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Published on: September 8, 2023
Abnormal Trabecular and Cortical Bone Microarchitecture in Chronic Hepatitis C Infection and Associations With Select
Erica J Weinstein1, Dean M Carbonari2, Craig W Newcomb2
1Division of Infectious Diseases, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Insights
Hepatitis C virus (HCV) infection is linked to lower bone density and structural deficits. Elevated tumor necrosis factor-alpha (TNF-α) in HCV patients may drive these bone changes, suggesting inflammation
Area of Science:
- Bone biology
- Hepatology
- Immunology
Background:
- Hepatitis C virus (HCV) infection is associated with reduced bone mineral density (BMD) and increased fracture risk.
- The structural basis for skeletal fragility in HCV and the role of inflammatory cytokines are not well understood.
Purpose of the Study:
- To compare skeletal parameters in individuals with and without chronic HCV using high-resolution peripheral quantitative computed tomography (HR-pQCT).
- To investigate the association between inflammatory cytokines and bone deficits in chronic HCV.
Main Methods:
- A cross-sectional study involving 58 participants with chronic HCV and 58 controls.
- HR-pQCT was used to assess volumetric BMD and cortical dimensions of the radius and tibia.
- Whole body dual-energy x-ray absorptiometry measured visceral fat and lean mass; serum cytokines (TNF-α, IL-6, IL-18) were quantified.
Main Results:
- Chronic HCV patients exhibited significantly lower radius and tibia trabecular volumetric BMD, and reduced cortical area and thickness compared to controls.
- Higher serum levels of tumor necrosis factor-alpha (TNF-α) were observed in the chronic HCV group.
- Elevated TNF-α correlated with decreased trabecular BMD and increased cortical porosity in the tibia.
Conclusions:
- Chronic HCV infection is associated with decreased bone mineral density and impaired cortical dimensions.
- Increased TNF-α levels in HCV patients may contribute to skeletal fragility.
- HCV-associated inflammation is a potential driver of bone deficits.
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]/cm3) and lower tibia trabecular volumetric BMD (-20.5 mg HA/cm3), cortical area (-20.9 mm2), and cortical thickness (-0.47 mm) than participants without HCV (all P < .05), independent of age, sex, visceral fat area, appendicular lean mass, and smoking. Mean log TNF-α was higher with chronic HCV (+0.1-log pg/mL; P < .001), but no differences in mean log interleukin 6 or interleukin 18 were observed. Higher log TNF-α was associated with lower radius trabecular volumetric BMD (-99.7 mg HA/cm3), lower tibia cortical volumetric BMD (-91.6 mg HA/cm3), and higher tibia cortical porosity (+1.39%) by HR-pQCT (all P < .05).
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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