To the editor

In their article, Skoczyńska et al¹ describe an interesting case of rheumatoid arthritis successfully treated with tuberculosis (TB) medicines. However, several issues remain unresolved.

There is no sharp distinction between TB and nontuberculous mycobacteria (NTM) pulmonary disease. The term “mycobacteriosis” is imprecise and rarely used in the literature. TB is an infectious disease caused by the Mycobacterium tuberculosis complex, which comprises distinct but related organisms, including M. tuberculosis, M. africanum, M. canetti, M. bovis, M. microti, M. caprae, M. pinnipedii, M. mungi, and M. orygis.² It is a notifiable disease with a reservoir only in humans, although many animals are susceptible to infection. The prognosis and treatment depend on the diagnosis of drug‑susceptible (DS) or drug‑resistant TB. TB infection can result in a latent period with a persistent risk of reactivation. NTM are ubiquitous, free‑living organisms that cause complex, noncontagious pulmonary diseases mainly in regions with a decreasing prevalence of TB.³ Patients with pulmonary diseases, such as cystic fibrosis, chronic obstructive pulmonary disease, bronchiectasis, and systemic immunosuppression, are at risk. The diagnosis of NTM infection involves both clinical and microbiological criteria, and treatment is tailored to the specific species.

The QuantiFERON‑TB test (QIAGEN, Venlo, the Netherlands) measures only antigen‑sensitized T cell‑mediated interferon release.⁴ It is primarily used for the detection of M. tuberculosis infection, but not for Mycobacterium spp. Early secreted antigenic target 6 and culture filtrate protein 10 are TB‑specific antigens. This test has poor specificity, as it cannot distinguish between an immune response to reactivated TB and a response to latent TB infection. Thus, it is not useful for confirming a diagnosis of TB.

Rapid molecular tests for TB and blood urine were performed according to the World Health Organization guidelines.⁴ However, after performing these tests, there were no results of TB cultures in the urine or blood.¹ Culture remains the gold standard for diagnosing TB. In immunosuppressed patients, the disease can be disseminated with extrapulmonary manifestations.

The patient was disqualified from the invasive procedures due to poor general condition. It is difficult to agree with the authors’ decision not to perform flexible bronchoscopy. Despite the presumed advanced malignancy and poor functional status, bronchoscopy is a key test used to exclude curable causes, such as TB. It is a safe procedure, and its diagnostic role is invaluable. Sputum induction has a similar diagnostic yield for smear‑negative pulmonary TB.⁵ Finally, endobronchial ultrasound–guided transbronchial needle aspiration is performed in the cases of unexplained mediastinal lymphadenopathy.

The current TB medicine regimen raises concerns. The regimen for DS TB comprises rifampicin, isoniazid, pyrazinamide, and ethambutol.² It does not typically include levofloxacin. The regimen for NTM infections primarily consists of rifampicin, ethambutol, and a macrolide. Amikacin is administered to patients with cavitary disease.

Finally, the authors did not specify the duration of treatment. The used 6‑month DS TB treatment is divided into the 2‑month intensive and the 4‑month continuation phase. Treatment extension beyond 6 months is not recommended, except for TB of the central nervous system or bone.² In NTM pulmonary infections, therapy is extended to 1 year after culture conversion. The report did not contain data on the adverse effects of the treatment. As hepatotoxic medications were used, it would be reasonable to screen for hepatotoxicity.

Containment of TB infection relies on an intact immune system. Antitumor necrosis factor α (TNF-α) therapy can negatively affect the maintenance of granuloma integrity. Granulomas serve as both immunological and mechanical barriers in the control of TB. Anti‑TNF-α agents, such as adalimumab and infliximab, substantially increase the risk of TB reactivation.⁴ However, they also increase the risk of NTM infection. Both TB and NTM infections have similar symptoms and radiographic features. The distinction between them is based on microbiological results.

Lung malignancies and TB share common risk factors and clinical manifestations. Their clinical presentation is usually straightforward, with radiological findings suggestive of a malignant tumor and common TB manifestations, such as cavities and heterogeneous consolidations involving the upper lobes and the superior segments of the lower lobes.⁶ In the report, the clinical picture was not immediately apparent, and a definitive diagnosis was not established.

This case report has significant educational implications. However, it would have been worthwhile to proceed with flexible bronchoscopy to reach an underlying diagnosis. Maximum effort should be made to determine the cause of the patient’s condition in order to initiate effective treatment. Therefore, it is essential to distinguish between TB and NTM infections. It is recommended to use the Xpert MTB/RIF assay (Cepheid, Sunnyvale, California, United States) to detect TB and resistance to rifampicin before the initiation of therapy.⁴ However, positive culture results are microbiological criteria for diagnosing NTM infection. Therefore, NTM infection should not be diagnosed in the absence of culture results.