Search Results (335)

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by progressive synovial inflammation, joint destruction, and metabolic abnormalities. In recent years, there has been growing interest in intermittent fasting (IF) as a potential dietary strategy for modulating inflammatory and immunometabolic processes in RA. Preliminary data suggest that IF may lead to reduced joint pain, lower inflammatory markers, improved well-being, and weight loss, but the available evidence is scattered and heterogeneous. The aim of this scoping review was to provide a comprehensive overview of the current state of knowledge regarding the effects of IF on inflammatory, immunological, and metabolic processes in patients with RA. Methods: The review was conducted in accordance with the Joanna Briggs Institute methodology and the PRISMA-ScR guidelines. The databases PubMed, Scopus, Web of Science, EBSCO, the Cochrane Library, and Google Scholar were searched (16 March to 12 April 2026) using the Population–Concept–Context model. Full-text observational and experimental studies, as well as reviews, on intermittent fasting in RA were included in the analysis. Results: Of the 137 publications identified, 9 studies were included in the review, covering populations from Iran, Luxembourg, Tunisia, Mexico, China, and Turkey. The results indicate that IF may lead to improvements in disease activity, quality of life, and selected metabolic parameters. Several studies reported a beneficial effect of IF on markers of oxidative stress and selected pro-inflammatory cytokines, although other analyses did not confirm significant changes in inflammatory biomarkers. Preclinical data have demonstrated strong anti-inflammatory and immunoregulatory effects of IF, including a reduction in pro-inflammatory cytokines and an increase in the Treg population. The heterogeneity of IF protocols, population differences, and small sample sizes limit the ability to interpret the results unequivocally. Conclusions: The available evidence suggests that intermittent fasting may represent a promising, nonpharmacological strategy to support the treatment of RA, particularly in terms of improving immunometabolic parameters and subjective disease symptoms. However, due to methodological limitations and the lack of long-term studies, further well-designed randomized clinical trials are needed to evaluate the efficacy and safety of IF in this population. Full article

Chronic pain continues to be a major global health burden and is frequently refractory to conventional pharmacologic and conservative therapies. Spinal cord stimulation (SCS) has emerged as an important neuromodulatory treatment for selected patients with chronic neuropathic and mixed pain syndromes. Since its introduction in the 1960s, SCS has evolved from paresthesia-based tonic stimulation into more adaptive and personalized neuromodulation. This review summarizes the current evidence regarding the mechanisms, clinical applications, technological advances, and future directions of SCS therapy. Mechanistically, SCS modulates nociceptive transmission through dorsal column and dorsal horn pathways, inhibitory neurotransmitter systems, wide-dynamic-range neuronal activity, and supraspinal pain-processing networks. Technological advances have expanded available stimulation paradigms, including burst stimulation, high-frequency stimulation, closed-loop evoked compound action potential-controlled systems, and differential target multiplexed stimulation. These approaches aim to improve analgesic durability, reduce the burden of paresthesia, and address mechanisms such as neuroinflammation and neural habituation. Clinically, SCS is used for conditions including failed back surgery syndrome, complex regional pain syndrome, painful diabetic neuropathy, ischemic limb pain, and emerging non-traditional pain states. However, outcomes remain variable and are influenced by psychological readiness, pain phenotype, anatomic factors, trial response, neurophysiologic markers, and patient engagement. Complications such as lead migration, infection, implantable pulse generator malfunction, and loss of efficacy remain important considerations. Future progress in SCS will likely depend on artificial intelligence, remote monitoring, biomarker-guided programming, and integration with multidisciplinary chronic pain care. Full article

