United States

Background
Strict glycemic control for management of diabetes can result in hypoglycemic episodes and the long-term, deleterious impacts of these episodes on health are unclear. Acute hypoglycemia causes a drop in microvascular density and perfusion of the retinal superficial capillary plexus. Additionally, severe hypoglycemia is associated with a higher incidence of retinopathy in patients with type 2 diabetes and proliferative disease in patients with type 1 diabetes. Understanding the influence of hypoglycemia on diabetes progression is an important question in guiding blood glucose control regimens to manage morbidity and mortality of this disease.

Methods
We performed a retrospective cohort study using the TriNetX platform including up to 200k patients per cohort across 70 US health care organizations, selected by blood glucose value or ICD-10 code. We evaluated the impact of hypoglycemia on the risk and progression of diabetic retinopathy, relative to both hyperglycemia and normoglycemia, in participants with type 1 and type 2 diabetes. We simultaneously assessed the effect of hypoglycemia on another microvascular complication, diabetic nephropathy.

Results
Participants with hypoglycemia were at an elevated risk for both non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) compared to both glycemic-controlled and hyperglycemic participants. Hypoglycemia increased risk by up to 3.56 (3.14, 4.05) for NPDR, 4.83 (4.53, 5.15) for PDR in persons with type 2 diabetes and comparably in those with type 1 diabetes, relative to normoglycemia. Relative to hyperglycemia, hypoglycemia increased risk by up to 1.68 (1.53, 1.85) for NPDR, 2.05 (1.96, 2.15) for PDR in participants with type 2 diabetes and comparably in those with type 1 diabetes. Additionally, hypoglycemia elevated risk of progression from NPDR to PDR to a similar degree as hyperglycemia, up to 1.99 (1.56, 2.54) in persons with type 2 diabetes, relative to normoglycemia.

In the kidney, hypoglycemia increased risk of chronic kidney disease (CKD) [2.11 (2.07, 2.14); 1.42 (1.40, 1.44)], end stage renal disease (ESRD) [6.64 (6.38, 6.91); 2.48 (2.41, 2.55)], and progression from CKD to ESRD [3.74 (3.61, 3.87); 1.53 (1.51, 1.58)], relative to both normoglycemia and hyperglycemia, respectively.

Conclusion
Hypoglycemia is associated with increased risk of diabetic retinopathy and comparable risk of retinopathy progression, compared with hyperglycemia. Additionally, both elevated risk and risk of progression for diabetic nephropathy are associated with hypoglycemia. This study underscores the significant role of hypoglycemia on ocular and renal morbidity and highlights the importance of appropriately cognizant blood glucose control strategies to mitigate these outcomes.

2025 AMA Research Challenge – Member Premier Access

Hypoglycemia Enhances Risk and Progression of Diabetic Retinopathy and Nephropathy

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Background
Invasive candidiasis is a growing health threat. In the last five years, the WHO has prioritized fungal pathogens, and the CDC has reported a more than 80% increase in nosocomial Candida infections. With resistance to first-line antimycotics also rising, new treatment and prophylactic measures are needed. Glycogen synthase kinase (GSK) is a potential target for fungal pathogens. Some GSK inhibitors have passed Phase 1 clinical trials for indications like bipolar disorder and Alzheimer’s disease. If the safety profiles of potential fungal medication are favorable, or if a potential medication has selectivity for fungal homologs of GSK, fungal GSK could be a novel drug target. Not much is known about the moonlighting functions of Candida GSK. This work screens GSK inhibitors against Candida to examine cell growth inhibition.

Methods
Candida parapsilosis (ATCC 22019) was grown planktonically in YM broth, containing penicillin and streptomycin, at 33°C. GSK inhibitors were purchased from AOBIOUS (Gloucester, MA) and dissolved in DSMO, with a final culture concentration of 0.5% DMSO. Inhibitor screens were run in triplicate in a clear, flat-bottom 96-well plate, and growth/inhibition was monitored by
OD600. Glycogen content in cell cultures was monitored by absorbance at 660 nm after iodine/potassium iodide stain. 

