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Pharmacokinetic effects of diphenhydramine or oxycodone in simulated acetaminophen overdose.
Halcomb SE, Sivilotti ML, Goklaney A, Mullins ME.
Division of Emergency Medicine, Washington University School of Medicine, Campus Box 8072, 660 South Euclid Avenue, St. Louis, MO 63110. mullinsm@wustl.edu.
OBJECTIVES: To determine the effects of co-ingested diphenhydramine (DPH) or oxycodone (OXY) on the absorption kinetics of simulated acetaminophen (APAP) overdose. METHODS: This was an institutional review board-approved, prospective crossover study of ten healthy human volunteers ingesting 5 grams of APAP, 5 grams of APAP + 250 mg of DPH (APAP+DPH), or 5 grams of APAP + 0.5 mg/kg of OXY (APAP+OXY). Serum APAP concentrations (APAPs) were measured hourly from zero through eight hours and again at 24 hours, and basic noncompartmental pharmacokinetic parameters were compared. RESULTS: For APAP alone, the mean parameters were: maximum APAP concentration ([APAP](max)) 71.8 mug/mL, time to peak [APAP] (t(max)) 1.71 hours, and area under the receiver operating characteristic curve (AUC(0-8)) 318.3 mug-hr/mL. For APAP+DPH, the mean parameters were: [APAP](max) 67.6 mug/mL, t(max) 1.90 hours, and AUC(0-8) 297.7 mug-hr/mL. For APAP+OXY, the parameters were: [APAP](max) 42.9 mug/mL, t(max) 2.87 hours, and AUC(0-8) 232.1 mug-hr/mL. Compared with APAP alone, APAP+OXY had a 27% lower AUC, a 40% lower [APAP](max), and a 68% longer t(max). Co-ingested DPH had no significant effect on APAP absorption, except a 6% decrease in the AUC. CONCLUSIONS: Co-ingested OXY, but not DPH, delayed absorption of APAP. This suggests a potential role for activated charcoal administration beyond one hour postingestion after mixed ingestions that include OXY.
PMID: 15692141 [PubMed - in process]
Methanol poisoning and heparin: a dangerous couple?
Hernandez MA, Holanda MS, Tejerina EE, Gonzalez C, Lopez M, Hernandez JL.
Publication Types:
PMID: 15666275 [PubMed - in process]
Fluorouracil-induced neurotoxicity presenting with generalized tonic-clonic seizure.
Elkiran ET, Altundag K, Beyazit Y, Guler N, Kars A.
Publication Types:
PMID: 15494386 [PubMed - indexed for MEDLINE]
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Recurrent acute hepatitis associated with use of cetirizine.
Pompili M, Basso M, Grieco A, Vecchio FM, Gasbarrini G, Rapaccini GL.
Department of Internal Medicine, Universita Cattolica del Sacro Cuore, Rome, Italy. mpompilii@rm.unicatt.it
OBJECTIVE: To describe a case of recurrent acute hepatitis related to the use of cetirizine, a selective histamine(1)-receptor antagonist approved for the treatment of common allergic diseases. CASE SUMMARY: A 26-year-old man was hospitalized with a week-long history of weakness, nausea, anorexia, and hyperchromic urine, which had developed after 6 days of therapy with oral cetirizine 10 mg/day for allergic rhinitis. Admission laboratory testing revealed evidence of acute hepatitis and seropositivity for liver-kidney microsome antibodies. Liver biopsy findings of diffuse portal tract and lobular inflammation with a prominent eosinophilic infiltrate were consistent with drug-related hepatitis. The patient was discharged after one week of treatment with tocopherol and glutathione. Three months after discharge, transaminase levels were normal. At 6 months, seropositivity for liver-kidney microsome antibodies was still present, but considerably less intense. The patient had suffered 2 previous episodes of "acute hepatitis of unknown origin," and both had occurred after cetirizine use. DISCUSSION: Use of the Naranjo probability scale indicated cetirizine as the probable cause of acute hepatitis, and the positivity for liver-kidney microsome antibodies is suggestive of an autoimmune mechanism for liver damage. As of September 13, 2004, ours is the fourth reported case of acute hepatitis associated with cetirizine and the second in which liver-kidney microsome antibodies have been documented. CONCLUSIONS: Although cetirizine is considered to have low potential for severe hepatic toxicity, the possibility that it can provoke autoimmune-mediated hepatotoxicity should be considered.
Publication Types:
PMID: 15383643 [PubMed - indexed for MEDLINE]
Hospital admissions for drug and alcohol use in people aged under 45.
Williams S, Hickman M, Bottle A, Aylin P.
Dr Foster Unit, Imperial College.
PMID: 15649927 [PubMed - indexed for MEDLINE]
Benefits of magnesium sulfate in the management of acute human poisoning by organophosphorus insecticides.
