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LETTERS TO THE EDITOR |
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Mt. Sinai School of Medicine, New York, New York, Brain and Perception Laboratory, University of California, San Diego, La Jolla, California, and Department of Psychiatry, University of Vermont, Burlington, Vermont
We read with great interest the important and fascinating paper of Modell et al. (1) in which they found bupropion to be clinically significantly effective for a majority of patients with psoriasis and atopic dermatitis. The patients were selected a priori, as well as demonstrated a posteori, not to be depressed. Modell et al. (1) conclude that a psychiatric effect is not the reason for the effectiveness of bupropion, and the mechanism by which bupropion might work in psoriasis and atopic dermatitis is not known. We suggest that bupropion works in these diseases by lowering the levels of the proinflammatory cytokine tumor necrosis factor-
(TNF). This would be consistent with our report that bupropion effected near complete clinical remission in patients with Crohn’s disease (2, 3), and our finding that bupropion can lower TNF. As well, an anti-TNF mechanism for bupropion is consistent with previous reports, discussed by Modell et al. (1) and us (4) of the effectiveness of monoamine oxidase inhibitors (MAO-Is) in psoriasis (1, 5), Crohn’s disease (6), and rheumatoid arthritis (7) (another disease associated with high levels of TNF).
While bupropion is typically thought of as an antidepressant, or a medication to aid in smoking cessation, we had found that a number of patients taking bupropion (2, 3) or a monoamine oxidase inhibitor (6) have experienced profound (to near normal bowel) and long-lasting (>2 years) remissions of their Crohn’s disease (CD). By increasing monoaminergic and dopaminergic tone, these medicines may be able to lower, via increased intracellular cAMP (8, 9) levels of the pathologically significant proinflammatory cytokine TNF (10). In one CD patient in whom we measured TNF, the value dropped from 29 pg/mL before treatment (Specialty Labs, Santa Monica, CA; normal <20 pg/mL) to 3 pg/mL on bupropion. We have seen seven other patients in whom TNF dropped dramatically on bupropion, six of these into the normal range. Consistent with the findings of Modell and colleagues (1), we have seen a patient whose psoriasis cleared nicely on bupropion, though we did not measure TNF in that patient. Psoriasis, like CD and rheumatoid arthritis is often associated with high levels of TNF, various drugs targeting TNF are being tried for these diseases (10). Atopic dermatitis is typically considered to be a disease with a different cytokine profile than psoriasis (more the Th-2 milieu). Nevertheless, in atopic dermatitis patients, TNF is increased in quiescent regions and in response to antigen (11), and TNF may play a role in disease pathogenesis, perhaps by increasing adhesion molecule expression (12). Larger trials of bupropion for psoriasis, atopic dermatitis, Crohn’s disease, and other diseases and conditions associated with high levels of TNF are warranted.
REFERENCES
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