Lupus, Latin for “wolf,” is a term used to describe many dermatologic conditions, some of which are related to underlying systemic lupus erythematosus, while others are distinct disease processes. Cutaneous lupus erythematosus includes a wide array of visible skin manifestations and can progress to systemic lupus erythematosus in some cases. Cutaneous lupus can be subdivided into three main categories: acute cutaneous lupus erythematosus, subacute cutaneous lupus erythematosus, and chronic cutaneous lupus erythematosus. Physical exam, laboratory studies, and histopathology enable differentiation of cutaneous lupus subtypes. This differentiation is paramount as the subtype of cutaneous lupus informs upon treatment, disease monitoring, and prognostication. This review outlines the different cutaneous manifestations of lupus erythematosus and provides an update on both topical and systemic treatment options for these patients. Other conditions that utilize the term “lupus” but are not cutaneous lupus erythematosus are also discussed.
1 The long-acting b 2 -adrenoceptor agonist, salmeterol (10 79 ± 10 75 M), inhibited the IgE-mediated release of histamine from human lung mast cells (HLMC) in a dose-dependent fashion. Additional badrenoceptor agonists were studied and the rank order of potency for the inhibition of histamine release from HLMC was isoprenaline4salmeterol4salbutamol. Approximate EC 50 values for the inhibition of histamine release were 10 nM for isoprenaline and 100 nM for salbutamol. An EC 50 value for salmeterol could not be calculated because maximal responses to salmeterol were not observed over the concentration range employed. 2 Both salmeterol and isoprenaline inhibited the generation of sulphopeptidoleukotrienes (sLT) more potently and more ecaciously than the release of histamine from immunologically-activated HLMC. Salmeterol (EC 50 50.1 nM) was more potent than isoprenaline (EC 50 0.4 nM) at attenuating sLT generation. 3 The b-adrenoceptor antagonist, propranolol (1 mM), and the selective b 2 -adrenoceptor antagonist, ICI 118,551 (0.1 mM), both caused rightward shifts in the dose-response curve for the inhibition of histamine release by isoprenaline. The antagonism of salmeterol eects by propranolol and ICI 118,551 was more complex. At lower concentrations (51 mM) of salmeterol, both antagonists shifted the dose-reponse curve to salmeterol rightward. At a higher concentration (10 mM) of salmeterol, neither ICI 118,551 nor propranolol was an eective antagonist of the salmeterol-mediated inhibition of histamine release. 4 Prolonged exposure (4 h) of HLMC to isoprenaline (1 mM) caused an approximately 50% reduction in the eectiveness of a second exposure to isoprenaline (10 mM) at inhibiting the release of histamine, whereas this pretreatment did not aect the salmeterol (10 mM) inhibition of histamine release. 5 Isoprenaline (10 79 ± 10 75 M) caused a dose-dependent increase in total cell cyclicAMP levels in puri®ed HLMC which paralleled the inhibition of histamine release. Salmeterol (10 79 ± 10 75 M) was considerably less potent than isoprenaline at increasing HLMC cyclicAMP levels. 6 In summary, these data indicate that salmeterol is an eective inhibitor of the stimulated release of mediators from HLMC. The present data also suggest that salmeterol may act to inhibit mediator release from HLMC by b-adrenoceptor-dependent and independent mechanisms.
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