SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.
Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.
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CLE patients who are smokers have a higher risk of disease. Quitting smoking can increase their response to treatment.
Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.
The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).
Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).
Dr. Jeffrey P. Callen
These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.
Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.
Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.
But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.
Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.
If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."
Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.
"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.
SDEF and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.