Background: Sickle cell disease (SCD) is a systemic disorder marked by chronic pain and neurocognitive deficits, yet the molecular drivers of these neurocognitive features remain poorly defined. Platelets, central to inflammation and vascular homeostasis, may reflect broad pathophysiologic processes in SCD. Methods: We performed high-resolution mass spectrometry on ultra-purified platelets from 16 adults with SCD and moderate to severe pain (self-reported ≥ 3/10 in the past year), identifying 4196 proteins, of which 1046 were significant (FDR < 0.05). Unsupervised clustering was used to stratify individuals into high- and low-pain phenotypes. Results: Contrary to expectations, canonical pain pathways were not enriched. Instead, significant alterations were observed in neurodegeneration, mitochondrial metabolism, ATP regulation, mitophagy, and tRNA aminoacylation pathways between high- and low-pain phenotypes. High-pain individuals exhibited elevated levels of proteins involved in proteostasis and neurodegenerative disease processes, whereas low-pain individuals showed increased expression of proteins linked to mitochondrial integrity, neuroprotection, and reduced oxidative stress. Protein-protein interaction networks revealed tightly connected clusters within neurodegenerative and central nervous system-related pathways. Disease association analysis ranked neurodegenerative and mitochondrial pathways above traditional hematologic and nociceptive mechanisms. Conclusions: These findings suggest that platelet proteomics may serve as a peripheral window into PNS or CNS vulnerability and cognitive risk in SCD. The enrichment of tRNA aminoacylation and mitochondrial regulation pathways underscores the metabolic complexity of SCD and highlights novel targets for biomarker development and therapeutic intervention. Full article

Endometriosis and irritable bowel syndrome (IBS) are chronic pain disorders that frequently coexist and share key pathophysiological features, including neuroinflammation, visceral hypersensitivity, peripheral sensitization, and central sensitization. Emerging evidence suggests that extracellular adenosine triphosphate (ATP)-mediated activation of the P2X3 receptor is a common mechanism driving persistent nociceptive signaling in both conditions. This narrative review examines the role of ATP–P2X3 signaling in the pathogenesis of endometriosis and IBS, highlighting its involvement in neuroimmune crosstalk, dorsal root ganglion plasticity, and cross-organ sensitization. We summarize experimental and clinical evidence supporting P2X3 as a therapeutic target and discuss the development of selective P2X3 antagonists, including gefapixant, eliapixant, sivopixant, and camlipixant. Although these agents have shown clinical benefit in refractory chronic cough, their application to endometriosis and IBS remains largely unexplored. Current evidence is predominantly preclinical, underscoring the need for biomarker-driven translational studies and clinical trials. Overall, ATP–P2X3 signaling represents a promising shared mechanistic pathway linking endometriosis and IBS and a potential target for the development of precision, nonopioid therapies for chronic pelvic and visceral pain. Full article

The rapid growth of multimodal neuroimaging research has produced fragmented literature that limits systematic characterization of cross-modal relationships and disease-specific knowledge structures. To address this, we constructed a multimodal neuroimaging knowledge graph from 1838 peer-reviewed studies (2016–2026) spanning fMRI, EEG, fNIRS, and PET, using an LLM-based extraction and retrieval-augmented semantic merging pipeline. The resulting graph comprised 4190 nodes and 7007 edges, exhibiting a scale-free topology with a dominant connected component covering 76.6% of nodes. Alzheimer’s disease, the hippocampus, and fMRI/PET emerged as the most central hubs linking disease, anatomical, and methodological dimensions. Louvain community detection identified 25 functional modules, with seven major communities—centered on Alzheimer’s biomarker integration, molecular/fluid imaging, and psychiatric functional connectivity—forming the field’s core structure. Cross-modal analysis revealed the strongest coupling between fMRI and PET, indicating high methodological convergence. At the disease level, Alzheimer’s disease displayed a mature, hierarchically organized biomarker system, whereas major depressive disorder and chronic pain showed diffuse, less consolidated knowledge structures. These results reveal pronounced disparities across neuroimaging research domains and demonstrate that LLM-augmented knowledge graphs can systematically uncover latent structural organization relevant to multimodal integration and biomarker discovery. Full article

Background/Objectives: Chronic orofacial pain disorders are highly heterogeneous and therapeutically challenging. Although current classifications such as the International Classification of Orofacial Pain (ICOP) and the concept of nociplastic pain have improved diagnostic consistency, patients with the same diagnosis may show substantial differences in symptom severity, underlying biology, and treatment response. This suggests that disease classifications may describe clinical phenotypes more effectively than the biological mechanisms sustaining persistent pain. This article proposes the Adaptive Hierarchical Domain Network (AHDN) as a conceptual framework for understanding chronic orofacial pain from a precision medicine perspective. Conceptual Framework: AHDN integrates concepts from systems biology, network neuroscience, predictive processing, biomarker research, and precision medicine. It organizes chronic pain across five hierarchically related but dynamically interacting layers: biological susceptibility, peripheral nociceptive drivers, central adaptive plasticity, behavioral adaptation, and social embedding. The framework is intended to complement, rather than replace, established diagnostic classifications. Implications: The proposed framework suggests that burning mouth syndrome, persistent dentoalveolar pain disorder, persistent idiopathic facial pain, occlusal dysesthesia, and subsets of temporomandibular disorders may represent different mechanistic configurations within a shared adaptive network. AHDN provides a hypothesis-generating structure for mechanistic phenotyping, biomarker development, and individualized management. However, the framework remains conceptual and requires prospective clinical validation, standardized assessment methods, and evaluation of its clinical utility before routine implementation. Full article

