Background: Adjustment to stress requires the involvement of coping strategies. Using maladaptive coping strategies may precipitate the onset or recurrence of psychiatric disorders. On the other hand, the illness itself may alter the coping mechanisms of an individual. This study aims to identify the coping strategies in patients with bipolar disorder (BD) and major depressive disorder (MDD) and determine the correlation between coping strategies and clusters of psychiatric symptoms. Material and Methods: Socio-demographic and clinical data were analyzed for 30 inpatients with BD and 30 inpatients with MDD. The SCL-90 questionnaire and COPE inventory were filled in by the participants. Results: Compared to the general population, the patients with BD had lower scores for functional coping strategies and higher scores for one dysfunctional coping strategy. The patients with MDD had lower scores for all active functional and two passive functional coping strategies. By contrast, they presented higher scores on one passive functional and one dysfunctional coping strategy. Positive reinterpretation and growth were negatively correlated with somatization, depression, anxiety, interpersonal sensitivity, hostility, and psychoticism. Behavioral disengagement was positively correlated with depression, anxiety, somatization, interpersonal sensitivity, and psychoticism. Substance use was positively correlated with the number of episodes. Distinct coping mechanisms were associated with certain symptom clusters. Conclusions: Although dysfunctional coping strategies may predispose to psychiatric disorders, in our study, they appear to be state-dependent rather than trait-dependent.

Background: Schizophrenia in adolescence disrupts neurodevelopment and long-term functioning. While symptom reduction remains a primary treatment goal, quality of life (QoL) represents a critical, patient-centered outcome. Pharmacogenetic variability, particularly in CYP2D6 metabolism of second-generation antipsychotics, may influence tolerability and subjective well-being beyond symptom control. Materials and Methods: Forty-seven adolescents (aged 14–18 years) diagnosed with schizophrenia (DSM-5) were followed in routine clinical care. CYP2D6 genotyping classified patients as normal metabolizers (NM, n = 27) or reduced-function metabolizers (RFM, including intermediate/poor, n = 20). Symptom severity was assessed with PANSS, QoL was assessed with the Pediatric Quality of Life Enjoyment and Satisfaction Questionnaire (PQ-LES-Q), and adverse effects (hyperprolactinemia, extrapyramidal symptoms, sedation, metabolic changes) were monitored. Non-parametric tests and multiple linear regression were applied. Results: At 12 months, RFM patients showed significantly higher PANSS scores, markedly more adverse reactions (95% vs. 48.1%), and lower PQ-LES-Q total and domain scores (all p < 0.0001) compared to NM patients. A regression analysis identified the metabolizer status (β = −0.410, p = 0.001), extrapyramidal symptoms (β = −0.248, p = 0.003), sedation (β = −0.193, p = 0.029), and hyperprolactinemia (β = −0.190, p = 0.012) as independent predictors of a reduced QoL, explaining 84% of the variance. The residual symptom severity was not independently associated. Conclusions: In adolescent schizophrenia, the CYP2D6-reduced metabolizer status is the strongest independent predictor of long-term QoL impairment, associated primarily through a substantially higher burden of treatment-related adverse effects (metabolic, endocrine, neurological, and sedative) rather than through persistence of psychotic symptoms alone. These findings support early pharmacogenetic testing to guide individualized dosing and improve tolerability and patient-reported outcomes.

Background and Objectives: Schizophrenia in adolescence severely impairs quality of life (QoL) and disrupts critical social, academic, and neurodevelopmental periods. Beyond symptom remission, functional recovery and subjective well-being have become central therapeutic goals; however, the specific contributions of pharmacogenetic, social–cognitive, and residual clinical factors to QoL in early-onset schizophrenia remain largely unexplored. This study investigated the contribution of CYP2D6 metabolizer status, social cognition (theory of mind and empathy), residual psychopathology, and family factors to subjective QoL in adolescents with schizophrenia. Materials and Methods: A cross-sectional study of 52 adolescents with DSM-5 schizophrenia (PAT-SCZ) and 51 matched healthy controls. QoL was measured with the Pediatric Quality of Life Enjoyment and Satisfaction Questionnaire (PQ-LES-Q). Social cognition was assessed using the revised Reading the Mind in the Eyes Test (RMET). Residual symptoms were rated with the Positive and Negative Syndrome Scale (PANSS). CYP2D6 genotyping classified patients as normal metabolizers (NMs) or reduced-function metabolizers (RM: intermediate/poor). Two multivariable OLS regression models examined predictors of QoL. Results: Patients showed markedly lower QoL, impaired theory of mind, lower empathy, and higher residual symptoms than controls (all p < 0.0001). Within patients, reduced-function metabolizer (RM) status was associated with poorer QoL, weaker social cognition, higher negative/general psychopathology, and lower IQ. Two multivariable regression models explained 84.2–84.3% of the variance in QoL (adjusted R²). Social cognition (RMET scores) and CYP2D6 reduced-function metabolizer status emerged as the strongest predictors (β = 0.363 and β = −0.362, respectively, both p < 0.0001), followed by negative symptom severity and dysfunctional family relationships (all p < 0.05). Conclusions: Pharmacogenetic (CYP2D6), social–cognitive, and clinical factors strongly determine QoL in adolescent schizophrenia. Routine CYP2D6 genotyping, social-cognition remediation, and family interventions should be integrated into early treatment to improve long-term well-being.

Background: Socio-cognitive deficits constitute a core and persistent feature of adolescent-onset schizophrenia, significantly impairing functional outcomes. However, the interplay between genetic metabolic markers such as CYP2D6 and specific socio-cognitive phenotypes remains poorly understood. Methods: This cross-sectional study included 73 adolescents with schizophrenia and 58 matched healthy controls. Theory of Mind (ToM) was evaluated using the Reading the Mind in the Eyes Test (RMET), while empathy was assessed with the Cambridge Empathy Quotient. Symptom severity was measured via the Positive and Negative Syndrome Scale (PANSS). CYP2D6 polymorphisms were genotyped using RT-PCR, classifying participants as Normal or Reduced (Intermediate) metabolizers. Hierarchical multiple regression analyses were performed, controlling for sex, IQ, and psychosocial factors. Results: Patients demonstrated significantly lower RMET and empathy scores compared to controls. Reduced CYP2D6 metabolizers exhibited poorer ToM performance and more severe negative symptoms. The final RMET model accounted for 88.8% of variance (p < 0.001), with CYP2D6 status emerging as a significant independent predictor (β = 0.178, p = 0.005), alongside IQ and negative symptoms. In contrast, the empathy model explained 49.0% of variance, with CYP2D6 effects fully mediated by negative symptom severity. Conclusion: Adolescents with reduced CYP2D6 metabolic activity exhibit greater negative symptom burden and impaired social-cognitive functioning. Our findings reveal a double dissociation: ToM functions as a stable, biologically anchored trait, while empathy serves as a state-dependent construct primarily driven by the negative syndrome. These insights advocate for the integration of pharmacogenetic stratification in the treatment of early-onset schizophrenia.