American International Medical University

Disclosure: R. Ali: None. A. Dixit: None. T. Jain: None. A.J. Augustine: None. P.R. Patel: None. S. Iftikhar: None. B. Padamati: None. G. Palaniswamy: None. V.A. Mendpara: None. N. Koduri: None. Background: Type 2 Diabetes Mellitus (T2DM) is a growing global health challenge, affecting over 537 million adults worldwide. While lifestyle factors like poor diet and lack of exercise are well-documented contributors, the role of alcohol consumption in increasing diabetes risk is often overlooked. Chronic alcohol use can lead to insulin resistance, obesity, and liver dysfunction, all of which heighten the likelihood of developing diabetes. Despite these metabolic effects, alcohol is rarely a focal point in diabetes prevention efforts. This study examines long-term trends in alcohol-related diabetes burden, focusing on mortality rates (ASMR), Disability (DALYs), and Future projections. Methods: This study analyses Global Burden of Disease (GBD) data from 1990 to 2021, tracking diabetes cases attributed to alcohol consumption. Time-series forecasting models (ARIMA and Exponential Smoothing) are used to predict trends through 2031. A Pearson correlation analysis (r = 0.85, p < 0.001) assesses the relationship between alcohol intake and diabetes burden over time. Additionally, a Vector Auto Regression (VAR) model evaluates the influence of alcohol taxation, obesity rates, and GDP per capita on diabetes prevalence. Results: The findings indicate a consistent rise in alcohol-related diabetes burden, with prevalence increasing from 0.015% in 1990 to 2.92% in 2021. Projections suggest this trend will continue, with alcohol-attributable diabetes burden expected to reach 1.7% by 2031 if no interventions are made. The Age-Standardized Mortality Rate (ASMR) due to alcohol-related diabetes increased from 4.59 in 1990 to 7.88 per 100,000 population in 2021, marking a 71.7% rise in diabetes-related deaths linked to alcohol consumption. Similarly, Disability-Adjusted Life Years (DALYs) due to alcohol-related diabetes increased from 4.45 million in 1990 to 7.72 million in 2021, a 73.4% rise, reflecting a growing impact on disability and reduced quality of life. Economic factors also play a key role—higher alcohol taxation is associated with lower diabetes rates while rising obesity levels and economic growth contribute to an increasing diabetes burden. Conclusions: The evidence points to alcohol consumption as a significant but often underestimated factor driving type 2 diabetes rates, impacting both mortality and disability. Without effective policy measures, the alcohol-related diabetes burden is projected to grow significantly in the coming years. Strategies such as higher alcohol taxes, public awareness campaigns, and integrating alcohol reduction into diabetes prevention programs could help mitigate these risks. Future research should focus on regional variations and long-term policy impacts to develop more effective interventions for reducing alcohol-related metabolic risks. Presentation: Monday, July 14, 2025

