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In new data presented at CCR West, investigators link smoking and ethnicity with organ damage of SLE patients.
Romy Kallas, MD
Smoking can be particularly harmful for those suffering from systemic lupus erythematosus (SLE), especially for African-Americans.
During the Clinical Congress of Rheumatology (CCR) West 2019 annual meeting in San Diego, CA, a team led by Romy Kallas, MD, from the Department of Medicine, Division of Rheumatology at Johns Hopkins University, examined the link between both smoking and ethnicity with the individual damage items from the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index.
The population of the 2629 patient study was 52.6% Caucasian and 39.3% African-American. The prevalence of ever smokers was also 35.8% in the study.
The investigators used a poisson regression to model the total SLICC/ACR Damage Index score against ever smoking and the Cox regression to assess the relationship between time to individual damage items and ever smoking.
The team also examined the relationship separately for African-American and Caucasian patients and compared SLICC/ACR Damage Index items among African-American and Caucasian ever smokers.
“There was no significant difference in total SLICC/ACR Damage Index score between ever smokers and never smokers after adjustment for ethnicity, gender, age at diagnosis, and years of education,” the authors wrote.
They also found that ever smokers had more atherosclerotic cardiovascular damage, such as angina, coronary bypass, myocardial infarction, and claudication, as well as skin damage compared to non-smokers.
In total, there were 186 cranial or peripheral neuropathy events (HR, .85 (95% CI, .63-1.16; P =.3046)).There were 109 incidents of this in Caucasians (HR, 1.24 (95% CI, .84-1.83; P =.2749)) and 71 events in African-Americans (HR, .49 (95% CI, .29-.83; P =.0081)).
Caucasian SLE patients who ever smoked were also more likely to have muscle atrophy and atherosclerosis than Caucasian non-smokers were.
There was 47 total muscle atrophy or weakness events (HR, 1.42 (95% CI, .78-2.6; P =.2489)). The investigators found that 26 of these events were from African-Americans (HR, .73 (95% CI, .31-1.72; P =.4737)) and 20 were from Caucasians (HR, 2.69 (95% CI, 1.08-6.72; P =.0337)).
The same pattern holds true for African-Americans in regard to skin damage, where ever smokers were more likely to suffer from skin damage than non-smokers.
African-American smokers were more likely to have multiple types of organ damage compared to Caucasians who smoked. The only 2 exceptions to this were gastrointestinal infarction and osteoporotic fracture, which were both more common in Caucasian smokers.
“Smoking is a modifiable factor for organ damage in SLE,” the authors wrote. “Our analysis proved its major effect on cardiovascular and cutaneous damage.”
However, the investigators said it was surprising that they found cardiovascular damage items had higher hazard ratios in Caucasian smokers than non-smokers, while skin damage items hazard ratios were higher in African-American smokers.
Overall, more damage items were increased in African-American smokers than Caucasian smokers.
Smoking is a known risk factor for SLE and has been associated with increased disease activity, as well as decreased hydroxychloroquine effectiveness in cutaneous lupus.
Earlier this year, investigators found that the long-term risks associated with smoking can linger for up to 3 decades.
Investigators from the Johns Hopkins Bloomberg School of Public Health performed an analysis that included more than 13,000 patients and found, even after cessation, cigarette smoking boosts a person’s risk of peripheral artery disease for up to 30 years after cessation.
To further evaluate long-term associations of cigarette smoking and its cessation with the incidence of coronary heart disease (CHD), peripheral artery disease (PAD), and stroke investigators performed an analysis using a sample of 13,355 patients within the Atherosclerosis Risk in Communities (ARIC) cohort.
When compared with those who never smoked, only cessation for 30 or more years had a similar risk for PAD as never smoking and smoking cessation for 20 to 30 years was still found to be associated with an elevated risk. In regard to CHD, the risk returned to baseline after about 20 years of smoking cessation.