A case of lead intoxication: clinical and biochemical studies.
A 23-year-old Japanese male with severe lead intoxication accompanied by hemolytic anemia was studied. The patient had taken 12 g to lead in about a month. He had moderate hemolytic anemia (Hb 8.9 g/100 ml) with reticulocytosis ranging from 2.5 to 11.7%. Peripheral blood smear showed nucleated red cells (42/200 white blood cells) and marked basophilic stippling in the red cells. Activities of erythrocyte enzymes were either normal or increased except for pyrimidine 5'-nucleotidase (P5N) and delta-aminolevulinic acid dehydratase (ALA-D) both of which were found to be decreased, being 48.8% and 4.1% of the normal controls respectively. Erythrocyte reduced glutathione (GSH) was high (145.6 mg/100 ml RBC). Erythrocyte pyrimidine nucleotides were accumulated up to 10.2% of total nucleotides. The level of lead in peripheral blood was 112 microgram per 100 ml blood. Ca2+-Na2-EDTA was given to the patient as treatment. The level of lead in the blood decreased gradually and hemolytic anemia improved. Basophilic stippling in the red cells disappeared. These results confirmed the findings of Valentine et al [1] that lead-induced deficiency of P5N resulted in basophilic stippling and hemolytic anemia just like hereditary hemolytic anemia due to P5N deficiency.
D015720:5'-Nucleotidase; D000328:Adult; D000743:Anemia, Hemolytic / Q000097:blood / Q000139:chemically induced*; D004912:Erythrocytes / Q000201:enzymology; D005978:Glutathione / Q000097:blood; D006801:Humans; D007855:Lead Poisoning / Q000097:blood* / Q000150:complications; D008297:Male; D009708:Nucleotidases / Q000172:deficiency*; D000623:Porphobilinogen Synthase / Q000172:deficiency; D011742:Pyrimidine Nucleotides / Q000097:blood
D011742:Pyrimidine Nucleotides; D009708:Nucleotidases; D015720:5'-Nucleotidase; D000623:Porphobilinogen Synthase; D005978:Glutathione