*Corresponding author:
Matteo Coen, Service of Internal Medicine, Department of Internal Medicine and Department of Pathology and Immunology, Geneva University Hospitals, Geneva, Switzerland, Geneva University Hospitals, rue Gabrielle Perret-Gentil 4, 1211, Geneva 14, SwitzerlandReceived: April 16, 2018; Published: April 25, 2018
DOI: 10.26717/BJSTR.2018.04.000999
To view the Full Article Peer-reviewed Article PDF
An 89-year-old man was admitted to our service for worsening asthenia and dyspnea over a period of 3 weeks. His history was positive for arterial hypertension, ischemic heart disease, and lowgrade non-Hodgkin’s lymphoma (lymphoplasmacytic lymphoma) treated with chemotherapy consisting of rituximab, prednisone, doxorubicin, cyclophosphamide and vincristine (R-CHOP). Moreover, he suffered multiple episodes of cold agglutinin anaemia secondary to lymphoma. Routine laboratory showed mild anemia (haemoglobin of 7.6 g/dl); the remainder of his laboratory evaluation was within normal limits apart from mild deficiency of folic acid and vitamin B-12. Because of his cardiac condition transfusion threshold was set at 8.0 g/dl and blood transfusion was ordered. Patient’s group was O Rh+. The hospital blood transfusion laboratory detected the presence of cold agglutinins. The nurse routinely verified recipient’s and donor’s group at the patient’s bedside prior to transfusion. The bedside blood grouping card showed the agglutination of the patient’s blood with both anti-A and anti-B antibodies as well as in the control well. Instead, the donor’s blood (“culot”) showed no reaction (Figure 1). Transfusion was performed using a blood warmer and proved uneventful. Yet, the peculiar results of blood grouping card drove our curiosity and prompted us to review the pathophysiology of cold agglutinin haemolytic anaemia. After transfusion, patient’s conditions rapidly ameliorated and was discharged at day 7.