Hidden consequences: Uncovering belimumab’s role in the development of Pneumocystis jirovecii pneumonia in a lupus patient

贝里穆马布 医学 强的松 耶氏肺孢子虫 肺炎 系统性红斑狼疮 内科学 免疫学 重症监护医学 疾病 B细胞 抗体 B细胞激活因子
作者
Maria Ng,Meggan Mackay,Pranisha Gautam‐Goyal,Sameer Goyal,Praveen Kumar Vikraman
出处
期刊:Lupus [SAGE Publishing]
卷期号:32 (10): 1227-1230 被引量:2
标识
DOI:10.1177/09612033231192334
摘要

Pneumocystis jirovecii is an opportunistic fungal organism that can cause fatal pneumonia in immunocompromised individuals. It is a disease associated with CD4+ T cell depletion or high-dose steroids. However, there is increasing evidence that B cell dysfunction may also play a role in this illness.A 33-year-old female with SLE, who was maintained on belimumab and low-dose prednisone (2.5 mg daily), presented with progressive cough and shortness of breath. She had been on monthly belimumab and prednisone 2.5 mg daily for 19 months, and her CD4 count was >200/uL, but her CD19+ B cell was <1% due to the belimumab. She developed a persistent cough and progressive dyspnea that did not respond to empiric antibiotic therapy for pneumonia. She went to the hospital for acute worsening of her dyspnea and cough. An extensive workup was performed, including a VATS procedure and surgical biopsy, which gave a definitive diagnosis of PJP. The patient was treated and discharged on trimethoprim-sulfamethoxazole. She made a complete recovery.Our report demonstrates the first confirmed case of pneumocystis jirovecii pneumonia in a patient with B cell depletion due to chronic maintenance therapy with belimumab. Our patient's diagnosis of PJP was unexpected, given her normal CD4+ count and the use of such a low dose of prednisone. We attribute her susceptibility to PJP infection to her profound B cell depletion in response to her belimumab therapy, supporting previous research indicating the importance of CD4+ T cells and B cells in the protective immune response against PJP. This case may help shape future clinical guidelines concerning PJP prophylaxis, particularly in SLE patients with deficient B lymphocytic activity and B cell depletion.
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