14 patients with heavy metal poisoning received 2,3-dimercaptosuccinic acid (DMSA). 12 subjects were given 30 mg/kg/day for 5 days; 1 subject was started on a lower dose because of a history of atopy; another subject was treated for 15 days because of very high initial blood lead concentrations. In the 9 subjects who had lead poisoning, DMSA decreased blood lead concentrations by 35 to 81%, and induced a 4.5- to 16.9-fold increase in mean daily urinary excretion of the metal. In the acutely arsenic-poisoned case, the plasma arsenic concentration on day 7 was half the pretreatment value, while no clear decrease was observed in a chronically exposed subject. In 3 mercury cases, DMSA increased daily mercury urinary excretion 1.5-, 2.8- and 8.4-fold, respectively, while blood mercury concentrations remained below detection limits. No serious side effects were observed and 3 weeks after administration of the drug the clinical condition of all subjects was either stable or improved. These results indicate the efficacy of DMSA for lead poisoning in humans and provide a rationale for further investigating its usefulness in mercury and arsenic poisoning cases.

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The physiopathology of metabolic bone disease described during long term total parenteral nutrition is poorly understood. We therefore prospectively assessed bone status of seven adult patients [mean age, 42 +/- 16 (SD) yr] treated with cyclic total parenteral nutrition for a period of 7 +/- 2 (SD) months. All patients had hypercalciuria (381 +/- 96 mg/day) associated with negative calcium balance in six of seven patients (-49 +/- 120 mg/day). A correlation was found (r = +0.74, P less than 0.01) between protein intake and calciuria. Two patients developed slight transient hypercalcemia. Serum magnesium and phosphate levels remained within the normal range. A high aluminum load due to the added phosphate solution (253 +/- 84 micrograms/day) was associated with increased serum aluminum levels (52 +/- 38 micrograms/liter). Normal serum levels of 25 hydroxyvitamin D (12 +/- 7 ng/ml) and low normal 1,25 dihydroxyvitamin D levels (21 +/- 8 pg/ml) were found. Serum PTH was normal in five and increased in two of the seven patients. However, in these two patients skeletal unresponsiveness to the action of PTH was found. A new histomorphometric picture of bone was observed; it consisted of a markedly reduced bone formation with subnormal osteoclastic activity leading to a low trabecular bone volume. No osteomalacia was found. The aluminum load may have played a role in these bone defects. The hypercalciuria with negative calcium balance was attributed to the cyclic amino-acid delivery during TPN.