Fibromyalgia and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are chronic multisystem disorders characterized by persistent fatigue, pain, cognitive dysfunction, sleep disturbances, and reduced quality of life. Increasing evidence implicates mitochondrial dysfunction, oxidative and nitrosative stress, immune dysregulation, and altered redox and nicotinamide adenine dinucleotide (NAD⁺) metabolism as interconnected mechanisms contributing to fatigue, although the strength of evidence varies across these pathways. Micronutrients are essential components of mitochondrial bioenergetics, antioxidant defense, and immune–metabolic regulation. This narrative review critically examines the mechanistic and clinical evidence supporting mitochondrial-oriented micronutritional interventions in fibromyalgia and ME/CFS, including NAD⁺ precursors, B-complex vitamins, magnesium, coenzyme Q10, alpha-lipoic acid, GlyNAC, L-carnitine, pyrroloquinoline quinone, taurine, and creatine. Mechanistic plausibility is distinguished from clinical efficacy, as disease-specific randomized controlled evidence remains limited for several interventions. We further discuss biomarkers, metabolic phenotyping, and precision nutrition within a systems-based micronutrition framework. Finally, we present the rationale for a future randomized, double-blind, placebo-controlled trial in fibromyalgia patients with clinically significant fatigue, which is planned for 2027, subject to ethics approval and prospective registration, as a strategy for future clinical validation. Full article

Background: Breast implant illness (BII) is a constellation of non-specific systemic and local symptoms—including fatigue, joint pain, cognitive dysfunction, and autoimmune-like manifestations—attributed to silicone breast implants. Although BII remains a controversial clinical entity, accumulating evidence suggests symptom improvement following implant removal; however, causal mechanisms and optimal surgical strategies remain uncertain. Objective: The objective was to evaluate the prevalence of BII symptoms and the effect of explantation with en bloc total capsulectomy on symptom resolution in affected women. Methods: A prospective case series of 50 women who underwent explantation with total capsulectomy between 2023 and 2025 was conducted (Level IV evidence). The BII Questionnaire of the American Society for Aesthetic Plastic Surgery (ASAPS) was administered to assess preoperative and one-year postoperative symptom burden. Perioperative data—including implant characteristics, capsular findings, and imaging results—were analyzed. Symptom changes were assessed using descriptive statistics and nonparametric tests. Results: The mean age at explantation was 43 years, with a mean age at implantation of 31 years. Implants were predominantly placed in the retropectoral plane (80%). Intraoperative rupture was identified in 34 patients (68%). At one-year follow-up, a statistically significant reduction in symptom burden was observed, with an 81.7% decrease in mean symptom frequency (preoperative mean: 10.79 vs. postoperative: 1.97; p < 0.001). The most pronounced improvements were noted in chronic fatigue, cognitive impairment, and delayed wound healing. No surgical complications were recorded, and aesthetic outcomes were satisfactory among patients who underwent single-stage mastopexy. Conclusions: Explantation with en bloc total capsulectomy is associated with substantial symptom improvement in women presenting with BII. Although the precise pathophysiology of BII remains elusive, these findings support a patient-centered approach incorporating thorough preoperative evaluation and shared decision-making. Future research should prioritize the development of standardized diagnostic criteria, biomarker validation, and patient subgroup stratification to optimize clinical management and further advance the understanding of BII. Limitations: The absence of a control group precludes causal inference. Objective clinical and immunological assessments were not performed. Patient-reported symptoms were not corroborated by formal clinical evaluation. Most patients were self-referred, introducing referral and expectation bias. The sample size was small. Full article

