Association between steatotic liver disease (MASLD, met-ALD, and ALD) with preserved ratio impaired spirometry: a population-based study

Abstract

Background

Preserved Ratio Impaired Spirometry (PRISm) is related to increased morbidity and mortality. Recently, metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated alcohol-related liver disease (Met-ALD), and alcohol-associated liver disease (ALD) have been recognized as systemic metabolic disorders. The association between these novel liver disease categories and PRISm remains unclear.

Methods

We analyzed data from 23,414 adults aged ≥ 40 years from the 2010–2019 Korean National Health and Nutrition Examination Survey. Participants with obstructive lung patterns were excluded. MASLD, Met-ALD, and ALD were defined based on hepatic steatosis index, cardiometabolic criteria, and alcohol consumption. PRISm was defined as FEV₁/FVC ≥ 0.7 and FEV₁ <80% predicted. Complex sample logistic regression was used to examine associations, adjusting for sociodemographic, behavioral, and clinical variables. Subgroup analyses by sex and sensitivity analyses using AST-to-platelet index (APRI) for advanced fibrosis and lower limit of normal (LLN)-based criteria for PRISm were performed.

Results

Among the study population, 3,182 had PRISm. MASLD, Met-ALD, and ALD were more prevalent in the PRISm group than in the normal spirometry group. In fully adjusted models, MASLD (OR 1.36; 95% CI, 1.19–1.55) and Met-ALD (OR 1.51; 95% CI, 1.14–2.01), and ALD (OR 2.38; 95% CI, 1.65–3.41) were associated with increased odds of PRISm. These associations were significant in males but not in females. Sensitivity analyses using LLN showed consistent results. Participants with advanced fibrosis (APRI ≥ 0.34) also had higher odds of PRISm in both sexes.

Conclusion

MASLD, Met-ALD, and ALD are associated with PRISm, particularly in men, suggesting a possible link between liver-based metabolic dysfunction and non-obstructive pulmonary impairment. These findings highlight the need for integrated approaches to managing metabolic liver disease and lung function decline.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12890-026-04152-y.

Introduction

Preserved Ratio Impaired Spirometry (PRISm) is a distinct but heterogeneous pattern of lung function impairment [1–3], defined by a reduced forced expiratory volume in one second (FEV₁) with a preserved FEV₁ over forced vital capacity (FVC) ratio. Unlike chronic obstructive pulmonary disease (COPD), PRISm does not meet criteria for airflow obstruction but is nonetheless associated with increased risks of respiratory symptoms, cardiovascular morbidity, and mortality [4, 5]. Recent studies have consistently shown that PRISm is associated with various metabolic abnormalities, including diabetes mellitus, hypertension, and dyslipidemia [6, 7]. These comorbidities are more prevalent in individuals with PRISm compared to those with normal spirometry, suggesting a shared pathophysiological basis. Given PRISM may evolve over time into either COPD or a normal spirometry pattern [8], this condition likely represents a dynamic state influenced by ongoing metabolic and pulmonary interactions.

Steatotic liver disease (SLD), recently reclassified into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated alcohol-related liver disease (Met-ALD), and alcohol-associated liver disease (ALD), is increasingly recognized as a systemic metabolic disorder rather than a purely hepatic condition. These liver phenotypes are characterized by insulin resistance, ectopic fat accumulation, dyslipidemia, and low-grade systemic inflammation—all of which may contribute to pulmonary injury and reduced lung function. Previous studies have reported associations between nonalcoholic fatty liver disease and reduced FEV₁; however, most have focused on obstructive lung patterns or used outdated liver disease classifications, without considering the updated MASLD, Met-ALD, and ALD frameworks or focusing on PRISm as a distinct entity.

In this context, our study hypothesizes that PRISm is associated with MASLD, Met-ALD, and ALD in the general adult population. This study aims to evaluate the relationship between newly defined subtypes of SLD and PRISm using a nationally representative Korean cohort, and to explore potential sex-specific associations and the role of hepatic fibrosis in this relationship.

Methods

Study participants

This study analyzed data from the Korean National Health and Nutrition Examination Survey (KNHANES) conducted between 2010 and 2019. The KNHANES is an annual nationwide survey administered by the Korean Centers for Disease Control and Prevention, designed to collect comprehensive health data from a representative sample of non-institutionalized Korean residents. The survey encompasses health interviews, physical examinations, and nutritional assessments, gathering detailed information about socioeconomic factors, health behaviors, physical measurements, and clinical markers of chronic diseases. Each year’s survey involved a randomly selected new group of participants, with the methodology detailed in previous publications [9].

