Although there is a wide range of systemic or topical agents available for the treatment of lupus, the use of topical corticosteroid therapy remains a key component of the management of lupus related skin conditions.
Corticosteroid drugs include any of several synthetic or naturally occurring substances with the general chemical structure of steroids. Corticosteroids are very powerful drugs that affect the entire body; even corticosteroids used on large areas of skin for long periods are absorbed in sufficient quantity to cause systemic effects.
Note: the enclosed information is a bit heavy on medical language, however this information does provide an excellent overview of how corticosteroids – steroid creams over time damage the structure of the skin which impedes healing and leaves skin vulnerable to subsequent damage.
Glucocorticoids (corticosteroid) mediated skin atrophy involves thinning of the epidermis and dermis (and even hypodermis), resulting in increased water permeability and, thus, in increased transepidermal water loss. The thinning is caused by a decreased proliferative rate of keratinocytes and dermal fibroblasts. The origin of the decreased proliferation lies in collagen turnover. Transforming growth factor β (TGF-β) is a signaling molecule that, among other actions, promotes production of collagen, using Smad proteins as second messengers. Activated GR negatively regulates Smad3 through a protein-protein interaction, in this way, blocking expression of the COL1A2 gene, which encodes a type I collagen chain.
Type I collagen represents roughly 80% of the total share of skin collagen. Therefore, glucocorticoids reduce collagen turnover through blocking of TGF-β actions. Coincidentally, TGF-β plays a central role in the epithelial-to-mesenchymal transition (EMT), an essential mechanism for cicatrisation (scar formation). Glucocorticoids also diminish synthesis of epidermal lipids.
Furthermore, glucocorticoids reduce collagenases, which are part of the matrix metalloproteinases (MMPs) and tissue inhibitors of the metalloproteinases TIMP-1 and TIMP-2. Striae (stretch marks) formation, which occurs in hypercortisolism and may occur after long-term topical treatment with glucocorticoids, may be explained by the skin tensile strength determined by type I and type III collagens. The thinning of epidermis caused by glucocorticoids’ long-term topical treatment appears also to be related with the repression of K5–K14 keratin genes, which are markers of the basal keratinocytes. Additionally, these drugs inhibit K6–K16 keratin genes, markers of activated keratinocytes, therefore promoting impaired wound healing.
Above Info Source From: Int J Endocrinol. 2012: 561018.
Mechanisms of Action of Topical Corticosteroids in Psoriasis
Luís Uva, Diana Miguel
Essentially, the ongoing use of topical corticosteroid often generates additional skin damage for lupus patients such as epidermal atrophy, degeneration of the dermal structure and collagen deterioration. Additionally, topical corticosteroids can inhibit the skin’s ability to fight against bacterial and fungal infections.
Maállo is a novel post steroid therapeutic skin cream for use after topical corticosteroid medication. As a daily maintenance therapeutic Maállo suppresses the stimulus of lupus related skin conditions and supports the structure and function of the skin to reduce the dependency on topical corticosteroids. To learn more about Maállo Cream click here.
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