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Allergic contact hypersensitivity reactions of the oral mucosa pose a significant medical concern for some patients. Oral hypersensitivity reactions can result from a vast number of allergenic chemicals, but occur commonly from dental materials, flavorings, and preservatives. Clinical presentation is varied and often overlaps with other oral conditions, complicating their diagnosis and management. The most common clinical entities associated with oral hypersensitivity reactions are oral lichenoid reactions and allergic contact cheilitis. In addition to reviewing these conditions and their most common corresponding allergens, this article summarizes the pathogenesis of oral hypersensitivity reactions and addresses patch testing pearls.

The American Contact Dermatitis Society recognizes the interest in the evaluation and management of metal hypersensitivity reactions. Given the paucity of robust evidence with which to guide our practices, we provide reasonable evidence and expert opinion–based guidelines for clinicians with regard to metal hypersensitivity reaction testing and patient management. Routine preoperative evaluation in individuals with no history of adverse cutaneous reactions to metals or history of previous implant-related adverse events is not necessary. Patients with a clear self-reported history of metal reactions should be evaluated by patch testing before device implant. Patch testing is only 1 element in the assessment of causation in those with postimplantation morbidity. Metal exposure from the implanted device can cause sensitization, but a positive metal test does not prove symptom causality. The decision to replace an implanted device must include an assessment of all clinical factors and a thorough risk-benefit analysis by the treating physician(s) and patient.

In recent years, there has been a growing interest in the use of skin patch testing to evaluate patients for orthopedic, implant-related adverse effects. This may be done preoperatively to avoid implanting a material to which an individual may be allergic or postoperatively to implicate sensitivity as a cause for implant failure. There is emerging evidence that patch testing might have utility in the workup of implant-related adverse events; however, the level of evidence at the present time is weak and based only on a collection of case reports, series, and retrospective cohort studies (level IV evidence as per United States Department of Health and Human Services guidelines); there are no randomized controlled trials (level I evidence) with which to guide medical decision making. Recent reports have advocated that patch testing be broadly used in the preoperative evaluation of all patients self-reporting a history of metal sensitivity. In addition, several authors have advocated that patch test results should guide preoperative implant selection and postoperative implant removal. It is the opinion of this author that these recommendations are premature, lacking robust clinical evidence, and unfeasible given the broad-reaching logistical impact and societal costs involved. More robust clinical data are needed, and thorough cost-benefit analyses must be performed before such far-reaching and costly systematic practices should be broadly implemented.

The following paper reviews the recent literature pertaining to allergic contact dermatitis in the pediatric population.

Papulopustular eruptions are a common side effect of treatment with agents that target the human epidermal growth factor receptor (HER1/EGFR). Use of these targeted therapies, which include cetuximab, erlotinib, and gefitinib, may also cause paronychial inflammation, hair changes, and xerosis, or “dry skin.” Although the etiology and pathogenesis of these cutaneous side effects are not well understood, most resolve with discontinuation of HER1/EGFR inhibitor therapy or even spontaneously. Treatment recommendations, though plentiful, are based on anecdotal information, as there have been no controlled clinical trials testing the efficacy of any specific modality. There is growing evidence that the papulopustular eruptions associated with the use of HER1/EGFR inhibitors might serve as a surrogate marker for tumor response and/or survival. This article reviews the clinical features of skin reactions to HER1/EGFR inhibitors and provides treatment recommendations for practicing dermatologists and oncologists.

For nearly 2 decades clinicians have been treating cutaneous T-cell lymphoma (CTCL) with regimens that combine interferon alfa with retinoid compounds. In December 1999 a new retinoid, bexarotene, was approved by the US Food and Drug Administration for the treatment of CTCL. At the manufacturer's recommended dose of bexarotene (300 mg/m2of body surface area), it has proven to be a highly effective therapy for all stages of CTCL. Nevertheless, this dose is typically associated with adverse effects including severe hyperlipidemia. Furthermore, there appears to be no standardization of dosing among physicians who treat CTCL.

Occupational health nurses should be cognizant of the myriad exposures that can result in dermal reactions among health care workers.

Leishmania are obligate intracellular protozoa that parasitize mononuclear phagocytes. Because mononuclear phagocytes are also the primary source of leukocytic pyrogen and of lymphocyte-activating factor, both considered properties of interleukin-1 (IL-1), we investigated in vitro production of leukocytic pyrogen and of lymphocyte-activating factor from human monocytes infected with Leishmania tropica. Despite parasitization of 95% of cells, 24- and 48-hr culture supernatants and cell lysates derived from L. tropica-infected monocytes did not contain IL-1. Leishmania that were killed by freezing or by glutaraldehyde treatment similarly did not induce monocyte production of IL-1. Of importance is the observation that human monocytes infected with L. tropica for 6 hr and then challenged with a potent IL-1 inducer (Staphylococcus epidermidisi) produced significantly less IL-1 than did uninfected monocytes that were similarly challenged (P <.001). This difference was not affected by the addition of indomethacin to the cultures. In contrast, soluble immune complexes prepared with an excess of L. tropica antigen and rabbit antibody to L. tropica induced high levels of IL-1 production from normal monocytes. Neither antigen nor antibody alone incubated with monocytes led to significant production of IL-1, however. Thus, these studies suggest that despite leishmanial adherence to, entrance into, and replication within human monocytes there is little or no stimulation of IL-1 production. This may represent a parasite evasion mechanism that retards the development of protective immune responses in leishmaniasis.