Objectives To investigate the lipid profile and subclinical atherosclerosis in patients with undifferentiated connective tissue disease (UCTD), in comparison with rheumatoid arthritis (RA) and healthy individuals. Methods This cross-sectional controlled study included 30 patients with UCTD, treated with conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs), 59 patients with RA receiving csDMARDs, and 31 age- and sex-matched healthy controls. All participants had no history or presence of coronary artery disease, hypertension, diabetes mellitus, dyslipidemia, thyroid disease, smoking, and none received diuretics, cholesterol-lowering drugs, or other agents affecting the lipid profile. Fasting serum lipid parameters such as total cholesterol (TC), triglycerides (TGL), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured in all patients and controls. Subclinical atherosclerosis was assessed by measuring carotid intima-media thickness (cIMT) using ultrasonography. Results UCTD patients exhibited significantly lower TC and HDL-C levels compared with controls (204.4 ± 43.0 mg/dL vs 238 ± 41.4 mg/dL, p < 0.004 and 50.6 ± 9.5 mg/dL vs 61.3 ± 13.3 mg/dL, p < 0.002 respectively). They also presented with increased cIMT compared to healthy controls (0.8 [0.6–1.5] mm vs 0.6 [0.5–0.7] mm, p < 0.001). No differences were observed in TGL and LDL-C among UCTD and healthy controls. RA patients demonstrated higher cIMT (in unadjusted analyses) and HDL-C compared to UCTD patients (0.9 [0.8–1.0] mm vs 0.8 [0.6–1.5] mm, p < 0.001 and 56.8 ± 15.2 mg/dL vs 50.6 ± 9.5 mg/dL, p < 0.004 respectively). However, after multivariable linear regression analysis adjusting for age, sex, ESR, and disease duration, disease type was not independently associated with cIMT (β = 0.02, 95% CI − 0.16 to 0.19; p = 0.86). Conclusions Subclinical atherosclerosis was observed in both RA and UCTD patients compared with healthy controls. Although RA patients exhibited higher cIMT values in unadjusted analyses, disease type was not independently associated with cIMT after multivariable adjustment. These findings suggest that cumulative inflammatory burden rather than diagnostic category alone may contribute to vascular alterations. Prospective longitudinal studies are required to clarify cardiovascular risk evolution in UCTD. <Table Float="No" ID="Taba"> <tgroup cols="2"> <colspec align="left" colname="c1" colnum="1" /> <colspec align="left" colname="c2" colnum="2" /> <tbody> <row> <entry align="left" nameend="c2" namest="c1"> Key Points • Patients with UCTD exhibit subclinical atherosclerosis despite conventional immunosuppressive treatment. • RA patients show a greater burden of subclinical atherosclerosis compared with UCTD patients in unadjusted analyses. • Quantitative lipid levels partly explain cardiovascular risk in inflammatory rheumatic diseases, highlighting the role of endothelial dysfunction and immune-mediated mechanisms. </entry> </row> </tbody> </tgroup> </Table>

Subclinical atherosclerosis in patients with undifferentiated connective tissue disease: comparison with rheumatoid arthritis

期刊论文
发表日期：

2026年3月23日

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Georgios V. Papamichail,
Nikolaos A. Georgiadis,
Vasileios G. Xydis,
Iro Rapti,
Christina A. Kapsali,
Athanasios Kitsakos,
Alexandros A. Drosos,
Paraskevi V. Voulgari

摘要

Objectives

To investigate the lipid profile and subclinical atherosclerosis in patients with undifferentiated connective tissue disease (UCTD), in comparison with rheumatoid arthritis (RA) and healthy individuals.

Methods

This cross-sectional controlled study included 30 patients with UCTD, treated with conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs), 59 patients with RA receiving csDMARDs, and 31 age- and sex-matched healthy controls. All participants had no history or presence of coronary artery disease, hypertension, diabetes mellitus, dyslipidemia, thyroid disease, smoking, and none received diuretics, cholesterol-lowering drugs, or other agents affecting the lipid profile. Fasting serum lipid parameters such as total cholesterol (TC), triglycerides (TGL), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured in all patients and controls. Subclinical atherosclerosis was assessed by measuring carotid intima-media thickness (cIMT) using ultrasonography.

Results

UCTD patients exhibited significantly lower TC and HDL-C levels compared with controls (204.4 ± 43.0 mg/dL vs 238 ± 41.4 mg/dL, p < 0.004 and 50.6 ± 9.5 mg/dL vs 61.3 ± 13.3 mg/dL, p < 0.002 respectively). They also presented with increased cIMT compared to healthy controls (0.8 [0.6–1.5] mm vs 0.6 [0.5–0.7] mm, p < 0.001). No differences were observed in TGL and LDL-C among UCTD and healthy controls. RA patients demonstrated higher cIMT (in unadjusted analyses) and HDL-C compared to UCTD patients (0.9 [0.8–1.0] mm vs 0.8 [0.6–1.5] mm, p < 0.001 and 56.8 ± 15.2 mg/dL vs 50.6 ± 9.5 mg/dL, p < 0.004 respectively). However, after multivariable linear regression analysis adjusting for age, sex, ESR, and disease duration, disease type was not independently associated with cIMT (β = 0.02, 95% CI − 0.16 to 0.19; p = 0.86).

Conclusions

Subclinical atherosclerosis was observed in both RA and UCTD patients compared with healthy controls. Although RA patients exhibited higher cIMT values in unadjusted analyses, disease type was not independently associated with cIMT after multivariable adjustment. These findings suggest that cumulative inflammatory burden rather than diagnostic category alone may contribute to vascular alterations. Prospective longitudinal studies are required to clarify cardiovascular risk evolution in UCTD.

Key Points

• Patients with UCTD exhibit subclinical atherosclerosis despite conventional immunosuppressive treatment.

• RA patients show a greater burden of subclinical atherosclerosis compared with UCTD patients in unadjusted analyses.

• Quantitative lipid levels partly explain cardiovascular risk in inflammatory rheumatic diseases, highlighting the role of endothelial dysfunction and immune-mediated mechanisms.