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Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

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ASU<br />

8644<br />

0-24 mcg/L<br />

Reference values apply to all ages.<br />

Clinical References: Caldwell KL, Jones RL, Verdon CP, et al: Levels of urinary total and speciated<br />

arsenic in the US population: National Health and Nutrition Examination Survey 2003-2004. J Expo Sci<br />

Environ Epidemiol 2009;19:59-68<br />

Arsenic, 24 Hour, Urine<br />

Clinical Information: Arsenic is perhaps the best known of the metal toxins, having gained notoriety<br />

from its extensive use by Renaissance nobility as an antisyphilitic agent and, paradoxically, as an antidote<br />

against acute arsenic poisoning. Even today, arsenic is still 1 of the more common toxicants found in<br />

insecticides, and leaching from bedrock to contaminate groundwater. The toxicity of arsenic is due to 3<br />

different mechanisms, 2 of them related to energy transfer. Arsenic covalently and avidly binds to<br />

dihydrolipoic acid, a necessary cofactor for pyruvate dehydrogenase. Absence of the cofactor inhibits the<br />

conversion of pyruvate to acetyl coenzyme A, the first step in gluconeogenesis. This results in loss of<br />

energy supply to anaerobic cells, the predominant mechanism of action of arsenic on neural cells that rely<br />

on anaerobic respiration for energy. Neuron cell destruction that occurs after long-term energy loss results<br />

in bilateral peripheral neuropathy. Arsenic also competes with phosphate for binding to adenosine<br />

triphosphate during its synthesis by mitochondria via oxidative phosphorylation, causing formation of the<br />

lower energy adenosine diphosphate monoarsine. This results in loss of energy supply to aerobic cells.<br />

Cardiac cells are particularly sensitive to this form of energy loss; fatigue due to poor cardiac output is a<br />

common symptom of arsenic exposure. Arsenic furthermore binds avidly with any hydrated sulfhydryl<br />

group on protein, distorting the 3-dimensional configuration of that protein, causing it to lose activity.<br />

Interaction of arsenic with epithelial cell protein at the sites of highest physiologic concentration, the<br />

small intestine and proximal tubule of the kidney, results in cellular degeneration. Epithelial cell erosion<br />

in the gastrointestinal tract and proximal tubule are characteristic of arsenic toxicity. Arsenic is also a<br />

know carcinogen, but the mechanism of this effect is not definitively known. A wide range of signs and<br />

symptoms may be seen in acute arsenic poisoning including headache, nausea, vomiting, diarrhea,<br />

abdominal pain, hypotension, fever, hemolysis, seizures, and mental status changes. Symptoms of chronic<br />

poisoning, also called arseniasis, are mostly insidious and nonspecific. The gastrointestinal tract, skin, and<br />

central nervous system are usually involved. Nausea, epigastric pain, colic abdominal pain, diarrhea, and<br />

paresthesias of the hands and feet can occur. Arsenic exists in a number of different forms; organic forms<br />

are nontoxic, inorganic forms are toxic. See ASFR/80375 Arsenic Fractionation, 24 Hour, Urine for<br />

details about arsenic forms. Because arsenic is excreted predominantly by glomerular filtration, analysis<br />

for arsenic in urine is the best screening test to detect arsenic exposure.<br />

Useful For: Preferred screening test for detection of arsenic exposure<br />

Interpretation: Normally, humans consume 5 to 25 mcg of arsenic each day as part of their normal<br />

diet; therefore, normal urine arsenic output is

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