Systemic immune-inflammatory index is associated with malignancy in Lung-RADS 4 lung nodules

Introduction

Lung cancer remains the leading cause of cancer mortality in the United States, with approximately 85% of lung cancer deaths in 2025 being attributed to cigarette smoking (1). The US Preventive Services Task Force (USPSTF) recommends annual low-dose computed tomography (LDCT) screening for adults aged 50 to 80 who have a 20-pack-year smoking history and currently smoke or have quit within the past 15 years (2). Five-year survival rates for early-stage lung cancer are 64%, compared to 9% when diagnosed at later stages (3). Annual LDCT has demonstrated a significant ability to reduce patient mortality in several, large randomized clinical trials (4-6). The Lung CT Screening Reporting and Data System (Lung-RADS) scoring system provides a systematic way to classify pulmonary nodules identified on imaging, ranging from 0 to 4 (7). Pulmonary nodules assigned Lung-RADS categories 1 and 2 have a less than 1% estimated risk of malignancy. Based on various nodule characteristics, nodules designated 4A have an approximate 5–15% risk of malignancy and those designated 4B or 4X have a greater than 15% risk of malignancy (8). Among pulmonary nodules denoted as Lung-RADS 4, the risk of further invasive measures and false positive results highlights the need to further stratify those at high risk for underlying malignancy.

Inflammation plays a pivotal role in cancer initiation, malignant transformation, tumor invasion, and metastasis (9). Several prognostic inflammatory and immune-based indices have been utilized to assist in assessing cancer survival and recurrence, including the neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) (10). The systemic immune-inflammatory index (SII) was created and identified as a powerful prognostic indicator of poor outcomes in patients with hepatocellular carcinoma who underwent curative resection (10). Since its creation, SII has been validated as a useful prognostic indicator in various solid tumors including non-small cell lung cancers (11-14). Given the key role of the immune system in cancer development, inflammatory indices represent a promising tool for prognosticating pulmonary nodules identified on annual LDCTs. One study reported that high levels of systemic inflammatory markers including NLR, PLR, and SII were associated with the risk of positive pulmonary nodules on LDCT and underlying lung cancer (15). However, a lack of additional studies analyzing this relationship highlights a gap in literature. Further investigation into the relationship between systemic inflammatory indices, specifically SII, and malignancy risk in Lung-RADS 4 nodules, is required. The objective of this study is to determine the association between SII and malignancy in Lung-RADS 4 nodules identified on annual LDCT. We present this article in accordance with the STARD reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0433/rc).

Methods

Study population

Patients were retrospectively identified from a single-center, prospectively maintained database of individuals who underwent LDCT lung cancer screening between 2015 and 2024. Individuals meeting National Comprehensive Cancer Network (NCCN) screening criteria with high-risk lung nodules, defined as Lung-RADS 4A, 4B, or 4X on LDCT, were included. Exclusion criteria included patients without a complete blood count (CBC) with differential performed within two months before or after the screening CT scan, as well as those with missing data on body mass index (BMI) or smoking history. Patients who were lost to follow-up or were found to have inflammatory nodules, defined as organizing pneumonia, granulomas, pulmonary Langerhans cell histiocytosis, pleuritis, bronchiolitis, or other inflammatory cell infiltrate, or metastases from other primary cancers upon biopsy were also excluded. Benign nodules were defined by stability or a downgrade in Lung-RADS designation on follow-up imaging or pathology (e.g., hematoma, benign fibrotic nodules/adenofibromas, hamartomas, benign bronchioloalveolar tissue, granular cell tumors, or unremarkable lung tissue). Additionally, patients with a new diagnosis of malignancy within 6 months prior to or following LDCT or actively undergoing cancer treatment were excluded. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. Approval for this retrospective review was obtained from the Rush University Medical Center Institutional Review Board (No. 24091203). Due to the retrospective nature of this study and minimal risk to participants, the need for informed consent was waived.

Inflammatory index calculation

The SII is designed to comprehensively reflect the inflammatory state of the body. For each patient, SII was calculated based on CBC performed no more than 8 weeks surrounding LDCT. SII utilized the raw counts of each cell type. The formula is shown below:

SII=Neutrophils×PlateletsLymphocytes[1]

Study variables and outcomes

Demographic data collected included age, gender, race, smoking history (pack-years), weight (kg), and height (cm). Comorbidity data included a history of chronic obstructive pulmonary disease (COPD), chronic steroid use, and prior malignancies. Nodule characteristics included size, type (benign or malignant) determined by pathology, stability on follow-up imaging, or treatment for primary lung cancer. The primary outcome was nodule type with the SII, analyzed as both continuous and categorical variables.

