Table 1.

The pathophysiological mechanisms governing the etiopathogenetic bidirectionality in mental-cutaneous disorders, whether proven or supposed.

Skin Disease	Psychiatric Comorbidities	Pathophysiological Mechanisms
Alopecia areata	Depressive, personality, and generalized anxiety disorders	(1)Acute stress-related HPA axis hyperactivation, subsequent mast cell degranulation, and catagen phase promotion; (2)Acute stress-related substance P overexpression and neurogenic inflammation promoting catagen phase entry; (3)Acute stress-related cholinergic hypertone and subsequent hyper-release of inflammatory cytokines by immune cells in the hair follicle.
Bullous pemphigoid	Schizophrenia, uni and bipolar disorders, personality disorders, depression, and psychosis	Cross-reactive neurocutaneous autoimmune (BP 180/BP230-mediated) response and subsequent neuroinflammation-neurodegeneration.
Pemphigus	Anxiety and depression	Proinflammatory habitus triggered by psychological stress related to previous adverse events.
Vitiligo	Depression	Stress-related HPA axis hyperactivation -> inflammation -> melanocytic oxidative damage.
Oral lichen planus	Anxiety, depression, and stress	(1)OLP-related oral and gut dysbiosis -> attempted microbiota neuroimmune regulation -> psychiatric disorders; (2)Stress-induced innate and adaptive immune dysregulation (Th1-Th2 shift) -> OLP.
Hidradenitis suppurativa	Major depression, anxiety, bipolar disorder, psychosis, substance abuse disorder, and suicide	Sharing of inflammatory pathways and involvement of the same cytokines.
Acne	Stress, anxiety, depression, obsessive-compulsive disorder, personality disorder, sexual dysfunction, and suicidal ideation/attempt	(1)Stress-related HPA axis activation and stress response at sebocyte level -> upregulation of lipogenesis, androgen metabolism, and pro-inflammatory cytokines; (2)Stress-induced dysfunction of skin barrier, wound healing, and enhanced susceptibility to certain bacterial infections.
Rosacea	Depression and social anxiety	(1)Shared inflammatory pathways with presumed involvement of matrix metalloproteinases (MMPs); (2)Dysregulation of the gut–brain–skin axis, also manifesting in alteration of both skin and gut microbiota.
Herpes simplex virus	//	Emotional stress-induced HPA axis and sympathetic system activation -> stress hormones-induced Th1-Th2 shift -> HSV-specific CD8+ memory T-cells functional inhibition -> viral reactivation.
Epstein–Barr virus	//	Chronic stress-induced HPA axis hyperactivation.
Atopic dermatitis	Anxiety, depression, attention deficit hyperactivity disorder, emotional problems, conduct disorder, and suicidal ideation	-Th2-mediated systemic inflammatory response, sympathetic hypertone, and HPA dysregulation as a consequence of chronic early-onset inflammation or chronic use of systemic corticosteroids; -Stress-induced functional synergy between HPA axis and neuro-endocrine-immunocutaneous system (NEICS) and aberrant parasympathetic response in supporting itch–stress interplay.