ABSTRACT Psoriasis is a chronic inflammatory skin condition that is often associated with systemic manifestations. It affects about 2 percent of U.S. adults, and can significantly impact quality of life. The etiology includes genetic and environmental factors. Diagnosis is based on the typical erythematous, scaly skin lesions, often with additional manifestations in the nails and joints. Plaque psoriasis is the most common form. Atypical forms include guttate, pustular, erythrodermic, and inverse psoriasis. Psoriasis is associated with several comorbidities, including cardiovascular disease, lymphoma, and depression. Topical therapies such as corticosteroids, vitamin D analogs, and tazarotene are useful for treating mild to moderate psoriasis. More severe psoriasis may be treated with phototherapy, or may require systemic therapy. Biologic therapies, including tumor necrosis factor inhibitors, can be effective for severe psoriasis and psoriatic arthritis, but have significant adverse effect profiles and require regular monitoring. Management of psoriasis must be individualized and may involve combinations of different medications and phototherapy.
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ABSTRACT: Psoriasis is a chronic inflammatory skin disease resulting from immune dysregulation. Regulatory T cells (Tregs) are important in the prevention of psoriasis. Traditionally, reactive oxygen species (ROS) are known to be implicated in the progression of inflammatory diseases, including psoriasis, but many recent studies suggested the protective role of ROS in immune-mediated diseases. In particular, severe cases of psoriasis vulgaris have been reported to be successfully treated by hyperbaric oxygen therapy (HBOT), which raises tissue level of ROS. Also it was reported that Treg function was closely associated with ROS level. However, it has been only investigated in lowered levels of ROS so far. Thus, in this study, to clarify the relationship between ROS level and Treg function, as well as their role in the pathogenesis of psoriasis, we investigated imiquimod-induced psoriatic dermatitis (PD) in association with Treg function both in elevated and lowered levels of ROS by using knockout mice, such as glutathione peroxidase-1-/- and neutrophil cytosolic factor-1-/- mice, as well as by using HBOT or chemicals, such as 2,3-dimethoxy-1,4-naphthoquinone and N-acetylcysteine. The results consistently showed Tregs were hyperfunctional in elevated levels of ROS, whereas hypofunctional in lowered levels of ROS. In addition, imiquimod-induced PD was attenuated in elevated levels of ROS, whereas aggravated in lowered levels of ROS. For the molecular mechanism that may link ROS level and Treg function, we investigated the expression of an immunoregulatory enzyme, indoleamine 2,3-dioxygenase (IDO) which is induced by ROS, in PD lesions. Taken together, it was implied that appropriately elevated levels of ROS might prevent psoriasis through enhancing IDO expression and Treg function.PLoS ONE 03/2014; 9(3):e91146. DOI:10.1371/journal.pone.0091146 · 3.53 Impact Factor
Article: Common Dermatologic Conditions[Show abstract] [Hide abstract]
ABSTRACT: This review discusses common dermatologic presentations as they would appear in a primary care office, exploring the differential diagnoses for each. Tips are provided on choosing an appropriate topical drug and vehicle and advising patients on its use. Etiology, differential diagnosis, and treatment options are discussed for the following: alopecias including androgenetic alopecia, female pattern hair loss, alopecia areata, and telogen effluvium; facial rashes including acne vulgaris, acne rosacea, periorificial dermatitis, seborrheic dermatitis, erysipelas/cellulitis, and systemic lupus erythematosus; intertriginous rashes including infections, intertrigo, and inverse psoriasis; and the inflamed leg including cellulitis and erysipelas, stasis dermatitis, and contact dermatitis.The Medical clinics of North America 05/2014; 98(3):445-485. DOI:10.1016/j.mcna.2014.01.005 · 2.80 Impact Factor
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ABSTRACT: Mood disorders have been recognised by the World Health Organization (WHO) as the leading cause of disability worldwide. Notwithstanding the established efficacy of conventional mood agents, many treated individuals continue to remain treatment refractory and/or exhibit clinically significant residual symptoms, cognitive dysfunction, and psychosocial impairment. Therefore, a priority research and clinical agenda is to identify pathophysiological mechanisms subserving mood disorders to improve therapeutic efficacy. During the past decade, inflammation has been revisited as an important etiologic factor of mood disorders. Therefore, the purpose of this synthetic review is threefold: 1) to review the evidence for an association between inflammation and mood disorders, 2) to discuss potential pathophysiologic mechanisms that may explain this association and 3) to present novel therapeutic options currently being investigated that target the inflammatory-mood pathway. Accumulating evidence implicates inflammation as a critical mediator in the pathophysiology of mood disorders. Indeed, elevated levels of pro-inflammatory cytokines have been repeatedly demonstrated in both major depressive disorder (MDD) and bipolar disorder (BD) patients. Further, the induction of a pro-inflammatory state in healthy or medically ill subjects induces 'sickness behaviour' resembling depressive symptomatology. Potential mechanisms involved include, but are not limited to, direct effects of pro-inflammatory cytokines on monoamine levels, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, pathologic microglial cell activation, impaired neuroplasticity and structural and functional brain changes. Anti-inflammatory agents, such as acetyl-salicylic acid (ASA), celecoxib, anti-TNF-α agents, minocycline, curcumin and omega-3 fatty acids, are being investigated for use in mood disorders. Current evidence shows improved outcomes in mood disorder patients when anti-inflammatory agents are used as an adjunct to conventional therapy; however, further research is needed to establish the therapeutic benefit and appropriate dosage.Progress in Neuro-Psychopharmacology and Biological Psychiatry 01/2014; DOI:10.1016/j.pnpbp.2014.01.013 · 4.03 Impact Factor