Sarcopenia: an overlooked predictor of the progression risk in pulmonary nontuberculous mycobacterial infections?

Abstract

Background

Pulmonary nontuberculous mycobacterial (pNTM) infection is increasingly diagnosed, particularly in elderly individuals with impaired immunity or comorbidities. While some patients remain stable without treatment, others experience disease progression despite therapy. This study aimed to investigate the association between radiologic progression of pNTM infection and sarcopenia, along with other clinical factors.

Methods

This single-center cohort included adults diagnosed with pNTM infection between January 1, 2021, and December 31, 2023, from the institutional picture archiving and communication system and electronic medical records using predefined clinical, radiologic, and microbiologic criteria; 64 patients were included (mean age 66.3±10.71 years). Sarcopenia was evaluated by measuring the cross-sectional area (CSA) of the erector spinae muscles (ESMs) at the T12 level on chest computed tomography (CT), normalized for height to calculate the skeletal muscle index at the level of T12 (T12MI, cm²/m²). Radiologic progression was defined as new or worsening lesions on follow-up CT and was verified through multidisciplinary review. Multivariate logistic regression analyzed associations between T12MI, prior tuberculosis (TB) history, pNTM treatment, and other clinical variables.

Results

Ten patients (16%) showed disease progression, including radiologic progression. Sarcopenia (low T12MI) was not significantly associated with progression. In contrast, recent pNTM treatment [odds ratio (OR) =7.167; 95% confidence interval (CI): 1.591–32.291; P=0.01] was significantly associated with progression, and previous TB infection showed a suggestive association (OR =3.500; 95% CI: 0.867–14.133; P=0.08).

Conclusions

Sarcopenia was not a significant predictor of radiologic progression in pNTM infection. Instead, treatment history and prior TB were more closely related to progression, suggesting that these clinical factors may be more relevant indicators for radiologic surveillance and management decisions.

Highlight box.

Key findings

• In 64 patients with pulmonary nontuberculous mycobacterial (pNTM) infection, 16% showed radiologic progression. Sarcopenia (measured by T12 muscle index) was not significantly associated with disease progression.

What is known and what is new?

• Previous studies suggested sarcopenia correlates with worse outcomes in chronic lung diseases like chronic obstructive pulmonary disease and interstitial lung disease. Report here about what is known.

• This study demonstrates that computed tomography-based sarcopenia assessment does not predict radiologic progression in pNTM infection, contrasting with findings in other respiratory diseases.

What is the implication, and what should change now?

• Absence of recent pNTM treatment (odds ratio =7.167) and prior tuberculosis history emerge as stronger progression indicators, suggesting these clinical factors should guide surveillance strategies rather than muscle mass assessment.

Introduction

The rising prevalence of pulmonary nontuberculous mycobacterial (pNTM) infections, particularly among older adults, has become an increasing concern in clinical practice because of the challenges in diagnosis and treatment. These infections often exhibit resistance to standard antibiotic regimens and show variable clinical courses, ranging from indolent to refractory disease. Although immunosenescence and chronic comorbidities have been implicated as risk factors, the underlying host susceptibility mechanisms remain poorly defined. Given the ubiquitous environmental presence of nontuberculous mycobacterial (NTM) organisms, accurate diagnosis requires integration of clinical, radiologic, and microbiologic criteria to distinguish between colonization from true infection (1-4).

Recent studies have highlighted the association of low body mass index (BMI), lean body composition, and subcutaneous fat depletion with pNTM susceptibility and severity (5,6). However, few studies have specifically examined sarcopenia—defined as the loss of skeletal muscle mass and function—as a predictor of pNTM disease progression. Given emerging evidence linking thoracic muscle area, particularly the erector spinae muscle (ESM) on computed tomography (CT), to pulmonary outcomes and mortality in chronic respiratory disease (7-9), sarcopenia may serve as a quantifiable imaging biomarker reflecting nutritional status and physiological reserve.

This study aimed to investigate the relationship between sarcopenia and radiologic progression of pNTM infection in a cohort of elderly patients. By exploring the interplay between aging, nutritional status, and disease progression, we sought to determine whether CT-based thoracic muscle metrics could offer prognostic value in pNTM. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1983/rc).