Disclosure: A. Dixit: None. T. Mareedu: None. G. Palaniswamy: None. P.R. Patel: None. B. Padamati: None. N. Koduri: None. A.J. Augustine: None. S. Sahu: None. S. Iftikhar: None. V.A. Mendpara: None. T. Jain: None. Background: Secondhand smoke (SHS) exposure has been widely recognized as a major public health concern, contributing to various non-communicable diseases, including Type 2 Diabetes Mellitus (T2DM). Despite extensive research on smoking-related illnesses, limited studies have quantified the direct impact of SHS on diabetes-related mortality, disability-adjusted life years (DALYs), and age-standardized mortality rates (ASMR) at a global scale. Given the increasing prevalence of diabetes and continued SHS exposure worldwide, this study aims to examine trends from 1990 to 2021 and predict future trajectories through 2035 using data from the Global Burden of Disease (GBD) Study. Methods: A dataset of 320 global observations covering 1990-2021 was analyzed to assess the relationship between SHS exposure and diabetes burden. Correlation and regression analyses were performed to evaluate associations between SHS exposure and diabetes prevalence, with a near-perfect correlation (r = 0.99998, p < 0.001). Linear and nonlinear regression models were used to validate the robustness of the association, where a nonlinear model provided a better fit (Residual Standard Error = 2619). ARIMA time-series modeling was employed to project changes in ASMR, DALYs, and diabetes-related deaths through 2035 to forecast future trends. Results: The Age-standardized mortality rate (ASMR) linked to SHS exposure has risen steadily from 8.2 per 100,000 in 1990 to 15.7 per 100,000 in 2021, reflecting a 91% increase. ARIMA projections indicate a further 8-12% rise in ASMR by 2032. Disability-adjusted life years (DALYs) due to SHS-induced diabetes have increased from 14.5 million in 1990 to 31.2 million in 2021, and the forecast suggests a 16% rise by 2032, highlighting the worsening impact on quality of life. Diabetes-related deaths due to SHS exposure have escalated from 1.6 million in 1990 to 3.2 million in 2021, with forecasts predicting over 3.5 million deaths by 2035. The near-perfect correlation between SHS exposure and diabetes burden raises concerns regarding potential collinearity, yet the data strongly indicate a causal relationship requiring further validation with stratified analyses. Conclusions: These findings emphasize the escalating burden of secondhand smoke exposure on diabetes prevalence, mortality, and disability. The projected rise in ASMR, DALYs, and Diabetes-related deaths suggests a growing global crisis unless immediate public health interventions are implemented. Stricter tobacco control policies, enhanced awareness campaigns, and targeted healthcare strategies are imperative to reduce SHS exposure and mitigate its metabolic consequences. Future research should focus on age-specific and regional variations to guide policy-making and intervention strategies that can effectively curb the impact of SHS-related diabetes worldwide. Presentation: Monday, July 14, 2025

Disclosure: V.A. Mendpara: None. S. Sahu: None. B. Padamati: None. K. Navyaja: None. G. Palaniswamy: None. A.J. Augustine: None. P.R. Patel: None. T. Mareedu: None. T. Jain: None. Background: Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder affecting reproductive-age women, characterized by hyperandrogenism, ovarian dysfunction, and metabolic disturbances. While obesity is often linked to PCOS, a distinct subset, lean PCOS, presents without obesity but still experiences metabolic and reproductive complications. The pathophysiology of lean PCOS differs from obese PCOS, making treatment more complex. Despite available pharmacological and lifestyle interventions, their long-term effects remain unclear. This meta-analysis assesses the efficacy of various treatment strategies in lean PCOS by evaluating weight change, insulin sensitivity, ovulation rate, and cardiovascular risk factors. Methods: A systematic search was conducted across PubMed, Scopus, Elsevier, Springer, BMC, and Google Scholar. Inclusion criteria comprised randomized controlled trials (RCTs) and prospective cohort studies assessing pharmacological (e.g., Metformin, Flutamide, oral contraceptives) and lifestyle interventions (e.g., dietary modifications, physical activity) in lean PCOS patients. Studies focusing solely on obese PCOS were excluded. Extracted outcomes included weight change, insulin sensitivity (HOMA-IR or glucose disposal rates), ovulation rate, and cardiovascular risk factors such as blood pressure. A random-effects meta-analysis was conducted to calculate pooled effect sizes with 95% confidence intervals (CIs). Statistical heterogeneity was assessed using the I-squared (I²) statistic. Sensitivity analyses were conducted to assess the reliability of the findings. Results: Five studies encompassing 299 lean PCOS patients were analyzed. The meta-analysis indicated a modest reduction in body weight (pooled effect size 0.40 kg, 95% CI: 0.23 to 0.57), suggesting weight management remains a challenge. Insulin sensitivity improved (SMD 0.36, 95% CI: 0.10 to 0.62), particularly with Metformin. Ovulation rates significantly increased (pooled OR 2.14, 95% CI: 1.30 to 2.98), highlighting reproductive benefits. However, the impact on cardiovascular risk factors was minimal, with blood pressure showing negligible changes (pooled effect size -0.18, 95% CI: -0.38 to 0.02). Moderate heterogeneity (I²: 30-50%) was detected, suggesting some variability across studies. Sensitivity analysis confirmed the reliability of the results. Conclusion: Metformin and Flutamide improve insulin sensitivity and ovulation rates in lean PCOS patients, but their effects on weight reduction and cardiovascular risks remain inconclusive. Further large-scale, long-term RCTs are needed to optimize treatment strategies. Standardized methodologies and well-defined clinical endpoints are essential to establish evidence-based guidelines for lean PCOS management. Presentation: Sunday, July 13, 2025

