Serum magnesium concentrations after repetitive magnesium cathartic administration

Severe hypermagnesemia has been reported by several authors after multiple doses of magnesium-containing cathartic are administered during management of a toxic ingestion. To evaluate the frequency and magnitude of serum magnesium elevations after the use of repetitive magnesium catharsis, we prospectively evaluated 102 patients who received multiple doses of magnesium citrate as a part of treatment of an overdose. Commonly ingested substances for which repetitive cathartic was administered were tricyclic antidepressants in 47%, aspirin in 17%, and phenytoin in 10%. For each case, serial electrolytes, blood urea nitrogen, creatinine, calcium and magnesium were obtained. Mean initial serum magnesium concentration was 1.8 +/- .03 mEq/L. After a mean 960 mL of magnesium citrate (9.22 g magnesium), final mean serum magnesium concentration was 2.5 +/- .05 mEq/L. Forty-seven patients (47%) developed an elevated (greater than 2.4 mEq/L) serum magnesium concentration, with 12 greater than 3.0 mEq/L. No correlation was found between total quantity of magnesium citrate administered and the increment in serum magnesium concentration. Our data indicate that serum magnesium concentrations consistently rise after repetitive magnesium citrate use. However, the magnitude of this rise appears modest. The elevation in serum magnesium concentration does not correlate with the quantity of magnesium administered. We conclude that with close monitoring, repetitive magnesium citrate can be administered without inducing severe hypermagnesemia (serum magnesium concentration greater than 5.0 mEq/L).     

In vivo metabolism of isoxicam in rats, dogs, and monkeys

Isoxicam is a long half-life nonsteroidal anti-inflammatory agent which undergoes extensive metabolism prior to elimination in animals and man. The major route of isoxicam transformation is hydroxylation of the methylisoxazole functionality to form hydroxymethylisoxicam, and cleavage of its benzothiazine moiety to give an oxoacetic acid metabolite. The metabolic pathway for scission of the benzothiazine moiety to the oxoacetic acid metabolite and to other potential metabolites is not known. To gain additional information on the metabolic fate of isoxicam, 14C-isoxicam labeled on the N-methyl group was administered to rats, dogs, and monkeys with urine and feces collected for metabolic profiling and identification. Identified as new metabolites of isoxicam were an open-ring sulfonamide, N-methylsaccharin, and saccharin. The formation of these metabolites suggests that isoxicam undergoes direct oxidative scission of its benzothiazine ring at carbon atom 3 to generate the observed open-ring sulfonamide, N-methylsaccharin, and oxoacetic acid metabolites.     

Cocaine exposure among children seen at a pediatric hospital

The results of 1,680 consecutive urine and serum toxicologic screens from 1,120 patients, performed in a children's hospital during a 19-month period were surveyed. Among this sample, 52 (4.6%) patients had specimens that contained cocaine and/or metabolite. Fifteen specimens contained ethanol, a benzodiazepine, or a narcotic in addition to cocaine. Four patients were neonates, whereas three were infants from 1 to 7 months of age. The remaining 45 patients were adolescents with a mean age of 19 years. Among the adolescents, 11 had a significant chronic illness. In 19 patients (37%), cocaine exposure was unsuspected until the results of testing for toxic substances were known. The reasons for hospital evaluation included depression/attempted suicide in 19 patients, seizure in five, chest pain in 5, motor vehicle accident in three, syncope in three, abdominal pain in two, pneumomediastinum in two, accidental self-immolation in one, and apnea in one. Twenty patients required medical hospitalization for a total of 268 patient-days. One patient, a neonate, died. There is a striking prevalence of cocaine exposure in the pediatric age group. Among adolescents, this exposure may occur despite the presence of chronic illness. Although the age distribution appears bimodal, infants and young children may also have unsuspected exposure to this toxin. Greater awareness of cocaine exposure in childhood will be needed by primary and tertiary care pediatricians to identify affected children and provide appropriate intervention.     

Rate of Disappearance of Infused Aged Albumin in Human Subjects

Human serum albumin stored for more than 10 years was studied. The biologic lifetime of this outdated albumin is only slightly shorter than that of freshly prepared human albumin. No determinations were done to determine safety or therapeutic efficacy.