Varashree Bolar Suryakanth

Objectives: To determine the pooled prevalence of sarcopenia phenotypes and synthesise the evidence on factors associated with sarcopenia among adults with type 2 diabetes mellitus (T2DM) in India. Design: Systematic review and meta-analysis. Data sources: PubMed, Embase, Scopus and Web of Science were searched from inception to 14 January 2026, supplemented by reference list and citation searching. Eligibility criteria for selecting studies: Cross-sectional studies of Indian adults (≥18 years) with T2DM reporting sarcopenia prevalence using Asian Working Group for Sarcopenia (AWGS) diagnostic criteria. Data extraction and synthesis: Two reviewers independently screened and extracted data. Methodological quality was assessed using the Joanna Briggs Institute prevalence checklist. Proportions were logit-transformed and pooled using random-effects models with Hartung-Knapp CIs and prediction intervals. Associated factors were synthesised narratively within a tiered framework separating adjusted from unadjusted ORs. Results: Seven studies (n=1359) were included. Pooled confirmed sarcopenia prevalence (AWGS 2019, k=6) was 27.4% (95% Hartung-Knapp CI 18.9% to 37.9%) but highly imprecise: I²=91.7% and the 95% prediction interval ran from 6.9% to 65.6%. Subgroup analysis showed 20.2% for dual-energy X-ray absorptiometry versus 31.7% for bioelectrical impedance analysis (Q between p=0.011). Severe sarcopenia was 11.0% (k=5) and sarcopenic obesity 25.2% (k=4); possible sarcopenia (65.6%, k=3; I²=98.6%) was too heterogeneous to interpret. In the two studies reporting adjusted estimates, hypertension (both studies) and diabetes duration ≥10 years (one study) were positively but imprecisely associated with sarcopenia. Certainty was very low for all prevalence outcomes (Grading of Recommendations Assessment, Development and Evaluation (GRADE)). Conclusions: Sarcopenia appears common among Indian adults with T2DM, at approximately one in four, but certainty is very low and the plausible prevalence in a new cohort spans roughly 7% to 66%. These estimates are not a sufficient basis for a screening recommendation, but justify greater clinical awareness and, above all, community-based, dual-energy X-ray absorptiometry-standardised prospective studies, including from South India. PROSPERO registration number: CRD420251251024.

Introduction: Pulmonary arterial hypertension (PAH) is relatively uncommon yet life-threatening morbidity in neonates and infants. South Asian countries including India may record a relatively higher incidence of pediatric PAH. The etiology of pediatric PAH is heterogeneous, and little evidence is available on the clinical spectrum of pediatric PAH from low- and middle-income countries. This descriptive study aims to describe the incidence and underlying causes of pediatric PAH at a tertiary care referral center in coastal Karnataka, India. Materials and Methods: This is a retrospective study which involved complete enumeration of pediatric PAH cases admitted at a tertiary care referral center in coastal Karnataka between January 2018 and December 2021 after prior approval from the Institutional Ethics Committee. Clinical data were retrieved from the electronic medical records. Results: The center documented a total of 165 cases of pediatric PAH, with an incidence of 1.19% among the total neonatal intensive care unit admissions within the study period. Persistent fetal circulation was the most common sub-classification (77.44%), with underlying inherited metabolic disorders (30%), infectious pathologies, and malnutrition being the final diagnosis in this group. Neonates subclassified under neonatal cardiac failure majorly showed underlying cardiac anomalies (80%), while 4% of the cases were attributed to other causes including hyperbilirubinemia-induced encephalopathy and COVID-induced multisystem inflammatory syndrome, viral endocarditis, etc. Conclusions: Inherited metabolic and cardiac anomalies, antenatal and postnatal maternal morbidities, nutritional deficiencies, and secondary infections are the major causes of neonatal and infantile PAH. Multilevel screening could substantially reduce the incidence and the morbidities associated with infantile PAH.

