Milk-specific IgE sensitization and cardiovascular outcomes: A retrospective cohort study.

BACKGROUND

Population-based studies have identified an association between milk-specific IgE and cardiovascular (CV) mortality. However, whether this sensitization reflects broader CV risk or adverse clinical outcomes remains unknown.

OBJECTIVE

To evaluate associations between milk-specific IgE sensitization and CV disease events and risk enhancers, including coronary artery calcium (CAC).

METHODS

A retrospective chart review of adults 50 years and older was performed within a multihospital health system. Patients with serum food-specific IgE testing were classified as milk IgE-negative (<0.10 kU/L), borderline (0.10-0.35 kU/L), or sensitized (>0.35 kU/L). Individuals with clinically confirmed milk allergy were excluded. Outcomes included myocardial infarction, cerebrovascular accident, coronary artery disease, and CAC, ascertained from electronic medical records using Current Procedural Terminology/International Classification of Diseases codes and imaging reports (2012-2024). Analyses used χ²/Wilcoxon tests and multivariable models adjusting for demographics and comorbidities.

RESULTS

Among the 1220 patients (mean age, 64.4 years; 63.6% female), 113 (9.3%) were milk IgE-sensitized. The CV events did not differ by milk sensitization status. Low-density lipoprotein (LDL) particle number was higher in elevated milk IgE (P < .001); associations with LDL particle metrics were inconsistent, likely reflecting limited nuclear magnetic resonance testing (n = 122). High-sensitivity C-reactive protein was not associated with milk sensitization. In a CAC-subsample (n = 104), the median CAC was higher with milk sensitization vs negative milk IgE (885.8 vs 145.2 Agatston units; P < .0001)

CONCLUSION

Milk-specific IgE sensitization was not associated with increased clinical CV disease events or systemic inflammatory markers. There was a dose-dependent relationship between milk-specific IgE and CAC in a small subset that may be explained by calcified, potentially more stable plaque biology. Prospective studies should evaluate temporality and mechanisms and clarify clinical implications.