The Role of Psychogenic Factors in Skin Diseases

Rostenberg, Adolph

doi:10.1001/archderm.1960.03730010085010

Cited by 31 publications

(14 citation statements)

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“…Many skin disorders, including psoriasis and atopic dermatitis, are initiated, exacerbated, or propagated by PS (20,31,35). The abnormalities in epidermal proliferation, epidermal differentiation, permeability barrier homeostasis, and SC integrity and cohesion could all contribute to the adverse effects of PS on cutaneous function.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, the mechanistic basis for the decrease in SC integrity, i.e., a reduction in corneodesmosomes, is also normalized by inhibition of GC action. Thus many of the adverse effects of PS on epidermal structure and function can be attributed to increased endogenous GC and conversely, approaches that either reduce GC production or action might benefit cutaneous disorders that are provoked or exacerbated by PS.RU-486; corticotropin-releasing hormone; stratum corneum integrity; barrier homeostasis PSYCHOLOGICAL STRESS (PS) is well recognized to provoke, exacerbate, or propagate many cutaneous dermatoses, including psoriasis and atopic dermatitis (20,31,35). Many of the disorders that are adversely affected by PS are also associated with abnormal permeability barrier function (17, 18).…”

mentioning

confidence: 99%

“…PSYCHOLOGICAL STRESS (PS) is well recognized to provoke, exacerbate, or propagate many cutaneous dermatoses, including psoriasis and atopic dermatitis (20,31,35). Many of the disorders that are adversely affected by PS are also associated with abnormal permeability barrier function (17,18).…”

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confidence: 99%

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Glucocorticoid blockade reverses psychological stress-induced abnormalities in epidermal structure and function

Choi¹,

Demerjian²,

Crumrine³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Recent studies have demonstrated that PS decreases epidermal proliferation and differentiation, impairs permeability barrier homeostasis, and decreases stratum corneum integrity. PS also increases the production of endogenous glucocorticoids (GC), and both systemic and topical GC cause adverse effects on epidermal structure and function similar to those observed with PS. We therefore hypothesized that increased endogenous GC in PS mediates its adverse cutaneous effects. To test this hypothesis, we used two independent approaches, administering either RU-486, a GC receptor antagonist that inhibits GC action, or antalarmin, a corticotropin-releasing hormone (CRH) receptor antagonist that prevents increased GC production in the face of PS. Inhibition of either GC action or production prevents the PS-induced decline in epidermal cell proliferation and differentiation, impairment in permeability barrier homeostasis, and decrease in stratum corneum (SC) integrity. Moreover, the pathophysiological basis for the abnormality in permeability barrier homeostasis; i.e., decreased lamellar body production and secretion, is restored toward normal by inhibition of GC action. Similarly, the mechanistic basis for the decrease in SC integrity, i.e., a reduction in corneodesmosomes, is also normalized by inhibition of GC action. Thus many of the adverse effects of PS on epidermal structure and function can be attributed to increased endogenous GC and conversely, approaches that either reduce GC production or action might benefit cutaneous disorders that are provoked or exacerbated by PS.RU-486; corticotropin-releasing hormone; stratum corneum integrity; barrier homeostasis PSYCHOLOGICAL STRESS (PS) is well recognized to provoke, exacerbate, or propagate many cutaneous dermatoses, including psoriasis and atopic dermatitis (20,31,35). Many of the disorders that are adversely affected by PS are also associated with abnormal permeability barrier function (17, 18). Studies in both rodents and human have demonstrated that PS perturbs permeability barrier homeostasis. While basal permeability barrier function is normal, the kinetics of barrier recovery following acute barrier disruption are delayed (2,7,8,16). This delay in barrier recovery is accounted for by a decrease in the production and secretion of lamellar bodies (LB) (5) with a resultant decrease in the formation of the extracellular lamellar membranes that mediate epidermal permeability barrier function (10). Epidermal lipid synthesis is essential for providing the lipids required for the formation of LB (11). Accordingly, the decrease in LB secretion in PS animals is explained by a decrease in epidermal lipid synthesis (5). Of note, the abnormality in barrier homeostasis induced by PS can be normalized by the topical applications of a mixture of barrier lipids, which normalize LB formation and secretion (5).In addition to adversely effecting barrier homeostasis, PS also decreases keratinocyte proliferation, impairs epidermal differentiation, and decreases stratum corneum (SC) ...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Glucocorticoid blockade reverses psychological stress-induced abnormalities in epidermal structure and function

