Excess mercury in the tissues is tightly bound to sulphur-containing amino acids and normally poorly excreted into the urine. The oral administration of 15 mg of DMSA per kg body weight is used to provoke the release and excretion of mercury; subjects with excess tissue storage of mercury will at least double their urine concentration of the metal over a 2.5 hour period post oral DMSA. In the absence of excess metal sequestration no significant increase in urinary mercury excretion will be observed.
DMSA will also chelate other heavy metals, so while this is primarily used as a challenge test for mercury overload, other toxic metals can also be usefully measured in the urine samples provided.
Mercury is a toxic metal with no known biological essentiality in man and its presence in any concentration can be regarded as harmful under certain circumstances.
There is no clearly defined reference interval for the increment in mercury production post DMSA; ideally the molar mercury/creatinine ratio in the basal sample should be less than 0.50, while that in the DMSA-provoked sample should be less than 1.00. The reference interval quoted on the report for the basal urine mercury/creatinine ratio (less than 2.00) reflects the current excessive dietary and environmental intake of mercury in this population.
However, a "normal" DMSA provocation test result (i.e. no excessive body mercury present) can be taken as an increase in urine mercury (corrected for creatinine concentration) of less than 100 % (= twice the initial value) and below 2.00 mmol Hg per mole of of creatinine.
Co-administration of chelating agents and other substances promoting metal excretion will influence the results of the DMSA provocation test, principally to raise the basal mercury/creatinine ratio and blunt the response to DMSA.
1. Aposhian HV. DMSA and DMPS water-soluble antidotes for heavy metal poisoning. Ann Rev Pharmacol Toxicol. 1983;23:193-215.
2. Daunderer M. Mobilisation test for environmental metal poisoning. Forum des Praktischen und Allgemenden-Arztes 1989;28:88.
3. Aposhian HV, Bruce DC, Alter W, Dart RC, Hurlbut KM, Aposhian MM. Urinary mercury after administration of DMPS: correlation with dental amalgam score. FASEB J 1992;6:2472-2476.
4. Hibberd AR, Howard MA, Hunnisett AG. Mercury from dental amalgam fillings: studies on oral chelating agents for assessing and reducing mercury burdens in humans. J Nutr Environ Med 1998;8:219-231.
5. Jones MM New developments in therapeutic chelating agents as antidotes for metal poisoning. Crit Revs in Toxicol 1991;21:209-233.
6. Liebelt EL, Shannon M, Graef JW. Efficacy of oral meso-2,3-dimercaptosuccinic acid therapy for low-level childhood plumbism. J Pediatr 1994;124:313-317.
7. Volans GN, Karalliedde L, Wiseman HM. Review of succimer for treatment of lead poisoning. Medical Toxicology Information Services, Mary Sheridan House, Guy's Hospital, London SE1 9RT, 2010.
8. Bridges CC, Joshee L, Zalups RK. Effect of DMPS and DMSA on the placental and fetal disposition of methylmercury. Placenta 2009;30:800-805.
9. Piepsz1A, Colarinha P, Gordon I et al. EANM guidelines on 99mTc-DMSA scintigraphy in children. Eur J Nucl Med. 200;28:37-41.
10. Miller NJ, Howard MA. Dimercaptosuccininc acid loading test for assessing mercury burden in healthy individuals. Ann Clin Biochem 2004;41:422-423.
11. Bradstreet J, Geier DA, Kartzinel JJ, Adams JB, Geier MR. A Case-Control Study of Mercury Burden in Children with Autistic Spectrum Disorders. J Am Phys Surg. 2003;8:76-79.