Research progress on febrile non-hemolytic transfusion reaction: a narrative review

BACKGROUND AND OBJECTIVE: About 1% of patients who receive blood transfusions will develop transfusion reactions. Febrile non-hemolytic transfusion reaction (FNHTR) is the most common type of transfusion reaction. It not only leads to misdiagnosis and delayed treatment, but also incurs a huge economic burden. This article reviews FNHTR systematically, aiming to make clinicians have a more comprehensive understanding of FNHTR and reduce the occurrence of this side effect. METHODS: A comprehensive search of the PubMed, Embase, and Cochrane Library databases was performed. Medical Subject Headings (MeSH) included Blood Transfusion, Transfusion Reaction, and Febrile Non-Hemolytic Transfusion Reaction. The searches and literature screening were performed by 2 researchers; any differences of opinion or results were resolved through negotiation. KEY CONTENT AND FINDINGS: The pathophysiological mechanisms of FNHTR mainly included immune and non-immune pathways. The former was associated with antibodies against human leukocyte antigen (HLA) produced in transfused patients, while the latter was associated with cytokines released from blood products during storage. Women with a reproductive history and those patients with multiple blood transfusions were more likely to experience FNHTR. Primary hematologic disease, malignant disease, and transfusion with over 6 units of leukocyte-depleted packed red blood cells were independent risk factors for the development of FNHTR. FNHTR could be diagnosed by accompaniment of the fever symptom (body temperature ≥38 ℃, maybe an increase of body temperature of more than 1 ℃ compared with that before blood transfusion) during or within 4 hours after transfusion, or the presence of chills, shakes, headache, and nausea, among other symptoms. FNHTR should be mainly differentiated from other types of transfusion reactions with similar symptoms. Prophylactic strategies for the routine use of antipyretic drugs before transfusion remain controversial. Removal of leukocyte components from blood could reduce the incidence of FNHTR significantly. CONCLUSIONS: The pathogenesis of FNHTR is mainly associated with anti-HLA antibodies and cytokines released from blood products during storage. Specific markers and effective detection methods for FNHTR are still lacking. Treatment for FNHTR is currently limited to antipyretic drugs, sedation, and other symptomatic treatment measures. More studies are warranted to focus on the pathological mechanism of FNHTR.