Background: The disruption of metabolic pathways in patients with community-acquired pneumonia (CAP) may provide insights into disease progression. We aim to identify early disruption in the serum metabolome of CAP patients using untargeted metabolic approaches. Methods: We conducted a single-centre, prospective case-control study involving 105 participants (70 with CAP and 35 healthy controls), between January 2025 and November 2025. We also performed a subgroup exploratory metabolomic analysis among the 70 CAP patients, comparing 60 patients with severe CAP requiring ICU admission with the 10 non-severe CAP patients who did not require ICU admission. Untargeted serum metabolomics was performed using gas chromatography-mass spectrometry (GC-MS) to investigate metabolic dysregulation in patients with CAP. The analysis of the clinical data was performed using SPSS version 25.0. The data of metabolomics was analyzed using MetaboAnalyst version 6.0. After the preprocessing, log ₁₀ transformation, normalization and scaling, 93 GC-MS metabolites were retained from the initial 300 metabolites. Principal component analysis was done for unsupervised clustering, which was then followed by OPLS-DA for supervised group discrimination. Model performance was assessed using R²Y and cross-validation-derived Q² values, and model robustness and overfitting exclusion was further evaluated using permutation testing. Discriminatory metabolites were identified using VIP scores, fold change, log₂ fold change and univariate testing with false discovery rate correction where applicable. ROC analysis, heatmap-based clustering and pathway enrichment analysis were performed. Results: The variable importance in projection (VIP) scores showed that out of 93 untargeted metabolites studied using GC-MS, the greatest differences between the CAP patients and healthy controls were about malic acid (VIP:3.374, fold change 2.591), 4-hydroxybenzeneacetic acid (VIP:2.459, fold change 27.97), 2-hydroxybutyric acid (VIP:2.059, fold change 4.779), and 4-hydroxyphenyllactic acid (VIP:1.882, fold change 20.67). Key disrupted pathways in CAP patients included propanoate, glyoxylate, and dicarboxylate; tricarboxylic acid cycle; nitrogen; tyrosine, cysteine, and methionine; and amino acid pathways. Comparison between the severe CAP patients (ICU admission required) and non-severe CAP patients (no-ICU admission), VIP analysis identified boric acid, ethylene glycol, ethanimidic acid, linoleic acid, oleic acid, cholesterol, 3-hydroxybutyrate, and α-tocopherol as the principal discriminating metabolites, while pathway analysis revealed perturbations in glutathione metabolism, amino acid metabolism, the tricarboxylic acid cycle, pyruvate metabolism, and arachidonic acid metabolism. Conclusions: CAP patients demonstrated early disruptions of key metabolic pathways compared with healthy controls, spanning energy metabolism, amino acid pathways, redox balance, lipid inflammatory signalling, and gut–host metabolic axes. These findings highlight the potential utility of metabolomic profiling as an adjunctive clinical tool for early risk stratification and biochemical phenotyping in CAP. Trial registration: Clinical trials Registry of India (CTRI 2024/12/078631) registration was done 27.12.2024.

Preeclampsia (PE) remains a major contributor of maternal and fetal morbidity and mortality worldwide, affecting 2%–8% of pregnancies. While genetic predisposition, placental dysfunction, and angiogenic imbalance remain central to PE pathophysiology, emerging observational evidence suggests potential associations between environmental factors, epigenetic modifications, and PE development. This review consolidates available research linking environmental exposures, particularly air pollution, maternal gut microbiome composition, and dietary habits, with changes in epigenetic markers during pregnancy that may influence PE susceptibility. We synthesize findings from epidemiological studies, mechanistic research, and biomarker studies across this research area. However, definitive causal evidence linking specific environmental exposures to PE through epigenetic mechanisms remains limited. The majority of existing studies employ observational designs or focus on biological mechanisms; well-designed prospective cohorts incorporating direct environmental measurements and randomized intervention trials are lacking. Circulating biomarkers, including microRNAs and DNA methylation patterns, show associations with both PE status and prior environmental exposure, providing biological support for the concept that environmental factors may influence PE development. The maternal gut microbiome demonstrates dysbiosis in PE patients, and mechanistic studies in animal models suggest that microbiota-derived metabolites may influence placental development through epigenetic pathways; however, clinical evidence in humans remains preliminary. Integration of environmental exposure assessment with multi-omics profiling in large prospective studies is necessary to establish whether environmental factors causally contribute to PE pathogenesis. Future research combining detailed environmental characterization, longitudinal epigenomic profiling, and rigorous causal inference methods will be essential to translate these mechanistic insights into prevention and therapeutic strategies.

Background/Objectives: Fatty acids, the building blocks of lipids, contribute to numerous crucial life processes and are implicated in numerous disease pathologies. Circulating fatty acids can be extracted/trans-esterified to their respective methyl ester forms and quantified from a variety of biological samples. This study aims to identify quantifiable fatty acids (through alkali trans-esterification) in human circulation, assess the correlation of the detectable fatty acid methyl esters (FAMEs) compounds between whole blood, serum and plasma matrices and propose the most ideal matrix for quantification of FAMEs. Methods: This anonymised study was carried out in a tertiary hospital after obtaining ethical approval and involved analysis of residual fasting whole blood, serum and plasma samples obtained from 20 apparently healthy subjects attending the routine health check services at the study centre. Fatty acids were converted to its methyl ester form by methanolic KOH trans-esterification and subjected to GCMS analysis. Paired t test, Pearsons’s correlation, linear regression and Bland Altman test were employed to assess the agreeability between matrices. Results: 9 out of 37 FAME compounds were detected in all three matrices. Strong correlations and statistically significant regression equations were obtained for the 9 compounds between plasma and serum matrices. Undecanoate, pentadecanoate, linolenate, and palmitate levels were lowest in plasma, while stearate, heptadecanoate levels were highest in whole blood. Myristate was highest in serum, dodecanoate was highest in plasma while docosahexanoate was found to be comparable in all three matrices. Methyl ester forms of dodeconate, myristate, pentadecanoate, palmitate, heptadecanoate, stearate, and linolenate were observed in higher concentrations in plasma when compared to serum. Conclusions: The current study shows similar & correlating FAME concentrations between serum and plasma matrix; however, whole blood FAME concentrations appear significantly different. Plasma serves as the most ideal matrix for detection and quantification of circulating fatty acids.

