Subclinical Atherosclerosis Can Be Detected in Rheumatoid Arthritis...

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Subclinical Atherosclerosis Can Be Detected in Rheumatoid Arthritis Patients

NEW YORK (Reuters Health) Aug 16 - In women with rheumatoid arthritis (RA),

subclinical atherosclerosis can be detected using carotid ultrasound, South

Korean researchers report.

This is noteworthy because the risk of an adverse lipid profile seems to be

increased in RA patients, as Dr. Soo-Kon Lee and colleagues, of Yonsei

University College of Medicine in Seoul, demonstrated previously. In fact,

this research group has shown that hyperlipidemia in patients with untreated

RA can be improved just by treating the RA, without using lipid-lowering

agents.

In the new study, which is reported in the July issue of Arthritis and

Rheumatism, Dr. Lee's group compared 53 women with RA and 53 women matched

for age and postmenopausal status. Evaluation by high-resolution B-mode

ultrasound showed that the average intima-media thickness of the left and

right carotid arteries was 0.77 mm in RA patients and 0.68 mm in controls (p

< 0.001).

" Possible causes of an increased cardiovascular disease risk among RA

patients include side effects of medication, decreased mobility, adverse

lipid profile, increased homocysteine level, increased levels of thrombotic

factors...and other inflammatory mechanisms, " the researchers report.

However, they found no correlation between carotid arterial wall thickness

and total homocysteine level, low-dose corticosteroid therapy, or

methotrexate therapy. Of more than 25 patient characteristics evaluated,

only five predicted increased arterial wall thickness: duration of RA,

duration of menopause, deformed joint count, cumulative C-reactive protein

level, and cumulative erythrocyte sedimentation rate.

" Recently, many similarities have emerged between the inflammation paradigm

in the pathogenesis of atherosclerosis (and unstable angina) and the

well-established inflammation mechanism in the pathogenesis of RA, " the

authors note. They suggest that " some of the shared inflammatory mechanisms

responsible for synovial lesions in RA patients may participate directly in

producing atherosclerotic lesions. "

Arthritis Rheum 2002;46:1714-1719.