Abstract 15430: Dramatic Reduction in Lipoprotein(a) With Immunosuppressant, Anti-Inflammatory, and Antimicrobial Therapy in a Patient With Multiple Inflammatory Diseases

Abstract

Background: Lipoprotein(a) (Lp(a)) is a potent, causative risk factor for ASCVD. Patients with inflammatory and autoimmune diseases are also at increased ASCVD risk. There is a complex, incompletely understood relationship between inflammation and Lp(a), including observations that IL-6 induces LPA gene expression. We present a unique case of dramatic Lp(a) lowering occurring with a combination of immunosuppressing, anti-inflammatory, and antimicrobial therapies. Case: A 50-year-old Black woman was referred to Lipid Clinic for Lp(a) of 138 mg/dL. Medical history included Crohn’s disease, total colectomy and end ileostomy, seronegative inflammatory polyarthropathy with psoriatic arthritis, and reactive neutrophilic dermatosis with suspected bowel-associated dermatitis-arthritis syndrome (BADAS). CT coronary calcium score was 0 Agatston units, but plaque was visible in her right coronary artery below the threshold for quantification. With rosuvastatin 5mg daily (which can increase Lp(a)), she experienced a ~25% reduction in LDL-C (baseline 102 mg/dL). She was not treated with niacin or PCSK9 inhibitors. Over the course of ~2.5 years, as the patient experienced BADAS flares she received extensive immunosuppressing, anti-inflammatory, and antimicrobial treatment including adalimumab (TNF-alpha inhibitor), sulfasalazine, dapsone, and doxycycline, and her Lp(a) decreased from 138 mg/dL to a low of 48 mg/dL (65% reduction) (Figure). Conclusion: Previous studies have shown that certain immunosuppressing therapies may lower Lp(a), and in this unique case we observed a dramatic reduction in Lp(a) during treatment with a complex regimen of immunosuppressing, anti-inflammatory, and antimicrobial therapies in a patient experiencing frequent flares of inflammatory diseases. The relationship between Lp(a), systemic inflammation, and the potential effects of anti-inflammatory and immunosuppressive therapies on Lp(a) deserves further study.