Background: It was observed that many people in the western coastal belt were found to have a high HDL cholesterol, the cause of which was not known. This study was done to learn about the factors contributing to the high HDL cholesterol in these patients and its effect on ASCVD risk. Methods: In this prospective, case control study, 150 patients were recruited, of which 63 were cases (patients with high HDL cholesterol), and 87 were controls (patients with normal HDL cholesterol). Details regarding their diet, sea-food consumption, habits, comorbidities, daily activity (using GPAQ questionnaire), and blood reports were collected. ASCVD risk score was calculated using an online ASCVD risk estimator. Blood samples of 96 patients (cases 40, controls 56) was tested for cholesterol esterase transfer protein (CETP) levels using ELISA, and the results were compared. Results: Patients with high HDL cholesterol were found to be physically more active and had median metabolic equivalent (METs) of 4680 (1200, 8580) compared with controls with median METs of 1680 (720, 5580), P-0.013. Cases had a lower mean BMI 23.09(SD-3.69), than in patients with normal HDL cholesterol with a mean of 24.41(SD-4.01), P-0.04. Cases also had a lower triglyceride level (91(69,118) in cases vs 121 (80,151) in controls, P-0.002. Alcohol and sea food consumption had no role on HDL levels in this study. The median CETP level was lower in patients with high HDL levels, 0.336(0.08, 0.336) versus 1.435(0.061, 2.893) in the control group although not statistically significant. Patients with high HDL cholesterol were found to have a significantly lower median 10-year ASCVD risk score 3.05 (0.6, 8.95), compared with patients with normal HDL 6.45 (2.7,14.2). Conclusion: Patients with high HDL cholesterol were found to be physically more active, had a lower BMI, a lower triglyceride level, and a lower ASCVD risk compared with controls. They also had a lower CETP level. Further research will be required to determine the normal CETP level in Indian population, their genetic makeup, and whether it has a role in cardiovascular protection.

Preeclampsia (PE) is a hypertensive disorder in pregnancy affecting multiple organ systems. This study hypothesized that oxidative stress and inflammatory responses contribute to the pathogenesis of Preeclampsia, and that selenium and N-acetylcysteine (NAC) could mitigate these effects. The study was initiated after approval from the Institutional Animal Ethics Committee. Twenty-four female Wistar rats were divided equally into four groups. Group I served as controls, while Groups II, III, and IV received Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) to induce hypertension from day 10 to 20 of gestation. Additionally, Group III received selenium (240 μg/kg/day) and Group IV received NAC (160 mg/kg). On day 20, Blood Pressure (BP) monitoring and urine protein estimation were carried out to assess hypertension and proteinuria, while blood samples were collected to measure malondialdehyde (MDA) and interleukin-6 (IL-6) levels, as markers of oxidative stress and inflammation, respectively. Statistical analysis was performed using GraphPad Prism 10.2. Selenium improved L-NAME-induced hypertension (Mean BP 107.63±5.22 mmHg vs 140.9±8.38 mmHg in disease control (DC) and proteinuria (65.5±4.09 vs 140.2±11.85 mg/day in DC) and significantly reduced the inflammatory response (IL-6 23.4±1.06 vs 50.63±3.35 pg/mL in DC) but had little effect on oxidative stress (MDA 0.21±0.02 vs 0.24±0.02 nmol/mL in DC). NAC did not lower BP (Mean BP 129.33±7.96 mmHg) but significantly reduced proteinuria (92.7±6.37mg/day), IL-6 levels (18.24±0.42 pg/mL), and oxidative stress (MDA 0.16±0.01 nmol/mL). These findings suggest that selenium and NAC play distinct protective roles in the pathophysiology of preeclampsia, potentially offering synergistic effects for cardiovascular and kidney health in hypertensive pregnancies.

Background: Preeclampsia (PE) is a hypertensive disorder in pregnancy affecting multiple organ systems. This study hypothesized that oxidative stress and inflammatory responses contribute to the pathogenesis of Preeclampsia, and that selenium and N-acetylcysteine (NAC) could mitigate these effects. Methods: The study was initiated after approval from the Institutional Animal Ethics Committee. ...

