Acute Pancreatitis as a Therapeutic Complication in Case of Paroxysmal Nocturnal Hemoglobinuria.

abstractParoxysmal nocturnal hemoglobinuria (PNH) is a rare acquired hematopoietic disorder requiring careful therapeutic management. In resource-limited settings, traditional treatments may carry significant risks. A 32-year-old female with PNH developed acute pancreatitis 10 months after initiation of danazol and deflazacort therapy. Initial presentation included typical hemoglobinuria, pancytopenia, and indirect hyperbilirubinemia. Flow cytometry confirmed PNH clones despite a negative Ham's test. Treatment with danazol 200 mg twice daily and deflazacort 30 mg daily initially provided clinical improvement. Subsequently, the patient developed pigment nephropathy requiring dialysis, followed by severe acute pancreatitis with markedly elevated pancreatic enzymes (amylase: 3370 U/L and lipase: 12,478 U/L). Ultrasonography revealed a bulky pancreatic head with heterogeneous echotexture. Other causes of pancreatitis were excluded. Both medications were discontinued, and conservative management led to clinical recovery. This case represents drug-induced pancreatitis, a rare but serious complication of PNH therapy. Both danazol and corticosteroids have been independently associated with acute pancreatitis in the literature, though reports remain sparse. The concurrent use of these agents may have contributed synergistically to pancreatic inflammation. The patient's clinical course, including androgenic side effects and temporal relationship with drug exposure, supports the causal association. Healthcare providers managing PNH in African settings must remain vigilant for drug-induced pancreatitis when using traditional therapies. Enhanced monitoring protocols and improved access to safer complement inhibitors are essential for optimizing patient outcomes while minimizing treatment-related complications in resource-limited environments.