From the initial pool of 103,465 participants during the study period, 80,860 individuals (78.2%) completed the survey. Since pulmonary function tests (PFT) were limited to participants aged 40 and older, 47,885 individuals without PFT data were excluded. Because this study focused on comparing normal PFT results with PRISm, we excluded 2,111 participants who showed obstructive patterns on PFT. We further excluded 9,803 cases due to insufficient data for calculating the hepatic steatosis index (HSI) or incomplete information needed to define MASLD and Met-ALD. The final analysis included 23,172 participants, comprising 20,047 individuals with normal PFT and 3,125 with PRISm.

Pulmonary function testing and PRISm

Pulmonary function testing was conducted using two different spirometry systems: the SensorMedics Model 2130 dry rolling seal spirometer (Yorba Linda, CA, USA) from 2010 to 2015, followed by the Vyntus Spiro (CareFusion, San Diego, CA, USA) from 2016 to 2019. All testing procedures adhered to the standardization guidelines established jointly by the American Thoracic Society and European Respiratory Society for calibration and quality control [10]. The prebronchodilator test measurements included forced expiratory volume in 1 s (FEV₁, L), forced vital capacity (FVC, L), and the FEV₁/FVC ratio (%). The KNHANES protocol did not include postbronchodilator testing. PRISm was defined by the presence of a normal FEV₁/FVC ratio in combination with an FEV₁% of the predicted value < 80 [3]. In addition, for sensitivity analysis, we categorized lung function testing based on lower limit of normal (LLN), where normal-LLN pattern of spirometry was defined as FEV₁/FVC ≥ LLN and FEV₁ ≥LLN and PRISm-LLN was defined as FEV₁/FVC ≥ LLN and FEV₁ < LLN [2]. Thresholds of LLN were calculated based on Global Lung Function Initiative reference equations [11].

SLD, MASLD, Met-ALD, and ALD

SLD was defined using the modified HSI, calculated as follows: HSI = 8×ALT/AST + BMI (+ 2 if female) [12, 13]. An HSI score ≥ 36 was used to define hepatic steatosis, with a reported sensitivity of 93.1% and specificity of 92.4% for detecting steatotic liver disease [12, 14]. Among individuals with hepatic steatosis, MASLD and Met-ALD were defined according to recently proposed diagnostic criteria based on the presence of cardiometabolic risk factors and alcohol intake [15]. MASLD was defined as hepatic steatosis in the presence of at least one cardiometabolic risk factor and non-excessive alcohol use. Met-ALD was defined as hepatic steatosis in individuals with excessive alcohol use (≥ 210 g/week in men, ≥ 140 g/week in women) and at least one cardiometabolic risk factor. For sensitivity analysis, an AST-to-platelet ratio index (APRI) cutoff of 0.34 was applied to define advanced fibrosis [16, 17].

Cardiometabolic criteria

The following cardiometabolic risk factors were used to define MASLD and Met-ALD, based on consensus definitions [15]. The following cardiometabolic risk factors were used to define MASLD and Met-ALD: (1) Waist circumference ≥ 90 cm in men or ≥ 80 cm in women, (2) fasting glucose ≥ 100 mg/dL or HbA1c ≥ 5.7% or current antidiabetic therapy, (3) blood pressure ≥ 130/85 mmHg or current use of antihypertensive medication, (4) plasma triglycerides ≥ 150 mg/dL or use of lipid-lowering drugs, and HDL cholesterol < 40 mg/dL in men or < 50 mg/dL in women.

Other variables

Other variables included age (years), sex (male or female), BMI (kg/m²), waist circumference (cm), systolic and diastolic blood pressure, smoking status (never, former, or current), and alcohol consumption level. Smoking status was categorized based on the National Health Interview Survey of the United States. Current smokers were defined as individuals who had smoked more than 100 cigarettes in their lifetime and currently smoked. Former smokers were defined as individuals who had smoked more than 100 cigarettes in their lifetime but had stopped smoking for more than one year. High-risk alcohol consumption was defined as more than seven drinks for men and more than five drinks for women on a single occasion. Laboratory examinations included levels of total cholesterol (mg/dL), LDL cholesterol (mg/dL), HDL cholesterol (mg/dL), triglycerides (mg/dL), HbA1c (%), fasting glucose (mg/dL), aspartate aminotransferase (IU/L), alanine aminotransferase (IU/L), total calorie intake, total carbohydrate intake, and total fat intake.