Results
Several GSK inhibitors, including tideglusib, were found to slow or block Candida growth at micromolar concentrations. Some GSK inhibitors had activities comparable to known antifungal agents tested. GSK inhibitors tested encompassed diversity in molecular structure, though some molecules like tideglusib and TDZD-8 shared pharmacophores. Besides inhibiting growth, treatment of GSK inhibitors at sub-MIC concentrations resulted in lower glycogen content.

Conclusion
Our results indicate growth inhibition of Candida with GSK inhibitors. This work is foundation chemical biology studies to elucidate moonlighting functions of fungal GSK. Next steps will be to perform synergy screens to test if the GSK inhibitors increase or decrease bioactivity of known antifungals, and vice versa. Future directions also include pursuing cloning of Candida GSK for biochemical screens of the active compounds.

Back to the Fungimentals: Antimycotic Activity of Glycogen Synthase Kinase

Introduction:
We compare the effects primary care and polytrauma care have on health care utilization and cost among veterans diagnosed with traumatic brain injury (TBI). Cohorts of veterans spanning from 2003 to 2023 were analyzed based on their usage of primary care, polytrauma care, both, or neither over three or more years.
Methods:
This study is a retrospective cohort analysis of LIMBIC Phenotype Study dataset linked with data from Veterans Health Administration (VHA). The cohorts were classified based on the presence or absence of a TBI diagnosis and whether veterans had no primary or polytrauma care, primary care for 3+ years, polytrauma care for 3+ years, or both primary care and polytrauma care for 3+ years. Care both within and outside of the VA system including total health care cost was documented as well. We used Propensity Score estimation method with augmented IPTW to compare utilization and cost across the groups. 
Results:
Veterans who did not use primary care or polytrauma care had an average year 1 utilization score of 3.22, which increased to a score of 22.8 by year 4. Similarly, healthcare costs for these individuals also rose from an average of $3505 to $10519. Veterans who used both primary care and polytrauma care experienced the opposite pattern: Utilization scores fell from an average of 73.66 to 39.34, and costs fell from $43092 to $16283. Veterans who only used primary care saw mild decreases in both utilization scores and costs, and those who only used polytrauma care saw little change in utilization and a large decrease in cost between Year 1 and 2 followed by minor changes across Years 2-4.
Conclusions:
When controlling for medical complexity, individuals with TBI who received regular combination of primary and polytrauma care for 3+ years continued to have lower health care utilization in subsequent years. Further analyses include identifying “surrogate” measures to identify the impact of care type and intensity on the quality and outcome of treatment. 


Impact of Primary & Polytrauma Care Services on Health Care Utilization of Veterans with All-Severity TBI

