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Am J Emerg Med 2003 Jan;21(1):89-90
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PMID: 12563594, UI: 22449945
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Ann Emerg Med 2003 Mar;41(3):396-399
Department of Emergency Medicine, New York University School of Medicine and the New York City Poison Control Center, New York, NY (Barrueto, Hoffman, Nelson), and the Department of Pathology and Laboratory Medicine, University of Louisville, Louisville, KY (Jortani, Valdes).
[Record supplied by publisher]
We describe a case of unintentional poisoning from a cardioactive steroid and the subsequent analytic investigation. A 36-year-old woman with no past medical history and taking no conventional medications ingested an herbal preparation marketed for "internal cleansing." Its ingredients were neither known to the patient nor listed on the accompanying literature. The next morning, nausea, vomiting, and weakness developed. In the emergency department, her blood pressure was 110/60 mm Hg, and her pulse rate was 30 beats/min. Her ECG revealed a junctional rhythm at a rate of 30 beats/min and a digitalis effect on the ST segments. After empiric therapy with 10 vials of digoxin-specific Fab (Digibind), her symptoms resolved, and she reverted to a sinus rhythm at a rate of 68 beats/min. Her serum digoxin concentration measured by means of the fluorescence polarization immunoassay (Abbott TDx) was 1.7 ng/mL. Further serum analysis with the Tina Quant digoxin assay, a more digoxin-specific immunoassay, found a concentration of 0.34 ng/mL, and an enzyme immunoassay for digitoxin revealed a concentration of 20 ng/mL (therapeutic range 10 to 30 ng/mL). Serum analysis by means of high-performance liquid chromatography revealed the presence of active digitoxin metabolites; the parent compound was not present. When the diagnosis of cardioactive steroid poisoning is suspected clinically, laboratory analysis can confirm the presence of cardioactive steroids by using immunoassays of varying specificity. An empiric dose of 10 vials of digoxin-specific Fab might be beneficial in patients poisoned with an unknown cardioactive steroid.
PMID: 12605208
Ann Emerg Med 2003 Feb;41(2):280; author reply 280
PMID: 12572561, UI: 22459774
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BMJ 2003 Mar 1;326(7387):466
[Medline record in process]
PMID: 12609925, UI: 22496640
JAMA 2003 Feb 19;289(7):836-8
PMID: 12599365, UI: 22485881
JAMA 2003 Feb 19;289(7):834-6
PMID: 12599363, UI: 22485879
Toxicol Sci 2002 Sep;69(1):279-85
Children's Research Institute, Center for Developmental Pharmacology and Toxicology, and Department of Pediatrics, Children's Hospital, The Ohio State University, Columbus, Ohio 43205, USA. rogersl@chi.osu.edu
The present studies were to test the hypotheses that glutathione reductase (GR), glutathione peroxidase (GPX), and glutathione S-transferase (GST) activities are expressed in nuclei and nucleoli of rat liver cells, and that differences in activities of these enzymes would correlate with the greater resistance of female than of male Fischer-344 rats to hepatic necrosis in vivo, mediated by reactive oxygen species generated by redox-cycling metabolism of diquat. Adult male and female Fischer-344 rats were treated with comparably hepatotoxic doses of diquat (0.1 or 0.2 mmol/kg, respectively), or equal volumes of saline, ip. Six hours later, the livers were harvested, and purified nuclei and nucleoli were isolated by differential centrifugation. Nuclear GR activities in male and female rats were 12 and 15 mU/mg protein, and nucleolar activities were 30 and 51 mU/mg protein, respectively, p < 0.05. Some differences between male and female rats in nuclear and nucleolar activities of GPXs and GSTs were observed, as were some differences in the respective diquat-treated animals, but implications of these differences for susceptibility to diquat-induced oxidant stress effects are not apparent. Nuclear GR, GPX, and GST probably contribute to antioxidant defense mechanisms, but the functions served by localization of GR and GPX in nucleoli are less evident.
PMID: 12215683, UI: 22204654
Toxicol Sci 2002 Sep;69(1):157-64
Department of Physiological Sciences, College of Veterinary Medicine, 264 Veterinary Medicine Building, Oklahoma State University, Stillwater, Oklahoma 74078, USA.
Pyridostigmine, a carbamate cholinesterase (ChE) inhibitor, has been used for decades in the treatment of the autoimmune disorder myasthenia gravis and was used prophylactically to protect soldiers from possible organophosphorus nerve agent exposures during the Persian Gulf War. Pyridostigmine is a charged, quaternary compound and thus would not be expected to easily pass the blood-brain barrier. Some studies have suggested, however, that stress may alter blood-brain barrier integrity and allow pyridostigmine to enter the brain. We evaluated the effects of acute and repeated restraint stress on functional signs of cholinergic toxicity (i.e., autonomic dysfunction and involuntary movements) and brain regional cholinesterase inhibition following either acute or repeated pyridostigmine exposures. The acute, oral maximum-tolerated dosage (MTD) of pyridostigmine was estimated at 30 mg/kg. Peak ChE inhibition in whole blood occurred from 0.5 to 4 h after MTD exposure, whereas minimal (<20%) brain ChE inhibition was noted. For acute restraint studies, rats were either (1) restrained for 90 min and then given pyridostigmine (30 mg/kg, po), (2) given pyridostigmine and immediately restrained for 60 min, or (3) restrained for 3 h, given pyridostigmine, and restrained for an additional 60 min. In all cases, rats were evaluated for cholinergic toxicity (SLUD signs and involuntary movements) and sacrificed 1 h after pyridostigmine treatment. Plasma corticosterone was significantly elevated immediately after a single 60-min session of acute restraint stress, but returned to control levels by 1 and 3 h later. Pyridostigmine-induced toxicity was not enhanced nor was brain ChE inhibition altered by acute restraint stress. Blood-brain barrier permeability, assessed by accumulation of horseradish peroxidase in brain regions following intracardiac injection, was not increased by restraint stress. For repeated restraint studies, rats were given pyridostigmine (0, 3, or 10 mg/kg/day) immediately prior to daily restraint (60 min) for 14 consecutive days. Plasma corticosterone was elevated at 1 and 7 days but not at 14 days. Pyridostigmine-treated rats in both dosage groups exhibited slight signs of toxicity for the first 3-5 days, after which cholinergic signs dissipated. Repeated restraint had little effect on functional signs of pyridostigmine toxicity, however. Whole blood and diaphragm ChE were markedly reduced 1 h after the last treatment, but stress had no influence on ChE inhibition in either peripheral or central tissues. The results suggest that acute and repeated restraint stress have little effect on pyridostigmine neurotoxicity or apparent entry of pyridostigmine into the brain.
PMID: 12215670, UI: 22204641