Mental disorders in patients with severe forms of chronic dermatoses: an observational cross-sectional study in a hospital-based consecutive sample

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Rationale

Patients with severe forms of chronic dermatoses demonstrate an increased prevalence of comorbid psychiatric disorders, a finding corroborated both by routine clinical practice and large-scale international cross-sectional and cohort studies indicating a stable inter-systemic relationship between cutaneous and psychiatric pathology [1, 2].

Severe forms of chronic dermatoses—characterized by extensive skin involvement, intense sensory symptoms (primarily pruritus and pain), life-threatening potential, high risk of disability, and the necessity of aggressive systemic therapy—create the conditions for the development of nosogenic psychiatric disorders [3]. Each dermatological nosology possesses distinct clinicopathogenetic features that influence the nature of psychosomatic interactions with comorbid psychiatric disorders.

Moderate-to-severe psoriasis (involving >10% of body surface area, or accompanied by erythroderma or pustular lesions) extends far beyond a purely dermatological condition, evolving into a systemic inflammatory disease [4]. Psoriatic arthritis develops in 25–30% of patients [5], often leading to structural joint damage and functional impairment; metabolic syndrome is identified in 40–50% [6], while a third exhibit an elevated risk of ischemic heart disease and cerebrovascular events [7]. Chronic inflammation, coupled with social stigmatization and the necessity of lifelong immunosuppressive therapy (including biologics), establishes a conducive background for the development of depressive, anxiety, and hypochondriacal disorders, fuelled by fears of systemic complication progression [8–11].

Lichen planus (LP), particularly in its widespread, erosive-ulcerative, and bullous forms, is associated with excruciating pruritus, painful oral mucosal lesions, and a high risk of secondary infection [12]. Additionally, LP may be associated with autoimmune liver diseases (notably primary biliary cholangitis in 10–20% of patients), Sjögren’s syndrome, and thymoma [13]. Long-term systemic glucocorticoid and cyclosporine use in severe cases does not always ensure sustained remission and carries risks of osteoporosis, arterial hypertension, hyperglycemia, and iatrogenic psychiatric disturbances, including steroid-induced euphoria [14].

Severe atopic dermatitis (AD) (SCORAD >50) is characterized by persistent, debilitating pruritus, sleep disturbance, secondary skin infections (including MRSA-associated), and a high frequency of comorbid allergic conditions—asthma, allergic rhinitis, and food allergy [15, 16]. Modern treatment of severe AD entails prolonged use of JAK kinase inhibitors and monoclonal antibodies (e.g., dupilumab); despite high efficacy, this approach carries risks of conjunctivitis, eosinophilia, and, rarely, systemic immune reactions [17, 18].

Acne vulgaris, contrary to common perception as merely “cosmetic,” constitutes a serious inflammatory disease in severe forms (conglobate or fulminant acne), leading to deep nodules, cysts, fistulae, and severe scarring [19]. Acne fulminans in particular presents with systemic manifestations: fever, polyarthralgia, hepatosplenomegaly, and leukocytosis [20]. Isotretinoin therapy, though highly effective, entails risks of pronounced cutaneous and mucosal dryness, hepatotoxicity, hyperlipidemia, as well as depression and suicidal ideation; thus, psychiatric status monitoring is an essential component of acne management [21, 22].

Rosacea, especially in severe forms, features persistent erythema and numerous papules and pustules; ocular rosacea may elevate the risk of keratitis and visual acuity impairment [23]. Despite the absence of direct life threat, severe rosacea causes profound social maladaptation, avoidance behaviors, and chronic anxiety [24]. Long-term antibiotic or isotretinoin regimens and laser therapies are associated with dysbiosis and emotional lability [25].

Chronic true eczema, particularly when complicated by secondary infection or progression to erythroderma, is accompanied by persistent pruritus, exudation, lichenification, and impaired epidermal barrier function [26]. Systemic corticosteroid and immunosuppressant therapies do not always induce remission and may, in some cases, increase the risk of opportunistic infections, nephrotoxicity, and endocrine disturbances [27, 28].

Severe seborrheic dermatitis with generalized cutaneous involvement may be accompanied by fever, lymphadenopathy, and electrolyte imbalance [29]. In adult patients with immunodeficiency (including HIV), seborrheic dermatitis often serves as a marker of disease progression [30]. Prolonged use of antifungal agents and topical corticosteroids leads to cutaneous atrophy, telangiectasias, and systemic adverse effects, reinforcing the perception of the disease as “uncontrollable” [31, 32].

