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Updated: Dec 22, 2025

Rat Model of Adhesive Capsulitis of the Shoulder
Published on: September 28, 2018
Association Between High-Sensitivity C-Reactive Protein and Idiopathic Adhesive Capsulitis
Hyung Bin Park1, Ji-Yong Gwark1, Jaehoon Jung1
1Departments of Orthopaedic Surgery (H.B.P. and J.-Y.G.) and Internal Medicine (J.J.), Gyeongsang National University School of Medicine and Gyeongsang National University Changwon Hospital, Changwon, Republic of Korea.
High-sensitivity C-reactive protein (CRP) is an independent marker for idiopathic adhesive capsulitis (IAC). Metabolic factors like dyslipidemia and hyperglycemia are associated with both CRP and IAC, suggesting chronic inflammation plays a role.
Area of Science:
- Orthopedics
- Rheumatology
- Clinical Chemistry
Background:
- Chronic inflammation is linked to idiopathic adhesive capsulitis (IAC).
- The association between high-sensitivity C-reactive protein (CRP) and IAC is not well-established.
- This study investigates the relationship between CRP levels and IAC, and associated metabolic factors.
Purpose of the Study:
- To determine if high-sensitivity CRP levels are associated with IAC.
- To identify metabolic factors linked to high-sensitivity CRP in patients with IAC.
Main Methods:
- A case-control study involving 202 IAC patients and 606 controls.
- Analysis of variables including BMI, diabetes, dyslipidemia, and serum levels of glucose, HbA1c, and CRP.
- Multivariable conditional logistic regression was used to evaluate associations.
Main Results:
- High-sensitivity CRP >1.0 mg/L was significantly associated with IAC (OR, 2.47).
- Diabetes, elevated fasting glucose, HbA1c, hypertriglyceridemia, hypo-high-density lipoproteinemia, and a high TG/HDL ratio were significantly associated with high-sensitivity CRP in IAC patients.
Conclusions:
- High-sensitivity CRP >1.0 mg/L is an independent marker associated with IAC.
- Dyslipidemia, insulin resistance, and hyperglycemia are linked to both high-sensitivity CRP and IAC.
- These findings support the role of chronic systemic inflammation in the development of IAC.
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