With an increasing prevalence during the past decades, atopic dermatitis has become a global health issue. A literature search following a targeted approach was undertaken to perform this non-systematic review, which intends to provide an overview of the epidemiology, pathophysiology, clinical features, comorbidities, and current therapies for the treatment of atopic dermatitis. In sum, this is a heterogeneous skin disorder associated with variable morphology, distribution, and disease course. Although not completely understood, its pathogenesis is complex and seems to result from a combination of genetic and environmental factors that induce skin barrier dysfunction, cutaneous and systemic immune dysregulation, skin microbiota dysbiosis, and a strong genetic influence. Diagnosis is based on specific criteria that consider patient and family history and clinical manifestations. Overall disease severity must be determined by evaluating both objective signs and subjective symptoms. Therapeutic goals require a multistep approach, focusing on reducing pruritus and establishing disease control. Patients should be advised on basic skin care and avoidance of triggers. Topical anti-inflammatory agents should be considered in disease flares or chronic/recurrent lesions. In case of inadequate response, phototherapy, systemic immunosuppressants and, more recently, dupilumab, should be added. Nevertheless, the treatment of moderate-to-severe atopic dermatitis remains challenging and novel, efficacious, safe and targeted treatments are urgently needed. In conclusion, although the last few years have seen important improvement in the understanding of the disease, future research in atopic dermatitis will continue exploring gene-environment interactions and how it affects pathophysiology, disease severity, and treatment outcomes.
Autoimmune diseases (AIDs) are characterized by a multifactorial aetiology and a complex genetic background, with the MHC region playing a major role. We genotyped for HLA-DRB1 locus 1228 patients with AIDs-213 with Systemic Lupus Erythematosus (SLE), 166 with Psoriasis or Psoriatic Arthritis (Ps + PsA), 153 with Rheumatoid Arthritis (RA), 67 with Systemic Sclerosis (SSc), 536 with Multiple Sclerosis (MS), and 93 with Myasthenia Gravis (MG) and 282 unrelated controls. We confirmed previously established associations of HLA-DRB1∗15 (OR = 2.17) and HLA-DRB1∗03 (OR = 1.81) alleles with MS, HLA-DRB1∗03 with SLE (OR = 2.49), HLA-DRB1∗01 (OR = 1.79) and HLA-DRB1∗04 (OR = 2.81) with RA, HLA-DRB1∗07 with Ps + PsA (OR = 1.79), HLA-DRB1∗01 (OR = 2.28) and HLA-DRB1∗08 (OR = 3.01) with SSc, and HLA-DRB1∗03 with MG (OR = 2.98). We further observed a consistent negative association of HLA-DRB1∗13 allele with SLE, Ps + PsA, RA, and SSc (18.3%, 19.3%, 16.3%, and 11.9%, resp., versus 29.8% in controls). HLA-DRB1∗13 frequency in the AIDs group was 20.0% (OR = 0.58). Although different alleles were associated with particular AIDs, the same allele, HLA-DRB1∗13, was underrepresented in all of the six diseases analysed. This observation suggests that this allele may confer protection for AIDs, particularly for systemic and rheumatic disease. The protective effect of HLA-DRB1∗13 could be explained by a more proficient antigen presentation by these molecules, favouring efficient clonal deletion during thymic selection.
Background: Psoriasis is a common, chronic, systemic inflammatory skin disease associated with numerous cardiovascular comorbidities. Much evidence of this association exists in the adult population, data available in childhood psoriasis is more limited. Objectives: To analyze the prevalence of excess adiposity, cardiovascular risk factors, metabolic syndrome and lipid profile in children with psoriasis comparing to control group with similar age and sex distribution. Materials & methods: A case-control study was conducted with children, 5-15 yearsold, with moderate-to-severe plaque-type psoriasis and a control group comprising children with other skin diseases without systemic inflammatory diseases. Results: Psoriatic children had a significantly higher prevalence and greater odds of excess adiposity compared to controls: BMI (≥85 th percentile; OR 4.4; 95%CI 1.2-15.6), waist circumference (>75 th percentile; OR 7.4; 95%CI 2.0-27.7) and waist-to-height ratio (>0.490; OR 4.6; 95%CI 1.3-17.0). A higher prevalence of metabolic syndrome was observed in children with psoriasis compared to controls (25% vs 3.7%; P = 0.07), and two components of the metabolic syndrome were significantly higher in the psoriasis group: waist circumference (75% vs 29.6%; P = 0.002) and the high blood pressure component (30% vs 3.7% P = 0.032). Finally, an altered and more atherogenic lipid profile was observed among psoriatic patients without excess adiposity. Conclusion: This study demonstrates that comorbidities known to be associated with adult psoriasis are also observed in childhood psoriasis, reinforcing the need for screening cardiovascular comorbidities in children with psoriasis and promoting healthy lifestyle choices in these patients. Moreover, it also suggests that its association with psoriasis may be in part genetically determined rather than uniquely acquired.
This study showed that psoriasis was associated with increased EAT volume independently of visceral abdominal fat and with subclinical atherosclerosis. Within psoriasis patients EAT volume was independently associated with CAC. EAT may be another important contributor to the higher cardiovascular risk observed in psoriasis.
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