Vitiligo, including extensive and rapidly progressive forms, despite being asymptomatic, is a systemic autoimmune disease driven by T-cell–mediated melanocyte destruction [33]. Its association with other organ-specific autoimmune disorders—such as chronic lymphocytic thyroiditis (Hashimoto’s disease), type 1 diabetes mellitus, and pernicious anemia—indicates a polyautoimmune syndrome, substantially amplifying patients’ perception of the disease as threatening not only appearance but also overall somatic health [34, 35].

Finally, pemphigus vulgaris represents a life-threatening autoimmune disorder characterized by painful bullae and erosions of the skin and mucous membranes, with a high risk of sepsis, hypoalbuminemia, and electrolyte disturbances [36]. Even during disease control, patients require lifelong high-dose glucocorticoid therapy, entailing risks of osteoporosis, diabetes mellitus, cataracts, infections, and neuropsychiatric complications [37, 38].

Aim of the present study: To develop a structured classification of comorbid psychiatric disorders, incorporating a comprehensive assessment of psychosomatic interrelationships in patients with severe forms of chronic dermatoses.

Methods

Between 2017 and 2025, 445 patients (158 males [35.5%], 287 females [64.5%]; mean age 42.3 ± 13.7 years) with severe forms of chronic dermatoses and comorbid psychiatric disorders verified according to ICD-10 criteria were examined at the V.A. Rakhmanov Clinic of Skin and Venereal Diseases of Sechenov University. Dermatological diagnoses included: psoriasis (n=121), atopic dermatitis (n=94), lichen planus (n=73), pemphigus vulgaris (n=56), true eczema (n=46), acne vulgaris (n=32), vitiligo (n=28), rosacea (n=21), and seborrheic dermatitis (n=14).

The study received approval from the Local Ethics Committee (LEC) of Sechenov University (Protocol No. 10-25, dated April 24, 2025). Study design: single-center cross-sectional investigation.

Inclusion criteria: Confirmed diagnosis of one of the aforementioned dermatoses in severe form: psoriasis (PASI ≥10); atopic dermatitis (SCORAD ≥50); pemphigus vulgaris (PDAI >45); lichen planus (LPASI >20); true eczema (EASI ≥21); acne (IGA ≥3); vitiligo (stage 2–3 by VETF); rosacea (RASI ≥18); seborrheic dermatitis (SDASI ≥30); presence of a comorbid psychiatric disorder diagnosed according to ICD-10; written informed consent.

Non-inclusion criteria: Pregnancy or lactation; life- or function-threatening non-dermatological conditions or other skin diseases; inability to undergo comprehensive clinical assessment due to intellectual disability, organic central nervous system lesions, progressive schizophrenia with marked personality changes, acute psychotic states, psychoactive substance use disorders, or malignant neoplasms.

Exclusion criteria: Patient’s voluntary withdrawal; failure to comply with the study protocol.

Study procedures:
– Clinical assessment: Conducted by specialists of the V.A. Rakhmanov Department of Skin and Venereal Diseases, Institute of Clinical Medicine, Sechenov University, using standardized dermatological severity scales: Clinical Symptoms Index (CSI); Dermatology Life Quality Index (DLQI); Behavioral Rating Scale (BRS) for pruritus intensity.
– Psychopathological assessment: Conducted by specialists of the Department of Psychiatry, Psychotherapy, and Psychosomatics (same institution), including preliminary evaluation using the Hospital Anxiety and Depression Scale (HADS), medical history collection (subjective and objective), psychiatric diagnosis per ICD-10, and expert clinical case review for psychosomatic status determination.

Statistical analysis was performed using IBM SPSS Statistics 26. Normality of distribution was assessed via the Kolmogorov–Smirnov test. For normally distributed variables, parametric methods were applied; results are presented as mean ± standard deviation (M ± σ). Non-normally distributed quantitative variables are presented as median [interquartile range: Q1–Q3]. Comparisons between two independent groups used Student’s t-test (t) for normal distributions and the Mann–Whitney U test for non-normal distributions. For ≥3 independent groups, the Kruskal–Wallis H test with Bonferroni correction was applied. Categorical variables were analyzed using Pearson’s χ² test; for tables >2×2 with significant χ², Cramér’s V was calculated to assess association strength, followed by post-hoc analysis of standardized residuals. Cells with |z| ≥ 2.58 (p < 0.01, two-tailed, Bonferroni-corrected) were deemed significant contributors to overall χ² significance. Correlation analyses between objective dermatological severity and subjective psychometric parameters employed Pearson’s r (normal distribution) or Spearman’s ρ (non-normal distribution). Correlation strength was interpreted as: weak (|r|/|ρ| = 0.10–0.29), moderate (0.30–0.49), strong (≥0.50). Statistical significance was set at p < 0.05.