Statistical analysis

The KNHANES was designed to represent the noninstitutionalized population of South Korea, utilizing a stratified multistage probability sampling method. As a result, all statistical analyses in this study accounted for the complex survey design by incorporating sampling weights, stratification, and clustering in SPSS. Continuous variables and categorical variables in the descriptive analysis were expressed as mean with standard error and percentages with standard errors, respectively.

Complex sample logistic regression analysis was applied to determine the odds ratios (OR) and 95% confidence intervals (CI) for PRISm. In the multivariable analysis, model 1 adjusted for age and sex. Model 2 additionally adjusted for residence, educational level, household income level, and smoking status. Subgroup analysis was conducted by sex. For sensitivity analysis, we adopted APRI index to calculate the odds of having PRISm. An additional analysis was conducted using LLN-based criteria for categorizing lung function testing. To further investigate potential confounding by BMI, analysis confined to individuals with obesity was also performed, because obesity itself could confound the association between SLD and PRISm.

All statistical analyses were conducted using SPSS version 24 for Windows (Chicago, USA). A P-value of < 0.05 was considered statistically significant for all analyses.

Results

Among the total study participants, 20,232 participants had normal lung function and 3,182 had PRISm (Table 1). The mean age was similar between groups. The PRISm group showed a higher proportion of males and had significantly higher BMI and waist circumference compared to the normal group. Participants with PRISm had higher prevalence of metabolic comorbidities including diabetes, hypertension, and dyslipidemia. Laboratory findings showed that the PRISm group had higher levels of fasting glucose, HbA1c, triglycerides, and liver enzymes.

Table 1.

Characteristics of study population

Age	Normal (n = 20 232)	PRISm (n = 3 182)	P
	53.5 (0.1)	53.8 (0.3)	0.293
Male	46.9 (0.5)	51.9 (1.4)	0.001
Body mass index	23.1 (0.0)	24.6 (1.0)	< 0.001
Waist circumference	80.5 (0.1)	84.9 (0.3)	< 0.001
Systolic BP	118.0 (0.2)	121.5 (0.5)	< 0.001
Diastolic BP	77.3 (0.1)	78.4 (0.3)	0.001
Diabetes	12.9 (0.4)	19.1 (1.1)	< 0.001
Hypertension	31.8 (0.5)	38.5 (1.4)	< 0.001
Dyslipidemia	42.3 (0.5)	48.8 (1.5)	< 0.001
Total cholesterol	197.3 (0.4)	196.5 (1.1)	0.492
LDL-cholesterol	117.5 (3.5)	120.9 (1.9)	0.373
HDL-cholesterol	50.6 (0.6)	49.1 (0.4)	< 0.001
Triglyceride	142.6 (1.3)	160.9 (4.1)	< 0.001
Heavy alcohol consumption	17.8 (0.4)	19.8 (1.2)	0.101
Smoking			< 0.001
Current	18.0 (0.4)	23.0 (1.3)
Former	22.7 (0.4)	24.0 (1.2)
Never	59.3 (0.5)	53.0 (1.3)
HbA1c (%)	5.7 (0.0)	6.0 (0.0)	< 0.001
Glucose, fasting	101.7 (0.3)	106.1 (0.8)	< 0.001
AST	22.2 (0.1)	24.3 (0.3)	< 0.001
ALT	21.6 (0.7)	24.9 (0.5)	< 0.001
Total calorie intake	1999.4 (10.4)	1987.6 (25.9)	0.667
Total carbohydrate intake	313.5 (1.6)	309.6 (3.7)	0.355
Total fat intake	41.7 (0.4)	41.9 (0.9)	0.777

Data are presented as mean (SE) for continuous variables and percentage (SE) for categorical variables

The percentage of MASLD was significantly higher in the PRISm group compared to the normal group (Table 2). Similarly, Met-ALD and ALD were more common in the PRISm group. The PRISm group also showed a higher burden of cardiometabolic risk factors compared to normal spirometry group (Table 2).

Table 2.