Spinal cord stimulation (SCS) is a widely used neuromodulatory therapy for chronic neuropathic pain, yet the cellular and molecular mechanisms underlying its clinical efficacy remain incompletely understood. This review synthesizes current literature on the neurophysiology of pain transmission and the mechanistic basis of major SCS paradigms (tonic, high-frequency, burst, and closed-loop stimulation), highlighting how each modality engages distinct dorsal horn circuits, glial and inflammatory pathways, as well as supraspinal networks involved in the affective dimension of pain. Particular attention is given to the evoked compound action potential (ECAP) as an emerging electrophysiological biomarker that enables real-time, feedback-guided stimulation and offers insight into the biophysical determinants of dorsal column activation. We also examine preclinical and clinical evidence linking SCS to modulation of central sensitization, neuroinflammatory signaling, and autonomic regulation, while identifying persistent gaps in mechanistic understanding. Finally, we discuss future directions, including AI-assisted, personalized SCS programming and expanding indications beyond classical neuropathic pain, underscoring the need for multimodal experimental approaches to more precisely define how SCS achieves analgesia. Full article

Uterine fibroids, the most common tumors in reproductive-age women, remain without a defined precursor tissue state. Unlike cervical dysplasia preceding cervical cancer, or colonic polyps preceding colorectal malignancy, no equivalent “at-risk” tissue marker exists for fibroids, and diagnosis relies on radiological imaging only after tumors are already well-established and often symptomatic including excessive menstrual bleeding, pelvic pain, infertility and obstetric complications. In this narrative review, we propose that a subset of women with unexplained AUB may harbor a chronic, non-infectious inflammatory condition of the myometrium, which we term Chronic Aseptic Myometritis (CAM). We synthesize mechanistic and human tissue evidence suggesting that sterile inflammation driven by damage-associated molecular patterns, NLRP3 inflammasome activation, oxidative DNA damage, and TGF-β–mediated extracellular-matrix remodeling may underlie the transition from normal myometrium (MyoN) to a pre-fibroid, inflamed and stiffened state (MyoF), and may contribute both to abnormal uterine bleeding (AUB) and to fibroid initiation. We propose a preliminary framework for future CAM research, including the identification of candidate biomarker categories and imaging correlates. We also discuss whether early mechanism-based interventions, such as vitamin D and epigallocatechin gallate (EGCG), may offer a potential pathway toward primary prevention. Because the components of this model derive largely from experimental and cross-sectional human studies, CAM is presented as a hypothesis-generating, myometrium-centered framework rather than a validated clinical entity, and prospective validation is required. Full article

Women with endometriosis experience chronic cyclic pelvic pain (CCPP) or chronic persistent pelvic pain (CPPP), both of which may be incapacitating even after treatment. Emotional dysregulation in endometriosis impedes patient recovery. This study evaluated the relationships among emotional state, pain perception, and inflammatory biomarkers (IL-1β, IL-6, and TNF-α) in women with endometriosis presenting with CCPP or CPPP. An exploratory, observational, descriptive, cross-sectional, comparative with repeated sampling study was conducted with 52 women diagnosed with endometriosis and experiencing either CPPP or CCPP. Participants completed a psychometric battery including the State-Trait Anxiety Inventory (STAI), Beck Depression Inventory (BDI-II), Goldberg General Health Questionnaire (GHQ-30), Hospital Anxiety and Depression Scale (HADS), and Mini-Mental State Examination (MMSE). Pain perception was assessed using the Wong–Baker Pain Rating Scale (FACES). Saliva samples were collected at baseline, during stressor and recovery phases, and concentrations of IL-1β, IL-6, and TNF-α were determined by ELISA. Fifty-two women with endometriosis were included (CPPP: n = 33; CCPP: n = 19). No significant between group differences were observed in emotional state (HADS: p = 0.682; BDI: p = 0.842), anxiety (STAI-State: p = 0.086; STAI-Trait: p = 0.615), general distress (GHQ-30: p = 0.730), or pain intensity (FACES: p = 0.705). The prevalence of depressive symptoms did not differ between groups (CPPP: 69.7% vs. CCPP: 73.7%; χ² = 0.093, p = 0.760). Salivary cytokine levels (IL-1β, IL-6, TNF-α) were comparable between groups across all measurement conditions. Spearman correlations revealed uncorrected significance between TNF-α and emotional distress: basal TNF-α correlated inversely with HADS (ρ = −0.292, p = 0.031) and BDI (ρ = −0.278, p = 0.041); TNF-α under stress correlated with HADS (ρ = −0.329, p = 0.014) and GHQ-30 (ρ = −0.271, p = 0.046); and TNF-α during recovery correlated with GHQ-30 (ρ = −0.363, p = 0.006). These findings indicate that CPPP and CCPP were not associated with statistically significant differences in emotional states or salivary cytokine profiles at the group level. Exploratory pos hoc analyses suggested that pain pattern may moderate the association between TNF-α and psychological burden, particularly in the CCPP subgroup; however, these findings require confirmation in larger studies with prespecified analyses. Exploratory analyses suggested patterns between salivary inflammation and psychological burden; however, these findings should be interpreted cautiously because of the small subgroup size, multiple comparisons, and lack of a matched healthy control group. Full article