Results

Among patients with severe chronic dermatoses, the following ICD-10 psychiatric disorders were diagnosed: adjustment disorders [F43.2] — 103 (23.1%); depressive episode [F32.0] — 66 (14.8%); hypochondriacal disorder [F45.2] — 63 (14.2%); recurrent depressive disorder [F33] — 55 (12.4%); personality disorders [F60] — 52 (11.7%); schizotypal disorder [F21] — 28 (6.3%); post-traumatic stress disorder [F43.1] — 18 (4.0%); generalized anxiety disorder [F41.1] — 12 (2.7%); bipolar affective disorder [F31] — 9 (2.0%); agoraphobia [F40.0] — 9 (2.0%); obsessive–compulsive disorder [F42] — 9 (2.0%); panic disorder [F41.0] — 8 (1.8%); social phobia [F40.1] — 7 (1.6%); hypochondriacal schizophrenia [F20.8] — 6 (1.3%).

Analysis of psychopathological phenomena revealed a unifying feature in the overwhelming majority of patients (n=400; 89.9%)—a transnosological hypochondriacal nosogenic complex—whereas a dysmorphic nosogenic complex was observed only in 45 patients (10.1%), primarily with facial rosacea, vitiligo, or acne. Given the overwhelming dominance of hypochondriacal-spectrum disorders, further analysis focused on this subgroup, where three clinical types were delineated:
– Depressive-hypochondriacal (n=250; 62.5%);
– Masked hypochondria (n=123; 30.8%);
– Aberrant hypochondria (n=27; 6.7%) (Table 1).

Comparative analysis showed similar objective dermatological severity across all three types: median CSI was 18 [16–20] in depressive-hypochondriacal, 17 [15–20] in masked, and 19 [17–21] in aberrant hypochondria (p = 0.38, Kruskal–Wallis). However, sharp differentiation was observed in subjective and behavioral parameters (p < 0.001 for all comparisons). Patients with depressive-hypochondriacal reactions exhibited the highest subjective distress: BRS = 7 [6–9]; DLQI = 23 [20–25]; HADS-anxiety = 16.4 ± 3.0; HADS-depression = 16.7 ± 2.9. Those with masked hypochondria occupied an intermediate position: BRS = 4 [3–6]; DLQI = 9 [7–13]; HADS-anxiety = 10.2 ± 3.1; HADS-depression = 4.5 ± 3.2. In contrast, patients with aberrant hypochondria, despite severe dermatological status, reported minimal subjective distress: BRS = 1 [0–2]; DLQI = 3 [1–6]; HADS-anxiety = 2.8 ± 2.1; HADS-depression = 1.9 ± 1.0 (p < 0.001 vs. depressive-hypochondriacal group).

To objectively verify psychosomatic parallelism, correlation analysis between CSI and psychometric measures was performed. In the full sample (n=400), statistically significant but weak correlations were observed between CSI and HADS-anxiety (r = 0.28, p < 0.001) and HADS-depression (r = 0.25, p < 0.001). However, subgroup analysis revealed qualitatively distinct patterns:
– In depressive-hypochondriacal cases (n=250), CSI significantly correlated with HADS-anxiety (r = 0.49, p < 0.001), HADS-depression (r = 0.52, p < 0.001), and DLQI (ρ = 0.46, p < 0.001);
– In masked hypochondria (n=123), correlations were non-significant (HADS-anxiety: r = 0.16, p = 0.09; DLQI: ρ = 0.14, p = 0.14);
– In aberrant hypochondria (n=27), no significant correlations emerged (e.g., HADS-depression: r = –0.21, p = 0.29).
Thus, a significant association between objective dermatological severity and subjective distress was observed only in the depressive-hypochondriacal subtype.

