Clinics in dermatology
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The immunopathogenesis of sarcoidosis has been difficult to charaterize given the heterogeneity of disease, the elusiveness of the causative antigen, and the lack of an adequate animal model. However, by examining well-defined clinical cohorts, the interplay between genetic predisposition and immunologic response has been increasingly informative. Technological advances in cellular analysis have allowed researchers to characterize the immune responses important in the maintenance of granulomatous inflammation. Finally, "new" clinical observations such as granuloma responsiveness to targeted biological therapies, sarcoid developing during immune restoration, and the relationship between sarcoidosis and Hepatitis C will provide future insight to the immunopathogenesis of sarcoidosis.
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Most of treatments for cutaneous sarcoidosis are extensions of the drugs tested for pulmonary sarcoidosis. There are some exceptions. These include drugs given topically and those with high concentrations in the skin. This review will examine the conventional treatments of cutaneous sarcoidosis and focus on the best available evidence to make recommendations on treatment.
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Sarcoidosis is a multisystem disease with cutaneous lesions present in 20%-35% of patients. Given the wide variability of clinical manifestations, it is one of the "great imitators," making it necessary to consider clinical, epidemiological, radiographic, laboratory, and histopathological criteria to make the diagnosis. Cutaneous lesions have been classified as specific and nonspecific, depending on the presence of noncaseating granulomas on histologic studies. ⋯ The most common nonspecific lesion is erythema nodosum. Others include calcifications, prurigo, erythema multiforme, nail clubbing, and Sweet syndrome. The importance of considering cutaneous sarcoidosis in the clinical differential diagnosis of a given skin lesion relies on the association with systemic involvement and the convenience of the skin as a tissue source for histologic analysis.
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The predisposition to sarcoidosis is genetically determined, and genetics appears also to account for the variability in clinical phenotype and behaviour. Many genetic loci have been investigated to date, mainly in case-control association studies. However, only a small number of human leukocyte antigen (HLA) alleles have been consistently associated with sarcoidosis susceptibility/phenotype. ⋯ Despite a number of intriguing hypotheses, what causes sarcoidosis remains obscure. Genetic studies and, importantly, functional analysis of candidate genes will provide insight into pathogenesis and disease risk. However, if, as many believe, sarcoidosis is a heterogeneous collection of disorders, a critical step will be to carefully refine the clinical phenotype, as genetic studies of complex diseases are more rewording if a very specific disease subset is addressed.
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Sarcoidosis is a systemic granulomatous disease of unknown cause. An infectious etiology of sarcoidosis has long been suspected, but only recently has scientific evidence provided a strong link between infectious agents and sarcoidosis. Moreover, recent advances in our understanding of the relationships between sarcoidosis phenotype and host genetic factors may further illuminate the mechanisms linking infection and sarcoidosis.