Statistical analysis

Continuous variables were analyzed using the Student’s t-test while the Wilcoxon rank sum test was used for continuous non-parametric variables, and categorical variables were compared using the Pearson chi-squared test. A univariable linear regression was first performed to assess the relationship between SII as a continuous variable and nodule type (benign vs. malignant) as the outcome, followed by a multivariable linear regression controlling for potential confounders known to influence both systemic inflammation and lung cancer risk. Subsequently, a receiver operating characteristic (ROC) curve analysis was conducted using SII as a continuous variable to determine the optimal cutoff value differentiating benign from malignant nodules on LDCT. The cutoff point was identified using Youden’s index, which maximizes the Youden’s index (sensitivity + specificity – 1) to achieve the best balance between sensitivity and specificity.

Finally, univariable and multivariable logistic regression analyses were performed to evaluate the association between the SII cutoff and nodule type, using a 95% confidence interval (CI). Covariates included age, race, gender, BMI, pack-years, COPD, history of cancer, chronic steroid use, and nodule size to account for the potential influence of tumor burden on SII. All analyses were conducted using R v4.3.2 (RStudio, Boston, MA, USA).

Results

A total of 123 patients met inclusion and exclusion criteria. Of these, 51.2% (63/123) were male and 54.4% (67/123) were White. The median age was 69 years [interquartile range (IQR), 63.5–74], and the median BMI was 27 kg/m² (IQR, 23–31). The median smoking history was 40 pack-years (IQR, 30–45), and the median nodule size was 1.2 cm (IQR, 0.9–1.7). Among patients with high-risk nodules, 63.4% (78/123) were diagnosed with lung cancer. The median SII for the overall cohort was 589 (IQR, 360–819). A detailed breakdown of baseline characteristics based on nodule type is reported in Table 1.

On multivariable linear regression analysis, after adjusting for age, sex, race, smoking history, medical comorbidities, BMI, and nodule size, individuals with malignant nodules had significantly higher SII compared to those with benign nodules (+272; 95% CI: 75–470; P=0.007). Compared with African American patients, White individuals and those belonging to other racial groups also demonstrated significantly higher SII values (+243; 95% CI: 54–433; P=0.01 and +363; 95% CI: 22–704; P=0.04, respectively). Larger nodule size, regardless of type, was independently associated with higher SII (β=94.3; 95% CI: 14–175; P=0.02) (Table 2). The optimal SII cutoff derived using Youden’s index analysis was 561, corresponding to an area under the curve (AUC) of 0.625, sensitivity of 64.1%, and specificity of 58.5% (Figure 1).

Figure 1 ROC curve (AUC 0.625) demonstrating the diagnostic performance of SII in differentiating benign versus malignant Lung-RADS 4 pulmonary nodules. AUC, area under the curve; Lung-RADS, Lung CT Screening Reporting and Data System; ROC, receiver operating characteristic; SII, systemic immune-inflammatory index.

On multivariable logistic regression analysis using a SII cutoff of 561, individuals with high SII had significantly greater odds of having malignant nodules [odds ratio (OR) 3.74; 95% CI: 1.42–9.85; P=0.008]. Older age was also associated with increased odds of malignancy (OR 1.09; 95% CI: 1.02–1.17; P=0.01). In contrast, White individuals were less likely than Black individuals to be diagnosed with malignant nodules, in line with the natural history of lung cancer (OR 0.10; 95% CI: 0.02–0.71; P=0.02) (2). Although larger nodule size was associated with malignancy on univariable analysis, this association was no longer significant after multivariable adjustment (Table 3).

Discussion

The goal of this study was to assess the association between SII and the diagnosis of primary lung cancer in Lung-RADS 4 nodules identified on screening LDCT. After risk adjustment, our results demonstrated that Lung-RADS 4 nodules that were diagnosed and/or treated as primary lung cancer were associated with a significantly higher SII value when compared to benign nodules. These findings highlight the role of inflammation in the development and promotion of lung cancer and suggest systemic inflammation may be an indicator of underlying lung cancer in high-risk pulmonary nodules.

