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Presentación de caso

Interaction between Severe Mental Illness and

Autoimmune Pathology: Schizophrenia and Psoriatic

Arthritis

Interacción entre enfermedad mental grave y patología

autoinmune: esquizofrenia y artritis psoriásica

Horacio Enrique Gaibor Mendoza1

José Alejandro Valdevila Figueira2,3,4

Bruno Nativi Merchan2

Indira Dayana Carvajal Parra2,4

1Universidad católica de Santiago de Guayaquil, Guayaquil, Ecuador

2Instituto de Neurociencias de Guayaquil. Guayaquil, Ecuador

3Universidad Ecotec. Guayaquil, Ecuador

4Red de Investigación en Psicología y Psiquiatría (RIPYP). Ecuador

Recibido: 25/02/2026

Aceptado: 29/02/2026

Editores: Salvador González Pal, Magdalena Sosa Sánchez

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Abstract

Introduction: A bidirectional association between schizophrenia and chronic inflammatory

diseases such as arthritis and psoriasis is now recognized. These disorders share common

pathophysiological mechanisms, including immune dysfunction, systemic pro-inflammatory

activation and alterations in the neuroimmune axis. Schizophrenia has been linked to a

chronic low-grade inflammatory state, while arthritis and psoriasis have a higher prevalence

of psychiatric disorders, suggesting a complex interaction between inflammation, genetics,

stress, and environmental factors, with relevant implications for a comprehensive clinical

approach.

Case Report: A female patient who suffered from acute or recurrent psychiatric symptoms,

accompanied by cognitive impairment, hand stiffness, and skin lesions in the auricular and

periauricular regions, with hand radiographs showing marked radiological signs of chronic

arthropathy.

Conclusión: This clinical case underscores the interconnection between chronic psychiatric

illnesses and autoimmune/inflammatory disorders, highlighting the brain-skin-joint axis. The

evolution of long-standing paranoid schizophrenia to psoriasis and psoriatic arthritis suggests

that persistent systemic inflammatory activation and chronic stress act as immunological

triggers. The importance of an interdisciplinary approach (psychiatry, dermatology,

rheumatology) for the comprehensive management of this patient is emphasized.

Keywords: schizophrenia; psoriatic arthritis; comorbidity

Resumen

Introducción: En la actualidad se reconoce una asociación bidireccional entre esquizofrenia

y enfermedades inflamatorias crónicas como la artritis y la psoriasis. Estos trastornos

comparten mecanismos fisiopatológicos comunes, entre ellos la disfunción inmunológica, la

activación proinflamatoria sistémica y alteraciones en el eje neuro inmunológico. La

esquizofrenia se ha vinculado a un estado inflamatorio crónico de bajo grado, mientras que

la artritis y la psoriasis presentan mayor prevalencia de trastornos psiquiátricos, lo que

sugiere una interacción compleja entre inflamación, genética, estrés y factores ambientales,

con implicaciones relevantes para el abordaje clínico integral.

Presentación del caso: Paciente femenina que presentó síntomas psiquiátricos agudos o

recurrentes, acompañados de deterioro cognitivo, rigidez en las manos y lesiones en piel de

regiones auricular y peri auricular, con radiografía de manos donde se evidencia marcados

signos radiológicos de artropatía crónica.

Conclusión: Este caso clínico subraya la interconexión entre enfermedades psiquiátricas

crónicas y trastornos autoinmunes/inflamatorios, destacando el eje cerebro-piel-

articulaciones. La evolución de una esquizofrenia paranoide de larga data hacia psoriasis y

artritis psoriásica sugiere que la activación inflamatoria sistémica persistente y el estrés

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crónico actúan como desencadenantes inmunológicos. Se destaca la importancia del manejo

interdisciplinario (psiquiatría, dermatología, reumatología) para el abordaje integral de la

paciente.

Palabras clave: esquizofrenia; artritis psoriásica; comorbilidad.

