In immunocompent patients, pNTM disease is usually limited to the

In immunocompent patients, pNTM disease is usually limited to the bronchi and lungs, but patients with human immunodeficiency virus (HIV) infection may progress to systemic disseminated disease. 2 Disseminated NTM (dNTM) disease is regarded as a sign of acquired immunodeficiency syndrome (AIDS) due to HIV infection, whereas dNTM disease without HIV infection is very rare. Recently, the existence of autoantibodies against interferon-gamma selleck chemical (IFN-γ) has been shown to be closely related to dNTM disease without HIV infection. 3, 4 and 5 A few reports on dNTM disease without HIV infection noted the existence of anti-IFN-γ autoantibody with strong neutralizing capacity.

5 We describe herein our dNTM patient who was HIV negative but was infected with M. kansasii. This patient did not have MAC infection but anti-IFN-γ autoantibody, with strong neutralizing capacity, was detected. A 53-year-old male was referred to our hospital because of dyspnea, decreased hemoglobin, and white blood cell (WBC) counts over 30,000/μL. He was admitted and his laboratory data and

radiological findings were evaluated. Clinical laboratory data on admission confirmed high WBC counts and decreased hemoglobin. A high serum total immunoglobulin-G level was also demonstrated. Biochemical data showed www.selleckchem.com/products/ABT-888.html elevated alkaline phosphatase and globulins and a low level of serum albumin. No serum M protein was detected. Serum C-reactive protein was elevated, indicating an inflammatory reaction. Soluble interleukin-2 receptor (sIL-2R) was elevated to 11,470 U/ml. Both anti-HIV and anti-human T-cell leukemia virus (HTLV) antibody were negative. Radiological findings on admission showed non-segmental and patchy consolidation

along bronchi in the bilateral lung parenchyma. Multiple mediastinal lymph nodes were enlarged (Fig. 1A–C). We initially suspected an abnormality of hematopoietic organs and thus evaluated his bone marrow. The specimens revealed mild hyperplasia with markedly increased atypical plasma cells. Several further studies, including flowcytometric analysis, were conducted to assess whether the abnormal cells showed any signs of malignancy. However, of these atypical cells were ultimately determined to represent benign reactive changes. To further evaluate the mediastinal lymphadenopathy, transbronchial aspiration cytology using endobronchial ultrasonography was performed, but no significant findings were obtained. Based on polyclonal hypergammmopathy by serology and plasma cells collected for the bone marrow analysis, MCD was highly suspected. To confirm this diagnosis, surgical biopsy specimens of mediastinal lymph nodes and the lung parenchyma sample were obtained on the 31st hospital day. However, a pulmonary specimen was obtained only from the right lung, and adequate mediastinal lymph node specimens could not be collected due to severe adhesion.

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