Baseline LDH as a prognostic biomarker of early treatment failure in lung cancer.

Abstract

e20023 Background: Despite advances in lung treatment modalities, outcomes still vary greatly and predicting treatment failure remains challenging. This highlights the need for effective prognostic biomarkers to guide lung cancer treatment such as Lactate Dehydrogenase (LDH). LDH is a preferred byproduct of cancer cells due to an inclination to metabolize pyruvate via anaerobic pathway despite oxygen availability. This metabolic shift affects the tumor microenvironment by enhancing the tumor’s ability to survive hypoxic environments, increase angiogenesis and facilitate an acidic environment that helps evade the host’s immune system. Previous meta-analyses have shown that patients with higher LDH levels may experience worse outcomes, especially among those being treated with immune checkpoint inhibitors. This study investigates the impact of baseline LDH levels on early treatment failure, which is defined as disease progression post-second treatment cycle in patients with lung adenocarcinoma, squamous cell carcinoma, and small cell lung cancer. Methods: This retrospective study included a cohort of over 200 patients diagnosed with lung cancer (adenocarcinoma, squamous cell carcinoma, or small cell lung cancer) at our institution. Demographic data, treatment outcomes and laboratory values were collected retroactively from electronic medical records. Inclusion criteria required patients having both a baseline LDH measurement at the time of diagnosis (with a two-week margin) and had imaging after two cycles of cancer treatment (immunotherapy, chemotherapy, radiation or combinations thereof). Disease progression was evaluated by radiologists according to RECIST criteria. Results: Following the application of inclusion criteria, the final sample consisted of 128 patients, with exclusions primarily due to missing baseline LDH measurements or unavailable imaging data. In this group, there were 41 patients that did not have disease progression post- 2 nd cycle of cancer treatment, with a mean baseline LDH of 244.78 (SD = 76.87). In contrast, there were 87 patients that had disease progression post- 2 nd cycle of cancer treatment, with a mean baseline LDH of 337.93 (SD = 236.00). Overall, higher baseline LDH levels were significantly associated with treatment failure in lung cancer patients (p = 0.001). Conclusions: These findings reaffirm the importance of LDH as a prognostic biomarker and its relation to treatment failure. Given the accessibility of LDH measurement, it could serve as an additional variable for guiding clinical decision-making in lung cancer treatment. However, the limitations of this study potentially include generalizability because the patient cohort were primarily seen at Wellstar MCG and resided in nearby geographic area. Future research should include elucidation of baseline LDH in relation to treatment response of specific immune checkpoint inhibitors.