Background
Addison’s disease is a rare endocrine disorder caused by failure of the adrenal cortex, most commonly due to autoimmune destruction of the adrenal gland. It presents with nonspecific symptoms such as fatigue, weight loss, hypotension, and hyperpigmentation, often delaying diagnosis. Acute adrenal crisis is a life-threatening complication requiring urgent treatment. Diagnosis is confirmed through ACTH stimulation testing and hormonal assays. Lifelong hormone replacement, follow up, and patient education are essential for management. When Addison’s disease coexists with diabetes mellitus and stroke, the clinical complexity increases significantly due to compounded cardiovascular and metabolic risks. This underscores the need for vigilant, individualized care to prevent complications and optimize outcomes.
Case Presentation
We present a 51-year-old female with a history of hypertension, multiple strokes, seizures, type 2 diabetes mellitus, and Addison’s disease who arrived at the ED with 10 days of weakness, dysphagia, and poor oral intake. Initial labs showed elevated BUN, creatinine, hyperchloremia, and hypoalbuminemia. She was admitted for management of severe dehydration and electrolyte disturbances. The family reported recurrent hospitalizations for dysphagia, dehydration, and hypoglycemia. On day one of hospitalization, she developed hypotension, hyperglycemia, and altered mental status, raising concern for adrenal crisis. MRI revealed severe basal ganglia atrophy with iron deposition; EEG showed left frontal seizure activity. By day two, she developed hyponatremia, hypokalemia, metabolic acidosis, and acute kidney injury. Echocardiogram showed preserved ejection fraction and mild valvular regurgitation. Treatment included IV hydrocortisone, insulin, levothyroxine, fluids, and nasogastric feeding.
Despite treatment, a code blue was triggered for severe hypoglycemia. She then required intubation, vasopressors, anticonvulsants, and broad-spectrum antibiotics for sepsis. The patient suffered three cardiopulmonary arrests but achieved return of spontaneous circulation.
Discussion
This case underscores the need for early recognition, aggressive management, and proactive cardiovascular risk reduction in complex endocrine-neurological patients. The patient presented with hypoglycemia, hypotension, and metabolic acidosis—hallmarks of adrenal crisis. Adrenal crisis represents a life‐threatening emergency, particularly in individuals with a known history of diabetes and cerebrovascular accidents. Cortisol deficiency disrupts cardiovascular and metabolic stability. Furthermore, stroke‐related autonomic dysfunction weakens the body’s cardiopulmonary reserve. Together, these factors significantly increase susceptibility to hypotension, hypoglycemia, and circulatory collapse, as exemplified by this patient. Additionally, precipitating events such as infection, dehydration, and inadequate oral intake may rapidly trigger decompensation. Despite timely and appropriate intervention, patients with Addison’s disease remain at increased risk of cardiovascular morbidity and mortality, particularly when concomitant comorbidities are present.

Addison’s Disease in a Patient with Stroke and Diabetes – A Fatal Lesson in Diagnostic Delay

Background: In recent years there has been a dramatic increase in the rates of syphilis within the US. Since 2021 reports of syphilis cases have increased by 17.3 %. Neurosyphilis can be clinically silent or present with symptoms such as meningitis, otologic and ocular deficits, Tabes dorsalis, and vascular damage. Coinfection with HIV is a complicated and serious concern for those affected by syphilis, with early neurosyphilis being more common among those living with HIV. When occurring simultaneously, distinguishing the etiology of a patient's neurologic changes can be difficult.
Case Presentation: We present the case of a 50-year-old Spanish only speaking unhoused male with no known medical history that presented to the ED after being found down on the side of the road. In the ED that patient was confused, hemodynamically stable without signs of trauma. On physical exam he appeared frail and disheveled with diffuse scaling of the scalp and under facial hair, thickening of the nails on the right hand and poor cognition without other pathologic findings. He was admitted for altered mental status of unknown cause. the initial work up yielded negative toxicology, WBC count of 2.7, normocytic anemia, and Brain CT showing small vessel ischemic disease. Due to non-specificity of patient presentation, subsequent workup consisted of a broad range of lab studies including UA, ammonia, TSH, B12, Folate, thiamine, copper, zinc, serum osmolality, and infectious disease panels/tests for HIV, Syphilis, Hepatitis, and TB. Results were positive for HIV-1 Ab with high viral load, CD4 count of 14, positive syphilis serology and RPR. CSF analysis later revealed elevated WBC and protein, negative VDRL and possible positive Borrelia burgdorferi antigen. A dual diagnosis of Advanced AIDS and Neurosyphilis were established and treatment with IV penicillin and antiretroviral therapy were initiated. The patient’s mental status remained the same throughout his 3 weeks of hospitalization.
Discussion: This case highlights the diagnostic challenge of altered mental status in a patient with concurrent HIV, neurosyphilis, and possible Lyme CNS involvement. While HIV-associated neurocognitive disorder and neurosyphilis are individually well-documented, their co-occurrence is rare and difficult to distinguish due to overlapping features. Our patient’s disorientation and lack of medical history required a broad workup. Neuroimaging revealed no enhancing intracranial lesions but showed mildly enlarged ventricles and cortical sulci, suggestive of cerebral atrophy. Coinfection can accelerate HIV progression and worsen neurologic outcomes. Early recognition and treatment are critical, especially in high-risk or underserved populations, to prevent irreversible complications.