HIV remains a persistent epidemic in the USA. Although newer and more effective screening and treatment regimens have reduced mortality, a significant disparity exists in urban and rural areas. This study aims to identify disparities in mortality in urban and rural areas for HIV using the CDC-WONDER database from 1999 to 2020 and to analyze any significant differences in mortality rates as well as demographic variables. The Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiological Research (CDC WONDER) database was used to investigate the Rural and Urban Mortality trends for HIV, ICD-10 codes B20–B24, from 1999–2020. The extracted data was systematically grouped by 10-year age range, gender, census region, and race, and analyzed for trends and patterns over time using the R Studio v4.3.2. package to give a statistically significant result with clear representative figures. The study showed that urban areas reported 194,717 deaths from HIV, whereas non-metropolitan/rural areas reported 16,009 deaths. The crude mortality rate (CMR)/100,000 population in urban areas declined from over 0.25 in 1999 to 0.05 in 2020. These rates were however always significantly greater than the CMR in rural areas (0.06 in 1999 and 0.01 in 2020). This disparity was most significant among males, the white race, and those between 35–65 years of age. This study highlights a statistically significant disparity in urban versus rural mortality rates of HIV especially amongst males, the white race, and people between 35–65 years of age.

Disclosure: T. Mareedu: None. T. Jain: None. P.R. Patel: None. A.J. Augustine: None. N. Koduri: None. G. Palaniswamy: None. B. Padamati: None. S. Iftikhar: None. Background: Hypothalamic hamartomas (HH) are rare, non-neoplastic congenital malformations associated with central precocious puberty (CPP) and gelastic seizures. These lesions are ectopic neuronal masses in the hypothalamus, capable of secreting gonadotropin-releasing hormone (GnRH), leading to early activation of the hypothalamic-pituitary-gonadal axis. Early diagnosis and management are crucial to prevent adverse psychosocial and metabolic consequences.Case Presentation: A 7-year-old male presented with signs of early puberty, including pubic hair development, accelerated growth velocity, and advanced bone age. Clinical examination revealed Tanner stage 3 pubertal development. Biochemical investigations showed elevated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels, with a testosterone concentration of 277 ng/dL (prepubertal reference <50 ng/dL), confirming a diagnosis of CPP. Thyroid function tests were normal. Brain MRI identified a hypothalamic hamartoma in the tuber cinereum region, consistent with the classic findings of HH-related CPP. Discussion: Hypothalamic hamartomas remain a diagnostic challenge due to their varied presentations, ranging from isolated CPP to epilepsy and cognitive impairments. The pathophysiology involves ectopic GnRH pulsatility, triggering the premature activation of the hypothalamic-pituitary axis. First-line treatment includes GnRH analogs, which effectively suppress pubertal progression and mitigate the psychosocial burden of early puberty. In cases refractory to medical therapy, surgical resection or gamma knife radiosurgery may be considered. Conclusion: This case underscores the importance of early recognition of hypothalamic hamartoma as a cause of precocious puberty. Timely intervention with GnRH analogs is essential to prevent complications such as early epiphyseal closure and psychosocial distress. Given its rarity, heightened clinical suspicion is required to differentiate HH from other causes of early puberty. Presentation: Sunday, July 13, 2025