Abstract During the last decade, different studies have converged to evidence the high prevalence of comorbidities in subjects with psoriasis. Although a causal relation has not been fully elucidated, genetic relation, inflammatory pathways and/or common environmental factors appear to be underlying the development of psoriasis and the metabolic comorbidities. The concept of psoriasis as a systemic disease directed the attention of the scientific community in order to investigate the extent to which therapeutic interventions influence the onset and evolution of the most prevalent comorbidities in patients with psoriasis. This study presents scientific evidence of the influence of immunobiological treatments for psoriasis available in Brazil (infliximab, adalimumab, etanercept and ustekinumab) on the main comorbidities related to psoriasis. It highlights the importance of the inflammatory burden on the clinical outcome of patients, not only on disease activity, but also on the comorbidities. In this sense, systemic treatments, whether immunobiologicals or classic, can play a critical role to effectively control the inflammatory burden in psoriatic patients.

Psoriasis is a chronic inflammatory, immune-mediated disease that affects 1% to 2% of the world's population. Immunobiological medications are prescribed for certain patients with severe forms of psoriasis, however, these drugs increase the risk of reactivation of viral diseases such as hepatitis B. We report the case of a patient with severe psoriasis with positive serology for the Hepatitis B virus, who received ustekinumab (a human monoclonal antibody against interleukin 12 and 23). In this patient, the use of ustekinumab did not reactivate the Hepatitis B virus. Given the high prevalence of chronic viral infections in patients who are candidates for biologic therapy, as well as the potential for reactivate chronic viral illness, randomized controlled studies are needed to assess the risks and benefits of such therapy in these populations.

A hipotricose congênita e a distrofia macular de Stargardt são desordens autossômicas recessivas raras de etiologias desconhecidas, caracterizadas respectivamente pela perda de cabelos, degeneração macular e redução pro gressiva e grave da visão de forma precoce. Encontram-se pouquíssimos relatos na literatura com a associação de ambas. Há estudos que demonstram que o gene defeituoso dessas doenças encontra-se no cromossomo I6q22.1 e implicam a participação da molécula caderina na patogênese das mesmas. O reconhecimento precoce dessas desor dens muitas vezes inicia por alterações capilares e deve alertar o dermatologista para uma análise oftalmológica para como forma de se evitar alterações oculares mais graves.

Congenital hypotrichosis and Stargardt macular dystrophy are rare autosomal recessive disorder of unk nown etiology respectively characterized by hair loss, macular degeneration and severe progressive vision reduc tion. There are few reports in the literature with this association. Studies show that the defective gene is on the chro mosome I6q22.1 and involve cadherin molecule in the pathogenesis. Early recognition of these disorders often starts with hair changes and should alert the dermatologist for an eye examination thereby avoiding more severe ocular defect.