# Patients with tuberculosis and diabetes show altered clinical and biochemical parameters during anti-TB treatment

**Authors:** Augustine Boadu Asare, Prince Asare, Michelle Yeboah-Manu, Stephen Osei-Wusu, Emelia Danso Konadu, Adwoa Asante-Poku, Yayra Klinogo, Abraham Adjei, Desmond Omane Acheampong, Jane S. Afriyie-Mensah, Atiase Yacoba, Dorothy Yeboah-Manu

PMC · DOI: 10.1038/s41598-026-36529-8 · 2026-02-04

## TL;DR

Patients with both tuberculosis and diabetes experience distinct metabolic and biochemical changes during treatment, requiring integrated care to manage risks and improve outcomes.

## Contribution

The study longitudinally evaluates clinical and biochemical changes in TB patients with and without diabetes, revealing specific metabolic derangements and management implications.

## Key findings

- TB-DM patients showed significantly lower chloride levels and higher hyponatremia prevalence compared to TB-only patients.
- Elevated liver enzymes in untreated TB-DM patients suggest delayed metformin initiation and a need for electrolyte monitoring.
- Dysregulated lipid profiles in TB-DM patients highlight increased cardiovascular risk requiring routine monitoring.

## Abstract

Type-2 diabetes mellitus (DM) increases tuberculosis (TB) risk and can worsen treatment outcomes. Both diseases and their treatments induce significant metabolic and biochemical perturbations that influence disease progression and management. This study longitudinally evaluated clinical, metabolic, and serum biochemical changes in patients with pulmonary TB with and without DM before and during anti-TB therapy. Ninety-five adult patients newly diagnosed with pulmonary TB in Ghana were stratified into TB-Only (n = 49; HbA1c < 6.5%) and TB-DM (n = 46; HbA1c ≥ 6.5%) groups, including treated (TB-DMt) and untreated (TB-DMnt) diabetes subgroups. Serum samples collected at baseline (t0), day 28 (t28), and day 56 (t56) were analyzed for electrolytes, renal function, liver enzymes, and lipid profiles using validated clinical chemistry analyzer. TB-DM cohorts exhibited significantly lower chloride levels at all time points relative to the TB-Only cohort (e.g., 98 vs. 100 mmol/L at t0, p < 0.001). Hyponatremia (serum sodium < 136 mmol/L) was prevalent during the intensive anti-TB treatment phase, affecting 53.1% of TB-Only patients, 61.1% of TB-DMt patients, and 70.0% of TB-DMnt patients. Liver function tests revealed elevated bilirubin, gamma-glutamyl transferase (g-GT), alkaline phosphatase (ALP), and alanine aminotransferase (ALT) levels, particularly in TB-DMnt patients, with normalization over time. Lipid profiles showed a pro-atherogenic pattern with elevated triglycerides and total cholesterol (p < 0.05). High-density and low-density lipoproteins were increased at select time points. Positive correlations were noted among albumin, cholesterol fractions, and electrolytes. Primary microbiological treatment outcomes, including sputum conversion and completion rates, were similar regardless of diabetic status. The distinctive metabolic and biochemical derangements in TB-DM, especially untreated diabetes, highlight the importance of integrated clinical management. Elevated hepatic enzymes in TB-DMnt may delay metformin initiation, suggesting a need to optimize timing post hepatic recovery, while the prevalence of hyponatremia underscores the need for routine electrolyte monitoring in TB patients with diabetes. The dysregulated lipid profile highlights cardiovascular risk that warrants routine monitoring. Despite metabolic challenges, effective TB treatment outcomes are achievable with comprehensive care.

The online version contains supplementary material available at 10.1038/s41598-026-36529-8.

## Linked entities

- **Diseases:** Type-2 diabetes mellitus (MONDO:0005148), tuberculosis (MONDO:0018076)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, ALPP (alkaline phosphatase, placental) [NCBI Gene 250] {aka ALP, PALP, PLAP, PLAP-1}
- **Diseases:** DM (MESH:D003920), atherogenic (MESH:D050197), pulmonary TB (MESH:D014397), Hyponatremia (MESH:D007010), Type-2 diabetes mellitus (MESH:D003924), TB (MESH:D014376)
- **Chemicals:** bilirubin (MESH:D001663), cholesterol (MESH:D002784), chloride (MESH:D002712), triglycerides (MESH:D014280), Lipid (MESH:D008055), sodium (MESH:D012964), metformin (MESH:D008687)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12923770/full.md

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Source: https://tomesphere.com/paper/PMC12923770