Background/Objectives: Gabapentin is a first-line treatment for neuropathic pain, classically understood to reduce neuronal excitability through binding to the alpha-2-delta-1 (α2δ-1) subunit of voltage-gated calcium channels. However, this neuron-centric model does not fully explain its variable clinical efficacy across pain syndromes. In parallel, chronic pain is increasingly conceptualized as involving neuron–glia–immune interactions, in which microglial activation, astrocytic signaling, and inflammatory mediators may contribute to central sensitization. Methods: A structured narrative review was conducted using PubMed, Web of Science, and Google Scholar for articles available through December 2025. The search focused on gabapentin/gabapentinoids, chronic and neuropathic pain, α2δ-1 mechanisms, neuron–glia interactions, neuroinflammation, central and peripheral sensitization, nociplastic pain, cytokine/chemokine signaling, and neuroimmune modulation. Basic science studies, animal models, translational studies, clinical trials, reviews, meta-analyses, and guidelines were narratively synthesized. Results: Preclinical evidence indicates that gabapentin reduces neuronal hyperexcitability and may secondarily attenuate neuron-to-glia signaling, glial activation, and cytokine- and chemokine-related pathways. However, these neuroimmune effects remain predominantly preclinical, model-dependent, and incompletely validated in humans. Clinical evidence supports gabapentin for selected neuropathic pain conditions, but human studies rarely evaluate glial activation, cytokine signaling, or neuroimmune biomarkers. Conclusions: Gabapentin remains best understood as a neuronal α2δ-1 modulator. Although preclinical and translational evidence suggests biologically plausible secondary effects on neuroimmune signaling, these mechanisms have not been validated as biomarkers or prescribing targets in humans. The conceptual framework presented in this review supports mechanism-informed clinical reasoning and individualized pain management but should not be interpreted as a biomarker-guided prescribing algorithm. Clinically, gabapentin should be prescribed selectively for patients with neuropathic or sensitized pain features, using predefined functional goals, appropriate renal dose adjustment, careful safety monitoring, and discontinuation when meaningful benefit is not achieved. Full article

Background/Objectives: Male chronic pelvic pain syndrome (CPPS) is a heterogeneous condition involving overlapping urinary, psychosocial, organ-specific, infectious, neurological, myofascial, and sexual phenotypes. This complexity limits the effectiveness of routine symptom assessment and empirical treatment strategies. Artificial intelligence (AI) may support more reproducible interpretation, differential diagnosis, phenotyping, and personalized management. This up-to-date narrative mapping review aimed to identify AI-assisted approaches that are directly or indirectly relevant to the assessment of males with CPPS, classify them according to UPOINTS phenotypic domains and clinical functions, and critically discuss the extent to which current evidence is disease-specific or extrapolated from related conditions. Methods: A literature search was performed in PubMed/MEDLINE, the Cochrane Library, and Google Scholar from database inception to May 2026 using terms related to male CPPS, UPOINTS domains, diagnosis, treatment, prognosis, digital solutions, artificial intelligence, machine learning, deep learning, natural language processing, computer vision, and decision support. Studies were included if they described AI-based or AI-adjacent computational approaches relevant to male CPPS or to related conditions important for UPOINTS-based phenotyping, differential diagnosis, or phenotype-specific assessment. Results: Available evidence remains fragmented and is largely extrapolated from related urological, chronic pain, pelvic floor, infectious, neurological, and sexual medicine conditions. AI applications were most developed in urinary and organ-specific domains, including uroflowmetry analysis, bladder volume assessment, cystoscopy, prostate imaging, urinary biomarkers, and differential diagnosis of lower urinary tract disorders. AI tools also showed potential for infection detection, psychosocial screening, chronic pain monitoring, neuroimaging-based phenotyping, pelvic floor dysfunction assessment, and evaluation of sexual dysfunction. However, male-CPPS-specific validation remains limited. Conclusions: AI has promising potential to improve differential diagnosis, multidomain phenotyping, and individualized management in males with CPPS. Current evidence is mainly translational and hypothesis-generating. Future studies should focus on prospective male-CPPS-specific cohorts, external validation, explainable multimodal models, and integration of AI tools into clinically meaningful, patient-centered workflows. Full article