Inflammation contributes to malignant phenotypic transition, tumor progression, and metastatic development and is recognized as a hallmark of cancer (16). Per the USPSTF, LDCT screening for lung cancer begins at age 50 following a 20-pack year smoking history (2). In 2025, approximately 85% of lung cancer deaths will be attributed directly to cigarette smoking (1). Numerous studies consistently link habitual cigarette smoking to increases in systemic inflammation, as evidenced by elevated inflammatory biomarkers such as C-reactive protein, fibrinogen, and interleukin-6 in smokers compared to non-smokers (17-19). At the cellular level, smoking impairs neutrophil bactericidal activity; however, a paradoxical increase in interleukin-8 production in smokers explains neutrophil accumulation despite functional impairment (20,21). Cigarette smoking contributes to increases in systemic inflammation as seen through elevation of inflammatory biomarkers, changes in immune cell profiles, and altered cytokine expression (17-21). Dysregulation of the host immune system seen in smokers likely contributes to malignant transition and propagation.

Following malignant transformation, various immune cells including platelets, neutrophils, and lymphocytes contribute to ongoing oncogenesis (22). The differential impact of malignancy on the innate and adaptive immune systems and the contribution of inflammation to cancer development have led to the creation of numerous prognostic inflammatory indices, including the NLR, PLR, and SII, to help predict outcomes across various malignancies (11-14). The SII is a comprehensive, novel inflammatory index where lymphocyte, neutrophil, and platelet counts are all considered (10). Studies comparing prior inflammatory indices such as NLR and PLR consistently demonstrate that SII serves as superior prognostic marker in non-small cell lung cancer (23,24).

Inflammation promotes malignant transition and degeneration; however, few studies have analyzed the role of inflammatory indices in lung cancer development. A large, prospective cohort study utilizing the UK Biobank, including approximately 440,000 participants, analyzed the pre-diagnostic association of systemic inflammatory markers and cancer risk for 17 cancer types. The strongest associations were observed between SII and colorectal and lung cancer risk (25). Only one single-center, retrospective study has been performed examining underlying lung cancer risk following the identification of a high-risk pulmonary nodule on LDCT, defined as any noncalcified nodule with a diameter greater than or equal to 6 mm, and systemic inflammatory indices demonstrating a U-shaped association between NLR and lung cancer. High PLR, NLR and SII were significantly associated with lung cancer risk in high-risk pulmonary nodules (15). Following the identification of high-risk pulmonary nodules on LDCT, our study similarly identified a significant association between an elevated SII and the subsequent diagnosis and treatment of primary lung cancer, suggesting that SII may serve as a valuable adjunct for further risk stratification.

In this study, we assigned patients with a Lung-RADS 4 nodule on LDCT into 4 separate categories: diagnosis of primary lung cancer, benign defined by pathology or established stability on follow-up imaging, infectious or inflammatory based on pathology, and malignancies other than primary lung cancer. Those found to have a primary malignancy other than lung cancer or diagnosis of an infectious/inflammatory lesion were excluded from this study. Prior studies have reported a significant impact of inflammatory lesions on SII values (26-28). Inflammatory pathologies such as sarcoidosis, pneumonia, and granuloma forming infectious diseases were clinically evident based on history and prior exposures. These nodules were excluded secondary to active inflammation being a confounding variable in the SII value.

In a broader clinical context, use of conventional risk stratification models, including biomarker-based tools such as SII, may be limited based on the underlying lung substrate. Smoking history and related comorbidities can elevate basal inflammation and alter lung architecture, potentially confounding inflammatory markers, leading to underestimation of malignancy risk. For example, in patients with interstitial lung disease, conventional nodule characteristics, aside from nodule size, may not reliably reflect high-risk features indicative of malignancy risk (29). However, patients with clinically evident lung disease may differ from asymptomatic patients with high-risk lung nodules detected during lung cancer screening with LDCT. Patient-specific factors such as prior cancer history, occupational exposures, other lung disease history, and exposure to infectious agents alter patient management and lung cancer screening pathways. These complex scenarios warrant special attention and individualized risk assessment. Biomarker-based risk stratification tools such as SII are likely limited in this clinical context due to altered systemic inflammation and immune cell profiles reducing its specificity for malignancy.

