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Photosensitive Dermatitis

»What is the definition of photosensitivity?
»What is the difference between a phototoxic reaction and a photoallergic reaction?
»What is the clinical appearance of a photodistributed eruption?
»Name some of the most common topical phototoxic and photoallergic agents and their action spectrums.
»Name some of the most common systemic phototoxic and photoallergic agents and their action spectrums.
»Give some examples of unique phototoxic reactions.
»What are some scenarios in which the skin may be more sensitive to ultraviolet radiation?
»What are the important questions to ask a patient with suspected photosensitivity?
»What are the most common causes of photosensitive dermatoses?
»What is persistent light reactivity?
»What is polymorphous light eruption (PMLE)?
»How is PMLE diagnosed?
»How is PMLE treated?
»What is actinic prurigo?
»What is solar urticaria?
»Discuss the differential diagnosis of photodermatoses in infants or young children.
»How do hydroa aestivale and hydroa vacciniforme differ?
»Which porphyrias are associated with photodermatoses?
»Describe the cutaneous changes in porphyria cutanea tarda.
»What causes porphyria cutanea tarda?
»How is porphyria cutanea tarda diagnosed?
»How is variegate porphyria distinguished from porphyria cutanea tarda?
»What treatments are used in porphyria cutanea tarda?
»What are the cutaneous findings in erythropoietic protoporphyria?
»How is a diagnosis of erythropoietic protoporphyria made?
»What treatments are used in erythropoietic protoporphyria?
»Do any other medical problems occur in patients with erythropoietic protoporphyria?
»Name some other photorelated disorders.

 
 
 

What causes porphyria cutanea tarda?

The porphyrias are due to specific enzyme deficiencies that lead to accumulation of porphyrins. Porphyrins absorb light in the 400- to 410-nm (Soret band) range, in the lower range of visible light. This absorbed light energy is then transferred to cellular structures or to molecular oxygen, causing damage to tissues. PCT is due to a deficiency of the enzyme uroporphyrinogen decarboxylase. There are two main categories of PCT patients, acquired and hereditary. Patients with acquired PCT have the enzyme deficiency in the liver only and often have attacks triggered by agents such as alcohol, estrogen, hexachlorobenzene, and iron. PCT may also develop in patients with chronic liver disease (e.g., hepatitis C infection or hemochromatosis). In hereditary PCT, uroporphyrinogen decarboxylase is deficient in most tissues, not just the liver. Both heterozygous and homozygous inheritances of enzyme deficiencies have been described.