When Infections Collide: Diagnostic Challenges of Unsuspecting Advanced
Disease in an Underserved Patient

Background:
Cervical artery dissection (CAD), including vertebral artery dissection (VAD), accounts for up to 25% of ischemic strokes in individuals under 45 years. Stroke risk following dissection is highest in the first two weeks, with a 1.25% absolute risk, decreasing to 0.18% by weeks 3–4 and becoming negligible thereafter. Delayed stroke beyond four weeks is rare but may result from persistent arterial wall instability, delayed thrombus formation, or genetic predispositions such as connective tissue disorders. Early diagnosis remains challenging due to non-specific symptoms, with misdiagnosis rates as high as 25%.

Case Presentation:
A 28-year-old male with no significant past medical history presented with acute right-sided weakness, facial droop, slurred speech, and amnesia. Imaging revealed a left P2 posterior cerebral artery occlusion, left vertebral artery occlusion, and left VAD. MRI showed infarcts in the left posterior inferior cerebellum, parahippocampal gyrus with hemorrhagic conversion, and left thalamus with petechial hemorrhage.

He underwent successful mechanical thrombectomy (TICI 3), with near-complete recovery except for mild sensory deficits. Notably, his only prior relevant history was a motor vehicle accident in 2018 and a concussion 7 months prior. Hypercoagulable workup was negative. There was no evidence of recent neck trauma, chiropractic manipulation, or family history of vascular disease.

He was diagnosed with ischemic stroke due to thromboembolism from VAD, despite the significant time lapse from prior minor trauma. He was treated with dual antiplatelet therapy for 90 days, followed by aspirin monotherapy for secondary prevention.

Discussion:
This case challenges the notion that stroke risk from VAD is negligible beyond four weeks. While most events occur early, delayed presentations like this suggest persistent thromboembolic risk in select individuals, possibly due to unresolved vascular injury or predisposition.

Current diagnostic approaches may miss such cases if relying solely on the traditional four-week cutoff. This case highlights the importance of considering vascular imaging in young patients with prior minor trauma or concussion, regardless of time elapsed. Clinicians must remain vigilant for subtle presentations of VAD and may need to extend monitoring and antithrombotic therapy in high-risk cases.

Further research is needed to define the optimal duration of antithrombotic therapy and identify patients at risk for delayed complications. Even remote minor trauma may predispose young patients to delayed stroke from vertebral artery dissection. Vascular imaging should be considered regardless of the time since injury, and prolonged antithrombotic therapy may be warranted in select cases to prevent catastrophic outcomes.

The Silent Countdown: When A Dormant Dissection Strikes A Young Brain

Background

Ovarian clear cell carcinoma (OCCC) is a rare subtype of epithelial ovarian cancer, accounting for 5–10% of cases in North America and up to 30% in East Asia. It is often associated with endometriosis and typically presents at an advanced stage. Prognosis is poor due to inherent resistance to platinum-based chemotherapy, late detection, and potential lymphatic spread. This case highlights delayed diagnosis of metastatic OCCC initially presenting as chronic thigh pain.

Case Presentation

A 66-year-old woman with stage III OCCC, previously treated with chemotherapy and radical hysterectomy, presented after a fall with diffuse left-sided musculoskeletal pain. Imaging showed degenerative joint changes and partial tendon tears but no acute fractures. Despite symptom improvement with physical therapy and injections, severe upper thigh pain persisted, predating her fall.

Concern for L3 radiculopathy led to lumbar spine MRI, which revealed a 6.7 cm paravertebral mass invading the L5–S1 vertebrae and encasing lumbar nerve roots. CT confirmed extension into the left psoas muscle and iliac vessels. Biopsy showed metastatic OCCC. Surgery was not feasible due to the tumor’s location and extent, so palliative radiation was administered. She received 71 cGy over 36 days using a targeted dosing strategy. One-month post-treatment, imaging showed marked tumor shrinkage and her thigh pain resolved. Follow-up imaging was deferred after the patient sustained cervical fractures in a separate fall.

