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Am J Gastroenterol 2003 Jan;98(1):175-9
Office of Drug Safety, Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20857, USA.
OBJECTIVE: Troglitazone, a thiazolidinedione antidiabetic agent, was withdrawn from the U.S. market in March, 2000, after 94 cases of acute liver failure (ALF) were reported with its use. Based on a literature review, the estimated background rate of hospitalization for idiopathic acute liver injury is 22 per million person-years and for idiopathic ALF, less than 1 per million person-years. This study was conducted to estimate the incidence rates of hospitalized idiopathic acute liver injury and ALF among troglitazone-treated patients. METHODS: An observational retrospective inception cohort of patients treated with troglitazone was assembled using claims data from a large multistate health care organization. Patients with at least 90 days of health plan enrollment before their first troglitazone prescription between April, 1997 and December, 1998 were enrolled. Hospitalized cases of potential troglitazone-induced acute liver injury or ALF were identified from claims data based on International Classification of Diseases, 9th Revision, coding. Primary medical records were reviewed for case validation, and incidence rates of acute liver injury were calculated using person-years of troglitazone exposure as the denominator. RESULTS: A total of 7568 patients contributed 4020 person-years of troglitazone exposure. Of these, five were hospitalized with acute liver injury attributed to the drug and not explained by other causes. Incidence rates (95% CI) per million person-years of acute idiopathic liver injury were as follows: hospitalization (n = 5), 1244 (404, 2900); hospitalized jaundice (n = 4), 995 (271, 2546); and ALF (n = 1), 240 (6.3, 1385). CONCLUSIONS: Troglitazone use was associated with a marked increase in risk of hospitalized acute idiopathic liver injury and ALF.
PMID: 12526954, UI: 22414482
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Ann Pharmacother 2003 Apr;37(4):538-542
Curtis E Haas PharmD, Department of Pharmacy Practice, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, Buffalo, NY; Medical Research Services, VA Western NY Healthcare System, Buffalo; Department of Surgery, School of Medicine and Biological Sciences, University at Buffalo.
[Record supplied by publisher]
OBJECTIVE: To report a case of nontraumatic rhabdomyolysis complicated by oliguric, acute renal failure following an intentional overdose of ethanol and diphenhydramine. CASE SUMMARY: A 21-year-old white man was admitted through the emergency department following an intentional overdose of ethanol and diphenhydramine. The patient subsequently developed acute renal failure, and a diagnosis of nontraumatic rhabdomyolysis was made. With the absence of other common causes in this case, the rhabdomyolysis was believed to be due to the combined ethanol and diphenhydramine overdose. DISCUSSION: Rhabdomyolysis is a severe and life-threatening syndrome caused by various insults to skeletal muscle, including drug-induced injury. Early detection and institution of effective treatments are essential to minimizing the complications of this syndrome. A delay in establishing the diagnosis in this case likely contributed to the severity of the renal failure. CONCLUSIONS: Nontraumatic rhabdomyolysis is an uncommon adverse outcome of drug and toxin ingestion. Due to the potential severity of the complications of this syndrome and the importance of early recognition and treatment to prevent renal failure, clinicians should have a high index of suspicion for rhabdomyolysis following overdoses that involve alcohol or antihistamines.
PMID: 12659612
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BMJ 2003 Mar 1;326(7387):498
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PMID: 12617072, UI: 22501455
BMJ 2003 Feb 22;326(7386):447
PMID: 12595392, UI: 22483328
Int J Dermatol 2002 Nov;41(11):801-3
Universidad Central de Venezuela, Caracas. rodriguf@camelot.rect.ucv.ve
BACKGROUND: Ant sting reactions are becoming an increasing problem in tropical countries. It is important for physicians to be aware of their possible cutaneous and systemic manifestations. METHODS: A child with a severe allergic reaction to an ant sting was examined and is discussed. This is the first case described in the literature caused by the ant Odontomachus bauri, and the biology of the ant and the clinical signs in the patient are described. RESULTS: A child developed a strong allergic reaction to an ant sting. The case was not associated with a previous ant sting. Treatment with the systemic antihistamine loratadine (Clarityn) was favorable in this patient. CONCLUSIONS: In tropical areas, ant stings are usually benign, self-limited pathologic processes. In some cases, however, severe allergic reactions can develop, including urticaria and anaphylactic shock. Physicians should be aware of the possible complications of ant stings.
PMID: 12453010, UI: 22341674
J Clin Psychiatry 2003 Feb;64(2):219
PMID: 12633136, UI: 22521211
JAMA 2003 Mar 12;289(10):1230, 1233
PMID: 12633165, UI: 22521446
Lancet 2003 Mar 1;361(9359):743-9
Department of Molecular Microbiology, Osaka University, Osaka, Japan.