Percentages (%) of no SLD, MASLD, Met-ALD, and ALD according to lung function groups

	Total	Normal	PRISm	P
				< 0.001
No SLD (n = 19 082)	80.9% (0.3)	81.7% (0.3)	75.1% (1.0)
MASLD (n = 3 540)	15.2% (0.3)	14.8% (0.3)	18.5% (0.9)
Met-ALD (n = 564)	2.7% (0.1)	2.6% (0.1)	4.0% (0.5)
ALD (n = 228)	1.1% (0.1)	1.0% (0.1)	2.4% (0.4)
#. Of cardiometabolic criteria				< 0.001
0	9.6% (0.2)	9.9% (0.3)	7.7% (0.6)
1	17.8% (0.3)	18.2% (0.3)	14.5% (0.8)
2	21.5% (0.3)	21.8% (0.3)	19.4% (0.9)
3	21.8% (0.3)	21.7% (0.3)	22.6% (1.0)
4	18.2% (0.3)	17.9% (0.3)	20.2% (0.9)
5	11.0% (0.3)	10.4% (0.3)	15.6% (0.9)

SLD  Steatotic liver disease, ALD  Alcohol-associated liver disease, MASLD  Metabolic dysfunction-associated steatotic liver disease, Met-ALD  Metabolic dysfunction-associated alcoholic liver disease, PRISm  Preserved ratio impaired spirometry, FVC  Forced vital capacity

In multivariable analysis, after adjusting for age and sex (Model 1), MASLD, Met-ALD, and ALD were associated with increased odds of PRISm (Table 3). These associations remained significant after additional adjustment for sociodemographic factors and lifestyle habits (Model 2). Among SLD subtypes, ALD showed the strongest association with the presence of PRISm lung function followed by Met-ALD and MASLD. The association was particularly strong in males in the fully adjusted model. However, these associations were not significant in females. In a sensitivity analysis in which PRISm was defined using LLN criteria, the results were consistent (Table 4). Additional analysis using the APRI score showed that participants with advanced fibrosis (APRI ≥ 0.34) had higher odds of PRISm (Table 5), and this association was consistent in both males and females. Finally, when we confined the analysis among individuals with obese, the association between PRISm and new classification of SLD was consistent only in males (Supplementary Table 1).

Table 3.

Odds ratio (OR) and 95% confidence interval (CI) of PRISm according to new SLD classification

Total	OR (95% CI)	P trend	Male	OR (95% CI)	P trend	Female	OR (95% CI)	P trend
Model 1		< 0.001	Model 1		< 0.001	Model 1		0.379
No SLD	Reference		No SLD	Reference		No SLD	Reference
MASLD	1.35 (1.18–1.54)		MASLD	1.59 (1.32–1.91)		MASLD	1.14 (0.95–1.37)
Met-ALD	1.59 (1.21–2.11)		Met-ALD	1.88 (1.39–2.53)		Met-ALD	0.67 (0.27–1.65)
ALD	2.53 (1.77–3.61)		ALD	2.96 (2.01–4.36)		ALD	1.07 (0.34–3.38)
Model 2		< 0.001	Model 2		< 0.001	Model 2		0.365
No SLD	Reference		No SLD	Reference		No SLD	Reference
MASLD	1.36 (1.19–1.55)		MASLD	1.61 (1.34–1.95)		MASLD	1.16 (0.96–1.40)
Met-ALD	1.51 (1.14–2.01)		Met-ALD	1.78 (1.31–2.42)		Met-ALD	0.66 (0.27–1.59)
ALD	2.38 (1.65–3.41)		ALD	2.77 (1.87–4.12)		ALD	1.04 (0.32–3.32)

ALD  Alcohol-associated liver disease, SLD  Steatotic liver disease, MASLD  Metabolic dysfunction associated steatotic liver disease, Met-ALD  Metabolic dysfunction-associated alcohol-related liver disease

Model 1 was adjusted for age and sex

Model 2 was additionally adjusted for residence, educational level, household income, and smoking status

Table 4.

Odds ratio (OR) and 95% confidence interval (CI) of PRISm classified by LLN according to new SLD classification

Total	OR (95% CI)	P trend	Male	OR (95% CI)	P trend	Female	OR (95% CI)	P trend
Model 1		< 0.001	Model 1		< 0.001	Model 1		0.474
No SLD	Reference		No SLD	Reference		No SLD	Reference
MASLD	1.52 (1.33–1.74)		MASLD	1.56 (1.34–1.82)		MASLD	1.24 (0.89–1.74)
Met-ALD	1.68 (1.33–2.13)		Met-ALD	1.71 (1.34–2.18)		Met-ALD	0.64 (0.15–2.71)
ALD	2.27 (1.61–3.22)		ALD	2.35 (1.63–4.36)		ALD	0.49 (0.07–3.61)
Model 2		< 0.001	Model 2		< 0.001	Model 2		0.346
No SLD	Reference		No SLD	Reference		No SLD	Reference
MASLD	1.52 (1.32–1.74)		MASLD	1.55 (1.32–1.81)		MASLD	1.28 (0.91–1.80)
Met-ALD	1.67 (1.31–2.13)		Met-ALD	1.69 (1.32–2.18)		Met-ALD	0.69 (0.16–2.97)
ALD	2.27 (1.59–3.25)		ALD	2.34 (1.60–3.42)		ALD	0.55 (0.07–4.05)

