Atopic dermatitis is a multifactorial, chronic relapsing, inflammatory disease, characterized by xerosis, eczematous lesions, and pruritus. The latter usually leads to an “itch-scratch” cycle that may compromise the epidermal barrier. Skin barrier abnormalities in atopic dermatitis may result from mutations in the gene encoding for filaggrin, which plays an important role in the formation of cornified cytosol. Barrier abnormalities render the skin more permeable to irritants, allergens, and microorganisms. Treatment of atopic dermatitis must be directed to control the itching, suppress the inflammation, and restore the skin barrier. Emollients, both creams and ointments, improve the barrier function of stratum corneum by providing it with water and lipids. Studies on atopic dermatitis and barrier repair treatment show that adequate lipid replacement therapy reduces the inflammation and restores epidermal function. Efforts directed to develop immunomodulators that interfere with cytokine-induced skin barrier dysfunction, provide a promising strategy for treatment of atopic dermatitis. Moreover, an impressive proliferation of more than 80 clinical studies focusing on topical treatments in atopic dermatitis led to growing expectations for better therapies.

The SARS-CoV-2 viral pandemic has had an immeasurable global impact, resulting in over 5 million deaths worldwide. Numerous vaccines were developed in an attempt to quell viral dissemination and reduce symptom severity among those infected. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of antinuclear autoantibodies (ANAs) with heterogenic clinical manifestations, secondary to immune complex deposition in a multitude of organ systems. There are scarcely reported cases of SLE development following COVID-19 mRNA vaccination. We present a case of a 24-year-old male without preexisting conditions or family history of autoimmune disorders, presenting with SLE following the first dose of the SARS-CoV-2 Pfizer-BioNTech mRNA vaccine.

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Background The association between acne keloidalis nuchae (AKN) and thyroid diseases is yet to be investigated. Objective To evaluate the risk of developing hypothyroidism and hyperthyroidism among patients with AKN and to characterize the patients who have AKN and thyroid comorbidities. Methods A population‐based cohort study was conducted comparing AKN patients (n = 2,677) with age‐, gender‐, and ethnicity‐matched control subjects (n = 13,190) with regard to incident cases of hypothyroidism and hyperthyroidism. Adjusted hazard ratios (HRs) were estimated by Cox regression analysis. Results The incidence rates of hypothyroidism among patients with AKN and controls were estimated at 2.15 (95% CI, 1.49‐2.99) and 0.82 (95% CI, 0.66‐1.00) cases/1000 person‐years, respectively. The crude risk of developing incident hypothyroidism was 1.85‐fold greater in patients with AKN (HR, 1.85; 95% CI, 1.24‐2.78; P = 0.003). The elevated risk persisted following the adjustment for putative confounders (adjusted HR, 1.72; 95% CI, 1.03‐2.89; P = 0.040). The risk of hyperthyroidism was comparable in patients with AKN and controls both in the crude (HR, 1.55; 95% CI, 0.57‐4.22) and adjusted (adjusted HR, 1.92; 95% CI, 0.59‐6.21) analyses. Patients with coexistent AKN and thyroid diseases were significantly older at the onset of AKN, had more prominent female preponderance, and had a higher burden of comorbidity. Conclusions Patients with AKN are at an increased risk of hypothyroidism. Screening for hypothyroidism should be considered in AKN patients with a compatible clinical picture.