A nutrition–inflammation index weighted toward disease burden: the lactate dehydrogenase-to-albumin ratio in TP53-mutated myeloid neoplasms
- 1Department of Clinical Laboratory, Ganzhou Hospital-Nanfang Hospital, Southern Medical University (Ganzhou People's Hospital) , , ,
Abstract
Background: Albumin-containing composite indices are frequently labeled as nutrition–inflammation biomarkers, although their biological meaning remains uncertain when direct nutritional assessment is unavailable. We investigated the construct validity and interpretive boundaries of the lactate dehydrogenase-to-albumin ratio (LAR) in TP53-mutated acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). Specifically, we examined whether pretreatment LAR more closely reflected disease burden or systemic inflammatory status, evaluated the relative contributions of its LDH and albumin components, and assessed its outcome associations and incremental prognostic information.
Methods: This retrospective cohort included 116 patients, with 114 adults included in the primary analysis. Associations of continuous log2-transformed LAR with prespecified disease-burden, acute-phase, and blood-count-derived markers were evaluated using Spearman correlations with false-discovery-rate control. Cox models assessed overall survival (OS), composite progression-free survival (PFS), and the cause-specific rate of progression or relapse. Sensitivity analyses additionally adjusted for the number of TP53 variants detected, co-occurring myeloid mutations and treatment category. Aalen–Johansen and Fine–Gray methods were used to evaluate progression cumulative incidence while accounting for death before progression as a competing event. Nonlinearity and incremental model performance were also examined.
Results: Among 114 adults, 74 deaths, 93 composite PFS events, 76 progression or relapse events, and 17 deaths before progression occurred. LAR correlated with white blood cell count (ρ = 0.406; q < 0.001) and marrow blast percentage (ρ = 0.298; q = 0.004), but showed no consistent correlation with available acute-phase markers. Component analyses indicated that LDH contributed more strongly than albumin to the outcome-related signal of the ratio. Each doubling of LAR was associated with shorter OS (adjusted hazard ratio [HR], 1.57; 95% confidence interval [CI], 1.20–2.05; p < 0.001) and composite PFS (adjusted HR, 1.44; 95% CI, 1.14–1.84; p = 0.003). These estimates were essentially unchanged after further adjustment for the number of TP53 variants, co-mutation number and treatment category (OS adjusted HR, 1.64; 95% CI, 1.21–2.21). However, the optimism-corrected increases in C-index were only 0.005 and 0.013, respectively. LAR was associated with the cause-specific rate of progression or relapse (adjusted HR, 1.39; 95% CI, 1.05–1.83; p = 0.021), but not with progression cumulative incidence in the pooled cohort after accounting for competing death (subdistribution HR, 1.02; 95% CI, 0.80–1.31; p = 0.855); this pooled estimate reflected the AML stratum, and in MDS the subdistribution HR was 1.73 (95% CI, 1.14–2.61). Associations with OS were present within both AML and MDS and were essentially unchanged in a diagnosis-stratified model (OS HR, 1.62; 95% CI, 1.23–2.13); the within-AML estimate for composite PFS was imprecise (HR, 1.33; 95% CI, 0.97–1.81).
Conclusion: In TP53-mutated AML and MDS, higher pretreatment LAR was associated with shorter OS, shorter composite PFS, and a higher cause-specific rate of progression or relapse, but provided only modest incremental discrimination beyond established clinical factors and, in the pooled cohort, was not associated with progression cumulative incidence after accounting for competing death. Its correlations with leukocyte count and marrow blast burden, together with the stronger contribution of LDH than albumin, are more consistent with a disease-burden-weighted signal than with a nutritional one. No validated nutritional assessment and no complete acute-phase marker panel were available, so a nutritional or inflammatory contribution to LAR can be neither confirmed nor excluded. LAR should therefore be interpreted as a disease-burden-weighted prognostic correlate whose nutritional significance requires direct validation, rather than as a standalone nutritional, prognostic, or treatment-selection tool.
