Guselkumab is a human monoclonal antibody directed against the p19 subunit of interleukin-23. This structured narrative review evaluates its pharmacologic rationale, efficacy, safety, durability, and therapeutic role in plaque psoriasis, psoriatic arthritis, Crohn’s disease, and ulcerative colitis. PubMed/MEDLINE and Europe PMC were searched from inception through 18 September 2026 using broad and disease-specific strategies; ClinicalTrials.gov was searched to link trial families and identify ongoing studies. Records were screened for directness, design, distinct contribution, and clinical relevance. The final synthesis included 64 PubMed-indexed articles and the current US prescribing information. In plaque psoriasis, guselkumab produces high and durable skin clearance rates and has demonstrated superiority over active comparators at prespecified time points. In psoriatic arthritis, it improves peripheral arthritis, skin disease, enthesitis, dactylitis, function, and patient-reported outcomes; long-term trials show low observed radiographic progression, whereas evidence for axial disease remains less definitive. In Crohn’s disease and ulcerative colitis, phase 3 programs demonstrate clinical and endoscopic efficacy with intravenous or fully subcutaneous induction and subcutaneous maintenance. Long-term trial data support a stable safety profile, although infection screening, tuberculosis assessment, vaccination review, and indication-specific liver monitoring remain important. Guselkumab may be clinically relevant when skin, joint, and bowel inflammation coexist, but treatment should remain domain based because efficacy cannot be assumed to be equivalent across manifestations. Direct within-class comparisons, validated response biomarkers, and dedicated axial and disease-modification studies remain priorities.
Background/Objectives: This retrospective study determined whether high-dose intravenous (IV) corticosteroid administered during biologic therapy for systemic sclerosis (SSc) was associated with scleroderma renal crisis (SRC). Methods: The outcomes in SSc patients who received high-dose IV methylprednisolone were compared to non-corticosteroid SSc controls. Blood pressure (BP), serum creatinine and glucose, urine protein, and episodes of SRC were determined at baseline, 4 h, 2 weeks, and 24 weeks after IV corticosteroid. Results: The SSc corticosteroid infusion (37 subjects) and non-corticosteroid (120 subjects) cohorts were similar in age, race, disease duration, antinuclear and topoisomerase-1 antibody positivity, interstitial lung disease, and pulmonary artery hypertension (all p > 0.05). However, the corticosteroid group was characterized by a higher proportion of men (18.9 vs. 6.7%, p = 0.04), diffuse cutaneous SSc (75.7 vs. 45.9%, p < 0.001), and anti-RNA polymerase III positivity (21.6 vs. 10%, p = 0.04). No patients in the control group developed SRC. In the corticosteroid group, after a total of 827 infusions (21 ± 23 infusions/subject) with 135 mg ± 66 mg methylprednisolone/infusion and a cumulative dose of 2983 mg ± 5198 mg methylprednisolone, none developed SRC. All-cause mortality (37.8 vs. 19.2%, HR 2.23, 95% CI 1.14–4.37, p = 0.02) during the mean 11.6 ± 6.2-year disease duration was increased in the corticosteroid group; however, 5-year (92% vs. 91%, p > 0.05) survival rates were similar. In the high-risk anti-RNA polymerase III antibody subgroup, there were no episodes of SRC or significant changes in blood pressure or renal function at 4 h, 2 weeks, and 24 weeks after corticosteroid. Conclusions: These data suggest that intermittent high-dose IV corticosteroid premedication for biologic infusions may have a lower risk for SRC.