Discussion

OCCC is the most chemoresistant epithelial ovarian subtype, often diagnosed late due to vague symptoms and lack of effective screening. Metastatic spread to lymph nodes or retroperitoneal structures, as seen in this case, is uncommon and can present as nonspecific pain, complicating timely diagnosis.
Immunohistochemistry is essential for accurate diagnosis, distinguishing OCCC (positive for HNF1B; negative for WT1, ER, PR, and p53) from high-grade serous carcinoma, which may respond better to chemotherapy. Misdiagnosis can delay appropriate care.
Currently, treatment for OCCC mirrors that of other ovarian cancers, though outcomes are poorer. Research into targeted therapies—such as angiogenesis inhibitors and metabolic pathway blockers—is underway. Agents like sunitinib show early promise. Additionally, identification of serum biomarkers (e.g., HAVCR1, IGFBP1, NEU3) may aid in earlier detection and monitoring.
This case illustrates the need for heightened clinical suspicion when evaluating unexplained chronic pain in patients with a history of OCCC and supports the pursuit of biomarker-driven screening and individualized treatment approaches.


Leg Pain in the Setting of Metastatic Clear Cell Carcinoma

Abstract Title

Gut-Feeling: A Cerebellar Infarct Masquerading as Gastrointestinal Illness

Background

Posterior circulation strokes, particularly those involving the cerebellum, can present with non-specific symptoms such as vertigo, nausea, vomiting, and headache, and may lack focal neurological findings. These symptoms often mimic benign gastrointestinal or vestibular conditions like viral gastroenteritis or labyrinthitis, leading to diagnostic delays. The compact anatomy of the posterior fossa increases the risk for rapid clinical deterioration from mass effect or hydrocephalus, making early identification critical. Up to one-third of cerebellar infarcts are missed on initial evaluation, especially when neuroimaging is delayed or not obtained.

Case Presentation
A 56-year-old woman with a medical history of hypertension, type 2 diabetes, and hypothyroidism presented to the emergency department with four days of dizziness, headache, nausea, vomiting, and heartburn. She denied neurological symptoms, chest pain, fever, or visual disturbances. Abdominal physical examination showed a non-distended, soft depressible abdomen. Neurologic examination was non-focal, with no evidence of gait ataxia, dysmetria, or nystagmus. Laboratory evaluation was notable for microcytic anemia, elevated RDW, neutrophilia/lymphopenia, hyperglycemia, and transaminitis. She had gastritis and peptic ulcer disease a month ago, so an abdominal and pelvic CT was obtained but produced no abnormalities. With ongoing symptoms, Non-Contrast Head CT as well as With/Without Contrast MRI of the Brain confirmed an infarct in the left cerebellar hemisphere. The patient was discharged with outpatient neurosurgical follow-up.

Discussion
This case highlights how cerebellar infarction may mimic gastrointestinal pathology, leading to missed or delayed diagnosis. The posterior vermis and nodulus have direct functional/anatomical connections with the central vestibular system and the brainstem vomiting centers, which normally mediate emesis. Without classical signs such as ataxia or nystagmus, the diagnosis of a cerebellar stroke may be delayed. The posterior fossa’s compact anatomy and subtle symptomatology require high clinical suspicion and early imaging to avoid missing potentially life-threatening strokes in acute settings here as per the American Stroke Association. Noncontrast CT, commonly used acute stroke evaluation, has low sensitivity for detecting early posterior ischemia. MRI with diffusion-weighted imaging is significantly more sensitive but is not always performed initially. The omission of detailed cerebellar assessment further contributes to misdiagnosis. Younger patients as well as patients seen by non-neurologists have a higher risk for missed misdiagnosis. This case emphasizes the importance of considering posterior circulation infarcts in patients with persistent vertiginous or emetic symptoms, particularly when GI workup is unrevealing, to ensure timely neurologic evaluation and appropriate management.