Methods

Study participants

A flowchart was provided in Figure 1. A retrospective observational cohort study was conducted of all chest CT examinations performed at Bucheon St. Mary’s Hospital between January 1, 2021, and December 31, 2023. Patients meeting the diagnostic criteria for pNTM infection were identified. A total of 64 patients were included.

Figure 1.

Study cohort. Illustration of study participant selection process. CT, computed tomography; pNTM, pulmonary nontuberculous mycobacterial.

Selection criteria

Eligible patients had chest CT findings suggestive of pNTM infection, including centrilobular nodules, ground-glass opacities (GGOs) or consolidation, bronchiectasis, and bronchial wall thickening. All patients underwent at least 6 months of follow-up imaging.

CT technique and image evaluation

All scans were performed in the supine position using a multi-detector CT scanner (Sensation 64-section CT, Siemens Medical Solutions, Forchheim, Germany). Standard-dose scans were acquired with 3-mm collimation at 3-mm intervals, gantry rotation time of 0.5 s, pitch of 1.0, tube voltage of 120 kVp, and tube current of 100 mAs, covering from the lower neck to the midlevel of the kidneys. Low-dose CT scans were performed at full inspiration with 3-mm collimation, pitch of 1.35, scanning speed of 0.8 s, 120 kVp, and 50 mA. Images were reconstructed in axial and coronal planes, with lung window settings [width 1,000–1,500 Hounsfield units (HU), level −700 HU] and mediastinal window settings (width 380 HU, level 50 HU).

Assessment of sarcopenia

CT-based assessment of thoracic muscle mass remains a promising biomarker in chronic pulmonary disease evaluation (7-11). The utilization of chest CT for sarcopenia assessment has garnered increasing attention in radiologic practice (12,13), particularly when abdominal imaging is unavailable (14,15).

Skeletal muscle measurements at the T12 vertebral level have demonstrated potential for sarcopenia diagnosis and may serve as outcome correlates in patients undergoing chest-limited CT examinations (16-19).

Thoracic skeletal muscle mass was quantified using chest CT images obtained at the time of initial pNTM diagnosis. The cross-sectional area (CSA) of the ESM at the T12 vertebral level was measured (Figure 2). Figure 2 illustrates the assessment of sarcopenia by comparing paraspinal thoracic muscles at the T12 level in patients with low (Figure 2A) and high (Figure 2B) skeletal muscle mass. Non-enhanced chest CT images were used to measure the CSA of the ESMs, which was performed semi-automatically using Syngo.Via Client (version 5.1.0090, Siemens Healthcare GmbH, Erlangen, Germany), with the CSA highlighted in yellow dotted lines as shown in Figure 2. Each CSA was normalized by patient height squared (m²) to calculate the skeletal muscle index (SMI, cm²/m²), with sex-specific cutoff values used to define sarcopenia.

Figure 2.

Assessment of sarcopenia. Comparison of paraspinal thoracic muscles at the T12 level in patients with low (A) and high (B) skeletal muscle mass. Non-enhanced chest CT images were used to measure the CSA of the ESMs, which was performed semi-automatically using Syngo.Via Client (version 5.1.0090, Siemens Healthcare GmbH, Erlangen, Germany). CSA of ESMs is highlighted in yellow dotted lines. CSA, cross-sectional area; CT, computed tomography; ESMs, erector spinae muscles.

Assessment of disease progression

Radiologic progression assessment

Radiologic progression or recurrence was determined by comparing baseline and follow-up CT scans according to established guidelines (20), which define disease progression as the development of new or worsening cavitation or fibrosis and the increase in nodules or tree-in-bud opacities. All images were independently reviewed by two radiologists, and a consensus was reached in cases of discrepancy.

Clinical and microbiologic confirmation of pNTM

Final diagnosis of pNTM was confirmed based on multidisciplinary clinical evaluation by pulmonologists and, when available, bronchoscopic culture results, in accordance with American Thoracic Society (ATS)/Infectious Diseases Society of America (IDSA) diagnostic guidelines (2).

