ABSTRACT
There are many dermatologic conditions that can involve the skin of the breast including malignancy, infections, and inflammatory conditions. These are summarized here including presentation and management options.
Subject(s)
Breast Neoplasms , Mammaplasty , Humans , Female , Nipples/pathology , Nipples/surgery , Skin , Breast Neoplasms/diagnosis , Breast Neoplasms/therapy , Breast Neoplasms/pathology , BreastABSTRACT
Plaque psoriasis is a chronic inflammatory disease driven by the proliferation of T cells and the production of several immunomodulators such as tumor necrosis factor (TNF) α. Tumor necrosis factor α plays a key role in multiple inflammatory conditions, including psoriatic arthritis, rheumatoid arthritis, and hidradenitis suppurativa. We present a patient with plaque psoriasis and sickle cell disease who began treatment with the TNF-α inhibitor adalimumab. With this treatment, the patient had improvement in both psoriasis and sickle cell disease symptoms. Tumor necrosis factor α inhibitors may be the drug of choice in patients with both psoriasis and sickle cell disease.
Subject(s)
Adalimumab/therapeutic use , Anemia, Sickle Cell/drug therapy , Psoriasis/drug therapy , Adult , Anemia, Sickle Cell/complications , Anemia, Sickle Cell/pathology , Antirheumatic Agents/therapeutic use , Female , Humans , Psoriasis/complications , Psoriasis/pathology , Tumor Necrosis Factor-alpha/antagonists & inhibitorsABSTRACT
Platelet-derived growth factor BB induced cyclin D1 expression in a time- and nuclear factor of activated T cells (NFAT)-dependent manner in human aortic smooth muscle cells (HASMCs), and blockade of NFATs prevented HASMC DNA synthesis and their cell cycle progression from G(1) to S phase. Selective inhibition of NFATc1 by its small interfering RNA also blocked HASMC proliferation and migration. Characterization of the cyclin D1 promoter revealed the presence of several NFAT binding sites, and the site at nucleotide -1333 was found to be sufficient in mediating platelet-derived growth factor BB-induced cyclin D1 promoter-luciferase reporter gene activity. In addition to its role in cell cycle progression, cyclin D1 mediated HASMC migration in an NFATc1-dependent manner. Balloon injury-induced cyclin D1-CDK4 activity requires NFAT activation, and adenovirus-mediated transduction of cyclin D1 was found to be sufficient to overcome the blockade effect of NFATs by VIVIT on balloon injury-induced vascular wall remodeling events, including smooth muscle cell migration from the medial to luminal region, their proliferation in the intimal region, and neointima formation. Together, these results provide more mechanistic evidence for the role of NFATs, particularly NFATc1, in the regulation of HASMC proliferation and migration as well as vascular wall remodeling. NFATc1 could be a potential therapeutic target against the renarrowing of artery after angioplasty.