ArticleInfection2026
Serum hepcidin as a host-derived biomarker of disease severity and risk stratification in tuberculosis.
Article in Infection, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepcidin is a key regulator of systemic iron metabolism. Hepcidin may reflect the inflammatory activity and disease burden in tuberculosis. However, prospective evidence on the prognostic value of serum hepcidin and other host-biomarkers in tuberculosis is limited. We evaluated the association of hepcidin with disease severity and outcomes.
methodsThis prospective cohort study enrolled consecutive adults (age ≥ 18 years) with newly diagnosed tuberculosis. Baseline serum hepcidin, adenosine deaminase (ADA), and creatine kinase-MB (CK-MB) levels were measured. Disease severity was assessed using a predefined tuberculosis severity score. The prognostic performance of biomarkers was evaluated using receiver operating characteristic analysis and multivariable logistic regression.
resultsAmong 140 patients (median age, 48 years; 67.1% male), 25% had pulmonary tuberculosis, 25% extrapulmonary tuberculosis, and 50% disseminated disease; HIV co-infection was present in 16.4%. The 3-month all-cause mortality rate was 22.1%. Serum hepcidin levels were significantly higher in severe than non-severe tuberculosis (201.5 vs. 145.9 ng/mL; p = 0.017), but were not associated with 3-month mortality. Conversely, CK-MB was significantly elevated among non-survivors (24.5 vs. 13.8 U/L; p < 0.001). CK-MB showed good predictive performance for mortality (AUC 0.795), while ADA demonstrated moderate discrimination (AUC 0.647). The ADA/CK-MB combination showed the highest discriminative performance for mortality prediction (AUC 0.82). Triple-marker panel (Hepcidin + ADA+CK-MB) provided the best discrimination for severe disease (AUC 0.717).
conclusionsSerum hepcidin was associated with disease severity in tuberculosis but was not associated with 3-month mortality. Combined biomarker models showed promising prognostic performance, warranting further validation in larger multicentre studies.
Indexed as
Identifiers
42878786What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.