Abstract
Fluri et al. recently described a case of a 68-year-old woman whose diagnosis of lead intoxication was based on urine and blood lead analyses.1 No study of erythrocyte aminolevulinic acid dehydratase (ALAD) activity was done, and excretion of urinary ALA was normal, but the urinary erythrocyte protoporphyrin level increased. Basophilic stippling of erythrocytes associated with macrocytic anemia has been interpreted as a sign of lead intoxication, in which the increased erythrocyte protoporphyrin level and microcytic anemia resemble iron deficiency. Normal levels of urinary ALA during acute tetraparesis is surprising. The authors suggest that the patient’s motor symptoms are due to lead intoxication, but the main mechanism of acute or subacute motor neuropathy in lead intoxication is the accumulation of ALA due to inhibition of ALAD in the heme biosynthesis, which should have been shown.2,3 Acute/subacute motor neuropathy of lead intoxication is clinically and biochemically similar to acute porphyria including obligatory elevation of ALA and porphyrins2,3 even if it develops during a chronic lead exposure.4 In a few cases, acute/subacute motor neuropathy caused by lead mimicked motor neuron disease. Seizures described in the patient with no symptoms of …
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