Poisoning urinary excretion

In mammals, phenobarbital and phenytoin increase serum ceruloplasmin concentrations (Aaseth and Norseth 1986). Chronic copper poisoning in sheep is exacerbated when diets contain heliotrope plants (Heliotropium sp., Echium spp., Senecio sp.). Aggravated effects of the heliotrope plants include reduced survival and a twofold to threefold increase in liver and kidney copper concentrations when compared to control animals fed copper without heliotropes (Howell et al. 1991). Rats given acutely toxic doses of 2,3,7,8-tetrachlorodibenzo-para-dioxin had elevated concentrations of copper in liver and kidney because of impaired biliary excretion of copper (Elsenhans et al. 1991). Morphine increases copper concentrations in the central nervous system of rats, and dithiocarbam-ates inhibit biliary excretion (Aaseth and Norseth 1986). In human patients, urinary excretion of copper is increased after treatment with D-penicillamine, calcium disodium EDTA, or calcium trisodium diethylenetriamine penta acetic acid (Flora 1991). 

Penicillamine is used chiefly for treatment of poisoning with copper or to prevent copper accumulation, as in Wilson s disease (hepatolenticular degeneration). It is also used occasionally in the treatment of severe rheumatoid arthritis (see Chapter 36). Its ability to increase urinary excretion of lead and mercury had occasioned its use in outpatient treatment for intoxication with these metals, but succimer, with its stronger metal-mobilizing capacity and lower adverse-effect profile, has generally replaced penicillamine for these purposes. 

Barbiturates such as phenobarbital are weak acids. The toxicity of the barbiturate is mainly the result of the effects on the central nervous system. Only the nonionized form of the drug will distribute into the central nervous system. The proportion ionized will depend on the pKa and the pH of the blood. By increasing the pH of the blood using sodium bicarbonate administration to the poisoned patient, ionization of the barbiturate will be increased and distribution to tissues such as the brain will be decreased. Urinary excretion of the barbiturate will also be increased because the urinary pH will be increased. 

Aspirin, salicylates, and thiazide diuretics should not be used with allopurinol. The dose of mercaptopurine should be reduced one-third or one-fourth when used with allopurinol. Acute poisoning of colchicine should be treated with gastric lavage and activated charcoal administration. Supportive maintenance measures for blood pressure and respiration should be provided. Probenecid is used by athletes to inhibit the urinary excretion of banned anabolic steroids.85... 

Zambrano A, Mandovano S. 1956. Urinary excretion of picric acid, picramic acid, and of sulfoconjugation products in experimental tetryl poisoning. Folia Med. (Naples) 39 162-171. (Italian)... 

Symptoms of chronic mercury poisoning have been reviewed (4-6). The symptoms are listed in Table 1. The urinary tract is very sensitive to poisoning by all forms of mercury, a sensitive indicator of early injury being a rise in the urinary excretion of A-acetyl-beta-D-glucosamini-dase (NAG) (7). 

In humans, dogs, and rats, 2-amino-4-nitrophenol was found to be the major excretory product. Humans can slowly eliminate both the unchanged compound and the previously mentioned metabolites. Urinary excretion is considered to be the main route of elimination of dinitrophenols. The half-life in the serum of a severely poisoned farmer was calculated to be 13.5 days. The residence half-life in humans is estimated to be 5-14 days. The elimination half-life for dinitrophenols in mice was 6 h. 

Myslak Z, Piotrowski JK, Musialowicz E. 1971. Acute nitrobenzene poisoning A case report with data on urinary excretion of p-nitrophenol and p-aminophenol. Arch Toxikol 28 208-213. 

Succimer, a heavy-metal-chelating agent, is used in the treatment of lead poisoning in children with blood levels about 45 mcg/dl. Succimer forms water soluble chelate with lead, increasing the urinary excretion. 

The concentration of lead in blood is an indication of recerd absorption of the metal. Clinical manifestations associated with increasing concentrations of lead in blood are shown in Figure 65-2. Children with concentrations of lead in blood >10 pg/dL are at risk ( developmental disabilities. Adults with concentrations <30 pg/dL exhibit no known functional injury or symptoms however, they will have a definite decrease in S-ALA dehydratase activity, a slight increase in urinary excretion of S-ALA, and an increase in erythrocyte protoporphyrin. Patients with a blood lead concentration of 30-75 pg/dL have all the preceding laboratory abnormalities and, usually, nonspecific, mild symptoms of lead poisoning. Clear symptoms of lead poisoning are associated... 

Lead is excreted in both urine and feces. However, true alimentary excretion is small and most of the lead in feces represents unabsorbed lead, while most absorbed lead is excreted by the kidneys. In normal individuals (no known exposure) the daily urinary excretion is 10-75 ng of lead, with the borderline at 80-100 /Ag/day (R4). Concentrations of 50 /ig/liter or greater generally indicate lead poisoning. Kehoe and co-workers have studied the excretion of lead in normal and lead-intoxi--cated individuals (K4-K6). Lead affects porphyrin metabolism (G7). 

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