SAN DIEGO – Smoking increases the effect of inflammation on x-ray damage in people with ankylosing spondylitis by more than fivefold, results from a Dutch study demonstrated. In addition, the effect is amplified by more than 13-fold in male smokers, compared with females who don’t smoke.
Those are the key findings from OASIS (Outcome in AS International Study), which followed ankylosing spondylitis patients for up to 12 years with biannual clinical assessments, including radiographs. Lead investigator Dr. Sofia Ramiro of the Academic Medical Center at the University of Amsterdam discussed the study during a press briefing at the annual meeting of the American College of Rheumatology.
Two reviewers independently scored the x-rays of 127 patients with ankylosing spondylitis according to the Modified Stoke Ankylosing Spondylitis Supine Score (mSASSS). Dr. Ramiro and her associates evaluated the relationship between the AS Disease Activity Score and x-ray damage over a period of 12 years by assessing the effect of inflammation at one point in time on the progression of damage 2 years later.
The mean age of the 127 patients was 41 years and 71% were male. Their mean symptom duration was 18 years, 82% were human leukocyte antigen B27 (HLA-B27) positive, and 40% were smokers.
Overall, smokers had a 5.5-fold higher effect of inflammation on x-ray damage, compared with nonsmokers, and male smokers had a 13.4-fold higher effect of inflammation on damage, compared with female nonsmokers. In addition, smokers with a short symptom duration – defined as those with fewer than 18 years of symptoms – had an 8.1-fold higher effect of inflammation on damage, compared with nonsmokers with long symptom duration.
"Smoking cessation, especially among young males, seems to be an important take-home message," Dr. Ramiro commented. "It will probably lead to less radiographic damage and to better long-term outcomes."
The press briefing’s moderator, Dr. Christie M. Bartels of the division of rheumatology at the University of Wisconsin in Madison, characterized the findings as "additional compelling evidence to say that smoking cessation would be an important process measure to look at in the rheumatology clinic, so that we can help our patients achieve their optimal outcomes."
As to the possible mechanism of action behind the relationship, Dr. Ramiro speculated that "it’s not really smoking itself that’s contributing to the worse outcomes. Smoking is increasing the impact of inflammation on radiographic damage. It’s inflammation that causes the damage."
In an interview, she acknowledged certain limitations of the study, including the fact that the sample size "is not large enough to split the data into several relevant subgroups. For instance, the number of females is rather small, as is the number of HLA-B27–negative males and females."
Dr. Ramiro said that she had no relevant financial conflicts to disclose.