Choi¹,

Demerjian²,

Crumrine³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Psychologic stress (PS) is well recognized to provoke, exacerbate, and propagate many cutaneous dermatoses associated with abnormal epidermal barrier function, such as psoriasis and atopic dermatitis (Rostenberg, 1960;Ghadially et al, 1996;Gupta and Gupta, 1996;Tausk and Nousari, 2001;Proksch et al, 2003;Sugarman et al, 2003). It is also well recognized that optimal management of these disorders mandates consideration, and where possible mitigation of co-existent emotional stressors.…”

mentioning

confidence: 99%

Mechanisms by Which Psychologic Stress Alters Cutaneous Permeability Barrier Homeostasis and Stratum Corneum Integrity

Choi

Brown

Crumrine

et al. 2005

Journal of Investigative Dermatology

173

141

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Although many skin disorders, including psoriasis and atopic dermatitis, are adversely affected by psychologic stress (PS), the pathophysiologic link between PS and disease expression remains unclear. Recent studies demonstrated PS-induced alterations in permeability barrier homeostasis, mediated by increased endogenous glucocorticoids. Here, we assessed the mechanisms by which PS alters stratum corneum (SC) function. Insomniac psychologic stress (IPS) altered both barrier homeostasis and SC integrity. IPS decreased epidermal cell proliferation, impaired epidermal differentiation, and decreased the density and size of corneodesmosomes (CD), which was linked to degradation of CD proteins (e.g., desmoglein1). Barrier compromise was linked to decreased production and secretion of lamellar bodies (LB), which in turn could be attributed to a decrease in de novo synthesis of epidermal lipids. Topical physiologic lipids (equimolar cholesterol, ceramides, and free fatty acids) normalized both barrier homeostasis and SC integrity in IPS mice, further evidence that lipid deficiency accounted for these functional abnormalities. Thus, PS inhibition of epidermal lipid synthesis results in decreased LB formation and secretion, as well as decreased CD, compromising both permeability barrier homeostasis and SC integrity. These studies suggest that topical treatment with epidermal physiologic lipids could be beneficial in stress-induced, barrier-associated dermatoses, such as psoriasis and atopic dermatitis.

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“…For the past several decades dermatolog ists have proposed a role for psychogenic fac tors in skin disorders [1,2], It is estimated that nearly 30-40% of dermatological dis eases may be linked with emotional disturbances [1,2], Use of psychotropics to treat skin disorders is on the increase as dermato logists realize the functional importance of these drugs in treating the spectrum of patient pathology they examine [3][4][5], Based on this, anxiolytics, antipsychotics, antidepressants and sedatives have been recommended and shown to be of benefit in the treatment of cer tain dermatological conditions (delusions of parasitosis, pruritus, chronic urticaria, post herpetic neuralgia, psoriasis and eczema) as sociated with emotional symptoms [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Skin Protein Kinase C by Psychotropic Drugs

Vaitla

Roshani

Holian

et al. 1997

Skin Pharmacol Physiol

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Lipid-soluble psychotropics are often used to treat skin diseases with psychosomatic indications. Although these drugs are known to exert their effects through the central nervous system, relatively little is known about their mechanism of action in skin. In this communication, several lipid-soluble psychotropic drugs have been examined for their ability to inhibit protein kinase C (PKC)-catalyzed phosphorylation of exogenous substrates and endogenous skin proteins. Phosphorylation of three discrete skin protein substrates at 64, 42 and 28 kDa and a group crowded together at 15-18 kDa was prevented by the antidepressants/antipsychotics. Inhibition was more pronounced in a phospholipid (PL) dependent system, but both drug-PL and drug-PKC interactions seem to be important in the mechanism of action of these drugs. In addition to the tricyclic nucleus, the propanamine side chain or its N-methyl form may influence the interaction of these drugs with PKC and its substrate(s). Chlorpromazine, imipramine, fluoxetine, doxepin, amitriptyline and hydroxyzine used in the practice of dermatology may exert their therapeutic effects by modulating skin PKC activity.

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The Role of Psychogenic Factors in Skin Diseases

Cited by 31 publications

References 0 publications

Glucocorticoid blockade reverses psychological stress-induced abnormalities in epidermal structure and function

Glucocorticoid blockade reverses psychological stress-induced abnormalities in epidermal structure and function

Mechanisms by Which Psychologic Stress Alters Cutaneous Permeability Barrier Homeostasis and Stratum Corneum Integrity

Inhibition of Skin Protein Kinase C by Psychotropic Drugs

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