Psoriasis is a chronic recurrent inflammatory autoimmune pathology with a significant genetic component and several interferences of immunological cells and their cytokines. The complex orchestration of psoriasis pathogenesis is related to the synergic effect of immune cells, polygenic alterations, autoantigens, and several other external factors. The major act of the IL-23/IL-17 axis, strongly influencing the inflammatory pattern established during the disease activity, is visible as a continuous perpetuation of the pro-inflammatory response and keratinocyte activation and proliferation, leading to the development of psoriatic lesions. Genome-wide association studies (GWASs) offer a better view of psoriasis pathogenic pathways, with approximately one-third of psoriasis’s genetic impact on psoriasis development associated with the MHC region, with genetic loci located on chromosome 6. The most eloquent genetic factor of psoriasis, PSORS1, was identified in the MHC I site. Among the several factors involved in its complex etiology, dysbiosis, due to genetic or external stimulus, induces a burst of pro-inflammatory consequences; both the cutaneous and gut microbiome get involved in the psoriasis pathogenic process. Cutting-edge research studies and comprehensive insights into psoriasis pathogenesis, fostering novel genetic, epigenetic, and immunological factors, have generated a spectacular improvement over the past decades, securing the path toward a specific and targeted immunotherapeutic approach and delayed progression to inflammatory arthritis. This review aimed to offer insight into various domains that underline the pathogenesis of psoriasis and how they influence disease development and evolution. The pathogenesis mechanism of psoriasis is multifaceted and involves an interplay of cellular and humoral immunity, which affects susceptible microbiota and the genetic background. An in-depth understanding of the role of pathogenic factors forms the basis for developing novel and individualized therapeutic targets that can improve disease management.

Dupilumab is the only available biological treatment for moderate-to-severe atopic dermatitis (AD). Even so, limited clinical data regarding its safety profile are available. Interactions with other drugs and the adverse effects of Dupilumab on patients with multiple comorbidities, such as chronic heart disease, diabetes, chronic kidney disease, etc., are not known yet. Moreover, there have been described cases of cutaneous lymphomas induced by Dupilumab. Therefore, the clinician that wants to start treatment for moderate-to-severe atopic dermatitis, which does not respond to conventional drugs, might be reluctant to choose biologic agents such as Dupilumab. In this paper, we reported a case of severe atopic dermatitis with multiple comorbidities in which the patient was successfully treated with Dupilumab despite numerous underlying conditions. We also conducted a review of the current literature on the safety profile of Dupilumab in special categories of patients with comorbidities, such as heart, kidney, and liver disease, oncologic conditions, and during pregnancy.

Malignant melanoma rarely develops in mucous membranes. Statistical data show that approximately 0.6–9.3% of patients with cutaneous malignant melanoma will develop metastases in the upper aerodigestive tract mucosa, and within these metastatic sites, the least common are the laryngeal and tracheobronchial ones. This exceedingly rare clinical entity has no clear treatment recommendations; radical surgery does not seem to benefit the patient in term of life expectancy. We present the case of a 56-year-old male patient diagnosed with laryngeal and tracheobronchial melanoma metastases. Prior to admission to our clinic the patient had a personal history of malignant melanoma of the nuchal region operated on 7 years ago, malignant melanoma of the gallbladder and metastatic left axillary polyadenopathy for which he underwent surgical treatment 3 months prior. Histopathological and immunohistochemical reports established the diagnosis of laryngeal metastasis of malignant melanoma. Genetic molecular analysis was positive for B-Raf (BRAF) gene and hence Vemurafenib was administered, with a favorable outcome at the one-year follow-up. Nevertheless, there are currently no clear universally accepted guidelines for the treatment of laryngeal melanoma, mainly due to the rarity of this clinical entity. We conducted a review of similar cases reported in the literature. Interestingly, reviewing the cases reported in the literature, it appears that laryngeal metastases of a primary cutaneous melanoma are more common in men, with an average time to metastasis of 4.3 years.

