Psoriasis is a lifelong, chronic, and immune-mediated systemic disease, which affects approximately 1–3% of the Caucasian population. The different presentations of psoriasis require different approaches to treatment and appropriate prescriptions according to disease severity. The use of topical therapy remains a key component of the management of almost all psoriasis patients, and while mild disease is commonly treated only with topical agents, the use of topical therapy as adjuvant therapy in moderate-to-severe disease may also be helpful. This paper focuses on the cutaneous mechanisms of action of corticosteroids and on the currently available topical treatments, taking into account adverse effects, bioavailability, new combination treatments, and strategies to improve the safety of corticosteroids. It is established that the treatment choice should be tailored to match the individual patient’s needs and his/her expectations, prescribing to each patient the most suitable vehicle.

Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease of unknown etiology with many clinical manifestations. The skin is one of the target organs most variably affected by the disease. The American College of Rheumatology (ACR) established 11 criteria as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. Cutaneous lesions account for four of these 11 revised criteria of SLE. Skin lesions in patients with lupus may be specific or nonspecific. This paper covers the SLE-specific cutaneous changes: malar rash, discoid rash, photosensitivity, and oral mucosal lesions as well as SLE nonspecific skin manifestations, their pathophysiology, and management. A deeper thorough understanding of the cutaneous manifestations of SLE is essential for diagnosis, prognosis, and efficient management. Thus, dermatologists should cooperate with other specialties to provide optimal care of SLE patient.

We reported earlier that urate may behave as a pro‐oxidant in Cu²⁺‐induced oxidation of diluted plasma. Thus, its effect on Cu²⁺‐induced oxidation of isolated low‐density lipoprotein (LDL) was investigated by monitoring the formation of malondialdehyde and conjugated dienes and the consumption of urate and carotenoids. We show that urate is antioxidant at high concentration but pro‐oxidant at low concentration. Depending on Cu²⁺ concentration, the switch between the pro‐ and antioxidant behavior of urate occurs at different urate concentrations. At high Cu²⁺ concentration, in the presence of urate, superoxide dismutase and ferricytochrome c protect LDL from oxidation but no protection is observed at low Cu²⁺ concentration. The use of Cu²⁺ or Cu⁺ chelators demonstrates that both copper redox states are required. We suggest that two mechanisms occur depending on the Cu²⁺ concentration. Urate may reduce Cu²⁺ to Cu⁺, which in turn contributes to formation. The Cu²⁺ reduction is likely to produce the urate radical (UH^·–). It is proposed that at high Cu²⁺ concentration, the reaction of UH^·– radical with generates products or intermediates, which trigger LDL oxidation. At low Cu²⁺ concentration, we suggest that the Cu⁺ ions formed reduce lipid hydroperoxides to alkoxyl radicals, thereby facilitating the peroxidizing chain reaction. It is anticipated that these two mechanisms are the consequence of complex LDL–urate–Cu²⁺ interactions. It is also shown that urate is pro‐oxidant towards slightly preoxidized LDL, whatever its concentration. We reiterate the conclusion that the use of antioxidants may be a two‐edged sword.