Therapy for Lead Poisoning

Graben, N; Doss, M; Klöppel, Heide; Wilhelms, W.; Tiepermann, R. v.

doi:10.1007/978-3-642-67002-2_36

Cited by 5 publications

(1 citation statement)

References 5 publications

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“…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).…”

Section: Discussionmentioning

confidence: 99%

Acute Lead Intoxication due to Intravenous Injection

Sixel-Dietrich¹,

Doss²,

Pfeil

et al. 1985

Human Toxicology

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A case of acute lead poisoning due to intravenous injection of lead acetate is reported. The patient developed clinical and biochemical symptoms characteristic for acute hepatic porphyrias. Elevated urinary 5-aminolaevulinic acid and low porphobilinogen correlated to a lead-induced inhibition of 5-aminolaevulinic acid dehydrase with diagnostically indicative reactivation rates by zinc and dithiothreitol. Urinary coproporphyrin excretion was also increased. Additional findings included anaemia and toxic hepatitis. Under the influence of elimination therapy with D-penicillamine pathologic parameters normalized. Except for transient neuralgic pains the patient did not experience any neurologic dysfunctions, thus contrasting the findings in chronic lead intoxication.

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Section: Discussionmentioning

confidence: 99%

Acute Lead Intoxication due to Intravenous Injection

Sixel-Dietrich¹,

Doss²,

Pfeil

et al. 1985

Human Toxicology

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Haematological Disturbances of Porphyrin Metabolism

Doss

1979

Strategies in Clinical Hematology

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Lead poisoning in inherited ?-aminolevulinic acid dehydratase deficiency

Doss

Laubenthal

Stoeppler

1984

Int Arch Occup Environ Heath

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delta-Aminolevulinic acid dehydratase (ALA-D), respectively porphobilinogen synthase, EC 4.2.1.24) activity can be lowered by toxic, metabolic and hereditary factors. A 30-year-old painter was suffering from lead poisoning with an acute abdominal-neurologic syndrome and anemia. Blood lead was measured at 414 micrograms/l. Urinary ALA and coproporphyrin excretion as well as erythrocyte protoporphyrin had increased extremely, whereas ALA-D activity in erythrocytes had decreased extremely to 8% of controls. Excretion parameters, protoporphyrin, hemoglobin and lead returned to normal after treatment, but four years later ALA-D activity still remained diminished (30% of controls). An inherited enzyme deficiency was assumed and found in the mother, analogous to the subnormal ALA-D activity in heterozygotes of four other families. The inherited enzyme deficiency sensitized the patient to lead exposure and intoxication, which is a toxogenetic disease in this case.

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Therapy for Lead Poisoning

Cited by 5 publications

References 5 publications

Acute Lead Intoxication due to Intravenous Injection

Acute Lead Intoxication due to Intravenous Injection

Haematological Disturbances of Porphyrin Metabolism

Lead poisoning in inherited ?-aminolevulinic acid dehydratase deficiency

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