Clobetasol under hydrocolloid occlusion in psoriasis results in a complete block of proliferation and in a rebound of lesions following discontinuation.
BACKGROUND
It is a well-established fact that very potent corticosteroids are highly effective in the treatment of psoriatic plaques, and that the addition of a hydrocolloid occlusive dressing (HCD) enhances its efficacy. It is known that topical steroids induce normal differentiation and diminish hyperproliferation during treatment of psoriatic plaques. These changes are reflected by an increase in keratin 10 (K10) and a decrease in keratin 6 (K6), respectively. However, the influence of class IV corticosteroids under HCD on K10 and K6 subpopulations has never been studied.


OBJECTIVE
The present study was performed to study quantitatively the influence of a class IV topical steroid under HCD on the dynamics of K10 and K6 subpopulations.


METHODS
In the present study, we treated moderately severe stable psoriatic plaques with clobetasol-17-propionate under HCD until clearance was achieved. We took biopsies prior to treatment, after clearance and at relapse. Using flow cytometry, we studied the dynamics of K10 and K6 subpopulations.


RESULTS
Prior to treatment, 41.8% of all cells expressed K6. After treatment-induced clearance, this proportion decreased to 1.2%, which is below the normal range. At relapse, pre-treatment levels were observed again. A trend to an increasing number of basal cells and an increase in the proliferative activity of these basal cells at relapse compared to the stable situation prior to treatment was observed.


CONCLUSIONS
We conclude that clobetasol under hydrocolloid occlusion induces virtually a total block of proliferation of the basal cell population and decreases hyperproliferation-associated keratins dramatically. Furthermore, based upon epidermal cell characteristics, we conclude that a rebound phenomenon occurs following discontinuation of therapy with clobetasol under hydrocolloid occlusion.
Mommers
J M
JM
Department of Dermatology, University Hospital Nijmegen, The Netherlands. R.Mommers@derma.azn.nl
van Erp
P E
PE
van De Kerkhof
P C
PC
D000287:Administration, Topical; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002990:Clobetasol / Q000627:therapeutic use*; D003102:Colloids / Q000627:therapeutic use*; D005434:Flow Cytometry; D005938:Glucocorticoids; D006801:Humans; D053550:Keratin-10; D007633:Keratins / Q000032:analysis; D009779:Occlusive Dressings; D011565:Psoriasis / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D012008:Recurrence; D012867:Skin / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D013997:Time Factors; D016896:Treatment Outcome
D000893:Anti-Inflammatory Agents; D003102:Colloids; D005938:Glucocorticoids; C507493:KRT10 protein, human; D053550:Keratin-10; D007633:Keratins; D002990:Clobetasol