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 ].
Weaker topical steroids are utilized for thin- skinned and sensitive areas, especially areas under occlusion, such as the armpit, groin, buttock crease, breast folds. Weaker steroids are used on the face, eyelids, diaper area, perianal skin, and intertrigo of the groin or body folds. Moderate steroids are used for atopic dermatitis , nummular eczema , xerotic eczema , lichen sclerosis et atrophicus of the vulva , scabies (after scabiecide) and severe dermatitis . Strong steroids are used for psoriasis , lichen planus , discoid lupus , chapped feet, lichen simplex chronicus , severe poison ivy exposure, alopecia areata , nummular eczema, and severe atopic dermatitis in adults. 
Gereç ve Yöntem: Mevsimsel alerjik rinit şikayeti olan ve bu nedenle yapılan prick test sonucu 3 ve 4 pozitif polen alerjisi taspit edilen yaşları 18-45 arasında bulunan 20 hasta çalışmaya alındı. Hatalara sistemik antihistaminik olan Levosetrizin 2-HCL ile beraber yarısına intranazal Azelastine HCL sprey, kalan yarısına da intranazal Triamsinolone Acetonide sprey kullanıldı. Hastaların şikayetleri 1 ay boyunca total semptom skorunu belirleyen bir anket ile günlük olarak değerlendirildi. Tüm hastalara tedaviye başlamadan önce bazal semptom değerlendirilmesi yapıldı.