Propylene glycol-induced proximal renal tubular cell injury.

Propylene glycol is a solvent that is used in many oral, injectable, and topical medications. Although uncommon, acute renal failure has been attributed to propylene glycol. The mechanism of propylene glycol-mediated renal injury is unknown. We report a case of acute renal failure in a 16-year-old boy given large doses of pentobarbital and phenobarbital, both of which are solubilized with propylene glycol. A renal biopsy showed proximal renal tubular cell swelling and vacuole formation. The data from this case suggest that the reversible acute renal failure caused by propylene glycol is attributable to proximal renal tubular cell injury.

Affinity-purified, mixed monospecific crotalid antivenom ovine Fab for the treatment of crotalid venom poisoning.

SUBJECT OBJECTIVE: To test the efficacy and safety of a new antivenom, affinity-purified, mixed monospecific crotalid antivenom ovine Fab, in human subjects with minimal or moderate crotalid envenomation. METHODS: We conducted a prospective multicenter clinical trial of 11 patients 10 years or older with progressive manifestations after mild to moderate crotalid snakebite. After giving their consent, subjects received four to eight vials of study drug and were then repeatedly examined over 48 hours and at 7 and 14 days after discharge. Each patient's clinical condition was evaluated serially with the use of a validated severity score, as well as on the basis of the investigator's assessment. RESULTS: In all 11 subjects to the antivenom was judged by the investigator to have had a beneficial response. The severity score for each patient remained the same or decreased over the first 4 hours. However, two subjects demonstrated worsened condition 12 to 15 hours after antivenom administration. In no subject did an allergic reaction develop. CONCLUSION: In this patient group, affinity-purified, mixed monospecific crotalid antivenom ovine Fab was associated with a halt of progressive crotalid venom poisoning. Initial safety data are promising but must be addressed further in subsequent studies.

Successful treatment of crotalid-induced neurotoxicity with a new polyspecific crotalid Fab antivenom.

STUDY OBJECTIVE: To report the effectiveness of a new polyvalent crotalid antivenom on neurotoxicity associated with North American rattlesnake envenomation. Two syndromes of crotalid-induced neurotoxicity have been reported. In severe envenomation by Crotalus scutulatus scutulatus (Mojave rattlesnake), weakness and fasciculations of various muscle groups, including those innervated by cranial nerves, may develop. Occasionally respiratory insufficiency develops. The second neurotoxic effects is myokymia, a type of fasciculation most frequently reported after bites by Crotalus horridus horridus (timber rattlesnake) and Crotalus atrox (Western diamondback rattlesnake). Conventional polyvalent antivenom is often ineffective in the treatment of venom-induced neurotoxicity. METHODS: We report a case series of three patients envenomated by North American rattlesnakes, one of which was identified as C scutulatus scutulatus. All three patients experienced neurotoxicity with weakness, paresthesias, and dramatic fasciculations, along with other signs and symptoms of crotalid venom poisoning. RESULTS: The administration of new polyspecific crotalid antivenom made of ovine Fab was successful in immediately and completely reversing neurotoxicity in each of these patients. CONCLUSION: We report the use of a new antivenom for North American crotalid envenomation that seems to have efficacy in reversing neurotoxicity associated with these bites.

Pharmacokinetics of meso-2,3-dimercaptosuccinic acid in patients with lead poisoning and in healthy adults.

We compared the pharmacokinetics of meso-2,3-dimercaptosuccinic acid (DMSA) in three children with lead poisoning, three adults with lead poisoning, and five healthy adult volunteers. All subjects received DMSA orally. Maximum blood concentration and time to maximum blood concentration of total DMSA concentration were not statistically different among the groups. Unaltered DMSA was detected in the blood of all poisoned patients but in only one of five healthy volunteers. Elimination half-life of total DMSA (parent drug plus oxidized metabolites) was longer in children with lead poisoning (3.0 +/- 0.2 hours) than in adults with lead poisoning (1.9 +/- 0.4 hours) and healthy adults (2.0 +/- 0.2 hours). Renal clearance of total DMSA was greater in healthy adults (77.0 +/- 13.2 ml/min per square meter) than in either adults (24.7 +/- 3.3 ml/min per square meter) or children with lead poisoning (16.6 ml/min per square meter); renal clearance of the metabolites of DMSA was also greater in healthy adults (64.6 +/- 10.1 ml/min per square meter) than in either adults (35.4 +/- 8.4 ml/min per square meter) or children with lead poisoning (19.5 ml/min per square meter). The DMSA appeared to enter the erythrocytes of patients with lead poisoning to a greater extent than in healthy adults. We conclude that renal clearance of DMSA and its metabolites may be impaired and that the distribution of DMSA in children with lead poisoning may be different from that in adults.