryana. Fifty-two patients of MDD (ICD-10) were randomly divided into two groups: Group F and Group V, allocated to receive fluoxetine and venlafaxine, respectively. The assessment was done during the enrolment and at the end of the 3rd, 6th, 9th, and 12th weeks of treatment using the ABC-Hamilton Depression Rating Scale (HAM-D) and Montreal Cognitive Assessment (MoCA) Scale. Statistical Analysis Used: The intragroup analysis was performed using repeated measures ANOVA while intergroup analysis was performed using unpaired “t”-test. p<0.05 was considered statistically significant. Results: Mean HAM-D score was clinically as well as statistically significant at the end of the 12th week of treatment as compared to baseline in both the groups while on the intergroup comparison, there was no statistically significant difference in both groups. The mean MoCA score was (25±2.19) in Group F and (23.76±6.97) in Group V at the end of the 12th week. On intergroup analysis at the 12th week, a statistically significant improvement in cognitive functions was observed in patients Group F as compared to Group V (p<0.05). Conclusions: The study of fluoxetine comparatively better improves cognition functions as compared to venlafaxine.

Objective: Psoriasiform drug eruptions can be induced by several drugs. Psoriasis is a chronic inflammatory disease characterized by T-cell-mediated cytokine production that drives the hyperproliferation and abnormal differentiation of keratinocytes. Drugs can cause new lesions when there is no prior history or family history of psoriasis. Based on the psoriatic drug eruption probability score, β‐blockers, synthetic anti‐malarial drugs, non‐steroidal anti‐inflammatory drugs (NSAIDs), lithium, digoxin and tetracycline antibiotics are relevant in psoriasis. Methods: A 58-year-old male was admitted to the Department of Respiratory Medicine at B. P. S G. M. C, Khanpur Kalan, Sonepat as a case of pulmonary tuberculosis and was put on anti-tubercular drugs CAT-I (according to RNTCP guidelines). The patient had a history of diabetes mellitus and hypertension for the past six years. On the third day of initiation of ATT, the patient started developing a psoriasiform rash. The psoriasiform rash began to improve within a few days after discontinuing the ATT. A causality assessment was done as per the WHO-UMC scale, which showed that the adverse events were likely caused due to the ATT. Results: Psoriasiform rash is a severe adverse drug reaction characterized by widespread lesions. Among all the various adverse drug reactions, lichenoid drug eruption is commonly associated with anti-tuberculosis medication and needs to be differentiated from psoriasiform eruption. The underlying pathomechanism of drug-induced psoriasiform eruptions remains uncertain, although several immunological interactions have been hypothesized. Conclusion: ATT has been reported to cause psoriasiform rash, and its drug component needs to be reconsidered in view of safer alternatives available.