ArticleOpen forum infectious diseases2025
Abnormal Trabecular and Cortical Bone Microarchitecture in Chronic Hepatitis C Infection and Associations With Select Inflammatory Cytokines.
Article in Open forum infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Bone health and chronic viral infections: A narrative literature review.World journal of virology · 2026Review
- Multiscale bone remodeling in COVID-19: from osteoimmune signaling to structural and mechanical impairment.Frontiers in bioengineering and biotechnology · 2026Review
- Changes in Bone Microarchitecture and Inflammatory Cytokines After Cure of Chronic Hepatitis C Infection With Direct-Acting Antiviral Therapy.Open forum infectious diseases · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
Background: Hepatitis C virus (HCV) infection is associated with reduced bone mineral density (BMD) and increased fracture risk. The structural underpinnings for skeletal fragility with HCV and contributions of inflammatory cytokines remain unknown. We used high-resolution peripheral quantitative computed tomography (HR-pQCT) to compare skeletal parameters by chronic HCV. Methods: We conducted a cross-sectional study among 58 participants with chronic HCV and 58 participants without HCV. Volumetric BMD and cortical dimensions of the radius and tibia were determined by HR-pQCT; visceral fat area and appendicular lean mass were assessed by whole body dual-energy x-ray absorptiometry; serum levels of tumor necrosis factor α (TNF-α), interleukin 6, and interleukin 18 were measured. Multivariable linear regression was used to estimate group differences in bone measurements and cytokines. Results: Participants with chronic HCV had lower radius trabecular volumetric BMD (-24.2 mg hydroxyapatite [HA]/cm Conclusions: Patients with chronic HCV had decreased trabecular volumetric BMD and cortical dimensions and higher TNF-α than individuals without infection, suggesting that HCV-associated inflammation might contribute to bone deficits.
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