Selective enhancement of production of IgE, IgG4, and Th2-cell cytokine during the rebound phenomenon in atopic dermatitis and prevention by suplatast tosilate.
BACKGROUND
Atopic dermatitis is a chronic inflammatory skin disease, which is commonly treated with topical steroids. It is, however, associated with rebound after therapy has been discontinued.


OBJECTIVE
This study was designed to elucidate the mechanisms of the rebound phenomenon, and to test the effect of an oral anti-allergic medication, suplatast tosilate, on atopic dermatitis.


METHODS
This is a randomized, placebo controlled study. Patients with atopic dermatitis who had been treated with strong steroid ointment (dexamethasone valerate) for several years were divided into two groups. One group (the control group, n = 15) was treated with a non-steroid anti-inflammatory ointment (bufexamac ointment), while the other group (the suplatast tosilate group, n = 17) was treated with the anti-allergic medications, suplatast tosilate and bufexamac ointment. In each group, in vitro production of immunoglobulins and cytokines before and after 2 weeks of treatment was measured.


RESULTS
In the control group, 15 of the 15 patients experienced rebound and mean production of IgE, IgG4, IL-4, IL-5, IL-10, and IL-13 was enhanced after 2 weeks. In contrast, only 2 of the 17 patients in the suplatast tosilate group experienced rebound. There was no enhancement of production of immunoglobulins and cytokines after 2 weeks of treatment.


CONCLUSIONS
Enhanced production of the Th2-cell cytokines, which selectively induces IgE and IgG4 production, may be involved in the pathogenesis of the rebound phenomenon, and that suplatast tosilate may prevent the rebound phenomenon by down-regulating the production of these cytokines.
Kimata
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Department of Allergy, Unitika Central Hospital, Uji-City, Kyoto Prefecture, Japan.
D000284:Administration, Oral; D000287:Administration, Topical; D000293:Adolescent; D000328:Adult; D018926:Anti-Allergic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use; D000917:Antibody Formation / Q000187:drug effects; D001190:Arylsulfonates / Q000008:administration & dosage / Q000627:therapeutic use*; D002019:Bufexamac / Q000008:administration & dosage / Q000627:therapeutic use; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000276:immunology; D003907:Dexamethasone / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D005260:Female; D006633:Histamine Antagonists / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007074:Immunoglobulin G / Q000096:biosynthesis*; D007378:Interleukins / Q000096:biosynthesis / Q000378:metabolism; D008222:Lymphokines / Q000378:metabolism*; D008297:Male; D013375:Substance Withdrawal Syndrome / Q000209:etiology / Q000276:immunology / Q000517:prevention & control*; D013452:Sulfonium Compounds / Q000008:administration & dosage / Q000627:therapeutic use*; D018418:Th2 Cells / Q000378:metabolism*; D016896:Treatment Outcome
D018926:Anti-Allergic Agents; D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D001190:Arylsulfonates; D006633:Histamine Antagonists; D007074:Immunoglobulin G; D007378:Interleukins; D008222:Lymphokines; D013452:Sulfonium Compounds; D007073:Immunoglobulin E; D002019:Bufexamac; D003907:Dexamethasone; C073028:suplatast tosilate; C030949:dexamethasone 17-valerate