Arch Dis Chilh 34:70-3, 1959, pp 70, 73

In 1926, McKhann described three cases of lead poisoning in small children; he noticed, among other symptoms and signs, that marked but transient glycosuria was present in two of the three cases. Seven years later McKhann and Vogt (1933) reviewed all the case notes of children with lead poisoning admitted to the Boston Infants and Children’s Hospitals between the years 1924 and 1933. These amounted to 89 cases, and the presence of glycosuria had been noted ‘frequently’ especially in the presence of encephalopathy. In a similar review from New York Goettsch and Mason (1940) collected records of 39 cases of lead poisoning between 1923 and 1938; in this series the incident of glycosuria was 20%. In one of the cases glycosuria persisted for five weeks. More recently Ennis and Harrison (1950) found glycosuria in four out of 10 cases of lead poisoning. Burrows, Rendle-Short and Hanna (1951) reported that glycosuria was commonly found in such cases. Six years ago, one of us (R.C.R.) in conjunction with Millichap and Llewellin (1952) reported five cases of lead poisoning in young children due to ingestion of paint. It was noticed at that time that two of the cases had had glycosuria for a short period at the onset, but the diagnosis in those cases had been established on other evidence.

Further reports of childhood lead poisoning have come from Zak and Finkelstein (1952), Gianattasio, Bedo and Pirozzi (1952), Wilson, Thomson and Dent (1953), Byers, Maloof and Cushman (1954), Marsden and Wilson (1955) Tanis (1955), and O’Donohoe (1956). In many of these cases it had been noticed that glycosuria was present.

However, it had apparently been an incidental finding and the purpose of this paper is to show the diagnostic value of glycosuria, especially in the cases of lead poisoning without encephalopathy. In the following three cases, seen consecutively, it was the presence of marked glycosuria in the absence of a raised blood sugar level that led to a search for other evidence of lead poisoning.

[Any] child who is otherwise unwell, the diagnosis of lead poisoning must always be considered.

The experience gained during the treatment of the cases with oral calcium di-sodium Versenate leads us to suggest that prolonged courses are without danger to the patient and, in addition, continue to enhance the renal excretion of lead in increased amounts. That the excretion of lead should be as complete as possible is shown by Henderson (1954) from Queensland, Australia, who gives evidence of the danger of chronic renal disease occurring in young adults who had been afflicted with lead poisoning in childhood. So far, no such series of cases has been reported in this country.

Three further cases of lead poisoning in children are described. The diagnosis of the condition was reached at an early stage after admission to hospital because of the discovery of glycosuria, which led to further tests for lead poisoning. The glycosuria persisted for three weeks. There was no evidence of residual renal damage at the end of six months. All three cases were treated with prolonged courses of oral calcium di-sodium Versenate resulting in prolonged excretion of lead in the urine.

Evidence is put forward to suggest that colored crayons of the yellow and orange ranges may be a danger to children on account of their content of lead chromate.

We are grateful to Dr. Helen Mackay, to Dr. C.T. Porter, and to Dr. Richard Dobbs for permission to publish these cases which were under their care: to Dr. J.A. Bonnell for much assistance, advice and many urine-lead estimations carried out in the Department for Industrial Medical Research at the London Hospital; to Dr. B. Levin for numerous laboratory investigations at the Queen Elizabeth Hospital.

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