Selective Immunoglobulin M Deficiency Among Clozapine-Treated Patients: A Nested Case-Control Study.

Clinicians are often encouraged to conduct studies that provide insight into the pathogenesis, diagnosis, prognosis, and treatment of different subsets of patients with schizophrenia and patients with psychotic disorders. Due to possible immunosuppressive action that may contribute to the antipsychotic efficacy, pharmacologic studies may need to extend beyond neurotransmitter activity.1 Clozapine is an atypical antipsychotic medication that possesses immunomodulatory properties and is indicated for patients who fail standard antipsychotic treatment. In fact, clozapine has been reported to mediate several effects on humoral immunity, such as altering the levels of antibody-producing cytokines, and has been speculated to possess immunosuppressant activity as a part of its antipsychotic properties.2 Selective immunoglobulin M immunodeficiency (SIgMD) is a rare form of dysgammaglobulinemia, which is characterized by a selective low level of IgM in conjunction with normal T cell numbers and function and no other identifiable immunodeficiency. SIgMD can occur as either a primary or secondary condition and has an estimated prevalence of 0.03%–3%.3 As a secondary condition, SIgMD can be associated with immunosuppressive treatments,4 including clozapine. Therefore, due to speculated immunosuppressive effects of clozapine as a part of its antipsychotic effect, which can alter levels of immunoglobulins and eventually may lead to SIgMD, we investigated the presence of SIgMD among clozapine-treated patients with the purpose of clinical management.