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Life sciences · Journal article
Frontiers in Immunology · September 17, 2026
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Background C-reactive protein (CRP) is routinely used to quantify systemic inflammation, yet its interpretation in hematologic disorders is complicated by marked biological heterogeneity. We characterized pretreatment CRP distributions across a broad hematologic disease spectrum and examined whether CRP–laboratory associations differed among clinically relevant subtypes. Methods This retrospective study included 4,823 patients aged ≥14 years with 21 hematologic disorders evaluated at Nanjing Drum Tower Hospital between 2009 and 2023. Baseline CRP and routine laboratory variables obtained before disease-directed therapy were analyzed across diseases and within acute myeloid versus acute lymphoblastic leukemia, chronic myeloid versus chronic lymphocytic leukemia, Hodgkin versus non-Hodgkin lymphoma, and multiple myeloma with versus without extramedullary disease. Spearman correlations and CRP-quartile analyses were used to characterize covariation with hematologic, biochemical, and nutritional measures. An unweighted exploratory analysis of six nonconsecutive National Health and Nutrition Examination Survey cycles compared participants reporting leukemia or lymphoma with non-cancer participants. Results Baseline CRP differed substantially across the 21 disorders (global P < 0.001), with the highest median values in hemophagocytic lymphohistiocytosis (44.6 mg/L) and thrombotic thrombocytopenic purpura (25.4 mg/L). Among 758 patients with acute leukemia subtypes, CRP was higher in acute myeloid than acute lymphoblastic leukemia (18.5 vs 9.2 mg/L; P = 0.004); increasing CRP was accompanied by lower albumin and higher lactate dehydrogenase in both subtypes. CRP did not differ between chronic myeloid and chronic lymphocytic leukemia (4.7 vs 3.8 mg/L; P = 0.150), although its laboratory correlation profile was broader in chronic myeloid leukemia. Hodgkin lymphoma showed higher CRP than non-Hodgkin lymphoma (17.2 vs 5.4 mg/L; P < 0.001), together with stronger leukocyte and platelet responses across CRP quartiles. In multiple myeloma, CRP was identical in patients with and without extramedullary disease (3.8 vs 3.8 mg/L; P = 0.712). In the NHANES sample, hs-CRP was highest among participants reporting leukemia, intermediate among those reporting lymphoma, and lowest among non-cancer participants; within the combined hematologic cancer group, hs-CRP correlated inversely with hemoglobin and albumin. Conclusions CRP is not a uniform marker across hematologic disorders. Its baseline concentration and accompanying laboratory phenotype depend on disease context, with prominent elevations in hyperinflammatory and selected aggressive disorders but limited value for identifying extramedullary myeloma. CRP should be interpreted as a context-dependent adjunct rather than a stand-alone diagnostic or prognostic marker.