Actinic prurigo is a  rare sunlight-induced, pruritic, papular or nodular skin eruption. Some medical experts use the term actinic prurigo to denote a rare photodermatosis that develops in childhood and is chronic and persistent; this rare photodermatosis, associated with the human leukocyte antigen HLA-DR4, is often called "Familial polymorphous light eruption of American Indians" or "Hereditary polymorphous light eruption of American Indians" but some experts consider it to be a variant of the syndrome known as polymorphous light eruption (PMLE). Some experts use the term actinic prurigo for Hutchinsons summer prurigo (aka hydroa aestivale) and several other photodermatoses that might, or might not, be distinct clinical entities. Symptoms
AP is characterized by itchy, inflamed papules, nodules, and plaques on the skin. Lesions typically appear hours or days after exposure of the skin to UV light, and follow a general pattern of sun-exposed areas. The face, neck, arms, hands, and legs are often affected, although lesions sometimes appear on skin that is covered by clothing and thus not exposed to UV light, thus making AP somewhat difficult to diagnose. AP is a chronic disease, and symptoms usually worsen in the spring and summer as the day lengthens and exposure to sunlight increases. Causes
The cause for actinic prurigo is unknown, however researchers believe that protein in our bodies may be a cause to the condition also:
•UV-A and UV-B light seem to be the main provoking agents.
Activation of these receptors causes adenylyl cyclase to convert ATP to cAMP, beginning the signalling cascade that ends with the inhibition of myosin phosphorylation and lowering the intracellular concentration of calcium ions (myosin phosphorylation and calcium ions are necessary for muscle contractions). The increase in cAMP also inhibits inflammatory cells in the airway, such as basophils, eosinophils, and most especially mast cells, from releasing inflammatory mediators and cytokines. Salbutamol and other β2 receptor agonists also increase the conductance of channels sensitive to calcium and potassium ions, leading to hyperpolarization and relaxation of bronchial smooth muscles.Salbutamol is either filtered out by the kidneys directly or is first metabolized into the 4′-O-sulfate, which is excreted in the urine. Chemistry
Salbutamol is sold as a racemic mixture. The (R)-(−)-enantiomer (CIP nomenclature) is shown in the image at right (top), and is responsible for the pharmacologic activity; the (S)-(+)-enantiomer (bottom) blocks metabolic pathways associated with elimination of itself and of the pharmacologically active enantiomer (R). The slower metabolism of the (S)-(+)-enantiomer also causes it to accumulate in the lungs, which can cause airway hyperreactivity and inflammation. Potential formulation of the R form as an enantiopure drug is complicated by the fact that the stereochemistry is not stable, but rather the compound undergoes racemization within a few days to weeks, depending on pH.