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Background: In the present study, we examined the association of immunosuppressant drug prescriptions with the growth of small abdominal aortic aneurysms (AAAs). Methods: Participants with an AAA measuring between 30 and 50 mm were recruited from four Australian centers. AAA growth was monitored by ultrasound. The immunosuppressant drugs included conventional disease-modifying antirheumatic drugs (eg, methotrexate, sulfasalazine, leflunomide), steroids, hydroxychloroquine, other immunosuppressant drugs (eg, cyclosporine, azacitidine), or a combination of these drugs. Linear mixed effects modeling was performed to examine the independent association of an immunosuppressant prescription with AAA growth. A subanalysis examined the association of steroids with AAA growth. Results: Of the 621 patients, 34 (5.3%) had been prescribed at least one (n = 26) or more (n = 8) immunosuppressant drug and had been followed up for a median period of 2.1 years (interquartile range, 1.1-3.5 years), with a median of three ultrasound scans (interquartile range, two to five ultrasound scans). No significant difference was found in AAA growth when stratified by a prescription of immunosuppressant drugs on either unadjusted (mean difference, 0.2 mm/y; 95% confidence interval [CI], −0.4 to 0.7; P = .589) or risk factor-adjusted (mean difference, 0.2 mm/y; 95% CI, −0.3 to 0.7; P = .369) analyses. The findings were similar for the unadjusted (mean difference, 0.0 mm/y; 95% CI, −0.7 to 0.7; P = .980) and risk factor-adjusted (mean difference, 0.1 mm/y; 95% CI, −0.6 to 0.7; P = .886) subanalyses focused on steroid use. Conclusions: The results from this study suggest that AAA growth is not affected by immunosuppressant drug prescription. Studies with larger sample sizes are needed before reliable conclusions can be drawn. : Clinical relevance: At present, it is unclear whether immunosuppression promotes or inhibits abdominal aortic aneurysm (AAA) progression. This has important implications for the management of AAA. With the increasing range of indications for which immunosuppressant medications are being prescribed, it is likely that more patients with AAAs will be prescribed these drugs for the treatment of comorbid diseases, such as rheumatoid arthritis, other autoimmune diseases, after organ transplantation, or coronary heart disease. The results from the present study suggest that patients prescribed a range of different immunosuppressant drugs for treating a variety of different inflammatory diseases did not experience a significantly different AAA growth compared with patients not receiving these medications. Our findings suggest that no strong case exists to either start or stop immunosuppressant drugs for AAA patients