BACKGROUND: Vibrio parahaemolyticus, a gram-negative marine bacterium, is a worldwide cause of food-borne gastroenteritis. V parahaemolyticus strains of a few specific serotypes, probably derived from a common clonal ancestor, have lately caused a pandemic of gastroenteritis. The organism is phylogenetically close to V cholerae, the causative agent of cholera. METHODS: The whole genome sequence of a clinical V parahaemolyticus strain RIMD2210633 was established by shotgun sequencing. The coding sequences were identified by use of Gambler and Glimmer programs. Comparative analysis with the V cholerae genome was undertaken with MUMmer. FINDINGS: The genome consisted of two circular chromosomes of 3288558 bp and 1877212 bp; it contained 4832 genes. Comparison of the V parahaemolyticus genome with that of V cholerae showed many rearrangements within and between the two chromosomes. Genes for the type III secretion system (TTSS) were identified in the genome of V parahaemolyticus; V cholerae does not have these genes. INTERPRETATION: The TTSS is a central virulence factor of diarrhoea-causing bacteria such as shigella, salmonella, and enteropathogenic Escherichia coli, which cause gastroenteritis by invading or intimately interacting with intestinal epithelial cells. Our results suggest that V parahaemolyticus and V cholerae use distinct mechanisms to establish infection. This finding explains clinical features of V parahaemolyticus infections, which commonly include inflammatory diarrhoea and in some cases systemic manifestations such as septicaemia, distinct from those of V cholerae infections, which are generally associated with non-inflammatory diarrhoea.
PMID: 12620739, UI: 22508454
MMWR Morb Mortal Wkly Rep 2003 Mar 14;52(10):199-201
[Medline record in process]
Illegally imported foreign products can result in domestic exposures to unusual toxic chemicals, and health-care providers might not be able to provide appropriate therapy because the chemical ingredients might not be listed or recognized even after translation of the product label. This report describes the first known case in the United States of exposure to a Chinese rodenticide containing the toxin tetramethylenedisulfotetramine (TETS), a convulsant poison. The report of this investigation highlights the need to prevent such poisonings through increased public education, awareness, and enforcement of laws banning the importation of illegal toxic chemicals.
PMID: 12653458, UI: 22539935
Toxicol Sci 2002 Oct;69(2):470-81
Department of Pharmacology and Toxicology, Institute for Environmental Toxicology, 214 Food Safety and Toxicology Building, Michigan State University, East Lansing, MI 48824, USA.
Noninjurious doses of bacterial endotoxin (lipopolysaccharide; LPS) enhance allyl alcohol-induced liver damage in rats in a Kupffer cell (KC)-dependent fashion. To investigate the mechanism by which KCs contribute to liver injury in this model, isolated KCs and hepatocytes (HCs) were cocultured. Addition of LPS to the cocultured cells did not enhance allyl alcohol-induced cytotoxicity. In addition, recirculating perfusion of isolated livers from naive rats with LPS for 2 h did not significantly enhance allyl alcohol-induced toxicity as measured by release of alanine aminotransferase (ALT). These results suggest an extrahepatic factor is required for LPS potentiation of allyl alcohol hepatotoxicity. To examine whether the coagulation cascade contributes to injury in this model, rats were given either warfarin at 42 and 18 h before LPS, or heparin at 1 h before LPS, and were treated with allyl alcohol 2 h after LPS. Warfarin and heparin each significantly blocked the decrease in plasma fibrinogen levels and attenuated the increase in plasma ALT activity in rats treated with LPS and allyl alcohol. To assess the role of thrombin in this injury, isolated livers from rats pretreated with LPS were perfused with thrombin or vehicle and allyl alcohol. Though LPS pretreatment enhanced the toxicity of allyl alcohol compared with livers from naive rats, perfusion with thrombin did not increase sensitivity to allyl alcohol. In summary, LPS augments the hepatotoxicity of allyl alcohol through a mechanism involving extrahepatic factors, one of which may be a component of the coagulation cascade.
PMID: 12377996, UI: 22266172
Toxicol Sci 2002 Oct;69(2):354-61
Department of Pharmacology and Toxicology, University of Otago, 18 Frederick Street, Rm. 238 Adams Building, Dunedin, New Zealand.
Recent investigations have demonstrated that polyphenolic catechins inhibit breast cancer cell proliferation and tumor growth. However, the ER-mediated effects of the three predominant catechins (EGCG, ECG, and EGC) have not been extensively examined in vitro or in vivo. Therefore, EGCG, ECG, and EGC were examined for their ability to compete with [(3)H]-17beta-estradiol ([(3)H]-E(2)) for binding to ERalpha and ERbeta and to elicit reporter gene activity in MCF-7 human breast cancer cells transiently transfected with either chimeric ERalpha or ERbeta. EGCG and ECG displaced [(3)H]-E(2) from GST-hERalphadef (D, E, and F domains of human ERalpha fused to GST) or from full-length human ERbeta. Additionally, only EGCG elicited Gal4-hERalphadef and Gal4-mERbetadef-mediated reporter gene expression (EC(50) values: 28 and 19 micro M, respectively) in MCF-7 cells cotransfected with a Gal4-regulated luciferase reporter gene. In cotreatment experiments, EGCG (1-50 micro M) and ECG (1 micro M) decreased E(2)-induced (1 nM) ERbeta-mediated gene expression 35-50%. In vivo, no catechin induced estrogenic responses (uterine weight or uterine peroxidase activity) in immature C57BL/6 mice. However, when mice were cotreated with E(2) (10 micro g/kg/day, 3 days) and either EGCG (30 and 50 mg/kg/day, 3 days) or ECG (50 mg/kg/day, 3 days), uterine peroxidase activity was increased 2.3-fold above that elicited by E(2) alone. In conclusion, EGCG and ECG bind to ERalpha and ERbeta, but only EGCG elicited ER-mediated gene expression in vitro. However, both of these compounds moderately increased E(2)-inducible responses in vivo.
PMID: 12377984, UI: 22266160