Louisiana Research Day Program Book 2025

Case Studies: Section 1

Case Studies: Section 1

Justin Nguyen, OMS-III 1 ; Matthew Overturf, PhD 1 ; Venu Kakarala, MD 2 1 VCOM-Louisiana; 2 Zachary Internal Medicine Clinic, Slaughter, Louisiana 76 IDENTIFYING ASPIRIN AS A CONTRIBUTING FACTOR TO PERSISTENT GOUT: A CASE REPORT

Dr. Deekshitha Manney, MD 1 ; Dr. Ram Kumar, MD 1 ; Dr. Edward Pierce, MD 1 ; Jessica O’Bryan, OMS-III 2 ; Trevor Perry, OMS-III 2 1 Department of Internal Medicine, St. Francis Medical Center, Monroe, LA; 2 VCOM-Louisiana 77 CLOSTRIDIUM CADAVERIS – A TIME OF DEATH INDICATOR BACTERIA FOUND IN DECAYING DEAD BODIES

Context/Impact: This case highlights a lesser-known cause of refractory gout: low dose aspirin’s potential to impair uric acid excretion, leading to persistent symptoms despite achieving target serum uric acid levels. It underscores the importance of recognizing medication side effects in patients with comorbid conditions such as hypertension, CKD, and cardiovascular risk. Report of Case: A 67-year-old African American male presented to a rural internal medicine clinic with severe right-hand pain and swelling lasting 3-4 days. He described the pain as sharp, constant, and exacerbated by wrist movement. The patient had a history of gout and prior treatment with colchicine and allopurinol, which he had discontinued. His medical history included hypertension, dyslipidemia, CKD stage 3, GERD, and a significant family history of cardiovascular disease. He denied alcohol or tobacco use and adhered to a low-purine diet. On examination, the right hand was tender and swollen, with pain elicited on joint manipulation. Laboratory testing revealed elevated uric acid levels (8.3 mg/dL), while x-rays were unremarkable. A diagnosis of gout was made, and the patient was restarted on allopurinol, NSAIDs, and

received an intramuscular ketorolac injection. Despite initial treatment, the patient experienced another gout flare within two weeks. Febuxostat was prescribed as an alternative to allopurinol, lowering uric acid to 5.3 mg/dL. However, his symptoms persisted. Upon further investigation, a detailed medication reconciliation revealed the patient was taking daily low-dose aspirin and was substituted in place of clopidogrel. This change resolved the patient’s symptoms, and his uric acid levels decreased to ~3.0 mg/dL. Over two years of follow-up, he remained symptom free, with no further flares. Comments/Conclusion: The patient’s presentation aligns with established knowledge of gout risk factors, including increased prevalence in African Americans and those with CKD. Aspirin’s effect on uric acid retention, though documented, is less frequently recognized in clinical settings. Studies by Hochberg (1995), Dalbeth (2013), and Zhang (2013) suggest low-dose aspirin inhibits renal uric acid excretion by interacting with URAT1 and MRP4 transporters. Substituting aspirin with clopidogrel provided symptom resolution, consistent with findings that clopidogrel does

not affect uric acid metabolism. This case underscores the importance of medication reviews in refractory gout and highlights a potential gap in widely used clinical resources like Epocrates and UpToDate, which do not emphasize this particular side effect of aspirin. Recognizing low-dose aspirin’s role in refractory gout can improve patient care, particularly for those with comorbid conditions requiring antiplatelet therapy. This case reinforces the value of personalized treatment strategies to optimize therapeutic outcomes.

Background: Clostridium cadaveris is a gram-positive, non-toxin-producing anaerobic bacterium that typically does not cause infections in humans. However, in rare instances, it can result in bacteremia in immunocompromised patients and may be fatal. Due to its low likelihood of prevalence, there are no established treatment guidelines. We aim to highlight a rare case of bacteremia through our case.

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2025 Research Recognition Day