The inflammatory process is controlled by the glucocorticoids’ activity, enhancing the transcription of anti-inflammatory genes and decreasing the transcription of inflammatory genes (Figure 3 ) [ 15 ].
Glucocorticoids induce the expression of annexin A1 (also known as lipocortin 1; encoded by ANXA 1) and ALXR (the annexin A1 receptor) by mechanisms still not known. Annexin A1 is a protein mainly located on basal keratinocytes of the basement membrane. Although in normal skin annexin A1 has been identified within cytoplasm, in diseased skin the intracellular localization of annexin A1 is apparently modified. In lesional psoriatic skin, annexin A1 appears only in the cell membrane, suggesting a translocation of the protein. This transition may occur to promote the binding of annexin A1 to phospholipids, therefore reducing the production of inflammatory prostanoids [ 37 ].
Annexin A1 inhibits phospholipase A 2 (PLA 2 ), thus blocking the synthesis of arachidonate-derived eicosanoids (prostaglandins, prostacyclins, leukotrienes, and thromboxanes) [ 32 ]. This blocking is furthered by the repression of glucocorticoid-mediated cyclooxygenase 2 transcription [ 38 – 41 ]. It remains unclear if the reduction of these substances levels come first and then plaque resolution, or if the normalization of prostanoid levels follows plaque clearance [ 37 ].
Exogenous and endogenous annexin A1 may regulate the innate immune cells activities controlling its levels of activation. Annexin A1 signals throw a formyl peptide receptor 2 (FPR2, ALXR in humans). Despite the activation of ALXR singnalling can occur by the annexin A1 autocrine, paracrine, and juxtacrine functions, the juxtacrine interaction seems to be the mechanism by which the anti-inflammatory process occurs. Concerning the innate response, it seems that the upregulation of the annexin A1 expression by leukocytes induced by glucocorticoids may be responsible for the inhibition of leukocytes response. Glucocorticoids also increase the secretion of annexin A1 by macrophages and the annexin A1 secreted by mast cells and monocytes, promotes the clearance of apoptotic neutrophils by macrophages. Endogenous annexin A1 is also released from apoptotic neutrophils and acts on macrophages promoting phagocytosis and removal of the apoptotic cells. The ALXR may be one mediator of this mechanism. Contrasting with the innate immunity, the adaptive immune system seems to act in a different way. Activation of T cells results in the release of annexin A1 and in the expression of ALXR. Although, glicocorticoids may reduce the annexin A1 expression within T-cell exposure as a consequence, there is an inhibition of T-cell activation and T cells differentiate into T helper 2 [ 42 , 43 ].
Clobetasol propionate is a man-made corticosteroid that is used on the skin (topically). It is available as foam, shampoo, cream, gel, lotion, ointment, solution, and spray. It is similar to alclometasone (Aclovate), hydrocortisone valerate (Westcort), halobetasol ( Ultravate ) and several others. Topical clobetasol is used to treat certain scalp and skin conditions such as psoriasis , rashes, and dermatitis . Corticosteroids have potent anti-inflammatory actions and also suppress the immune response. Clobetasol is a very potent topical corticosteroid and should only be used for a short period of time. Long term use of topical clobetasol propionate can cause serious systemic side effects and should be avoided.
The obvious priority is immediate discontinuation of any further topical corticosteroid use. Protection and support of the impaired skin barrier is another priority. Eliminating harsh skin regimens or products will be necessary to minimize potential for further purpura or trauma, skin sensitivity, and potential infection. Steroid Atrophy   is often permanent, though if caught soon enough and the topical corticosteroid discontinued in time, the degree of damage may be arrested or slightly improve. However, while the accompanying Telangectasias may improve marginally, the Striae is permanent and irreversible.