Delta-Aminolevulinic Acid, 24-Hour Urine

Diagnose porphyrias: Δ-ALA may be increased in attacks of acute intermittent porphyria, hereditary coproporphyria, and porphyria variegata; evaluation of certain neurological problems with abdominal pain; diagnosis of lead or mercury poisoning. Urinary Δ-ALA is not a sensitive indicator of lead poisoning in children because it does not increase until blood lead concentration is 40 μg/dL, well above the recommended level <15 μg/dL. ALA is increased also in tyrosinemia.^1,2 Porphobilinogen and δ-aminolevulinic acid are the tests of choice for acute intermittent porphyria. Recently the molecular lesions have been identified in a severely affected homozygote with δ-aminolevulinate dehydratase deficient porphyria.³

ALA may be normal during latent period of acute intermittent porphyria, hereditary coproporphyria, porphyria variegata. For the diagnosis of lead poisoning, measurement of blood and urine lead, and free erythrocyte protoporphyrin are other available options.

This test was developed, and its performance characteristics determined, by LabCorp. It has not been cleared or approved by the Food and Drug Administration.

Conversion of ALA to porphobilinogen is inhibited by lead and mercury; thus, lead poisoning causes increased urinary Δ-ALA, as well as increases of coproporphyrin and of free erythrocyte protoporphyrin.

1. Labbe RF, Lamon JM. Porphyrins and disorders of porphyrin metabolism. In: Tietz NW, ed. Fundamentals of Clinical Chemistry. 3rd ed. Philadelphia, Pa: WB Saunders Co;1987:825-841.

2. Hereditary tyrosinaemia. Lancet. 1990 Jun 23; 335(8704):1500-1501. PubMed 1972437

3. Plewinska M, Thunell S, Holmberg L, et al. ?-Aminolevulinate dehydratase deficient porphyria: Identification of the molecular lesions in a severely affected homozygote. Am J Hum Genet. 1991 Jul; 49(1):167-174. PubMed 2063868