Clinical characteristics

Clinical information was obtained from electronic medical records, including sex, age, smoking history, alcohol consumption, BMI, pathologic diagnosis and causative organism, antibiotic treatment history, recurrence, concurrent pulmonary tuberculosis (TB), and underlying comorbidities (diabetes mellitus, hypertension, hyperlipidemia, chronic kidney disease (CKD), chronic lung disease (CLuD), chronic liver disease (CLD), chronic heart disease, prior stroke, malignancy, and history of surgery). Nutritional and physiological status were assessed using documented screening results for malnutrition and pressure sore risk, as well as laboratory data within 3 months of the initial CT scan. Laboratory parameters included white blood cell (WBC) count, hemoglobin, platelet count, fasting blood sugar (FBS), blood urea nitrogen (BUN), creatinine, estimated glomerular filtration rate (eGFR), C-reactive protein (CRP), serum albumin, total bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Pulmonary function test (PFT) parameters—forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC—were also collected when available. When available, additional nutritional biomarkers such as transthyretin and retinol-binding protein were also reviewed, in accordance with previous literature linking nutritional status to pNTM severity (6).

Statistical analysis

All statistical analyses were performed using R software (version 4.0.3; R Foundation for Statistical Computing, Vienna, Austria). Baseline demographic and clinical characteristics were compared between patients with and without radiologic progression or recurrence of NTM lung disease. Categorical variables were analyzed using Pearson’s Chi-squared test or Fisher’s exact test, as appropriate, and continuous variables were compared using the Student’s t-test or analysis of variance (ANOVA). Univariate logistic regression was performed to evaluate associations between potential risk factors and disease progression. Variables with P<0.10 in univariate analysis were entered into a multivariate logistic regression model to identify independent predictors, with results expressed as odds ratios (ORs) and 95% confidence intervals (CIs). A two-sided P value <0.05 was considered statistically significant.

Ethical statement

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the institutional review board (IRB) of Bucheon St. Mary’s Hospital (IRB No. HC23RISI0027) and individual consent for this retrospective analysis was waived.

Results

Baseline characteristics

Of the 64 patients included in the study, 10 (15.6%) experienced radiologic progression or recurrence of NTM lung disease during follow-up (Table 1). The mean age was similar between the progression and non-progression groups (65.5±11.05 vs. 66.4±10.74 years, P=0.80). Females accounted for a slightly higher proportion in both groups (70.00% vs. 59.26%, P=0.53). BMI, height, weight, and SMI at the level of T12 (T12MI) did not significantly differ between groups. The prevalence of comorbidities, including hypertension, hyperlipidemia, diabetes mellitus, CKD, CLD, and CLuD, was low in the recurrence group and showed no significant association with disease progression. Smoking status showed no difference was not statistically significant (P=0.29).

Table 1. Characteristics of the patients diagnosed pNTM infection.

Characteristics	Data (n=64)
Age (years)	66.3±10.71
Sex (M:F)	39:25
BMI (kg/m2)	20.2±3.0
Smoking
No	47
Ex-smoker	8
Current smoker	7
No available information	2
Underlying disease
Hypertension	16 (25.0)
Hyperlipidemia	6 (9.4)
Diabetes	9 (14.1)
CKD	1 (1.6)
CLD	4 (6.3)
CLuD	13 (20.3)
COPD	10 (76.9)
Asthma	1 (7.7)
ILD	2 (15.4)
Past TB history	17 (26.6)
No pNTM treatment	11 (17.2)
T12MI (cm2/m2)
Initial CT	43.96±14.5
FU CT	43.49±14.5

Data are presented as mean ± SD, number, or number (%). BMI, body mass index; CKD, chronic kidney disease; CLD, chronic liver disease; CLuD, chronic lung disease; COPD, chronic obstructive pulmonary disease; CT, computed tomography; F, female; FU, follow-up; ILD, interstitial lung disease; M, male; pNTM, pulmonary nontuberculous mycobacterial; SD, standard deviation; T12MI, skeletal muscle index at the level of T12; TB, tuberculosis.

Nutritional and clinical parameters

Nutritional screening scores, disease severity, and pressure ulcer risk assessments were comparable between the two groups. Laboratory results—including WBC count, hemoglobin, platelet count, CRP, BUN, creatinine, eGFR, serum albumin, bilirubin, AST, ALT, FEV1, FVC, and FEV1/FVC—showed no significant associations with progression.

