The correct answer is D. Ferrochelatase.

This pediatric patient has erythropoietic protoporphyria (EPP), characterized by the rapid onset pf painful burning followed by erythema and edema after sun exposure. Urinary porphyrins are not elevated in EPP patients unlike other porphyrias, such as hereditary porphyria and variegate porphyria. It is associated with jaundice and the development of pigment gallstones, a leading cause of gallstones in the pediatric population. It is caused by a genetic, either autosomal recessive or dominant, deficiency in the enzyme ferrochelatase. Ferrochelatase normally converts protoporphyrin into heme in the mitochondria of erythrocytes as part of the heme synthesis pathway.

Porphobilinogen deaminase is deficient in acute intermittent porphyria, but this disease does not have any cutaneous manifestations. Uroporphyrinogen decarboxylase is deficient in porphyria cutanea tarda, the most common porphyria characterized by bullae on sun-exposed areas. Coproporphyrinogen oxidase is deficient in hereditary coproporphyria. Protoporphyrinogen oxidase is deficient in variegate porphyria, a mostly silent disease exacerbated by infection and drugs.

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Porphobilinogen deaminase is deficient in acute intermittent porphyria, but this disease does not have any cutaneous manifestations. Uroporphyrinogen decarboxylase is deficient in porphyria cutanea tarda, the most common porphyria characterized by bullae on sun-exposed areas. Coproporphyrinogen oxidase is deficient in hereditary coproporphyria. Protoporphyrinogen oxidase is deficient in variegate porphyria, a mostly silent disease exacerbated by infection and drugs.