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.
Cytophagic histiocytic panniculitis (CHP) is a rare panniculitis that is associated with systemic features including fevers, hepatosplenomegaly, lymphadenopathy, pancytopenia, hepatic abnormalities, hypertriglyceridemia, and coagulopathy without an elevated erythrocyte sedimentation rate. The panniculitis lesions show adipose tissue lymphocytic and histiocytic infiltration along with hemophagocytosis, which may also appear in bone marrow, spleen, lymph nodes, and liver. Patients may have a rapidly fatal disease course, a longer disease course with intermittent remissions and exacerbations for many years prior to death, or a nonfatal acute or intermittent course responsive to treatment. The cytophagocytic disorder in these patients is a hemophagocytic lymphohistiocytosis (HLH), similar to the infection-activated reaction associated with perforin mutations found in familial hemophagocytic lymphohistiocytosis. HLH is a group of autoinflammatory disorders, which include macrophage activation syndrome and infection-associated hemophagocytic syndrome, which if not treated rapidly, can be fatal. The relationship of CHP and HLH is discussed. CHP associated diseases include: subcutaneous panniculitis-like T cell lymphomas; infections, connective tissue diseases, other malignancies, and the molecular disorders that cause HLH. Treatment of CHP includes: glucocorticoids in combination with cyclosporine, combined chemotherapeutic medications and most recently, anakinra, an Interleukin-1 receptor antagonist; along with supportive care, search for underlying malignancies and treatment thereof, and control of associated infections.
Leprosy, or Hansen's disease (HD), is caused by Mycobacterium leprae, a slowly dividing mycobacterium that has evolved to be an intracellular parasite, causing skin lesions and nerve damage. Less than 5% of people exposed to M. leprae develop clinical disease. Host cell-mediated resistance determines whether an individual will develop paucibacillary or multibacillary disease. Hansen's disease is a worldwide disease with about 150 new cases reported annually in the United States. Effective anti-mycobacterial treatments are available, and many patients experience severe reversal and erythema nodosum leprosum reactions that also require treatment. Leprosy has been the target of a World Health Organization multiple drug therapy campaign to eliminate it as a national public health problem in member countries, but endemic regions persist. In the United States, the National Hansen's Disease Program has primary responsibility for medical care, research, and information.
Cutaneous metabolism and pharmacology have been the focus of increased scientific inquiry in the past 2 decades. However, in the past few years, attention has been focused specifically on the effects of topically applied drugs in infants as different qualitatively or quantitatively from their effects in adults. Prior to 1972, it was known that brain damage occurred in animals with prolonged blood levels of 2 microgram/ml hexachlorophene, and that washing newborn babies with a standard 3% hexachlorophene liquid soap for 3-5 days resulted in significant blood levels of the compound. However, this knowledge was not disseminated widely enough to prevent the tragic deaths of infants after the use of baby powder contaminated with 6.6% hexachlorophene [1]. This incident highlighted the need for increased understanding of drug effects not only from the viewpoint of the skin as a target organ, but also of percutaneous penetration and resultant blood levels; the affinity of other body tissues for drugs and their metabolites, metabolites which may result from the effect of the skin itself acting on the drug; and the infant's much greater ratio of surface area to body weight, allowing the infant to percutaneously absorb proportionately greater quantities of topical medication than an adult. Although tissue distribution of most drugs has not been studied in infants, it is known that such distribution often depends on age. For example, in infants and children with a given plasma level, of drugs such as barbiturates, morphine and tetracycline, the brain tissue level may exceed that of the adult. Thus, drugs and chemicals that penetrate infant skin may produce effects different than those penetrating adult skin.
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