The significant increase in the incidence of stress-related dermatitis is largely due to stress and mental health issues.
Vanesa Micolucci, director of Cosmetic Latam, reported a 900% increase in stress-related dermatitis.
The significant increase in the incidence of stress-related dermatitis is largely due to stress and mental health issues. Constant stress and daily worries can trigger or worsen skin conditions like stress-related dermatitis, underscoring the importance of maintaining emotional balance for healthy skin and overall well-being.
Atopic dermatitis (AD) is considered one of the most common and debilitating skin diseases.
The pathogenesis of this chronic inflammatory disease involves the upregulation of the type II immune response through the activation of type II helper T cells.
This disease particularly leads to deficient colonization of normal skin flora, such as Staphylococcus aureus. Patients may present with severe, moderate, or mild forms of AD, depending on the presentation of the skin lesions.
Psychological stress can trigger the activation of numerous physiological responses, including the endocrine, nervous, and immune systems. Several studies have hypothesized that the release of substances (adrenaline, epinephrine, etc.) by the adrenal medulla during “pain and intense emotions” (fear, anger, and suffocation) was an evolutionary adaptation for survival. However, the connotation of emotional distress as a survival adaptation has changed drastically for most modern humans.
A plausible interprofessional area of collaboration between dermatology and psychiatry is elucidated by studies of outpatients in dermatology clinics who exhibit psychiatric morbidity. In fact, coexisting psychiatric disorders in patients with skin disorders show a prevalence of approximately 30%.
Innate Immune Responses to Stress
The stratum corneum is a terminally differentiated epidermis that forms the outermost layer of the skin. The corneocytes that make up the stratum corneum arise from underlying keratinocytes, although unlike their predecessors, corneocytes lack a nucleus and most cellular organelles. The intercorneocyte spaces contain high concentrations of nonpolar lipids that contribute to the water impermeability of the stratum corneum.
The stratum corneum plays an integral role in maintaining tissue hydration, and its mechanical or chemical disruption results in transepidermal water loss. In addition to its role in hydration, the stratum corneum is normally shed, potentially removing microorganisms from the skin, including potential pathogens.
Finally, the stratum corneum contains melanin derived from melanocytes, which protects the skin from ultraviolet radiation. Researchers concluded that stress-induced changes in epidermal function can act as triggers for dermatosis.
Adaptive immune responses to stress
The adaptive immune response requires the interaction of antigen-presenting cells (i.e., dendritic cells) with antigen-specific lymphocytes (i.e., T cells). Activation of lymphocytes requires their complex interaction with antigen-presenting cells and costimulatory molecules on the surfaces of both cell types, as well as the production of cytokines.
Results from various studies have suggested that elements of the adaptive immune response are required for immune enhancement induced by acute stress, since irritants do not elicit immunological memory. The impact of chronic stress on skin immune responses has also been investigated. Chronic stress has been reported to lead to immunosuppression in several systems, including skin graft rejection.
Among the factors that may explain the psychologically stress-induced changes in the adaptive immune response are changes in the number, proportions, and distribution of immune cells. Previous studies have found that psychological stress significantly decreases white blood cell counts. Furthermore, psychological stress can modulate the activity of immune cells.
Therefore, psychological stressors and stress-related molecules (e.g., epinephrine, glucocorticoids, and noradrenaline) have been shown to affect various cell behaviors, co-stimulatory molecule expression, and cytokine profiles of immune cells in adaptive immune responses of the skin, including dendritic cells and lymphocytic immune cell subsets.
Psychological Stress and Nervous Dermatitis
Atopic Dermatitis
Atopic dermatitis is a dermatological disorder initially characterized as an acute, TH2-mediated disease that becomes TH1-polarized with chronicity. Atopic dermatitis appears to worsen in patients who are psychologically stressed, and adult patients with atopic dermatitis have a constellation of psychological conditions that may put them at risk for this dermatitis. Patients with atopic dermatitis have been reported to have an attenuated HPA axis response and a hyperactive sympathoadrenomedullary system that may exacerbate the disease.
Managing the Patient at the Intersection of Dermatology and Psychiatry
Psychotropic medications (antipsychotics, lithium, antidepressants, and anticonvulsants) can cause skin rashes and allergies, as well as severe skin reactions (Stevens-Johnson syndrome associated with anticonvulsant treatment). On the other hand, adverse psychiatric effects of dermatological medications and treatments can include depression (e.g., treatment with isotretinoin and IFN) and psychosis (treatment with dapsone).
The apparent psychophysiological responses of many dermatoses may suggest that treatment programs structured at the dermatology/psychiatry interface could be useful for patient management, including programs that incorporate psychotherapy, biofeedback, hypnosis, and cognitive behavioral methods.
Treatments
Moderate to severe dermatitis is often refractory to first-line topical treatments, and while systemic immunosuppressants have been shown to be effective, they have significant adverse effects. The scarcity of basic treatments has contributed to the development of targeted topical and systemic immunotherapies based on the use of small molecules and biologics that can interact directly with the pathogenic pathways of atopic dermatitis. These represent a new era of therapeutic innovation. Additional new treatments are desirable because atopic dermatitis is a heterogeneous disease characterized by different immunological phenotypes.
Among the drugs in development, biologics targeting novel interleukin receptors such as interleukin-31, interleukin-22, and interleukin-2 are being discussed, along with a new pathway analyzing the OX40-OX40L interaction. Oral agents and small-molecule therapies such as Janus kinase inhibitors, sphingosine-1-phosphate modulators, and Bruton’s tyrosine kinase inhibitors are also being investigated, along with various novel topical medications.
Recently approved topical treatments such as phosphodiesterase-4 and JAK inhibitors are highlighted, while the potential of tapinarof and emerging microbiome-targeted therapies are explored. Beyond conventional approaches, unconventional therapies are currently being studied.
CutiBiome CLR™ is a cosmetic active ingredient designed to strengthen the skin microbiota and reduce inflammation.
It has been shown to help with conditions such as acne and dandruff by acting on the skin ecosystem and reducing the growth of harmful bacteria, such as virulent strains of Cutibacterium acnes. While its primary focus is on combating acne and dandruff, its anti-inflammatory properties and ability to balance the skin microbiota could also be beneficial for treating nervous dermatitis.
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