Update on the dermatologic use of systemic glucocorticosteroids

Jackson, Scott M.; Gilchrist, Heidi; Nesbitt, Lee T.

doi:10.1111/j.1529-8019.2007.00133.x

Cited by 46 publications

(44 citation statements)

References 59 publications

(66 reference statements)

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“…Steroids also inhibit the expression of tumor necrosis factor-a (TNF-a), IL-2, and interferon g, which are all proinflammatory cytokines. There are no data showing a direct effect of steroids on melanocyte proliferation, therefore, the eruption of nevi in steroidtreated patients is probably a consequence of the immunosuppressive action of this agent [47]. FK506 (tacrolimus) is a calcineurin inhibitor approved for the prevention of allograft rejection in organ transplant recipients and topically for atopic dermatitis [48,49].…”

Section: Immunosuppression and Melanocyte Proliferationmentioning

confidence: 99%

Immunosuppression and melanocyte proliferation

et al. 2009

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Melanocytes are pigmented cells derived from the neural crest; their proliferation is restrained by immune system. The eruption of nevi after an immunosuppressive condition is a peculiar phenomenon indicating that the immune system may play a major role in limiting proliferation of melanocytes. In this review, we analyze the role of immunosuppressive regimens on melanocyte proliferation. In particular, we discuss the eruptive nevi phenomenon, which is determined by the inability of the immune system to inhibit melanocyte proliferation. These clinical observations indicate that the immune system has a pivotal role in restraining melanocyte proliferation. However, although the role of the immune system in the development of nonmelanoma skin cancer has been shown clearly in several studies involving organ transplant patients, the role of immunosuppression in melanoma genesis has not yet been established. Further investigations are required to establish the real immunogenicity of melanoma, particularly in the light of the dichotomy between the eruptive nevi phenomenon in immunosuppressed patients and the low incidence of melanoma in transplanted patients.

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Section: Immunosuppression and Melanocyte Proliferationmentioning

confidence: 99%

Immunosuppression and melanocyte proliferation

et al. 2009

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“…Unfortunately, there is very little information as to whether an endogenous steroideal system exist in human skin and what data have been reported relate to the presence of steroidogenic enzymes in dermal fibroblasts [Hammami and Siiteri, 1991] and melanocytes [Slominski et al, 2004]. Furthermore, it is not known whether epidermal keratinocytes can synthesize hydrocortisone de novo on stimulation with ACTH.Glucocorticoids are exogenously administered to treat a large number of diseases that require anti-inflammatory activity and immunosuppression [Hengge et al, 2006;Jackson et al, 2007;Stahn and Buttgereit, 2008]. Topical and systemic preparations of corticosteroids are probably most widely used in Dermatology and Oral Medicine but the mechanisms by which they induce disease remission are unclear.…”

mentioning

confidence: 98%

Keratinocytes synthesize and activate cortisol

Cirillo¹,

Prime²

2011

J. Cell. Biochem.

105

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The bioavailability of circulating and/or endogenous hydrocortisone (cortisol) in epidermal cells is a key determinant in inflammatory disease and chronic wounds. It is not known, however, whether epidermal cells can regulate tissue cortisol and whether they are capable of producing endogenous glucocorticoids. In the present study, we show by microarray analysis that epidermal cells express mRNAs to all the major enzymes involved in the metabolic chain from cholesterol to cortisol, including cytocrome P450 chain, 11β-hydroxysteroid dehydrogenases (HSD11Bs), adrenocorticotropic hormone (ACTH) receptor (MC2R), and glucocorticoid receptor. The two enzymes mediating activation/deactivation of cortisone to cortisol, namely HSD11B1 and HSD11B2, were expressed at the protein level in cultured keratinocytes as well as human skin samples, as shown by Western blotting and immunohistochemistry, respectively. In functional assays, we show that keratinocytes are not only able to activate cortisone to cortisol in a HSD11B-dependent manner but also silencing of either HSD11B1 or HSD11B2 specifically modulates the bioavailability of the inactive glucocorticoid and the active steroid, respectively. A further key observation was that keratinocytes responded to stimulation with ACTH by a significant increase in the de novo synthesis of cortisol. Taken together, we provide evidence for a novel non-adrenal steroideal system in human keratinocytes.

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“…Similarly, systemic glucocorticoids are important in a broad range of acute and chronic disorders (e.g., allergic contact dermatitis, atopic dermatitis, lichen planus, and herpes zoster) [27]. Their use is limited by the risk of hypothalamic-pituitary-adrenal axis suppression, cushingoid symptoms, and a host of other potential metabolic, hematologic, and infectious complications.…”

Section: Anti-inflammatory Agentsmentioning

confidence: 99%

Dermatotherapeutic Agents

Gendimenico

2015

Ullmann's Encyclopedia of Industrial Chemistry

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Update on the dermatologic use of systemic glucocorticosteroids

Cited by 46 publications

References 59 publications

Immunosuppression and melanocyte proliferation

Immunosuppression and melanocyte proliferation

Keratinocytes synthesize and activate cortisol

Dermatotherapeutic Agents

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