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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV0350

Mast cell activation syndrome and psychiatric symptoms: diagnostic validity, neuroimmune evidence, and nosological implications

MAST CELL ACTIVATION SYNDROME AND PSYCHIATRIC SYMPTOMS: DIAGNOSTIC VALIDITY, NEUROIMMUNE EVIDENCE, AND NOSOLOGICAL IMPLICATIONS

Although the neuroimmune rationale for MCAS is biologically plausible, its current definition lacks the diagnostic precision, discriminant validity, and evidence of treatment response required for recognition as a psychiatric diagnostic entity.

The aim is to assess whether mast cell activation syndrome (MCAS) constitutes a valid psychiatric diagnostic entity, given that its proposed psychiatric association derives more from theory than from clinical evidence. PubMed, Embase, and PsycINFO were searched for the period 2010–2025; proposed MCAS diagnostic criteria, neuroimmune studies of mast cell–brain interactions, and clinical case series were examined in a critical integrative review for conceptual coherence, biological plausibility, and discriminant validity. The Molderings 2013 study yielded an estimated prevalence of approximately 17% in the German population based on a self-report symptom questionnaire, with a rate of 46% among first-degree relatives; however, diagnostic criteria were not applied and mediators were not measured. By contrast, in the Zaghmout and Gülen 2024 study, idiopathic MCAS was confirmed in only 4.4% of 703 consecutive patients referred for suspected mast cell disease when the three consensus criteria were applied. In mastocytosis, an established disease entity, the Moura 2011 and 2012 studies (288 and 57 patients) reported depression in 64% and cognitive impairment in 38.6%, with cognitive impairment found to be independent of depression. In the Jendoubi 2021 study of 139 patients with mastocytosis, memory loss was identified in 52%, difficulty concentrating in 40%, and depression in 49%; none was associated with tryptase levels, KIT status, or disease subtype. Of the two sets of criteria compared, the Valent 2012 consensus requires involvement of at least two organ systems, an event-related rise in tryptase, and a response to treatment, whereas the Afrin 2020 consensus accepts any multisystem pattern, does not require elevated mediator levels, and considers treatment response merely supportive. As the criteria broaden, the disease category expands, but the evidence for a psychiatric phenotype does not. Anxiety, brain fog, fatigue, palpitations, dizziness, and insomnia occur in MCAS, anxiety disorders, postural orthostatic tachycardia syndrome (POTS), and somatic symptom disorder, making these symptoms nondiscriminatory. The authors state that they are not arguing that the symptoms are imaginary or that mast cells have no connection to the brain; their criticism is directed at the construct itself, not at patients, and a subgroup meeting strict criteria with documented tryptase elevation may be identified in the future. In conclusion, the proposed next steps are a placebo-controlled trial of mast cell–stabilizing treatment with preregistered psychiatric outcomes; validation of a mediator panel comprising tryptase, N-methylhistamine, and PGD2 against psychiatric symptom status; and a direct comparison of strict and broad criteria in terms of discriminant validity.

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