Juan David Leal Serrano

Neuroimmune interactions have emerged as a central framework for understanding the complexity of gastrointestinal diseases, integrating immune regulation, neural signaling, and microbiota-driven mechanisms within the gut–brain axis. This review synthesizes current evidence on the role of neuroimmune pathways in both inflammatory and functional gastrointestinal disorders, with particular emphasis on inflammatory bowel disease and irritable bowel syndrome. The analyzed literature demonstrates that gastrointestinal symptom generation and disease expression result from dynamic interactions among immune cells, enteric and autonomic neural circuits, microbial signaling, and stress-related modulation rather than from isolated pathological processes. In inflammatory conditions, immune dysregulation and macrophage-mediated pathways predominate, while neural and autonomic mechanisms contribute to symptom persistence and variability. In functional disorders, immune–neural coupling, mast cell–nerve interactions, and visceral sensory sensitization emerge as key drivers of pain and altered bowel habits despite minimal structural abnormalities. Across both disease categories, the intestinal microbiota acts as a cross-cutting regulator influencing immune tone, barrier integrity, and neural responsiveness. From a clinical and diagnostic perspective, these findings support a mechanism-based approach that complements traditional inflammatory and structural assessments with neuroimmune-informed reasoning. This integrative framework has particular relevance for medical education and clinical practice in diverse healthcare settings, including Latin America, where resource variability necessitates strong pathophysiological interpretation. Overall, neuroimmune models provide a coherent and biologically grounded perspective for advancing diagnosis, teaching, and future translational strategies in gastroenterology.

Chronic inflammatory skin disorders have traditionally been regarded as localized dermatologic entities; however, increasing evidence from cutaneous immunology supports their interpretation as visible manifestations of underlying immune dysregulation. Across a broad spectrum of inflammatory, autoimmune, and autoinflammatory dermatoses, reproducible immune pathways have been shown to drive stable clinical phenotypes, positioning the skin as a sentinel organ of systemic immune imbalance. This review synthesizes current immunopathological evidence linking major chronic inflammatory skin disorders with dominant immune-dysregulation domains, including polarized cytokine-driven inflammation, cytotoxic T-cell–mediated autoimmunity, innate immune hyperreactivity, autoantibody-mediated tissue injury, and immune-driven fibrosis. By comparatively analyzing mechanistic, clinical, and therapeutic literature, the review identifies shared and disease-specific immune signatures that explain phenotypic diversity while supporting a unified conceptual framework. The findings highlight that conditions such as psoriasis, atopic dermatitis, vitiligo, alopecia areata, hidradenitis suppurativa, chronic urticaria, autoimmune bullous diseases, cutaneous lupus erythematosus, rosacea, and systemic sclerosis can be systematically interpreted through their immunological architecture rather than solely by morphology. Framing chronic inflammatory dermatoses as markers of immune dysregulation enhances diagnostic reasoning, strengthens medical education, and reinforces the clinical relevance of dermatologic findings in recognizing broader immune-mediated disease, particularly in diverse international healthcare settings.

The skin frequently reflects internal pathological processes, making cutaneous manifestations valuable indicators of systemic disease. This narrative integrative review analyzes current scientific evidence on dermatologic findings that function as early or concurrent markers of underlying systemic disorders. The study synthesizes peer-reviewed literature addressing renal–metabolic, inflammatory–immune, malignancy-related, and vascular–calcific conditions, emphasizing recognizable cutaneous patterns and their clinical context. Results demonstrate that paraneoplastic dermatoses are commonly described as early indicators that may precede the diagnosis of internal malignancy, whereas renal–metabolic and vascular–calcific manifestations are more frequently reported as concurrent expressions of established systemic disease. Inflammatory and immune-mediated dermatoses exhibit variable timing, reflecting heterogeneous triggers and systemic associations. Across categories, cutaneous findings consistently mirror immune dysregulation, metabolic imbalance, vascular injury, or neoplastic activity. This review highlights the diagnostic and educational relevance of dermatologic examination in general medical practice, particularly in settings where access to advanced diagnostic resources may be limited. Integrating systematic skin assessment into routine clinical evaluation can strengthen diagnostic reasoning, support earlier recognition of systemic illness, and promote a more holistic approach to patient care.