Gut-Feeling: A Cerebellar Infarct Masquerading as Gastrointestinal Illness

Background 
Immune-checkpoint inhibitors (ICIs), including nivolumab, have revolutionized the treatment of advanced melanoma. However, their expanding use has led to a rise in the incidence of immune-related adverse events (irAEs), which can affect multiple organs and mimic systemic illnesses such as sepsis. Prompt recognition and appropriate management result in favorable outcomes. 

Case Presentation 
A 56-year-old female with stage IIIB melanoma of the left leg presented with acute confusion 24 hours post-infusion of nivolumab (OPDIVO 480 mg) — prior regimens included the combination of nivolumab + ipilimumab and nivolumab + relatlimab for the past 10 months—. 
On presentation: T-104°F, RR-32, SpO₂-89% → 95%- O₂ 2 L/min, HR-115, BP-75/42 mmHg, refractory to IV fluids resuscitation (30 cc/kg) requiring norepinephrine (0.63 mcg/kg/min). In addition to the known melanoma lesion, a diffuse erythematous rash involving the face, neck, chest, and extremities was noticed. Urine output was 0 cc/kg/hr. 
Labs showed WBC 23.20 (8.48), procalcitonin 10, lactic acid 3.4, CRP 15.8, LDH 303, Cr 2.94 → 3.52 (baseline 0.68), BUN 18 → 20, GFR 18 → 14 (baseline 102), HCO₃ 18 → 17, bilirubin 2.2 → 1.7, albumin 2.9 → 2.4, with normal ESR 15, calcium 9.0, and uric acid 5.3. 
Urinalysis showed hematuria, pyuria, proteinuria +, and amorphous crystals. FeNa suggested intrinsic renal injury. Nephrotoxic drugs, infection, obstruction, among other etiologies were ruled out. 
Troponin rose from 77 → 416 → 1295. ECG: sinus tachycardia, and echocardiogram: hyperdynamic LVEF:70%. 
CT chest/abdomen revealed new diffuse bilateral ground-glass opacities and colonic wall thickening. 
Empiric high-dose IV corticosteroids were initiated for suspected ICI-induced ATIN, leading to rapid clinical improvement within 24 hours and full renal recovery by day 5. 

Discussion 
This case highlights the diagnostic challenge of distinguishing irAEs with multiorgan involvement from systemic illness such as sepsis. Early recognition reduces the unnecessary use of antibiotics and escalation. The patient lacked traditional ICI-AKI/ATIN risk factors: age, gender, comorbidities, low GFR, gastrointestinal loss, and drugs, being the combination of PD1-CTLA-4 inhibitors and long-term therapy with Nivolumab the only recognized factors. ICI-induced ATIN often presents later during the course of therapy, reinforcing the role of time and cumulative dose as dependent effects. Avoiding other nephrotoxic drugs reduces the risk of ICI-induced ATIN. Corticosteroid can result in full recovery regardless of the severity. Rechallenging ICIs can be dangerous. Establishing clear pathways for patients who have experienced irAEs is essential. Co-treatment with steroids might be explored due to melanoma progression being a big concern.

Immune Checkpoint Inhibitor-Induced Acute Kidney Injury with Multisystem Involvement Mimicking Septic Shock in a Patient with Advanced Melanoma: A Diagnostic Challenge

Enhancing Surgical Skill Acquisition: Assessment of a Novel 3D Printed Laparoscopic Trainer (Non-Inferiority Trial)

