Urinary δ-Aminolevulinic Acid as a Biological Indicator throughout Penicillamine Therapy in Lead Intoxication

Abstract

A group of 121 patients with occupational lead exposure was studied. Saturnism was confirmed in 42 of them. Patients were given D-penicillamine in doses of 0.75 and 1.5 g/day. Urinary delta-aminolevulinic acid was selected as a toxicity biological indicator; its concentrations were quantified daily during therapy. Urinary delta-aminolevulinic acid is considered a good biological indicator throughout penicillamine therapy and also in the detection of lead intoxication. Likewise, the chelating test is considered an excellent method to confirm the diagnosis of lead poisoning.

Implications of oxidative stress in occupational exposure to lead on a cellular level

“…Accumulation of EPP IX and CP reflects the disturbance of the final step in heme synthesis, suggesting biochemical effect of active deposits of lead in bone marrow tissue (Sakai et al 2000). ALA-U was also previously reported to be a valuable measure of metabolically active lead (Molina-Ballesteros et al 1978). We determined high levels of ALA-U in exposed group, which could contribute to an oxidative stress increase through alterations in the heme synthesis pathway.…”

Acute Lead Intoxication due to Intravenous Injection

“…Except for very intensive neuralgic pains, neurologic functions were not impaired, suggesting a differentiation of short-term and long-term effects: longterm lead exposition will lead to a chronic disease process with histo-morphologic damage to the nervous system, possibly being mediated by the lead-induced 5aminolaevulinic acid elevation as well as by lead itself. Furthermore, 5-aminolaevulinic acid and coproporphyrin serve as good biologic indicators for monitoring lead elimination with D-penicillamine (Molina-Ballesteros et al, 1978) and ethylenediaminetetraacetate (Green et al 1978) as they decrease continuously throughout detoxication treatment (Graben et al, 1978). Individuals with hereditary 5-aminolaevulinic acid dehydrase deficiency have consequently been shown to react to lead exposition at lower blood lead levels with the development of an acute syndrome and the increase of urinary 5-aminolaevulinic acid and also coproporphyrin (Doss & Mfller, 1982;Doss et al , 1984).…”

Lead Intoxication Treated With D-Penicillamine

“…A high urinary δ-ALA concentration or blood zinc protoporphyrin level may therefore be useful for diagnosing lead intoxication, especially in patients with an acceptable blood lead concentration despite symptoms of lead intoxication. Furthermore, re-elevation of the urinary δ-ALA level due to tissue redistribution of lead can indicate the need for additional administration of chelating agents [9]. Measurement of the total urinary lead excretion the day after Ca-EDTA infusion (30 mg/kg, up to 2 g) is the most direct method of estimating the total body lead burden, and this test is positive if a 24-h urine collection after chelation contains more than 2.89 µmol (0.6 mg) [3].…”