Severe aplastic anemia as a rare autoimmune complication of ankylosing spondylitis

Rationale: Aplastic anemia (AA) is a rare, life-threatening bone marrow failure syndrome, most often driven by immune-mediated destruction of hematopoietic stem and progenitor cells. Ankylosing spondylitis (AS) is a chronic inflammatory spondyloarthropathy characterized by aberrant T-cell activity and elevated pro-inflammatory cytokines. Although both diseases share immune dysregulation as a common pathogenic feature, their coexistence has not been previously documented in the literature. Patient concerns: A 42-year-old male with a known history of AS presented with recurrent mucocutaneous bleeding, severe fatigue, and progressive transfusion dependence. Diagnoses: Laboratory work-up revealed pancytopenia. Bone marrow biopsy showed marked hypocellularity (5%–10%), consistent with severe AA. Secondary etiologies were systematically excluded, confirming the diagnosis of severe AA in the setting of underlying AS. Interventions: The patient was started on immunosuppressive therapy comprising antithymocyte globulin, cyclosporine, and eltrombopag. Antithymocyte globulin was discontinued due to serum sickness, while cyclosporine and eltrombopag were maintained. For active AS, golimumab (an anti-tumor necrosis factor-alpha agent) was subsequently added. Outcomes: Over a follow-up period of 6 months, the patient achieved normalization of peripheral blood counts and complete remission of rheumatologic symptoms, with no major adverse events reported. Lessons: This case suggests a possible immunological link between AA and AS, given their shared pathways of T-cell-mediated cytotoxicity and cytokine activation. However, this single observation should be interpreted with caution and does not establish causation. It may nonetheless contribute to the emerging literature on potential pathophysiological overlaps between rheumatologic disorders and bone marrow failure syndromes.