Urine glycolic acid

Biodegradation of the aliphatic polyesters occurs by bulk erosion. The lactide/gly-colide polymer chains are cleaved by random nonenzymatic hydrolysis to the monomeric lactic and glycolic acids and are eliminated from the body through the Krebs cycle, primarily as carbon dioxide and in urine. 

In six men exposed one-arm only to 50 ppm [ 2] 2-butoxyethanol for 2 hours, about two-thirds of the 2-butoxyacetic acid excreted in the urine was in the form of the A-butoxyacetyl glutamine conjugate (Corley et al. 1997). No free 2-butoxyethanol, free or conjugated ethylene glycol ether, or glycolic acid (a metabolite of ethylene glycol) were detected in the urine. 2-Butoxyacetic acid was eliminated in the urine primarily during the first 12-hour collection period. 

It is impossible to distinguish these two types of oxaluria without careful biochemical investigation of the blood and the urine, and without direct attempts to identify the enzyme defect. The crucial difference between glycolic and glyceric aciduria is precisely that in addition to oxalate, glycolic acid accumulates in primary oxaluria, whereas glyceric acid accumulates in the second type [106, 107]. 

Dietzen DJ, Wilhite TR, Kenagy DN, Milliner DS, Smith CH, Landt M Extraction of glyceric and glycolic acids from urine with tetrahydrofuran utility in detection of primary hyperoxaluria. Clin Chem 1997 43 1315-1320. 

Pronethalol, adrenergic blocker . Metabolized.via 2 pathways (a), N-dealkylation follo /ed by oxidation, forming 2-naphthyl-glycollic acid (m) which is oxidatively decarboxylated (m) ( ), ring hydroxylation at C-7 and glue. UP (t) in urine. species difference in pathway. 

Three stages of ethylene glycol overdose occur. Within the first few hours after ingestion, there is transient excitation followed by CNS depression. After a delay of 4-12 hours, severe metabolic acidosis develops from accumulation of acid metabolites and lactate. Finally, delayed renal insufficiency follows deposition of oxalate in renal tubules. The key to the diagnosis of ethylene glycol poisoning is recognition of anion gap acidosis, osmolar gap, and oxalate crystals in the urine in a patient without visual symptoms. 

Only minimal amounts of a topically applied dose are absorbed through normal stratum corneum. Percutaneously absorbed propylene glycol is oxidized by the liver to lactic acid and pyruvic acid, with subsequent utilization in general body metabolism. Approximately 12-45% of the absorbed agent is excreted unchanged in the urine. 

Twenty-four-hour or spot urine should be collected in the presence of HC1. Add 10 ml of 20% (v/v) HC1 per liter of urine. Keep samples frozen at -20°C. Before injection into the HPLC system, dilute the urine (1) for oxalate 0.2 ml of centrifuged (3000 xg for 5 min) urine with 1.8 ml of 0.3 M boric acid (see below) (2) for glycolate and glycerate 0.2 ml of centrifuged (3000 xg for 5 min) urine with 1.8 ml of water. 

When Rinaldo analyzed Ryan s blood serum, he found high concentrations of methylmalonic acid, a breakdown product of the branched-chain amino acids isoleucine and valine, which accumulates in MMA patients because the enzyme that should convert it to the next product in the metabolic pathway is defective. And particularly telling, he says, the child s blood and urine contained massive amounts of ketones, another metabolic consequence of the disease. Like Shoemaker, he did not find any ethylene glycol in a sample of the baby s bodily fluids. The bottle couldn t be tested, since it had mysteriously disappeared. Ri-naldo s analyses convinced him that Ryan had died from MMA, but how to account for the results from two labs, indicating that the boy had ethylene glycol in his blood Could they both be wrong ... 

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