The present study is aimed at assessing the presence and prevalence of subclinical entheseal changes in Psoriasis (PsO) patients using musculoskeletal ultrasonography (US), conjoined with the analysis of possible differences in terms of demographic, clinical, or biological features. We carried out an observational study on 54 patients with PsO and 40 controls. Subclinical enthesopathy, according to OMERACT definitions, was identified in 20 of the psoriasis patients (37.03%), a significantly difference compared to the controls (5 patients; 10.20%). A comparison between US examinations for psoriasis patients and controls indicates that all the examined areas manifested changes in a significantly higher percentage of patients than the controls. The most common structural changes were represented by thickened tendon (85%), calcification (65%), erosions (35%), power Doppler (PD) signal (20%), and bursitis (5%). The difference in mean MASEI (Madrid Sonographic Enthesitis Index) score between the psoriasis and control groups was statistically significant (10.56 + 2.96 vs. 2.9 + 2.20; p < 0.0001). In conclusion, ultrasound is an easily accessible and vital follow-up method for psoriasis patients to enable an early, subclinical detection of entheseal involvement, i.e., the first red-flag sign for a future transition to psoriatic arthritis (PsA).

Sweet syndrome (SS) is a rare neutrophilic dermatosis often associated with hematologic malignancies, particularly myelodysplastic syndromes (MDSs). We report a case of SS-like dermatosis in a patient with MDS who subsequently developed peripheral T-cell non-Hodgkin lymphoma (NHL). We review the literature on Sweet syndrome to contextualize this atypical presentation Methods: We present a case report of a 77-year-old male with leukopenia and known MDS, admitted for a persistent, infiltrated erythematous eruption. The patient underwent repeated dermatologic assessments, and serial skin and bone marrow biopsies with histopathologic and immunohistochemical analysis. A literature review was also conducted, focusing on SS in association with hematologic malignancies, including T-cell NHL. Results: Initial skin biopsies were inconclusive, and SS was diagnosed clinically based on lesion morphology and a prompt response to corticosteroids, despite the absence of definitive neutrophilic infiltrates. During follow-up, the patient’s condition progressed with worsening cytopenias and recurrent febrile episodes. Repeat biopsies eventually confirmed the diagnosis of peripheral T-cell NHL with secondary hemophagocytic lymphohistiocytosis (HLH). Conclusions: This case illustrates the diagnostic uncertainty of SS-like eruptions in hematologic patients when histopathological findings are atypical or absent. Corticosteroid responsiveness may guide early diagnosis.

Background/Objective: Psoriasis is a systemic inflammatory disease often associated with metabolic comorbidities, including hyperuricemia. While biological therapies effectively target inflammatory pathways, their specific impact on serum uric acid (SUA) levels remains debated. This study aimed to evaluate whether biological therapy, while reducing systemic inflammation, influences SUA levels in patients with moderate-to-severe plaque psoriasis. Methods: A prospective longitudinal cohort study was conducted involving 30 patients with moderate-to-severe plaque psoriasis. Patients received biological treatment (adalimumab, secukinumab or ustekinumab) and tsDMARDS (apremilast). Clinical severity was assessed using the Psoriasis Area and Severity Index (PASI). C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), SUA levels and other laboratory markers were measured at baseline and after 48 weeks of therapy. Results: Biological therapy led to a significant reduction in PASI scores (from 21.6 ± 10.7 at baseline to 0.4 ± 0.86 after 48 weeks of therapy, p < 0.001), and CRP decreased from a median of 5.75 mg/L at baseline to 3.55 mg/L, p < 0.001. ESR also declined from 26.2 ± 11.4 mm/h to 19.0 ± 8.06 mm/h, p < 0.001. However, no statistically significant change was observed in mean SUA levels 5.49 ± 1.55 vs. 5.55 ± 1.60 mg/dL; p = 0.758. Subgroup analysis revealed that SUA levels remained stable regardless of the specific biological agent used or the degree of clinical improvement. Conclusions: Our findings suggest that while biological therapy is highly effective in controlling skin and systemic inflammation in psoriasis, it does not modify SUA levels. These results imply that hyperuricemia in psoriasis may be driven by metabolic factors independent of the primary inflammatory pathways targeted by current biologics.