Hematological Factors in Pulmonary Tuberculosis

Pulmonary tuberculosis remains a leading cause of infectious mortality worldwide, and its course is closely intertwined with alterations in the blood. Anemia is among the most common comorbidities, reflecting both the host’s inflammatory response and nutritional deficiencies. Two principal forms of anemia are observed: the anaemia of chronic disease, driven by inflammatory cytokines and iron sequestration, and iron deficiency anaemia, arising from malnutrition or blood loss. Beyond haemoglobin levels, patients frequently exhibit elevated acute-phase reactants such as C-reactive protein and erythrocyte sedimentation rate, while white cell and platelet counts may fluctuate in response to mycobacterial burden and co-infection status. Iron-regulatory hormones, notably hepcidin, orchestrate iron availability during infection but may also contribute to persistent inflammation. More recently, dysregulation of T-cell subsets and innate lymphoid populations has been linked to iron status, suggesting that haematological factors not only serve as biomarkers of disease severity but also modulate immune control of Mycobacterium tuberculosis. Routine assessment of these parameters offers a window on prognosis, guides adjunctive interventions and underscores the global imperative to integrate haematological screening into tuberculosis programmes.

Research from Nature Portfolio

Systematic aggregation of African cohorts has revealed that nearly three quarters of newly diagnosed pulmonary tuberculosis patients present with anaemia, predominantly of the chronic disease type. This meta-analysis also details the distribution of anaemia severity and highlights marked gender disparities, thereby advocating routine haemoglobin screening at the point of diagnosis. In a complementary study, multidimensional profiling of patients before and during antitubercular therapy uncovered a distinct inflammatory signature in anaemic individuals, characterised by persistent elevations in uric acid, C-reactive protein and erythrocyte sedimentation rate. These findings demonstrate that inflammation-driven anaemia only partially resolves with standard treatment and that residual biosignatures may predict slower clinical improvement.

Hematological Factors in Pulmonary Tuberculosis publication trend

The graph below shows the total number of articles in hematological factors in pulmonary tuberculosis across all publications each year (not limited to Nature Index journals).

Technical terms

Anaemia of chronic disease: Reduction in haemoglobin concentration caused by inflammation-driven iron sequestration and impaired erythropoiesis.

Iron deficiency anaemia: Haemoglobin deficit resulting from inadequate iron intake, absorption or excess loss, commonly coexisting with chronic infection.

Hepcidin: Liver-derived peptide hormone that regulates iron absorption and distribution by controlling ferroportin activity during inflammation.

C-reactive protein (CRP): Acute-phase protein produced by the liver in response to inflammatory cytokines, used as a marker of systemic inflammation.

Erythrocyte sedimentation rate (ESR): Laboratory measure of red blood cell aggregation rate, elevated in the presence of acute or chronic inflammation.

References

1. Interplay between systemic inflammation, anemia, and mycobacterial dissemination and its impact on mortality in TB-associated HIV: a prospective cohort study. Frontiers in Immunology (2023).
2. Iron Status and Supplementation during Tuberculosis. Microorganisms (2023).
3. Relationship between iron deficiency and severity of tuberculosis: Influence on T cell subsets. iScience (2024).
4. Prevalence and types of anemia among people with tuberculosis in Africa: a systematic review and meta-analysis. Scientific Reports (2023).
5. Tuberculosis-associated anemia is linked to a distinct inflammatory profile that persists after initiation of antitubercular therapy. Scientific Reports (2019).