Most cases of<unk>  are results of inborn errors of metabolism but the metabolic defect in some patients may be acquired. Mutation of the gene that encodes for ferrochelatase in the long arm of chromosome 18 is found in majority of the cases. Ferrochelatase (FECH) catalyzes the insertion of ferrous iron into the<unk>  IX ring to form heme.<unk>  exhibits both recessive and dominant patterns of inheritance and a high degree of allelic heterogeneity with incomplete penetrance. Most heterozygotes are asymptomatic. Symptoms do not occur unless FECH activity is less than 30% of normal, but such low levels are not present in a majority of patients.
Erythropoietic protoporphyria
Xeroderma pigmentosum
Pseudoporphyria
Harderoporphyria
Thalassemia
Scurvy
Hemoglobinemia
Megavitamin-B6 syndrome