title: Distinct clinical features in nontuberculous mycobacterial disease with or without latent tuberculosis infection.
abstract: Nontuberculous mycobacteria (NTM) diseases are in the face of a progressive increase even in immune-competent subjects, and the clinical features of NTM diseases are heterogenous. The decision to institute treatment of the patients should be made after a period of follow up, because therapy is often prolonged, and frequently ineffective. The reasons why some patients develop severe NTM diseases are not clear. Here we observed the involvement of latent tuberculosis infection (LTBI) in clinical and laboratory features of NTM diseases. We evaluated various tuberculosis-related inflammatory markers including osteopontin (OPN), pentraxin-3 (PTX-3), and soluble IL-2 receptor (sIL-2R) in NTM infected patients with or without LTBI. Eight NTM and 5 tuberculosis (TB) patients, and 5 healthy subjects were enrolled. Polymerase Chain Reaction (PCR) analysis confirmed the absence of tuberculosis specific gene (RD1 region), among clinical isolates from NTM patients. Interferon-γ (IFN-γ) release assay (IGRA) using Early Secreted Antigenic Target-6 (ESAT-6) and CFP-10, the RD1-encoded protein, was employed for determining LTBI. IGRA was positive in 4/8 NTM (NTM with LTBI, 50%) and 5/5 TB patients. Only 2 of 4 NTM with LTBI were under chemotherapy among all NTM patients, and others were followed up. The plasma levels of OPN, PTX3 and sIL-2R were significantly higher in NTM patients with LTBI than in those without LTBI (P < 0.05). The two patients under therapy showed the highest OPN levels that persisted after treatment. The increased inflammatory levels in NTM patients with LTBI indicate enhanced inflammatory reaction. Extensive therapy may be necessary in such patients.
authors.affiliation: Division of Emerging Infectious Diseases, Graduate School of Medicine, Tohoku University, Sendai, Japan.
authors.forename: Umme Ruman
authors.initials: UR
authors.lastname: Siddiqi
authors.forename: Haorile
authors.initials: H
authors.lastname: Chagan-Yasutan
authors.forename: Chie
authors.initials: C
authors.lastname: Nakajima
authors.forename: Hiroki
authors.initials: H
authors.lastname: Saitoh
authors.forename: Yugo
authors.initials: Y
authors.lastname: Ashino
authors.forename: Osamu
authors.initials: O
authors.lastname: Usami
authors.forename: Beata
authors.initials: B
authors.lastname: Shiratori
authors.forename: Motoki
authors.initials: M
authors.lastname: Usuzawa
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Toshio
authors.initials: T
authors.lastname: Hattori
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D004269:DNA, Bacterial / Q000235:genetics; D005260:Female; D006801:Humans; D055985:Latent Tuberculosis / Q000175:diagnosis* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009165:Mycobacterium Infections, Nontuberculous / Q000175:diagnosis* / Q000276:immunology; D015269:Mycobacterium avium Complex / Q000235:genetics* / Q000302:isolation & purification; D009169:Mycobacterium tuberculosis / Q000235:genetics* / Q000302:isolation & purification; D053495:Osteopontin / Q000097:blood; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D000683:Serum Amyloid P-Component / Q000378:metabolism; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D004269:DNA, Bacterial; D053495:Osteopontin; D015375:Receptors, Interleukin-2; D000683:Serum Amyloid P-Component; D000099153:Pentraxins