LLN  Lower limit of normal, ALD  Alcohol-associated liver disease, SLD  Steatotic liver disease, MASLD  Metabolic dysfunction associated steatotic liver disease, Met-ALD  Metabolic dysfunction-associated alcohol-related liver disease

Model 1 was adjusted for age and sex

Model 2 was additionally adjusted for residence, educational level, household income, and smoking status

Table 5.

Odds ratio (OR) and 95% confidence interval (CI) of PRISm according to fibrosis index

Total	OR (95% CI)	P	Male	OR (95% CI)	P	Female	OR (95% CI)	P
Model 1			Model 1			Model 1
APRI < 0.34	Reference		APRI < 0.34	Reference		APRI < 0.34	Reference
APRI ≥ 0.34	1.35 (1.20–1.52)	< 0.001	APRI ≥ 0.34	1.26 (1.07–1.48)	0.006	APRI ≥ 0.34	1.36 (1.13–1.63)	0.001
Model 2			Model 2			Model 2
APRI < 0.34	Reference		APRI < 0.34	Reference		APRI < 0.34	Reference
APRI ≥ 0.34	1.29 (1.15–1.46)	< 0.001	APRI ≥ 0.34	1.25 (1.06–1.47)	0.008	APRI ≥ 0.34	1.36 (1.13–1.64)	0.001

APRI  AST to platelet ratio index

Model 1 was adjusted for age and sex

Model 2 was additionally adjusted for residence, educational level, household income, and smoking status

Discussion

In this nationally representative Korean population-based study, we found that MASLD, Met-ALD, and ALD were independently associated with increased odds of PRISm, even after adjusting for a wide range of sociodemographic and cardiometabolic factors. These associations were particularly pronounced in men, whereas no significant associations were observed in women. Furthermore, elevated APRI scores, suggestive of advanced hepatic fibrosis, were consistently associated with PRISm in both sexes. To our knowledge, this is the first study to comprehensively examine the relationship between PRISm and the newly redefined categories of steatotic liver disease—MASLD, Met-ALD, and ALD—based on updated diagnostic criteria.

The newly reclassified form of SLD has been recognized as a systemic condition and it is a broad term encompassing liver diseases characterized by excessive fat accumulation, including MASLD, MetALD, ALD, and cryptogenic SLD [18, 19]. Several previous studies have suggested that steatotic liver disease, particularly NAFLD, is associated with reduced lung function [20]. However, these prior studies largely focused on obstructive spirometry patterns such as COPD or did not distinguish between spirometric subtypes. Our study extends the existing literature by applying the new MASLD, Met-ALD, and ALD definitions to a large, nationally representative cohort, and by focusing specifically on their relationship with PRISm. Importantly, we conducted sex-stratified analyses to reveal that the association was particularly significant in men. Additional sensitivity analysis using LLN-based PRISm classification further strengthens the observed findings. We also incorporated APRI as a surrogate for hepatic fibrosis to examine the effect of fibrotic progression, which showed consistent associations with PRISm across both sexes. These findings suggest that PRISm may reflect the pulmonary component of systemic metabolic disease and highlight the need for integrative approaches in evaluating metabolic and respiratory health.

Interestingly, in our study, there was a stepwise gradient in the presence of PRISm, increasing sequentially from individuals without SLD to those with MASLD, Met-ALD, and ALD. There are several previous reports supporting this observation. For example, multiple nationwide cohort studies have shown that the risk of decompensated cirrhosis, hepatocellular carcinoma, and cholangiocarcinoma was highest in individuals with ALD, followed by Met-ALD and MASLD [21, 22]. Another meta-analysis similarly revealed that individuals with Met-ALD exhibited poorer outcomes in liver-related events and all-cause mortality than those with MASLD [23]. Based on their definitions, Met-ALD reflects MASLD with concomitant moderate alcohol consumption, while ALD represents a condition driven by substantial alcohol exposure. Accordingly, the stepwise gradient in association appears biologically plausible; however, further mechanistic and pathophysiological studies are required to elucidate the mechanisms underlying these observations.