The depressive-hypochondriacal type (n=250; 62.5%) predominated in individuals with premorbid anxious and dramatic personality cluster traits and neurotic somatoperceptive accentuation. Clinical presentation was defined by tight correlation between skin lesion extent and depth of affective suffering. Hypotimia co-occurred with somatopsychic hyperesthesia, tearfulness, irritability, insomnia, inner tension, and hypochondriacal fears (e.g., fear of lifelong disfigurement, malignant transformation, or systemic complications). In 48 patients (19.2% of this subgroup) with recurrent depressive disorder temporally linked to dermatosis exacerbation, a “double depression” nosogenic reaction developed—residual affective symptoms persisted even after dermatological remission.

Masked hypochondria (n=123; 30.8%) manifested as a rational, coping-oriented behavioral style despite severe skin disease. Patients, typically with premorbid sthenic traits—emotional detachment, perfectionism, high stress resilience—integrated treatment into daily routines, adhered strictly to medication regimens, and preserved occupational and physical activity. Medical consultation was prompted not by lesion extent but by disruption of “functional comfort”—e.g., persistent pruritus, pain, or insomnia perceived as barriers to productivity. Although DLQI and HADS-anxiety scores were mild-to-borderline and dermatological severity substantial, patients did not regard the dermatosis as a serious health threat; nonetheless, unlike the aberrant group, they demonstrated high treatment compliance and responsibility.

Aberrant hypochondria (n=27; 6.7%) was characterized by a paradoxical mismatch between objective dermatological severity and subjective illness perception. Despite massive, often ulcerated lesions, functional impairment, and need for caregiver assistance, patients exhibited no anxiety regarding their health, denied risk of death or disability, and ignored potential hazards of immunosuppressive therapy. Premorbidly, such individuals belonged predominantly to affective and eccentric personality clusters, exhibited deficits in bodily self-awareness (body image), and displayed emotionally impoverished perception of personal suffering. High pain/pruritus tolerance combined with lack of initiative in seeking care (referrals occurred only upon insistence by relatives or employers) and disregard for medical advice—absent external supervision—signified profound dissociation between somatic and mental status.

Distribution of clinical types of comorbid psychiatric disorders with transnosological hypochondriacal complex by dermatosis type is presented in Figure 1.

Analysis of type distribution across dermatoses revealed the following patterns:
– Depressive-hypochondriacal type occurred across all nosologies—including life-threatening conditions (pemphigus), chronic somatic exhaustion and high systemic risk (psoriasis, AD), and dermatoses with massive lesions (vitiligo), intense inflammation, intractable pruritus, chronic exudation, lichenification, and insomnia (LP, acne, rosacea, seborrheic dermatitis, eczema).
– Masked hypochondria was observed in all dermatoses, most frequently in psoriasis, AD, acne, seborrheic dermatitis, and vitiligo.
– Aberrant hypochondria (6.7% of cases) occurred only in pemphigus, psoriasis, AD, and acne.

Association between dermatosis type and clinical psychiatric subtype was assessed via Pearson’s χ² test. A statistically significant deviation from expected distribution was found (χ² = 57.96; df = 16; p < 0.001), confirming linkage between psychiatric subtype and dermatological nosology. Cramér’s V = 0.27 indicated a weak association strength.

Post-hoc standardized residual analysis (|z| ≥ 2.58, p < 0.01) identified the following significant deviations:
– Psoriasis: excess of masked hypochondria (z = +2.8, p = 0.005);
– Pemphigus: excess of aberrant hypochondria (z = +2.8, p = 0.005);
– Acne: excess of aberrant hypochondria (z = +3.0, p = 0.003);
– Lichen planus: excess of depressive-hypochondriacal type (z = +2.7, p = 0.007).

Discussion

This study aimed to characterize the structure and psychosomatic interrelationships of comorbid psychiatric disorders in patients with severe chronic dermatoses. The identified hypochondriacal nosogenic complex represents a transdiagnostic construct manifesting within various psychiatric diagnostic categories. On one hand, it constitutes a universal response to severe nosogenic stress; on the other, it underlies the formation of three distinct clinical types of comorbid psychiatric disorders (depressive, masked, aberrant hypochondria), shaped by dermatological and psychiatric status, as well as premorbid and somatoperceptive personality traits.

This approach aligns with contemporary psychosomatic trends emphasizing pathophysiological constructs beyond categorical nosology [39], where somatogenic triggers often serve as dominant syndromogenic factors [40].

In depressive hypochondria, subjective distress directly correlates with dermatological severity. In contrast, dissociation between objective dermatosis severity and subjective psychopathological expression defines masked and aberrant hypochondria.

