Psychiatric disorders often coexist with internal medical conditions, posing significant challenges to diagnosis, treatment, and overall patient outcomes. This study examines the bidirectional relationship between these conditions, emphasizing their impact on morbidity, treatment adherence, and quality of life. Through a comprehensive review of the peer-reviewed literature, we explore the physiological, neuroinflammatory, and psychosocial mechanisms that underpin these interactions. Key psychiatric disorders, including depression, anxiety, cognitive impairments, and psychosis, are identified as critical contributors to diagnostic complexity and therapeutic hurdles. Our findings underscore the importance of integrated, multidisciplinary care models, advocating for early detection, routine mental health screening, and personalized treatment strategies. Challenges such as overlapping symptoms, diagnostic ambiguities, and potential drug interactions are critically analyzed, with practical, evidence-based recommendations proposed for clinical practice. Despite advancements, significant research gaps persist, particularly the lack of longitudinal studies and the limited application of precision medicine tailored to this population. Future directions focus on enhancing diagnostic tools, developing innovative therapeutic approaches, and integrating mental health services into routine care. This study highlights the critical need for holistic, patient-centered approaches to manage comorbid psychiatric and internal medical conditions, offering actionable insights to improve outcomes and bridge existing gaps in research and practice.

Obesity represents a complex, multifactorial syndrome that represents a high burden for public health systems worldwide. Serotonin is an important factor in feeding behavior and weight regulation and their interplay implies multiple mechanisms that could explain the correlation with obesity, so understanding these interconnections is essential for developing targeted therapeutic strategies. A systematic review of the literature was conducted using PubMed and Scopus databases, using articles published between 1 January 2015 and 1 December 2024, based on predefined inclusion and exclusion criteria. After the selection process, 22 studies were selected for detailed analysis, focusing on the role of serotonin in obesity. Serotonin significantly influences appetite control and energy homeostasis through multiples pathways, including insulin resistance, high-fat diets, gut microbiota, low-grade inflammation, interferences with tryptophan metabolism, psychiatric modifications, genetic alterations of serotonin receptors, serotonin implications in eating behavior, and neurohormonal regulation of appetite. This review highlights the multidimensional characteristics of the serotonin–obesity association, along with its significance in metabolic and psychiatric pathologies. In order to develop more efficient methods for managing obesity, future studies should concentrate on serotonergic regulation and complex management strategies involving the neurohormonal axis.

Background/objectives: Psoriasis is a chronic inflammatory autoimmune disease with important systemic and psychosocial impacts. The association with metabolic syndrome (MS) impairs disease severity and negatively influences patient-reported outcomes, particularly their quality of life as measured by the Dermatology Life Quality Index (DLQI). This study aims to investigate the relationship between systemic inflammation, DLQI scores and disease severity, focusing on the persistent impact of MS on patient outcomes after one year of treatment. Methods: This retrospective cross-sectional study included 150 psoriasis patients, with 74 also meeting the diagnostic criteria for MS. Clinical and inflammatory markers such as systemic immune–inflammatory index (SII), cytokines (IL-17A, IL-23), leptin, BMI and triglycerides were analyzed alongside PASI and DLQI scores. Results: Patients with MS had significantly higher PASI and DLQI scores compared to those without MS, reflecting worse disease severity and quality of life (p < 0.01). Elevated SII levels were strongly associated with higher DLQI scores (p < 0.01). Despite considerable reductions in PASI scores over one year of treatment, DLQI scores indicated a persistent negative impact of MS on quality of life. Notably, markers of systemic inflammation, such as SII, leptin and cytokines, correlated positively with both PASI and DLQI scores, highlighting the role of systemic inflammation in disease burden. Conclusions: This study underlines the significant role of systemic inflammation and metabolic comorbidities in amplifying the burden of psoriasis. The persistent impact of MS on quality of life despite clinical improvement underscores the need for comprehensive treatment approaches targeting systemic inflammation, metabolic health and psychosocial factors to improve long-term outcomes.

Background/Objectives: Psoriasis is a chronic inflammatory autoimmune disease with important systemic and psychosocial impacts. The association with metabolic syndrome (MS) impairs disease severity and negatively influences patient-reported outcomes, particularly their quality of life as measured by the Dermatology Life Quality Index (DLQI). This study aims to investigate the relationship between systemic inflammation, DLQI scores, and disease severity, focusing on the persistent impact of MS on patient outcomes after one year of treatment. Methods: This retrospective cross-sectional study included 150 psoriasis patients, with 74 also meeting the diagnostic criteria for MS. Clinical and inflammatory markers such as systemic immune-inflammatory index (SII), cytokines (IL-17A, IL-23), leptin, BMI, and triglycerides were analyzed alongside PASI and DLQI scores. Results: Patients with MS had significantly higher PASI and DLQI scores compared to those without MS, reflecting worse disease severity and quality of life (p < 0.001). Elevated SII levels were strongly associated with higher DLQI scores (p < 0.0001). Despite considerable reductions in PASI scores over one year of treatment, DLQI scores indicated a persistent negative impact of MS on quality of life. Notably, markers of systemic inflammation, such as SII, leptin, and cytokines, correlated positively with both PASI and DLQI scores, highlighting the role of systemic inflammation in disease burden. Conclusions: This study underlines the significant role of systemic inflammation and metabolic comorbidities in amplifying the burden of psoriasis. The persistent impact of MS on quality of life despite clinical improvement underscores the need for comprehensive treatment approaches targeting systemic inflammation, metabolic health, and psychosocial factors to improve long-term outcomes.

Background: In the last few decades, it has been emphasized that dopamine, a well-known neurotransmitter with multiple roles in central nervous system, is also implicated in the activity of peripheral tissues and organs, more specifically influencing the gastrointestinal system (GI). Methods: We registered a protocol under the CRD42024547935 identifier in the Prospero register of systematic reviews. Furthermore, using the Population, Intervention, Comparison, Outcome, and Study Design strategy to guide our study rationale, and under the Preferred Reporting Items for Systematic reviews and Meta-Analyses recommendations, we conducted a qualitative systematic literature search based on the PubMed, Scopus, and Web of Science databases using the “gastric cancers AND dopamine” search criteria. We obtained 68 articles from PubMed, 142 articles from Scopus, and 99 articles from the Web of Science database. Results: Within gastric cancer biology, dopamine has notable effects on STAT-3 and DARPP-32. STAT-3, a transcription factor involved in cellular proliferation and invasion, plays a significant role in cancer progression. Conclusions: Understanding the roles of dopamine in cancer, beyond aspects such as cancer cell invasion, immune response modulation, or tumor growth, could guide the development of new cancer therapies by modulating its pathways, especially the DARPP-32/CXCR4/CXCL-12 complex axis, in order to improve the morbidity and mortality caused by this type of cancer.