PRISm, which was previously conceived as a restrictive lung disease [24], is considered to have systemic inflammatory process [25]. An elevation of several endocrine and inflammatory markers such as IL-6 and TNF levels was observed in individuals with PRISm which was similar to that in patients with COPD [26]. Phenotypic studies show several metabolic abnormalities like obesity and dyslipidemia are higher in PRISm than in normal spirometry [2, 27]. Although the association between metabolic liver dysfunction and pulmonary impairment may appear intuitive given their shared inflammatory pathways, several mechanisms underline the observed findings. MASLD, Met-ALD, and ALD are characterized by systemic low-grade inflammation, insulin resistance, and ectopic fat accumulation, all of which have been implicated in the pathogenesis of extrahepatic diseases including lung dysfunction [28, 29]. Fatty liver disease is associated with reduced lung function, particularly FEV₁ and FVC [30]. While direct evidence linking pro-inflammatory cytokines such as TNF-α and IL-6 to pulmonary decline in SLD is limited, subclinical systemic inflammation and insulin resistance are proposed mechanisms underlying this association [31]. Further experimental studies are warranted to clearly elucidate the underlying pathophysiologic pathways within the body that connect hepatic metabolic dysfunction with structural and functional impairment of the lungs.

We also found that individuals with a high APRI score, indicative of advanced hepatic fibrosis, had a greater probability of having PRISm. This finding aligns with prior evidence suggesting that fibrosis in different organs—including liver and lung—may be driven by shared genetic and molecular pathways, as demonstrated by overlapping fibrosis-associated gene signatures across multiple tissues [32–35]. Furthermore, fibrosis is increasingly recognized as a ubiquitous consequence of chronic inflammation and disrupted metabolic homeostasis, mediated by processes such as TGF‑β signaling and extracellular matrix remodeling [36]. These insights challenge the traditional paradigm that views organ-specific fibrosis in isolation and suggest the possibility that metabolic liver disease–induced systemic inflammation may predispose to fibrotic changes in the lung. Therefore, our results call for future longitudinal and mechanistic studies to investigate whether hepatic fibrosis may serve as an early indicator—or even a mediator—of pulmonary fibrogenesis in metabolic disease contexts.

Our study has several limitations. First, due to the cross-sectional nature of the KNHANES dataset, we cannot establish a causal relationship between MASLD, Met-ALD, ALD, and PRISm. Second, hepatic steatosis and fibrosis were assessed using surrogate indices rather than imaging or biopsy, which may lead to misclassification. Third, the lack of post-bronchodilator spirometry in KNHANES may introduce uncertainty in distinguishing PRISm from early or reversible obstructive lung disease. Fourth, residual confounding from unmeasured variables such as physical activity, diet, or environmental exposures cannot be excluded. Lastly, given the high global prevalence of SLD, our findings might not be interpreted as supporting population-wide screening for PRISm. Rather, PRISm should be viewed as a potential risk marker that may warrant opportunistic spirometric assessment in selected high-risk individuals, rather than as a target for routine screening.

Conclusion

MASLD, Met-ALD, and ALD are significantly associated with PRISm in a nationally representative adult Korean population, particularly in men. The findings suggest a potential shared pathophysiological mechanism linking metabolic liver dysfunction and restrictive spirometric impairment. Elevated APRI scores, reflecting advanced liver fibrosis, were also associated with increased PRISm risk in both sexes. These results highlight the importance of recognizing PRISm as a possible pulmonary manifestation of systemic metabolic disease. Future longitudinal and mechanistic studies are warranted to clarify causal pathways and to assess whether early detection and management of liver disease could help prevent or mitigate pulmonary dysfunction.

Authors’ contributions

S.J: Writing - original draft, H.C: Validation, Data Collection, Formal analysis, Methodology, and Writing - review & editing, J.L: Writing - review & editing, and T.K: Conceptualization; Data Collection, Formal analysis, Methodology; Validation; Visualization; Supervision, and Writing - review & editing; All authors reviewed the manuscript.

Funding

None.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

The study protocol was approved by the Institutional Review Board of the Korea Disease Control and Prevention Agency (2010-02CON-21-C, 2011-02CON06-C, 2012-01EXP-01–2 C, 2013-07CON-03–4 C, 2013-12EXP-03–5 C, 2018-01-03-P-A, and 2018-01-03-C-A). Written informed consent was obtained from all individuals. The study protocol and was conducted in accordance with the principles of the Declaration of Helsinki. All procedures were performed in accordance with the relevant guidelines and regulations.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.