Introduction

Psoriasis arthritica (PsA) is a chronic inflammatory disease of immunological origin that

affects both the skin and joints. Its pathophysiology is characterized by the activation of T

cells and the release of proinflammatory cytokines such as interleukin (IL) 17, IL 23, and

tumor necrosis factor alpha (TNF α), which generate a state of persistent systemic

inflammation in affected patients. (1,2) This chronic inflammation is associated with metabolic

and cardiovascular comorbidities, as well as psychiatric manifestations, including depression

and anxiety, at a higher rate than in the general population. (3,4)

Schizophrenia is a complex neuropsychiatric disorder characterized by disturbances in

thought processes, perception, and behavior. Its etiology is multifactorial and not yet fully

elucidated, with emerging evidence linking systemic inflammation to its pathogenesis,

suggesting the involvement of immunological mechanisms similar to those observed in

chronic autoimmune diseases. Recent studies have identified shared pathways of T-cell

activation and production of proinflammatory cytokines (such as TNF-α and IL-6),

demonstrating a possible common biological basis between peripheral inflammatory

processes and neuroimmunological dysfunction associated with psychotic disorders. (5)

Explicit comorbidity between psoriasis and schizophrenia is not widely described in the

literature; however, recent genetic analyses point to possible causal relationships mediated

by chronic inflammation and oxidative stress pathways, as well as alterations in the

hypothalamic-pituitary-adrenal axis that could predispose to the coexistence of these

pathologies. (6) Given the clinical and therapeutic impact that these two conditions can have

together, it is relevant to analyze cases in which these entities coexist, in order to contribute

to a better understanding of their interrelated mechanisms and possible integrated

management approaches.

The mutual influence of coexisting psoriasis arthriticus (PsA) and schizophrenia may occur

primarily through shared systemic inflammatory mechanisms. PsA is a chronic inflammatory

disease mediated by cytokines, with evidence that persistent inflammation contributes to

comorbidities beyond joint and skin involvement, including neuropsychiatric disorders. (7) In

patients with schizophrenia, inflammation and proinflammatory cytokines such as IL-6 and

Interacción entre enfermedad mental grave y patología autoinmune: esquizofrenia y artritis psoriásica,

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TNF-α have also been described as playing a role in the pathophysiology of the disease and

in modulating brain functions related to affect and perception. (8,9) Increased systemic

inflammation from active PsA flares could exacerbate psychotic or emotional symptoms,

while decompensation of schizophrenia (with increased stress and immune dysfunction)

could exacerbate peripheral inflammation, promoting more severe PsA activity.

Furthermore, psychiatric treatments can have immunomodulatory and metabolic effects that

influence the course of PsA. Both typical and atypical antipsychotics have been shown to

alter cytokine production, decreasing some pro-inflammatory mediators such as IFN-γ and

modulating other immune factors, which can lead to changes in the patient's inflammatory

balance. (10) However, prolonged use of second-generation antipsychotics is also associated

with metabolic alterations (such as weight gain and metabolic syndrome), which are related

to chronic pro-inflammatory states that can worsen systemic inflammatory diseases such as

PsA. (11) Therefore, comprehensive management should consider both the control of

psychiatric symptoms and the systemic and metabolic effects of the drugs, in order to

minimize the exacerbation of inflammatory comorbidities and improve the patient's overall

outcome.

This case report was prepared following the 2013 CARE (Case REport) guidelines, (12) which

establish standardized criteria for the presentation of individual clinical reports. These

guidelines provide a structured framework that includes detailed information on patient

history, clinical findings, interventions, clinical course and outcomes, as well as ethical

considerations and informed consent. Using the CARE guidelines ensured that clinical

information was documented completely, clearly, and reproducibly, facilitating transparency

and the case's usefulness for clinical practice and research, while also ensuring compliance

with international quality standards for case report communication.

Case report

A 59-year-old female patient with a history of paranoid schizophrenia (ICD-10 F20.0)

presented with a clinical course that chronologically documented the subsequent onset of

psoriasis and its progression to psoriatic arthritis. The psychiatric condition began in 2002

with hospitalization under a diagnosis of organic mental disorder (F06.8). Laboratory tests

were within normal parameters, and partial improvement was observed upon discharge.