Factors associated with progression

The associations between clinical and radiologic factors and NTM lung disease progression are presented in Table 2. A previous history of TB infection demonstrated a suggestive association with pNTM progression (OR =3.500; 95% CI: 0.867–14.133; P=0.08). Notably, radiologic progression of pNTM infection was significantly more frequently observed in patients who had not recently received treatment for pNTM compared to those who had received recent treatment (50.00% vs. 11.11%; OR =7.167; 95% CI: 1.591–32.291; P=0.01). When translated into absolute risk, radiologic progression was observed in 50.00% of patients without recent pNTM treatment compared with 11.11% of those with recent treatment, indicating an absolute risk increase of 38.89% during the follow-up period. Other clinical conditions evaluated in Table 2, including prior stroke, cancer history, and previous operation history, were not significantly associated with progression risk.

Table 2. Association between progression of pNTM disease and clinical/radiologic factors.

Parameters	Non-event (n=54)	Progression or recurrence (n=10)	Univariate analysis
			OR (95% CI)	P value
Age (years)	66.4±10.74	65.5±11.05	0.992 (0.930, 1.057)	0.80
Sex
Male	22 (40.74)	3 (30.00)	1.604 (0.374, 6.889)	0.53
Female	32 (59.26)	7 (70.00)
Continuous value
BMI (kg/m2)	20.34±3.05	20.41±2.24	1.008 (0.780, 1.303)	0.95
Height (m)	1.60±0.08	1.59±0.09	0.067 (0.000, 988.751)	0.58
Weight (kg)	52.19±8.79	51.58±8.95	0.992 (0.910, 1.081)	0.85
T12MI (cm2/m2)
Before	16.23±4.63	18.89±5.87	1.116 (0.959, 1.297)	0.16
After	16.04±4.51	18.20±6.11	1.097 (0.941, 1.279)	0.23
Underlying disease
Hypertension	16 (29.63)	0	0	>0.99
Hyperlipidemia	6 (11.11)	0	0	>0.99
Diabetes	8 (14.81)	1 (10.00)	0.639 (0.071, 5.755)	0.69
CKD	1 (1.85)	0	0	>0.99
CLD	4 (7.41)	0	0	>0.99
CLuD	12 (22.22)	1 (10.00)	0.389 (0.045, 3.383)	0.39
COPD	10	0	0.2 (0.010, 3.703)	0.34
Asthma	1	0	1.7 (0.060, 44.610)	>0.99
ILD	1	1	5.630 (0.530, 60.010)	0.29
Smoking
No	39 (72.22)	8 (80.00)
Ex-smoker	8 (14.81)	0	0	>0.99
Current smoker	6 (11.11)	1 (10.00)	0.792 (0.083, 7.512)	0.84
No available information	1 (1.85)	1 (10.00)	4.750 (0.268, 84.175)	0.29
Past TB history	12 (22.22)	5 (50.00)	3.500 (0.867, 14.133)	0.08
No pNTM treatment	6 (11.11)	5 (50.00)	7.167 (1.591, 32.291)	0.01
Nutritional screening scores
0	15 (27.78)	3 (30.00)
1	14 (25.93)	4 (40.00)	1.429 (0.270, 7.549)	0.67
2	7 (12.96)	1 (10.00)	0.714 (0.063, 8.150)	0.79
3	6 (11.11)	1 (10.00)	0.833 (0.072, 9.688)	0.88
4	5 (9.26)	0	0	>0.99
5	2 (3.70)	0	0	>0.99
Disease severity (score)	17.43±4.80	16.33±1.94	0.936 (0.771, 1.136)	0.50
Pressure ulcer risk (score)	21.88±2.43	20.00±7.55	0.906 (0.777, 1.055)	0.20
Stroke	3 (5.56)	1 (10.00)	1.889 (0.176, 20.237)	0.60
Cancer	21 (38.89)	3 (30.00)	0.653 (0.152, 2.813)	0.57
WBC (×109/L)	7.15±3.74	6.23±2.16	0.909 (0.709, 1.165)	0.45
Hemoglobin (g/dL)	12.73±1.55	13.05±1.40	1.157 (0.727, 1.841)	0.54
Platelet (×109/L)	244.82±135.74	223.2±64.10	0.998 (0.991, 1.005)	0.62
CRP (mg/L)	25.56±45.48	9.29±13.30	0.983 (0.946, 1.022)	0.39
BUN (mg/dL)	15.19±5.08	11.76±6.40	0.883 (0.749, 1.041)	0.14
Creatinine (mg/dL)	0.79±0.19	0.75±0.12	0.282 (0.002, 37.059)	0.61
eGFR (mL/min/1.73 m2)	86.47±20.21	74.31±34.12	0.978 (0.946, 1.011)	0.19
Albumin (g/dL)	5.15±6.32	4.30±0.20	0.953 (0.664, 1.367)	0.79
Bilirubin (mg/dL)	0.59±0.96	0.40±0.14	0.155 (0.001, 27.973)	0.48
AST (U/L)	25.29±10.79	23.75±8.19	0.984 (0.907, 1.067)	0.70
ALT (U/L)	21.44±14.51	19.13±11.51	0.987 (0.928, 1.049)	0.67
FEV1 (%pred)	89.86±23.5	89.43±23.3	0.999 (0.965, 1.034)	0.96
FEV1/FVC (%)	70.98±11.7	73.14±11.6	1.017 (0.946, 1.095)	0.65
FVC (%pred)	88.93±18.1	86.43±18.1	0.992 (0.949, 1.037)	0.73
Previous operation	24 (44.44)	4 (40.00)	0.806 (0.203, 3.189)	0.76

