Calcutta National Medical College

Abstract Background: Hypertension commonly coexists with chronic kidney disease (CKD), accelerating renal decline and increasing cardiovascular risk. Optimal blood pressure (BP) control is crucial to prevent CKD progression. Among antihypertensives, calcium channel blockers and diuretics are key components. This study compared the efficacy and renal safety of two combinations – amlodipine–torsemide and amlodipine–chlorthalidone – in hypertensive CKD patients. Materials and Methods: A prospective, observational, comparative study was conducted over 12 months among 90 adults with CKD (estimated glomerular filtration rate [eGFR]: 30–90 mL/min/1.73 m 2 ) and hypertension. Participants were randomly assigned to receive either amlodipine + torsemide (Group A) or amlodipine + chlorthalidone (Group B). Primary endpoints included changes in systolic BP (SBP) and diastolic BP, eGFR, and urine albumin-to-creatinine ratio (ACR). Data were analyzed using SPSS v22, with statistical significance set at P < 0.05. Results: Both the regimens produced significant BP reductions from baseline ( P < 0.001) with no intergroup difference (mean SBP fall: 23.0 ± 3.7 vs. 24.5 ± 4.1 mmHg; P = 0.18). The chlorthalidone group showed a significantly greater reduction in ACR (119.7 ± 17.6 vs. 88.7 ± 14.8 mg/g; P = 0.021) and a slower decline in eGFR (−7.3 ± 3.1 vs. −10.2 ± 2.8 mL/min/1.73 m 2 ; P = 0.043), suggesting superior renal preservation. Ultrasonographic kidney dimensions remained unchanged, and adverse effects were mild and comparable. Conclusion: Both the combinations effectively controlled BP in hypertensive CKD, but amlodipine–chlorthalidone offered better renoprotective benefits without added safety concerns. Larger multicentric trials are recommended to confirm these findings.

Aims: Adolescent suicide is a leading cause of mortality worldwide, yet prediction remains limited by symptom-based clinical assessment. This study aimed to synthesise genetic, biological, neuroimaging and sociocultural evidence to develop a mechanistically informed framework for adolescent suicide risk, moving beyond single-domain or correlational models. Methods: We conducted a PRISMA-compliant systematic review and meta-analysis registered with PROSPERO (CRD420251020839). Searches of PubMed, EMBASE, PsycINFO, CENTRAL, Scopus and Web of Science identified studies published between 2005 and 2025 involving adolescents aged 10–19 years reporting suicidal ideation, suicide attempts or death by suicide. Eligible studies contributed data from at least one domain: genome-wide association studies or polygenic risk scores, neuroimaging, inflammatory or neurotrophic biomarkers, sociocultural risk factors, or treatment outcomes related to lithium, sodium valproate or electroconvulsive therapy (ECT). Random-effects meta-analysis generated pooled effect sizes, with heterogeneity quantified using I². Machine-learning analyses used harmonised study-level estimates only, employing XGBoost with nested cross-validation and SHAP interpretation. Mendelian randomisation was applied to explore genetically informed pathways. Results: A total of 140 studies comprising 1,526,000 adolescents from 80 countries were included. The pooled effect size for suicide risk across domains was d=0.71 (95% CI 0.58–0.83; I²=78%). Significant predictors included polygenic risk for major depressive disorder (r=0.21), elevated interleukin-6 (r=0.38) and C-reactive protein (r=0.32), ventromedial prefrontal cortex hypoactivity (r=−0.31), childhood trauma (r=0.42) and sexual and gender minority stress (r=0.44) (all p<0.001). An integrative Bio-Psycho-Social Suicide Risk Index achieved an internally validated area under the curve of 0.93, interpreted as hypothesis-generating. Mendelian randomisation supported genetically informed pathways linking liability to inflammation and neural dysfunction. Secondary exploratory analyses suggested associations between lithium and reduced inflammatory markers, sodium valproate and improved inhibitory neurotransmission, and ECT and increased hippocampal volume. Conclusion: Adolescent suicide reflects interacting genetic, neurobiological and sociocultural processes. This global meta-analysis provides the most comprehensive mechanistic synthesis to date and proposes a biologically informed framework to complement clinical judgement. Prospective external validation is required before clinical implementation.

Psoriasis is a chronic, debilitating disease of inflammatory dermatoses. IL-17 plays a pivotal role in the pathogenesis of psoriasis. It acts as a driving force in psoriasis and has a significant role in keratinocyte proliferation, plaque progression, neutrophil recruitment, forming an amplification loop, and formation of tissue-resident memory T helper cells causing relapse. Ixekizumab is a humanized IgG4 monoclonal anti-IL-17 antibody approved for psoriasis in 2016. We are reporting a series of 22 patients presented with moderate to severe psoriasis treated with ixekizumab. 31.8% of patients had pre-existing comorbidities like Hypertension, diabetes, or hypertriglyceridemia. After 14 weeks of treatment, the Mean ± SD PASI improved from 30.82 ± 7.06 to 2.82 ± 3.12. At the end of treatment (14th week), PASI75, PASI 90, and PASI 100 were achieved by 95.45%, 68.18%, and 27.27% of patients, respectively. Friedman's ANOVA shows a significant decrease (P < 0.05) in PASI, BSA, and sPGA scores starting from the 1st follow-up (2 weeks) onwards. Paired t-test shows a significant decrease in PAsI, BSA, and sPGA reduction, P < 0.0001 between baseline and 7th follow-up visit (14 weeks). No significant side effects were noted in this period. The present study illustrates the experience with ixekizumab in real-world clinical practice, confirming its effectiveness and safety in the management of plaque psoriasis patients.