Background
As laparoscopic operations yield reliable outcomes across specialties, the need for specialized skills underscores the importance of effective, accessible, and affordable training devices. The acquisition of these techniques traditionally relies on hands-on instruction in the operating room or simulation labs equipped with expensive training devices. Beyond these settings, student exposure is largely limited to observation. Those at institutions with limited access to simulation facilities face an even greater challenge in gaining familiarity with laparoscopic techniques. Current literature describes “do-it-yourself” trainers that attempt to mitigate costs and accessibility; however, material pricing, ease of use, and simulation realism can still be improved. This study validates a novel 3D (three dimensional)-printed laparoscopic trainer designed to provide training outcomes comparable to those of commercial simulators at a fraction of the cost. 
Methods
In this IRB-approved study, we designed a 3D-printed laparoscopic trainer prioritizing affordability, portability, and accessibility. Our device was modeled using Autodesk Fusion 360 software and printed with PLA (polylactic acid) material. The trainer features compact size, enhanced user-friendliness with multi-device compatibility, and a production cost of $11.01. To test its functionality, twenty medical students (M1–M4) with no prior laparoscopic training were randomized into two groups to train on either a commercial simulator (SIMULAB LapTrainer) or the 3D-printed trainer. Participants were taught a threading technique and timed on task completion before and after a one-hour training session.
Results
A paired one-sided t-test revealed no significant differences in task completion times between the two devices for both pre-training (p > 0.05) and post-training (p > 0.05) trials, indicating comparable effectiveness. Additionally, all participants demonstrated improved task completion times in their post-training trials.
Conclusion
These findings validate the potential of 3D-printed trainers as cost-effective alternatives for basic laparoscopic skills training. Future iterations will focus on improving ergonomics and realism to better replicate surgical environments, promote wider accessibility, and advance medical education in resource-limited areas.

Enhancing Surgical Skill Acquisition: Assessment of a Novel 3D Printed Laparoscopic Trainer (Non-Inferiority Trial)

Abstract Title
Cardiovascular Disease Burden and Industrial Environmental Contamination: A
Community-Based Cohort Study in Rural India

Background
The global rise in cardiovascular disease amid declining healthcare workforce availability necessitates urgent implementation of prevention strategies, particularly in low and middle-income countries. This study examined the disproportionate cardiovascular disease burden, including heart failure, in rural Indian communities exposed to industrial wastewater contamination from distillery operations, which raised public health concerns. We investigated the prevalence of heart failure risk factors and other acute and chronic health conditions associated with environmental toxin exposure while assessing how socioeconomic disparities influence cardiovascular disease outcomes.

Methods
A cross-sectional analysis encompassed 4,885 individuals across three villages (Mahianwala Kala, Ratol Rohi, Mansoorwaal Kalan) through door-to-door surveys and health camps conducted over nine months. All participants underwent screening by at least two separate medical teams on different days. Trained physicians and medical personnel collected comprehensive data including medical histories, socio-demographic information, and environmental exposure details. The study focused on cardiovascular outcomes including hypertension, heart disease, stroke, arrhythmia, and heart failure precursors. Logistic regression analyses assessed associations between disease prevalence, socioeconomic status, and environmental factors. Concurrent groundwater testing was performed around the ethanol factory by our team.

Results
The study population demonstrated an alarming disease burden with cardiovascular disease affecting 34% of adults. Stage II hypertension was present in 39% of the cohort, while 21.3% of households reported family members with myocardial infarction history. Adjusted analyses revealed increased odds of heart disease (OR 1.42; 95% CI 1.31-1.51) and respiratory conditions (OR 1.34; 95% CI 1.21-1.42), frequently accompanied by dyspnea and fatigue, which are early indicators of heart failure. Hypertension prevalence exceeded national averages by over 50%, with significantly higher rates among lower socioeconomic groups. Additionally, 10.5% of families reported cancer histories and 60% experienced dermatological conditions, suggesting systemic toxin exposure. Groundwater testing revealed cyanide(0.3 mg/L), heavy metals like lead (0.16 mg/L), and elevated chemical oxygen demand COD (320 mg/L) near the ethanol factory.

Conclusion
Our findings demonstrate a critical association between industrial pollution and elevated disease burden in rural India, particularly heart failure risk factors including hypertension and ischemic heart disease. These results underscore the persistent environmental injustice with marginalized communities bearing disproportionate health burdens. Urgent policy interventions are required to regulate industrial toxin discharge, expand clean water access, and implement targeted cardiac screening programs in underserved communities. Longitudinal studies are warranted to assess pollution-related disease trajectories, especially heart failure progression, in this vulnerable population.

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