Background and Aims: Proper sagittal alignment and postural control are important for functional independence. This exploratory cross-sectional study evaluated the sagittal vertical axis (SVA), as measured by spinal radiography, in individuals with axial spondyloarthritis (iwaxSpA), and examined its associations with postural sway parameters, derived from plantar pressure via baropodometry, as well as with handgrip strength (HGS). Methods: Twenty-one iwaxSpA and 20 controls underwent whole-spine lateral radiography for SVA measurement, baropodometric assessment, and HGS testing. Results: An SVA ≥ 50 mm was observed in 9/21 (42.8%) iwaxSpA and 4/20 (20.0%) controls. Median SVA was higher in iwaxSpA than in controls (31 [16–53] vs. 26.5 [9.50–36.7] mm), but the between-group comparison was not statistically significant after correction for multiple testing (adjusted p = 0.802). No baropodometric parameter or mean HGS differed significantly between groups after multiplicity correction. Within the iwaxSpA group, SVA showed nominal positive correlations with age (ρ = 0.511, unadjusted p = 0.017) and maximal mediolateral displacement (ρ = 0.452, unadjusted p = 0.039), but neither association remained statistically significant after Benjamini–Hochberg adjustment (adjusted p = 0.356 and p = 0.395, respectively). Conclusions: In iwaxSpA, there are numerical trends toward poorer postural assessment and balance control, as measured via spinal radiography and baropodometry, though no significant differences remain after adjusting for multiple comparisons. No significant associations were found between spinal alignment (as assessed by spinal radiography), baropodometric parameters, and HGS. Due to the exploratory nature of the study and its limited statistical power, larger controlled multicenter trials are needed to better define the roles of spinal radiography and baropodometry in this population.
The clinical and pathogenetic intersection of Familial Mediterranean Fever (FMF) and axial spondyloarthritis (axSpA) represents a compelling frontier in modern rheumatology, challenging the traditional binary classification of inflammatory diseases. FMF is a monogenic autoinflammatory disorder caused by mutations in the MEFV gene, characterized by dysregulation of the pyrin inflammasome and surges in interleukin-1β (IL-1β), while axSpA is an immune-mediated condition linked to the HLA-B27 antigen and the IL-23/IL-17 axis. Following a structured search of PubMed/MEDLINE and Scopus, this review integrates PRISMA-informed screening of epidemiological data with a comprehensive narrative synthesis of the molecular pathogenesis and clinical management of this association. The analysis demonstrates a substantially elevated prevalence of spondyloarthritis among FMF patients compared to the general population. It explores the molecular “bridge” where innate immune activation provides the requisite cytokine milieu for the expansion of Th17 cells that drive spinal inflammation. Clinical evidence defines a distinct FMF-associated spondyloarthritis phenotype, characterized by a balanced sex distribution, early onset, and high risk of destructive hip involvement and AA amyloidosis, particularly in M694V carriers. Management strategies focus on dual biologic blockade in refractory cases, targeting both the upstream IL-1 pathway and downstream TNF or IL-17 effectors. This report identifies critical knowledge gaps, emphasizing the need for large-scale clinical trials to optimize outcomes for this complex patient population.
Background/Objectives: Psoriatic disease (PsD) is a chronic, systemic inflammatory disorder characterized by a wide spectrum of clinical manifestations extending beyond skin and joint involvement. Increasing evidence suggests a relevant role of the gut microbiota in the pathogenesis of psoriatic arthritis (PsA), although a clear causal relationship remains to be fully established. The aim of this review is to summarize current evidence on the role of the gut microbiome in PsD, with a focus on immune modulation, disease pathogenesis and potential therapeutic implications. Methods: A narrative review of the literature was conducted, focusing on studies investigating gut microbiota composition, dysbiosis patterns, and microbiome-related mechanisms in PsD and PsA, as well as emerging microbiota-targeted interventions. Results: Recent advances in high-throughput sequencing technologies have identified distinct microbial signatures associated with PsA onset and progression. Dysbiosis appears to influence immune system regulation, contributing to systemic inflammation through mechanisms involving intestinal barrier dysfunction and immune activation. Patients with PsA exhibit specific alterations in gut microbial composition compared to healthy controls. Emerging therapeutic strategies targeting the microbiota—including dietary interventions, probiotics, and fecal microbiota transplantation—show potential as adjunctive approaches in disease management, although clinical evidence remains limited. Conclusions: The gut microbiome represents a promising area of research in PsD, offering novel insights into disease mechanisms and potential therapeutic targets. Further studies are needed to clarify causal relationships and to define the clinical applicability of microbiota-based interventions.