Data are presented as mean ± SD, number (%), or number, unless otherwise stated. ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; BUN, blood urea nitrogen; CI, confidence interval; CKD, chronic kidney disease; CLD, chronic liver disease; CLuD, chronic lung disease; COPD, chronic obstructive pulmonary disease; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity; ILD, interstitial lung disease; OR, odds ratio; pNTM, pulmonary nontuberculous mycobacterial; T12MI, skeletal muscle index at the level of T12; TB, tuberculosis; WBC, white blood cell.

Discussion

pNTM infection is an increasingly prevalent respiratory disease worldwide and represents a significant clinical challenge, particularly in elderly populations. While most prior research has focused on risk factors for initial disease development or severity at diagnosis, relatively few studies have examined determinants of disease progression and recurrence after diagnosis. In this study, we investigated whether sarcopenia—quantified by thoracic SMIs (T12MI) derived from chest CT—was associated with radiologic progression of pNTM infection. Our results demonstrated no significant relationship between sarcopenia and disease progression.

Several previous studies have explored the relationship between sarcopenia and CLuDs, with mixed results. In chronic obstructive pulmonary disease (COPD), sarcopenia has consistently been associated with worse clinical outcomes, including exacerbation risk, hospitalization, and mortality (21-23). Similarly, sarcopenia has been linked to adverse outcomes in interstitial lung disease (ILD) (24,25) and aspiration pneumonia (26), suggesting that skeletal muscle mass and function may reflect systemic vulnerability across diverse pulmonary conditions.

In contrast, studies investigating sarcopenia in the context of pNTM infection have yielded more heterogenous findings. Some reports have demonstrated that reduced muscle mass or strength and disease susceptibility or severity (5,8,21,27). For example, quantitative assessment of ESM CSA on chest CT has been linked with more severe pNTM and mortality, though not with radiologic progression (8). Other studies evaluated body composition through bioelectrical impedance and found abdominal fat ratio—not muscle mass—associated with disease progression (5).

Several investigations have reported no clear association between sarcopenia and radiologic progression in pNTM. In addition, recent studies suggest that functional measures such as handgrip strength or physical inactivity may better reflect clinically relevant sarcopenia in pNTM than measures of muscle mass alone obtained from CT (21,28).

Our study employed routine institutional assessments, including nutritional screening scores, disease severity evaluations, and pressure ulcer risk stratification, to assess the functional aspects of sarcopenia. However, these surrogate measures may not fully reflect functional impairment, suggesting that muscle quality or strength could be more relevant than quantitative CSA alone (27).

Considering that sarcopenia is predominantly an age-related process in elderly populations (29-31) and progressive pNTM tends to occur in relatively younger individuals, age-related confounding may partly explain the lack of association observed. In addition, multiple comorbidities frequently seen in elderly patients may independently contribute to sarcopenia (32-35).

The decision to initiate antimicrobial treatment for pNTM is often difficult, as no absolute criteria exist (2). Many patients with pNTM remained clinically and radiologically stable for considerable periods of time without treatment (36,37), whereas long-term combination therapy is frequently accompanied by significant side effects (2,38-42). Because treatment does not guarantee a complete cure (2,38,41), initiation of treatment for pNTM should be guided by clinical factors, the infectious organism, and the patient’s treatment goals (2,20,41,43). Radiologically, the cavitary lung lesion is generally considered an indication for treatment initiation; however, this remains a conditional recommendation (41). Although treatment-related variables appeared as secondary findings in our analysis, the primary objective of this study was not to evaluate treatment outcomes but to explore whether sarcopenia reflects radiologic disease behavior in pNTM. Therefore, treatment considerations were described only briefly and interpreted as supplementary observations.