Patients with masked hypochondria, despite comparable dermatological severity and symptom burden (pruritus/pain/insomnia), exhibited high tolerance, preserved physical activity and work capacity, integration of therapy into daily routines, and strict medication adherence.

Patients with aberrant hypochondria, despite extremely severe disease, showed minimal social maladaptation, anxiety, or depression; paradoxical pain/pruritus tolerance; disregard of vital risks and disabling complications; absence of health-related concern; continuation of physically demanding or trauma-inducing work; and inability to autonomously seek help.

Clinically, these findings enable differentiated psychopharmacological and psychotherapeutic strategies:
– For depressive hypochondria, first-line psychosomatic psychopharmacotherapy combined with cognitive–behavioral therapy targeting catastrophic thinking is indicated [41, 42];
– For masked hypochondria, psychotherapy should focus on sustaining treatment compliance and preventing emotional burnout [43];
– For aberrant hypochondria, the primary task is establishing treatment motivation via motivational interviewing and involving significant others in the therapeutic process [44].

Conclusion

In patients with severe chronic dermatoses, comorbid psychiatric disorders span diverse diagnostic categories—from adjustment and personality disorders to recurrent depression and schizotypal disorder. Yet beneath this nosological heterogeneity lies a robust clinical commonality: the identified psychiatric disorders arise temporally and thematically in connection with dermatological manifestations, forming a unified response to severe nosogenic stress via the transnosological hypochondriacal nosogenic complex. Beyond dermatological severity, the clinical phenotype of each of the three psychosomatic syndrome types—including the paradoxical dissociation between subjective distress and objective severity, as well as amplification and somatization of pruritus—is critically shaped by premorbid personality structure, somatoperceptive accentuation, and the psychopathological architecture of the comorbid psychiatric disorder.

As decades of clinical experience confirm, differentiating comorbid psychiatric disorders dominated by the transnosological hypochondriacal nosogenic complex into clinical subtypes significantly enhances diagnostic precision and lays the foundation for personalized psychopharmacological and psychotherapeutic interventions.

Additional Information

Authors’ Contributions
I.Yu. Dorozhenok — project administration, study design, data collection and processing, manuscript writing, data analysis;
O.Yu. Olisova — study design, manuscript writing, manuscript editing;
D.A. Koriakin — manuscript writing, manuscript editing, statistical data analysis.
All authors approved the final manuscript (version for publication) and agreed to be accountable for all aspects of the work, ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Ethical Approval
The study was approved by the Local Ethics Committee (extract from Protocol No. 10-25, dated April 24, 2025).

Funding
None.

Disclosure of Interests
The authors declare no relationships, activities, or interests—financial or non-financial—with third parties (commercial or non-commercial) over the past three years that could be perceived as influencing, or being influenced by, the content of this article.

Originality
The authors confirm that no previously published material (text, figures, or data) was used in the preparation of this manuscript.

Data Availability
All data generated or analysed during this study are included in this published article.

Generative Artificial Intelligence
No generative artificial intelligence (AI) tools or technologies were used in the preparation of this manuscript.

Peer Review Process
This manuscript was submitted to the journal on the authors’ initiative and underwent standard peer-review procedures. Review was carried out by two independent external reviewers and the journal’s scientific editor.

Table 1. Comparative psychometric characteristics of three types of mental disorders comorbid with chronic dermatoses and transnosological hypochondriacal complex

Figure 1. Distribution of clinical types of comorbid mental disorders with transnosological hypochondriacal complex depending on the nosological form of dermatosis (n=400)

About the authors

Igor Yu. Dorozhenok

The First Sechenov Moscow State Medical University (Sechenov University); Scientific Center for Mental Health

Author for correspondence.
Email: idoro@bk.ru
ORCID iD: 0000-0003-1613-2510
SPIN-code: 8701-7958

MD, Cand. Sci. (Medicine), Assistant Professor

Russian Federation, 4/1 Bolshaya Pirogovskaya st, Moscow, 119991; Moscow

Olga Y. Olisova

The First Sechenov Moscow State Medical University

Email: olisovaolga@mail.ru
ORCID iD: 0000-0003-2482-1754
SPIN-code: 2500-7989

MD, Dr. Sci. (Medicine), Professor, Corresponding Member of the Russian Academy of Sciences

Russian Federation, Moscow

Danila Koriakin

Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russian Federation

Email: Danila110920021@gmail.com
ORCID iD: 0000-0003-3619-206X
SPIN-code: 8253-7096
Russian Federation

References

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