A 46-year-old man with non-Hodgkin lymphoma (NHL) in remission since 2014 presented with progressive dizziness, fatigue, and dark-colored urine. Laboratory workup revealed hemoglobin levels of 5.9 g/dL, elevated lactate dehydrogenase (LDH), hyperbilirubinemia, low haptoglobin, and a positive direct Coombs test for IgG, C3, and poly-specific antibodies, confirming warm autoimmune hemolytic anemia (wAIHA). Immunoglobulin profiling showed low IgM and IgA with high-normal IgG, suggesting chronic immune dysregulation, whereas abdominal imaging revealed mesenteric calcifications, raising concern for residual lymphomatous tissue potentially driving ongoing autoimmune activation. Despite corticosteroids and intravenous immunoglobulin (IVIG), persistent hemolysis necessitated four units of packed red blood cell (PRBC) transfusions and escalation to rituximab, after which gradual clinical stabilization was achieved, highlighting the refractory nature of wAIHA in the setting of previous lymphoproliferative malignancy. Serial monitoring of hemoglobin, reticulocyte count, and LDH throughout the clinical course demonstrated dynamic trends consistent with partial but meaningful immunosuppression, underscoring the value of longitudinal laboratory surveillance in guiding therapeutic escalation decisions. The presence of mesenteric calcifications, combined with a skewed immunoglobulin profile, provided important structural and immunologic clues to the underlying pathophysiology, illustrating how multimodal diagnostic evaluation can reveal occult contributors to delayed autoimmune phenomena even in the absence of overt malignancy recurrence. This case underscores the importance of recognizing delayed AHA in NHL survivors and the necessity of long-term hematologic surveillance, periodic cross-sectional imaging, and a low threshold for multidisciplinary consultation even after prolonged remission.
Azinge et al. (Mon,) studied this question.