Viêm bàng quang xuất huyết do virus BK ở bệnh nhân sau ghép tế bào gốc tạo máu: Báo cáo ca bệnh

BK virus (BKV) is a ubiquitous pathogen that typically causes asymptomatic infection in immunocompetent individuals. However, in the context of hematopoietic stem cell transplantation (HSCT), BKV reactivation frequently leads to hemorrhagic cystitis (HC), a severe and potentially life-threatening urological complication. This condition significantly increases hospitalization duration and mortality rates. Despite its clinical impact, a universally standardized treatment protocol for BKV-associated hemorrhagic cystitis remains elusive, particularly in resource-constrained environments. This case report aims to highlight a successful management strategy for this challenging complication in a patient undergoing HSCT, offering valuable insights into current therapeutic approaches in settings where specific antiviral agents are unavailable, emphasizing supportive care and immunosuppression tapering.

Các bác sĩ lâm sàng, chuyên gia huyết học, cấy ghép tế bào gốc, niệu khoa, và các nhà nghiên cứu y học quan tâm đến quản lý biến chứng nhiễm trùng sau cấy ghép tế bào gốc, đặc biệt là trong bối cảnh các quốc gia đang phát triển.

This case report details the successful management of BKV-associated hemorrhagic cystitis in a 4-year-old female patient who underwent allogeneic hematopoietic stem cell transplantation for beta-thalassemia. Following a rigorous conditioning regimen and transplant from an HLA-identical sibling donor, the patient developed classic symptoms of cystitis with a urinary BKV load exceeding 10^10 copies/mL. Given the unavailability of specific antiviral medications in this resource-limited setting, a comprehensive supportive care strategy was implemented. This approach included intensive hydration, diuretics, and the administration of intravenous immunoglobulin, alongside careful tapering of immunosuppression. Clinically, the patient's urinary symptoms, including dysuria and frequency, significantly improved, and microscopic hematuria resolved. Although the urinary BKV load remained elevated at day +30 post-transplant, it remarkably decreased to 2880 copies/mL by day +60. The patient also achieved good neutrophil engraftment and showed no signs of graft-versus-host disease, leading to a safe discharge. This case underscores that a combined approach of supportive measures, judicious immunosuppression reduction, and intravenous immunoglobulin can be an effective and safe alternative for managing BKV-associated hemorrhagic cystitis following HSCT, particularly in environments where conventional antiviral agents are not accessible. The findings also suggest a complex relationship between viral load and clinical presentation, warranting further investigation. Future, larger prospective studies are essential to establish standardized treatment protocols for this challenging complication, especially in developing countries like Vietnam.