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BibTeX
@article{xin2026nutritioninflammation,
title = {{A nutrition–inflammation index weighted toward disease burden: the lactate dehydrogenase-to-albumin ratio in TP53-mutated myeloid neoplasms}},
author = {Xiaoqin Xin and Zongqi Wang},
journal = {Frontiers in nutrition},
year = {2026},
month = oct,
doi = {10.3389/fnut.2026.1966874},
url = {https://europepmc.org/article/PMC/PMC13719407},
note = {CC BY},
}
RIS
TY - JOUR
TI - A nutrition–inflammation index weighted toward disease burden: the lactate dehydrogenase-to-albumin ratio in TP53-mutated myeloid neoplasms
AU - Xiaoqin Xin
AU - Zongqi Wang
PY - 2026
DA - 2026/10/16
JO - Frontiers in nutrition
DO - 10.3389/fnut.2026.1966874
UR - https://europepmc.org/article/PMC/PMC13719407
AB - Background: Albumin-containing composite indices are frequently labeled as nutrition–inflammation biomarkers, although their biological meaning remains uncertain when direct nutritional assessment is unavailable. We investigated the construct validity and interpretive boundaries of the lactate dehydrogenase-to-albumin ratio (LAR) in TP53-mutated acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). Specifically, we examined whether pretreatment LAR more closely reflected disease burden or systemic inflammatory status, evaluated the relative contributions of its LDH and albumin components, and assessed its outcome associations and incremental prognostic information. Methods: This retrospective cohort included 116 patients, with 114 adults included in the primary analysis. Associations of continuous log2-transformed LAR with prespecified disease-burden, acute-phase, and blood-count-derived markers were evaluated using Spearman correlations with false-discovery-rate control. Cox models assessed overall survival (OS), composite progression-free survival (PFS), and the cause-specific rate of progression or relapse. Sensitivity analyses additionally adjusted for the number of TP53 variants detected, co-occurring myeloid mutations and treatment category. Aalen–Johansen and Fine–Gray methods were used to evaluate progression cumulative incidence while accounting for death before progression as a competing event. Nonlinearity and incremental model performance were also examined. Results: Among 114 adults, 74 deaths, 93 composite PFS events, 76 progression or relapse events, and 17 deaths before progression occurred. LAR correlated with white blood cell count (ρ = 0.406; q < 0.001) and marrow blast percentage (ρ = 0.298; q = 0.004), but showed no consistent correlation with available acute-phase markers. Component analyses indicated that LDH contributed more strongly than albumin to the outcome-related signal of the ratio. Each doubling of LAR was associated with shorter OS (adjusted hazard ratio [HR], 1.57; 95% confidence interval [CI], 1.20–2.05; p < 0.001) and composite PFS (adjusted HR, 1.44; 95% CI, 1.14–1.84; p = 0.003). These estimates were essentially unchanged after further adjustment for the number of TP53 variants, co-mutation number and treatment category (OS adjusted HR, 1.64; 95% CI, 1.21–2.21). However, the optimism-corrected increases in C-index were only 0.005 and 0.013, respectively. LAR was associated with the cause-specific rate of progression or relapse (adjusted HR, 1.39; 95% CI, 1.05–1.83; p = 0.021), but not with progression cumulative incidence in the pooled cohort after accounting for competing death (subdistribution HR, 1.02; 95% CI, 0.80–1.31; p = 0.855); this pooled estimate reflected the AML stratum, and in MDS the subdistribution HR was 1.73 (95% CI, 1.14–2.61). Associations with OS were present within both AML and MDS and were essentially unchanged in a diagnosis-stratified model (OS HR, 1.62; 95% CI, 1.23–2.13); the within-AML estimate for composite PFS was imprecise (HR, 1.33; 95% CI, 0.97–1.81). Conclusion: In TP53-mutated AML and MDS, higher pretreatment LAR was associated with shorter OS, shorter composite PFS, and a higher cause-specific rate of progression or relapse, but provided only modest incremental discrimination beyond established clinical factors and, in the pooled cohort, was not associated with progression cumulative incidence after accounting for competing death. Its correlations with leukocyte count and marrow blast burden, together with the stronger contribution of LDH than albumin, are more consistent with a disease-burden-weighted signal than with a nutritional one. No validated nutritional assessment and no complete acute-phase marker panel were available, so a nutritional or inflammatory contribution to LAR can be neither confirmed nor excluded. LAR should therefore be interpreted as a disease-burden-weighted prognostic correlate whose nutritional significance requires direct validation, rather than as a standalone nutritional, prognostic, or treatment-selection tool.
SN - 2296-861X
ER -