Subsequent re-evaluations culminated in 2008 with the confirmation of paranoid

schizophrenia. Regular follow-up was maintained between 2009 and 2020, during which

episodic crises were treated with antipsychotics. In 2022, she experienced a severe psychotic

decompensation characterized by aggression, disorganized behavior, global insomnia,

affective lability, and suicidal ideation, requiring prolonged hospitalization. Additional

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studies ruled out cardiovascular involvement and epileptiform activity, and cognitive

assessment showed mild impairment attributable to the chronicity of the disorder. Following

stabilization and adequate therapeutic adherence, in 2023 erythematous-dequamative skin

lesions appeared on the dorsal region (fig. 1 A-B-C), lower extremities, and scalp in a guttate

pattern, confirming the dermatological diagnosis of psoriasis, initially guttate and later

reclassified as unspecified. Topical treatment with periodic follow-up was initiated. During

this period, concomitant systemic alterations began to be documented (anemia under

investigation, episodes of leukopenia, and mild liver dysfunction), which were interpreted

collectively as the expression of a chronic inflammatory state. Finally, in 2026, during a new

hospitalization for psychiatric decompensation, the patient presented with marked asthenia

and polyarthralgia.

Physical examination revealed active psoriatic lesions associated with peripheral

inflammatory joint involvement with dactylitis and characteristic digital deformity (fig. 2),

confirming the clinical diagnosis of psoriatic arthritis (CASPAR criteria, table 1) despite

negative immunological studies. Disease-modifying therapy with methotrexate and

interdisciplinary follow-up were initiated. The temporal sequence (long-standing

schizophrenia, subsequent onset of psoriasis, and progression to psoriatic arthritis) supports

the hypothesis of an interaction between severe mental illness, persistent inflammatory

activation, and systemic immune dysfunction, demonstrating the brain-skin-musculoskeletal

axis as an integrating mechanism in this clinical case.

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Fig. 2. Anteroposterior view radiograph of hands showing signs of erosion, osteolysis and pencil-in-cup

deformities in interphalangeal joints, consistent with advanced psoriatic arthritis

Table 1. Results of the application of the CASPAR criteria (13)

Evidence of psoriasis:

(one of a,b,c)

Current psoriasis: Psoriatic skin or scalp disease present today as

judged by a rheumatologist or dermatologist (2 Points)

Psoriatic nail dystrophy

Typical psoriatic nail dystrophy including onycholysis, pitting and

hyperkeratosis observed on current physical examination (0 Points)

A negative rheumatoid factor

By any method except latex but preferably by ELISA or

nephelometry, according to the local laboratory

reference range (1 Point)

Dactylitis (a or b)

0 Points

Radiological evidence of juxta-

articular new bone formation (Fig. 2)

1 Point

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Discussion

Patients with autoimmune diseases, including rheumatoid arthritis (RA), psoriatic arthritis

(PsA), and psoriasis, have a high burden of psychiatric comorbidity, particularly anxiety and

depression, reflecting the complex interplay between chronic inflammation, psychological

stress, and mental health. Recent meta-analyses indicate that the lifetime prevalence of

depressive disorders in patients with RA can reach up to 32.4 %, while anxiety affects 22.2

% of these patients. (14) Specific subtypes such as major depressive disorder (MDD) and

generalized anxiety disorder (GAD) show higher prevalence than other, suggesting the need

to prioritize these diagnoses in clinical evaluation and systematic screening.

In patients with psoriasis, the psychological impact is equally significant. Data from a

Spanish study of 746 patients show that the disease directly affects mood (87.1 %), self-

esteem (74.9 %), and social life (52.1 %), and is associated with anxiety, sadness, stress, and

sleep disturbances in more than 70 % of cases. (15) Furthermore, most patients feel they do

not receive adequate information or resources to manage their emotional distress. These

findings reflect the insufficient integration of mental health into clinical psoriasis care, which

could limit treatment adherence and overall prognosis.

