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Multiple eruptive dermatofibromas are a rare presentation of dermatofibroma which are frequently associated with underlying diseases such as human immunodeficiency virus infection or lupus erythematosus. Eruptive dermatofibromas generally present a characteristic histology with a poorly circumscribed lesion showing hyperplasia of the epidermis, prominent bundles of collagen and a diffuse proliferation of fibrocytes. We report an unusual case of multiple eruptive dermatofibromas showing massive depositions of mucin within the dermis. A 20-year-old woman presented with nearly 100 red to yellowish papules and nodules distributed symmetrically all over the integument which developed over a period of 9 years. Comprehensive clinical and laboratory diagnostics showed no signs indicating any underlying disease. To our knowledge this is the first report of multiple eruptive myxoid dermatofibromas. We consider this case to be a unique presentation of multiple eruptive dermatofibroma showing massive deposition of mucin.

Side effects after tattoos are being observed with greater frequency in dermatological practice. The complications that occur can be classified into systemic and local reactions. The time course of cutaneous side effects ranges from direct complications during or following tattooing to reactions that first appear several years thereafter. The majority of allergic complications can be explained by the delayed degradation of the color pigment used for the tattoo and then release of potent allergens sometimes not until years later.

Atopic dermatitis (AD) is a common, chronic inflammatory skin disease with a highly variable clinical phenotype and heterogeneous pathophysiology. Its pathogenesis is associated with alterations to both the skin barrier and the immune system, which may in turn be influenced by genetic mutations and the patient's environment. Basic and translational research, as well as clinical trials, have helped broaden our knowledge of the molecular mechanisms underlying the development of AD and to identify potential treatment targets and approaches. These include new ways of reducing transepidermal water loss and the shedding of corneocytes, new ways of interacting with established molecular targets (such as histamine receptors and interleukins and other T-cell cytokines), and the identification of new molecular targets (such as toll-like receptors and tight junction proteins). Well-established treatment options such as emollients, corticosteroids and topical calcineurin inhibitors will clearly continue to have a role in treating AD. Among the new agents that could be joining them in the near future are sphinganin (a precursor of ceramides 1 and 3), cannabinoids, highly targeted monoclonal antibodies and subcutaneous immunotherapy.