Abstract / Summary
Abstract Acute methanol poisoning is a life-threatening emergency, and early risk stratification at admission is critical. The leukocyte glucose index (LGI), a marker of systemic inflammation and stress hyperglycaemia, has prognostic value in acute illness but has been studied in only one small methanol cohort. We evaluated admission LGI in clinically diagnosed acute methanol poisoning at two tertiary emergency departments in Türkiye. We conducted a two-centre retrospective study of adults (≥ 18 years) with clinically diagnosed acute methanol poisoning (compatible history, characteristic features, and high anion-gap metabolic acidosis; serum methanol was not measured) admitted between January 2021 and December 2025. LGI was calculated as (WBC [× 103/µL] × plasma glucose [mg/dL])/1000 from the first admission panel. The primary outcome was a composite of in-hospital mortality, invasive mechanical ventilation, or haemodialysis; mortality alone was a key secondary outcome. Discrimination was assessed by ROC analysis with paired (DeLong) comparisons, and adjusted associations by logistic regression, including a Firth model containing venous pH, Glasgow coma scale (GCS), and creatinine. Among 83 patients (mean age 40.7 ± 17.4 years; 71.1% male), the composite outcome occurred in 34 (41.0%): mortality 21, intubation 30, and haemodialysis 29. Admission LGI was approximately threefold higher in patients with an event (median 2.75 vs. 0.91; p < 0.001) and correlated with acid–base markers, lactate, GCS, and APACHE-II (all p < 0.001). For the composite outcome, LGI yielded an AUC of 0.879 (95% CI 0.790–0.950), not significantly different from venous pH, GCS, bicarbonate, or creatinine on paired comparison; an exploratory cut-off of 1.24 gave 82.4% sensitivity and 79.2% specificity. For mortality alone, AUC was 0.857 (95% CI 0.733–0.962). Adjusted for age and GCS, log-transformed LGI remained independently associated with the outcome (adjusted OR 12.08, 95% CI 1.70–85.92; p = 0.013), although this estimate was imprecise. After adjustment for venous pH, GCS, and creatinine, LGI retained an independent association (Firth aOR 4.70, 95% CI 1.30–31.52; p = 0.017) but improved discrimination only marginally (ΔAUC + 0.020, 95% CI − 0.003 to + 0.044). In clinically diagnosed acute methanol poisoning, admission LGI was independently associated with adverse short-term outcomes, including mortality alone, with discrimination numerically similar to that of established acid–base and clinical severity markers. It added little discrimination once venous pH, GCS, and creatinine were available; its potential value lies in rapid risk stratification where blood-gas analysis is unavailable or delayed. The cut-off of 1.24 is exploratory. Because serum methanol was not measured and two composite components are treatment decisions, prospective external validation in analytically confirmed cohorts is required before clinical implementation.