PsA represents a critical intermediate point between psoriasis and RA, as it combines skin

and joint involvement. The presence of chronic stress and inflammatory symptoms activates

the hypothalamic-pituitary-adrenal (HPA) axis, modulating the immune response and

exacerbating systemic inflammation, resulting in greater disease severity and more intense

psychological symptoms. (16) This bidirectional cycle between inflammation and

psychological distress is reinforced by psychosocial factors, such as stigmatization,

functional limitations, and concerns about appearance, which can worsen depression and

anxiety and perpetuate the decline in quality of life.

Psychiatric disorders in autoimmune diseases have also been linked to deeper

neuroimmunological alterations. Evidence from Danish population studies indicates that the

presence of autoimmune diseases and hospitalizations for severe infections significantly

increases the risk of schizophrenia and mood disorders, suggesting a synergistic effect

between immune activation, inflammation, and environmental exposure. (17,18)

The relationship between autoantibodies and neuropsychiatric symptoms, also observed in

long COVID, supports the hypothesis that autoimmunity may directly contribute to

psychiatric manifestations, especially invulnerable subgroups. (19,20) The clinical findings of

this case report reinforce the importance of early detection of psychiatric symptoms in

patients with autoimmune diseases. Anxiety and depression not only affect emotional well-

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being but are also associated with reduced self-care, decreased treatment adherence, and a

poorer disease prognosis. (21,22) In this context, the recognition of autoimmune psychosis,

characterized by isolated psychiatric symptoms and a partial response to conventional

treatments, highlights the need for a multidisciplinary approach that combines

immunomodulation, psychiatric pharmacological therapy, and continuous follow-up, since

early intervention with steroids can prevent recurrences and improve clinical outcomes. (23)

Additionally, sociodemographic and disease-related factors, such as sex, age, educational

level, disease severity, and duration of diagnosis, influence vulnerability to anxiety and

depression. (24) This underscores the need for personalized mental health prevention and

management strategies, including patient education, psychosocial support programs, and a

comprehensive approach to physical and psychological symptoms. Available evidence

suggests that integrating quality of life and mental health assessments into clinical practice

is crucial for improving prognosis and treatment adherence in patients with autoimmune

diseases.

Conclusion

The interconnection between chronic psychiatric illnesses and autoimmune/inflammatory

disorders demonstrates the shared involvement of the brain-skin-joint axis. The evolution of

long-standing psychoses with comorbidities such as psoriasis and psoriatic arthritis suggests

that persistent systemic inflammatory activation and chronic stress act as immunological

triggers.

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Conflicts of interest

The authors declare that there are no conflicts of interest related to the research presented.

Author contributions

Conceptualization: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza; Bruno

Nativi Merchan; Indira Dayana Carvajal Parra

Data curation: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza

Formal analysis: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza; Bruno Nativi

Merchan; Indira Dayana Carvajal Parra

Funding acquisition: José Alejandro Valdevila Figueira

Investigation: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza

Methodology: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza; Bruno Nativi

Merchan; Indira Dayana Carvajal Parra

Project administration: José Alejandro Valdevila Figueira

Resources: José Alejandro Valdevila Figueira

Software: José Alejandro Valdevila Figueira

Supervision: José Alejandro Valdevila Figueira

Validation: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza

Visualization: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza

Writing – original draft: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza; Bruno

Nativi Merchan; Indira Dayana Carvajal Parra

Writing – review & editing: José Alejandro Valdevila Figueira; Horacio Gaibor Mendoza;

Bruno Nativi Merchan; Indira Dayana Carvajal Parra

Funding Source

The research and/or preparation of this article did not receive funding from any sponsor. The

study design; data collection, analysis, and interpretation; report writing, and the decision to

submit the article for publication were not supported by any funding source.

Data Availability Statement

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The anonymized data supporting the findings of this study are available from

the corresponding author upon reasonable request.