Background/Objectives: Adenomyosis is a chronic gynecological disorder characterized by the presence of endometrial tissue within the myometrium, causing pelvic pain, abnormal uterine bleeding, and infertility. Despite its high prevalence, the molecular mechanisms underlying disease initiation and progression remain incompletely understood. Current evidence implicates disruption of the endometrial–myometrial interface, epithelial–mesenchymal transition, and progesterone resistance in driving tissue invasion and remodeling. Diagnosis relies mainly on imaging modalities, while reliable non-invasive biomarkers are lacking. MicroRNAs, as stable post-transcriptional regulators of gene expression, have emerged as key modulators of proliferation, inflammation, and hormonal signaling, and represent promising candidates for novel diagnostic strategies. Methods: A systematic review was conducted in accordance with PRISMA guidelines and registered with PROSPERO (CRD42025637752). A comprehensive search of the Medline, Embase, Scopus, and Cochrane databases was performed in April 2025. Studies investigating miRNA expression in patients with adenomyosis compared with controls were included. The quality of the studies and the risk of bias were assessed using the Newcastle–Ottawa scale. Two reviewers independently performed study selection, data extraction, and quality assessment. Results: Twenty-seven studies published between 2015 and 2025 met the inclusion criteria. Thirty-nine distinct miRNAs were reported as significantly dysregulated in adenomyosis. Recurrently altered miRNAs included let-7a, miR-145, miR-10b, miR-30c-5p, miR-141-3p, miR-143, and miR-191. Functional analyses have consistently implicated miRNAs in key pathogenic pathways, including Hippo-YAP, PI3K/AKT, MAPK/ERK, JAK/STAT, and Wnt/β-catenin signaling. These alterations were associated with enhanced epithelial–mesenchymal transition, increased cellular proliferation and migration, progesterone resistance, chronic inflammation, and immune modulation. Emerging evidence highlights exosomal and circulating miRNAs as promising non-invasive biomarkers, with a few studies already demonstrating diagnostic potential using serum, plasma, or urine samples. However, substantial heterogeneity in tissue types, sampling timing, and analytical methods precluded meta-analysis. Conclusions: MiRNAs play a central role in the molecular pathogenesis of adenomyosis and show strong potential as non-invasive diagnostic biomarkers. However, large-scale validation studies and standardized methodologies are required before clinical implementation. Full article

Generalized pustular psoriasis (GPP) is a rare, potentially life-threatening, chronic cutaneous inflammatory disease characterized by unpredictable, recurrent acute flares of painful sterile pustules on a widespread erythematous background. In addition to cutaneous manifestations, patients may experience fever, pruritus, pain, chills, and general malaise, which may be further complicated by secondary infection, sepsis, and organ failure, thus requiring urgent medical treatment and, in some cases, hospitalization. Prompt therapeutic management of the acute phase is crucial for severe cases, and proactive treatment to prevent flares should always be considered. However, early recognition of acute flares can be challenging due to the low frequency of the disease, the rapid onset of flares, the lack of hematological biomarkers and the absence of standardized diagnostic criteria. Moreover, despite the approval of new targeted therapies, there are still several unmet needs, as these treatments are highly expensive, not always readily available, and may have limited efficacy in patients with advanced or complicated disease. For these reasons, multidisciplinary round-table discussions and shared diagnostic and therapeutic algorithms involving dermatologists, who are responsible for diagnosing and treating GPP, and other medical specialists are desirable to facilitate prompt referral to dermatologists for accurate diagnosis and appropriate treatment. We report the updated literature discussed during a multidisciplinary meeting with the aim of providing practice recommendations for clinicians involved in GPP management. Full article