Vydehi Institute of Medical Sciences and Research Centre (VIMS) is in Whitefield, Bangalore, India. It is an independent medical institute dedicated to education, research and patient care. VIMS was established in 2000 and is promoted by Srinivasa trust.
Vascular disorders of the intestine (VDI) and ischemic heart disease (IHD) are linked by shared atherosclerotic risk factors including diabetes, hypertension, and smoking. Their coexistence poses a significant threat to population health, with associated high morbidity and mortality. While advances in care have improved outcomes, evolving trends and disparities remain under-investigated at the national level. This study assessed national mortality trends and demographic disparities in deaths attributed to vascular disorders of the intestine and ischemic heart disease among all age groups in the United States from 1999 to 2023. We used the CDC WONDER Multiple Cause of Death database (1999–2023) and identified deaths in which ICD-10 code K55 (vascular disorders of the intestine) and ICD-10 codes I20–I25 (ischemic heart disease) were concurrently listed on the same death certificate. Age-adjusted mortality rates were calculated and stratified by sex, race/ethnicity, and U.S. census regions. Joinpoint regression analysis was applied to evaluate temporal trends and compute annual percent change with 95
Psoriasis is a chronic, systemic inflammatory disease characterized by combined epidermal and immunological pathology. It is becoming recognized as a metabolic inflammatory disorder caused by interleukin (IL)-23/Th17 axis imbalance and lipid metabolism dysfunction. Peroxisome proliferator-activated receptors (PPARs), including peroxisome proliferator-activated receptor alpha (PPARα), peroxisome proliferator-activated receptor beta/delta (PPARβ/δ), and peroxisome proliferator-activated receptor gamma (PPARγ), regulate metabolic homeostasis and immune tolerance, making them potential targets for treating the psoriatic march of comorbidities such as obesity, insulin resistance, psoriatic arthritis, non-alcoholic fatty liver disease, and accelerated atherosclerosis. This review aims to summarize current evidence on PPAR isoform-specific roles in psoriatic pathogenesis, explore the molecular mechanisms that link PPARs to cutaneous and systemic inflammation, and assess the therapeutic potential and translational challenges of PPAR-directed pharmacotherapy. Peer-reviewed research on PPAR biology in psoriasis, metabolic comorbidities, and the clinical effectiveness of PPAR ligands was identified by a comprehensive literature search of PubMed/MEDLINE, Scopus, and Web of Science (2014-2024, with seminal papers from 2000+). Real-world evidence, randomized controlled trials, and mechanistic studies were given priority in the analysis. In psoriatic lesions, PPARγ is downregulated, leading to nuclear factor-κB and signal transducer and activator of transcription 3 deregulation. This promotes keratinocyte hyperproliferation and Th17 cell differentiation. PPARβ/δ is overexpressed, leading to anaerobic glycolysis and peroxisomal fatty acid β-oxidation. This depletes structural barrier lipids and maintains hyperplasia. Reduced PPARα inhibits lipogenesis at the epidermal barrier. Thiazolidinedione agonists (pioglitazone, rosiglitazone) have modest but clinically significant anti-psoriatic efficacy when combined with traditional systemic medicines, resulting in cardiometabolic benefits. Preclinical studies suggest that PPAR-selective antagonists, such as 4-chloro-N-(2-{[5-trifluoromethyl)-2-pyridyl] sulfonyl} ethyl)benzamide 3 (GSK3787) for PPARδ, outperform broad agonism. Topical PPAR ligand bioavailability remains inadequate, necessitating innovative delivery strategies. Although PPAR modulation offers a dual-benefit treatment approach that simultaneously suppresses metabolic dysregulation and cutaneous inflammation, there are still significant gaps between genetic potential and clinical reality. Future directions include patient biomarker stratification, dual/selective agonists (glitazars), and sensible combination with biologics that target tumor necrosis factor-alpha/IL-17/IL-23. This review reframes PPARs as key players in the relationship between psoriasis and metabolic syndrome by synthesizing molecular understanding and clinical data.
Background: Progressive dilation of the ascending aorta after aortic valve replacement (AVR) is increasingly recognized and may coexist with aneurysms of supra-aortic vessels such as the innominate artery. Concomitant pathology in the ascending aorta and innominate artery presents complex technical challenges, particularly in a redo sternotomy setting. Case presentation: We describe a 30-year-old male with prior mechanical AVR who was incidentally found on routine imaging to have a dilated ascending aorta with a saccular aneurysm of the innominate artery. After multidisciplinary evaluation, he underwent elective redo median sternotomy with ascending aorta and hemiarch replacement and re-implantation/reconstruction of the innominate artery. Cerebral protection strategies and meticulous surgical technique were used. The postoperative course was uneventful; the patient was extubated on day 1, ambulated on day 2 and discharged in stable condition with preserved neurological function. Conclusion: With careful preoperative planning, cerebral protection, and experienced surgical execution, redo sternotomy with hemiarch replacement and innominate artery reconstruction can be carried out safely in selected patients. Vigilant imaging surveillance after AVR permits elective intervention prior to emergent complications. Keywords: Ascending aortic aneurysm, Innominate artery aneurysm, Redo sternotomy, Hemiarch replacement, Cerebral protection, Aortic valve replacement
The accuracy of computed tomography (CT) parameters in the preoperative diagnosis of benign adrenal lesions, such as adrenal schwannoma (AS) and adrenal ganglioneuroma (AG), has not been systematically studied. Hence, we aimed to analyze CT features of AS/AG to distinguish them from other lipid-poor, poor-washout adrenal masses. Description of our AS/AG cohort, along with systematic review of literature for histopathologically confirmed AS/AG and available CT characteristics (providing unenhanced, early venous, and delayed venous phase attenuation). These were compared with our previously published cohort of other lipid-poor, poor-washout adrenal masses (n = 47). The cohort included AS (n = 30; literature:25, our center:5), AG (n = 27; literature:25, our center:2). AS and AG were similar, except AG patients were younger (28 vs. 49.5 years, p = 0.003). All AS and 92.5
Venolymphatic malformations (VLMs) are rare congenital disorders involving the vascular and lymphatic systems. They are characterized by altered endothelial differentiation rather than true neoplastic proliferation, with lesion enlargement occurring in response to hormonal or inflammatory stimuli. We report a case of a 15-year-old male who presented with slow-growing swelling over the right parotid region that worsens with trauma, requiring multidisciplinary care. Clinical examinations and imaging findings on ultrasound and magnetic resonance imaging were suggestive of VLM, a low-flow venous malformation, and a cystic epidermoid lesion of the right parotid gland. The patient went under image-guided sclerotherapy under interventional radiology guidance. This case highlights the importance of multimodal imaging in establishing the diagnosis of VLM and demonstrates the role of sclerotherapy as an effective minimally invasive treatment option for selected head and neck swellings.