The sustainable developmental goals emphasize good health, reduction in preventable neonatal and under-five mortalities, and attaining zero hunger. However, South Asian countries report a higher incidence of neonatal and under-five mortalities when compared to the Western world, many of which are attributed to maternal and perinatal micronutrient deficiencies. Isolated nutrient deficiency in the absence of calorie deficit poses a diagnostic challenge since such deficiencies present with acute multisystemic and enigmatic manifestations. Thiamine (vitamin B1) is a micronutrient of prime importance which exerts indispensable roles in energy metabolism. Deficiency of thiamine can lead to catastrophic consequences. This review provides insight into the biochemical actions of thiamine in energy metabolism, the compromised aerobic metabolism resulting from thiamine deficiency, and the crucial role of thiamine in the proper functioning of the nervous, cardiovascular, and immune systems. The review also explores the acute life-threatening consequences of thiamine deficiencies in neonates and infants and the speculative role of thiamine in other pathologies like encephalopathy, sepsis, and autism spectrum disorders. However, routine assessment of thiamine in pregnant women and neonates is yet to be implemented, due to the lack of affordable and automated diagnostic techniques, and the cost-intensive nature of mass spectrometry-based quantification. Conclusion: Physicians are recommended to have a low threshold for suspecting thiamine deficiency especially in vulnerable populations. Laboratory diagnosis of thiamine deficiency needs to be implemented as a standard of care, especially in endemic regions. Further, public health policies on food fortification, mandatory supplementation, and surveillance are imperative to eliminate thiamine deficiency-induced health hazards. What is Known:• South Asian countries report a higher incidence of neonatal and under-five mortalities, many of which are attributed to maternal and perinatal micronutrient deficiencies.• Preventable causes of neonatal/ infantile deaths include birth factors (low birth weight, birth asphyxia), infectious diseases (pneumonia, diarrhoea, tetanus, tuberculosis, measles, diphtheria, malaria, acute infections), deficiency diseases and genetic diseases (vitamin & mineral deficiencies, IEMs, congenital heart disease, unexplained PPHN, SIDS etc). What is New:• Acute thiamine deficiency presenting as multisystemic syndromes, has unfortunately been a long standing unresolved public health concern. However, accessible surveillance and diagnostic strategies remain elusive in most clinical settings.• Despite decades of reports and emerging guidelines, diagnosis of thiamine deficiency is often missed and policy mandates at national level are yet to be implemented even in endemic countries.• This review provides a comprehensive summary of the biochemical role of thiamine, its key functions and effects on major organ systems, the diagnostic gap, the enigmatic presentation of acute thiamine deficiency, the plausible role of thiamine in other pathologies and the preventive measures at individual and community level.

About 10 to 20% of reported pregnancies have complications like spontaneous abortion (SA), preeclampsia (PE), preterm birth (PTB), and fetal growth restriction (FGR); 60% are attributed to maternal nutritional alterations. Multiple micronutrients (MMN) are supplemented in the antenatal period, but no proper validation/guidelines are available regarding dosing/time, the need for initiation, and the duration of supplementation. Studies have reported adverse pregnancy complications related to the overuse/unwanted use of multiple micronutrient supplementations during pregnancy. Identifying the exact population requiring supplementation is necessary to prevent its abuse. This article attempts to review the impacts of micronutrient deficiency/supplementation in cases of SA, FGR, and gestational diabetes mellitus (GDM), preterm delivery and PE. The study used a literature search using PubMed, Google Scholar, Mendeley, and Scopus Databases using search words pregnancy, spontaneous abortion, gestational diabetes mellitus (GDM), fetal growth restriction (FGR), preterm delivery, preeclampsia (PE) or “adverse pregnancy” associated with minerals, micronutrients, or supplementation. The review also considered in-house literature databases, a single-window search at Kasturba Medical College (KMC) Health sciences library, MAHE (Manipal Academy of Higher Education). The figures included in the study were created by Biorender.com. Micronutrients play multiple roles during pregnancy and fetoplacental growth stimulating growth hormone secretion, Lysyl oxidase (LOX), involved in the crosslinking between collagen and elastin in the amniotic membrane, downregulation of interleukin (IL)-1 alpha, IL-1 beta, IL-4, IL-6, Il-10, IL-12, tumor necrosis factor (TNF)-alpha and several chemokines involved in hypertension, immune-inflammatory pathways, attenuate insulin resistance, structural development of neurons and glia. Over-supplementation has led to complications such as spontaneous abortion and gestational diabetes mellitus. Since there is a lack of standardization concerning micronutrient supplementation during pregnancy, there is a need for systematic study related to the role of micronutrients during each trimester of pregnancy to optimize its supplementation and to prevent hazards associated with its abuse.