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This study found that about one-third of the patients on AIs experience arthralgia. Of these symptomatic patients, many also had tenosynovial changes upon more detailed rheumatologic examination. These various findings in these patients, suggests a multifactorial etiology for AI-related arthralgia.
STUDY IN CONTEXT
Aromatase inhibitors (AIs) block the aromatase enzyme, therefore effectively reducing the levels of estrogen in postmenopausal women. Several clinical trials have shown the superiority of AIs over tamoxifen, leading to their use as the gold standard for adjuvant endocrine therapy in postmenopausal women with breast cancer. Compared with tamoxifen, AIs are associated with a greater frequency of musculoskeletal events, including arthralgias, loss of bone mineral density, and fractures. The fractures and loss of bone mineral density have been attributed to estrogen deprivation; the mechanism of AI-associated arthalgia is less well understood. It is possible that estrogens also play a role in the functioning of joint and muscular tissues.
This study investigated the prevalence of AI-related arthralgia using a detailed rheumatologic assessment. The rheumatologic assessment included autoimmune serology, musculoskeletal sonography, and electromyography (EMG).
The study was conducted in Ankara, Turkey. A total of 120 patients were included, of which 92 were being treated with AIs and 28 were controls, having not received any hormone therapy (n = 26) or having taken hormone therapy 5 or 10 years earlier (n = 2). Approximately 32% of the patients taking AIs reported new AI-related arthralgia or worsening arthralgia. The joints most commonly affected were the wrist (70%), knee (70%), hand (63%), and back (17%).
Sonography was performed in 85 patients. Effusion was the most common finding, especially in the knee joint. In addition, the tendons in patients receiving AIs were thicker than those in patients not taking AIs (P < .001). EMG detected more findings suggestive of carpal tunnel syndrome in patients with AI-related arthralgia than in those without arthralgia. Laboratory investigations did not find any significant differences between the controls and the study subjects in antinuclear antibodies, anti−double-stranded DNA, rheumatoid factor, and anti−cyclic citrullinated peptide.
Prior studies have reported a prevalence between 5% to 47% for AI-related arthralgia. In this study, the prevalence was 32.6%. This study also provided important insight into tenosynovial pathology that may be seen in patients on AIs. The tenosynovial changes were frequently seen in patients on AIs who reported arthralgias, yet some symptomatic patients lacked tenosynovial findings. Such observations suggest a multifactorial etiology for AI-related arthralgia.
Abstract:
http://jco.ascopubs.org/cgi/content/...2008.20.5435v1
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