Although nodule characteristics including size, attenuation, and growth pattern increase suspicion for underlying lung cancer, there remains a need to further stratify the likelihood of malignancy in high-risk nodules (8). The results of this study further elucidate the role of the immune system and inflammation in lung cancer pathogenesis and progression. This study established a cutoff SII value below which pulmonary nodules are likely to be benign, which can supplement clinical decision making in high-risk individuals. An exceedingly high SII value should elicit pause in interpretation of results as these may signify an underlying inflammatory process. The exclusion of inflammatory pathologies from this study was inherent to manage the confounding effect of inflammatory processes on the primary outcome. However, some aspect of confounding remains given the elevated basal level of inflammation intrinsic to this patient population with a long-standing smoking history. While calculation of an SII value may serve as a useful adjunct for risk stratification in patients undergoing LDCT, clinical correlation must be applied when interpreting SII values as they apply to lung cancer prognostication.

Limitations of our study are inherent to any retrospective, single-center study design with a relatively small cohort. The malignancy rate (63.4%) among this cohort is inflated secondary to the small sample size and nature of the exclusions required to limit confounding variables, which may reduce generalizability to typical LDCT screening populations which incorporate pulmonary nodules with a Lung-RADS 0–4 designation. While Lung-RADS 1–3 nodules are generally considered benign, or probably, benign warranting short-term follow-up, this study intentionally focused on the diagnostic uncertainty of high-risk pulmonary nodules with a Lung-RADS 4 designation, where a higher baseline malignancy rate is expected, further contributing to the elevated rate observed in our cohort (7). Additionally, the impact of advanced disease driving the SII at the time of diagnosis could not be assessed as we utilized a single SII measurement. Given the retrospective nature of this study, an 8-week window around LDCT timing was utilized to obtain CBC components. This interval balances routine clinical workflow and follow-up timelines associated with high-risk pulmonary nodules that may prompt biopsy or serial imaging, while capturing the potential influence of inflammation on lung cancer development. Although intercurrent illnesses may impact CBC values, these findings are likely evident upon chart review or follow-up imaging. Importantly, an 8-week window is narrow enough to assume biological stability of CBC parameters with minimal variation over short intervals, while reflecting the practical realities of routine clinical care (30).

Despite these limitations, we have identified a significant association between SII and primary lung cancer in Lung-RADS 4 nodules on LDCT. To our knowledge, this is the first study to use a contemporary cohort utilizing the Lung-RADS designation to further stratify an at-risk population for underlying lung malignancy risk. While our findings do not identify a causal relationship between SII and underlying lung cancer risk, the systemic immune response is a principal pre-clinical feature in lung cancer development, and the use of blood cell ratios could serve as important biomarkers for underlying malignancy risk. This study is the first to identify a specific cut-off value for SII in individuals who have high-risk pulmonary nodules defined by a Lung-RADS 4 designation. These findings further delineate the role of inflammation in cancer pathogenesis in a high-risk patient population prone to inflammatory activation secondary to habitual cigarette smoking. Calculation of an SII value in individuals with Lung-RADS 4 nodules can assist clinicians in further stratifying patients at high-risk for primary lung cancer and serve as a valuable supplement to existing risk-stratification measures. Expanding upon our findings with longitudinal SII assessment, external validation, and prospective evaluation in larger, multi-institutional cohorts may improve the power of this study to further support SII in predicting underlying malignancy in Lung-RADS 4 nodules.

Conclusions

Lung cancer remains the leading cause of cancer mortality in the United States with LDCT screening providing a great opportunity for early detection to mitigate lung cancer deaths; however, the need for further stratification of high-risk pulmonary nodules identified on screening LDCT exists. Inflammation plays a key role in malignant phenotypic transition and propagation. Utilizing readily available blood cell ratios to calculate a novel, comprehensive inflammatory index, we found that an elevated SII was associated with malignancy in non-inflammatory Lung-RADS 4 nodules identified on annual LDCT. While external validation and prospective evaluation in larger, multi-institutional cohorts are needed, this study highlights the pre-clinical role of inflammation in cancer development and suggests SII calculation can assist clinicians in further stratifying patients at high-risk for primary lung cancer.

Acknowledgments

The abstract was presented at the Annual Meeting of the Southern Thoracic Surgical Association, Fernandina Beach, FL, Nov 6–9, 2025.

Footnote

Reporting Checklist: The authors have completed the STARD reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0433/rc

Data Sharing Statement: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0433/dss

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0433/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0433/coif). The authors have no conflicts of interest to declare.

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. Approval for this retrospective review was obtained from the Rush University Medical Center Institutional Review Board (No. 24091203). Due to the retrospective nature of this study and minimal risk to participants, the need for informed consent was waived.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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