Systematic reviews and meta-analyses (44) have identified several factors significantly associated with radiologic progression in pNTM disease, including increasing age, ILD, cavitation, consolidative pattern, anemia, and leukocytosis. In our cohort, patients with disease progression were more likely to have lacked recent pNTM treatment. While this finding suggests that treatment history may influence radiologic trajectories, it should be interpreted cautiously, as treatment-related variables were not the primary focus of our study and may reflect clinical decision-making rather than intrinsic disease behavior.

A previous history of TB demonstrated a suggestive association with pNTM progression (P=0.08), consistent with evidence that post-TB structural lung damage—including bronchiectasis, parenchymal scarring, and compromised local immunity—predisposes patients to recurrent or progressive disease (44-48). These observations indicate that baseline structural vulnerability, rather than muscle mass, may play a larger role in determining radiologic outcomes in pNTM. In contrast, sarcopenia did not show meaningful predictive value for short-term radiologic progression. This differs from its role in COPD, ILD, and aspiration pneumonia, where sarcopenia—and particularly respiratory muscle dysfunction—is strongly linked to symptom burden, exercise intolerance, and mortality (21-25,28,49). In COPD, disease severity correlates with skeletal muscle dysfunction characterized by muscle atrophy, weakness, reduced endurance, and fatigue, as well as respiratory muscle impairment leading to exercise capacity limitations (exercise intolerance) (22,50,51). Similarly, ILD causes respiratory muscle dysfunction due to reduced lung compliance, resulting in dyspnea and exercise intolerance (24). Multiple factors in ILD patients, including hypoxemia, inflammation, steroid use, inactivity, and malnutrition, contribute to both respiratory and limb muscle dysfunction (52), with age-related decline in inspiratory muscle strength (53-55) helping explain why sarcopenia emerges as a mortality risk factor in this population. In elderly patients, sarcopenic dysphagia increases aspiration pneumonia susceptibility through impaired swallowing function (26,56). These observations suggest that the critical factor may be the presence or absence of a direct pathophysiologic connection between respiratory disease mechanisms and the core sarcopenia criteria (57,58): low muscle strength, low muscle quantity or quality, and low physical performance. While sarcopenia in chronic infections such as pNTM may compromise host immune defense and overall physiologic reserve, its prognostic impact appears to depend on disease phase, causative organism, and patient characteristics. Our results suggest that the prognostic utility of sarcopenia for predicting radiologic progression in established pNTM disease may be limited. Although our study aimed to identify radiologic indicators that could assist in pNTM treatment decisions, changes (44) in existing pulmonary imaging findings may currently provide the most clinically relevant information for disease monitoring.

Limitation

This study has several limitations. First, its retrospective, single-center design may introduce selection bias and limit generalizability. Second, although all included patients met microbiologic diagnostic criteria—most confirmed by bronchoscopy—the requirement for multidisciplinary clinical-radiologic consensus and pathologic confirmation inherently restricted the sample size. This diagnostic rigor, while necessary to avoid misclassification in a disease with highly nonspecific imaging findings, limited statistical power for detecting small effect sizes. Third, comprehensive microbiologic subtyping of NTM species was not available for all patients, and species-specific differences in pathogenicity, clinical courses, radiologic features, and therapeutic response patterns may have influenced the results (41).

Prospective, multi-institutional studies with larger cohorts, standardized imaging protocols, complete species identification, and incorporation of validated functional sarcopenia assessments such as handgrip strength, gait speed, and short physical performance battery (SPPB) are needed to clarify the relationship between sarcopenia and radiologic progression in pNTM (57,58).

Conclusions

Sarcopenia was not significantly associated with radiologic progression of pNTM infection in elderly patients. Although recent treatment history appeared to correlate with progression, this represents a secondary exploratory finding and requires further investigation in future studies.

Supplementary

The article’s supplementary files as

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the institutional review board (IRB) of Bucheon St. Mary’s Hospital (IRB No. HC23RISI0027) and individual consent for this retrospective analysis was waived.

Data Sharing Statement

Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1983/dss

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DOI: 10.21037/jtd-2025-1983