BZellAplasie

BZellAplasie, also known as B-cell aplasia, is a medical condition defined by the absence or severe depletion of CD19-positive B lymphocytes in the peripheral blood and secondary lymphoid tissues, leading to impaired humoral immunity. It is typically acquired, though rare congenital forms exist.

Causes of BZellAplasie include therapeutic depletion of B cells and certain immunodeficiency disorders. Anti-CD20 monoclonal antibodies (such as rituximab, obinutuzumab, or ofatumumab), and other B cell–depleting therapies can induce B-cell loss. Chimeric antigen receptor (CAR) T-cell therapies targeting CD19, as well as hematopoietic stem cell transplantation, can result in prolonged B-cell aplasia. Less commonly, genetic or acquired primary immunodeficiencies and certain viral infections may contribute. The resulting lack of mature B cells leads to reduced production of immunoglobulins and a heightened risk of recurrent infections.

Clinical features typically include recurrent sinopulmonary and other bacterial infections, poor response to vaccines, and laboratory evidence of hypogammaglobulinemia with very low or absent CD19+ B cells. Diagnosis relies on flow cytometry showing depleted B cells and serum immunoglobulin measurements, along with assessment for underlying causes and exclusion of other immunodeficiencies.

Management focuses on protecting against infections and restoring humoral defense. Immunoglobulin replacement therapy (intravenous or subcutaneous) is commonly used to provide passive antibodies. Antimicrobial prophylaxis and vaccination planning may be indicated, with vaccines often ineffective during active B-cell depletion. In cases related to therapy, B-cell recovery may occur over time after cessation or waning of treatment, but persistent BZellAplasie requires ongoing management. Prognosis depends on the cause and the ability to reconstitute B-cell function.