Response to Treatment with Chelating Agents of Anaemia, Chronic Encephalopathy, and Myelopathy Due to Lead Poisoning.

Chronic lead poisoning is a well-known clinical entity which is now becoming uncommon as a result of improvements in industrial hygiene applied to workers with lead. The patient with chronic lead poisoning presents commonly with abdominal pain and constipation, less commonly with a neuropathy, and rarely with a refractory anaemia. Encephalo-pathy due to lead poisoning is common in childhood but rare in adult life. The diagnosis is usually confirmed by the finding of an excess of lead in the blood and urine. The present case showed rather unusual features of chronic lead poisoning; special techniques were involved in the investigation of the neurological and haematological abnormalities and the results provide information of fundamental interest on the effects of lead on these systems. METHODS The routine investigations were carried out by the accepted standard laboratory methods. The radioactive chromium (51Cr) technique for estimating haemolysis was based on the method of Mollison and Veall (1955) and carried out as described by Goldberg and Seaton (1960). Red cell volume was calculated from the radioactivity in a sample of venous blood obtained 20 minutes after the injection of the 5'Cr-labelled cells, by the dilution principle. Radioiron (59Fe) uptakes and utilization tests were carried out as described by Ledlie and Baxter (1954) and Wetherley-Mein, Hutt, Langmead, and Hill (1956). Serum B12 assay was carried out by the Fuglena gracilis method of Hutner, Bach, and Ross (1956). Electroencephalography was carried out by routine techniques. Co-axial needle electrodes with conventional amplification and cathode-ray oscilloscope recording were used for electromyography, and motor nerve conduction velocity was determined by the method of Simpson (1956). Neuromuscular transmission was investigated according to the method of Harvey and Masland (1941). The patient was a 39-year-old man employed as an acetylene burner for over 20 years and treated in 1949 for abdominal pain and constipation caused by lead poisoning. In 1955 he began to have giddy turns and occasional 'blackouts' if working in confined spaces and by October 1957 these attacks were more frequent. His blood pressure then was 110/70 mm.Hg and he had moderate anaemia (Hb 76%) with reticulocytosis (6-5 %). About this date he noticed weakness and wasting of his right hand. Radiographs of the cervical spine did not reveal a cause for the weakness. In January 1960 he was admitted to the Western Infirmary of Glasgow as the severity of his weakness was such that he was unable to feed …