Pajoumand A, Shadnia S, Rezaie A, Abdi M, Abdollahi M.
Poison Control Center, Loghman-Hakim Hospital, School of Medicine, Shaheed-Beheshti University of Medical Sciences, Tehran, Iran.
Organophosphorus chemicals (OPs) are the pesticides most often involved in serious human poisoning. Treatment of intoxication with OPs conventionally involves atropine for reduction of muscarinic signs and oximes that increase the rate of hydrolysis of the phosphorylated enzyme acetylcholinesterase (AChE). Although atropine and oximes (pralidoxime or obidoxime) are traditionally used in the management of such poisoning, their efficacy remains a major issue of debate; thus, the goal of this prospective clinical trial was to elaborate the value of magnesium sulfate (MgSO4) in the management and outcome of OP insecticide poisoning. This unicenter, randomized, single-blind trial study was conducted on patients who were acutely poisoned with OPs and admitted to the Poisoning Center of Loghman-Hakim Hospital in Tehran, Iran. In a systematic sampling, every fourth eligible patient was chosen to undergo MgSO4 treatment. Magnesium sulfate was administered at dose of 4 g/day i.v. continued for only the first 24 hours after admission. The mean daily oxime requirement and the mean daily atropine requirement were not statistically significant between two treated groups. The mortality rate and hospitalization days of patients who received MgSO4 treatment were significantly lower than those who had not received MgSO4 (P < 0.01). It is concluded that administration of MgSO4, in a dose of 4 g/day concurrent to conventional therapy, in OP acute human poisoning is beneficial by reducing the hospitalization days and rate of mortality.
PMID: 15688984 [PubMed - in process]
Phenprocoumon-induced liver disease ranges from mild acute hepatitis to (sub-) acute liver failure.
Schimanski CC, Burg J, Mohler M, Hohler T, Kanzler S, Otto G, Galle PR, Lohse AW.
First Department of Internal Medicine, University of Mainz, Langenbeckstrasse 1, 55101 Mainz, Germany. dr_schimanski@yahoo.de
BACKGROUND/AIMS: Except for bleeding complications, other serious adverse reactions of coumarin anticoagulants such as hepatotoxicity or skin necrosis are comparatively rare. Nonetheless, a small number of coumarin-induced (sub-) acute liver failures has been published. METHODS: A retrospective analysis was performed of patients treated for liver disease between 1992 and 2002 at our department to evaluate the incidence, clinical findings and histopathology of coumarin-induced hepatotoxicity. RESULTS: The retrospective analysis revealed eight cases of phenprocoumon-induced hepatotoxicity, including three cases of (sub-) acute liver failure which resulted in two orthotopic liver transplantations and one fatal outcome. Five patients with phenprocoumon-induced hepatitis recovered well after anticoagulation was switched to another coumarin derivate or subcutaneous low molecular weight heparin. In all patients liver injury was predominantly of an hepatitic type. In the cases of (sub-) acute liver failure massive confluent liver cell necroses were histologically present, whereas among patients without liver failure mild portal to moderate active lobular hepatitis were observed. A retrospective analysis by BfArM (German Federal Institute for Drugs and Medical Devices) revealed 4390 cases of possible phenprocoumon-related adverse reactions since 1990, 2% of which had presented with hepatitis and 0.2% with liver failure. CONCLUSIONS: Phenprocoumon-induced liver disease is an uncommon complication, which can, however, cause (sub-) acute liver failure.
Publication Types:
PMID: 15246210 [PubMed - indexed for MEDLINE]
A federal agency's role in fulfilling the public health core functions: the childhood lead poisoning prevention program model.
Niskar AS, Buchanan S, Meyer PA.
National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
The Institute of Medicine identified 3 core functions of public health: assessment, policy development, and assurance. Federal, state, and local public health agencies all have an obligation to provide these vital functions to ensure conditions in which people can be healthy. However, the few publications that provide core function applications only focus on applications at the local or state levels. The Centers for Disease Control and Prevention's Childhood Lead Poisoning Prevention Program uses a comprehensive public health approach. This article describes the Centers for Disease Control and Prevention's leading role in applying the core public health functions to prevent childhood lead poisoning.
PMID: 15692293 [PubMed - in process]
Erratum in:
- MMWR Morb Mortal Wkly Rep. 2005 Jan 28;54(3):76.
Elevated blood lead levels in refugee children--New Hampshire, 2003-2004.
Centers for Disease Control and Prevention (CDC).
As a result of reductions in lead hazards and improved screening practices, blood lead levels (BLLs) in children aged 1-5 years are decreasing in the United States. However, the risk for elevated BLLs (> or =10 microg/dL) remains high for certain populations, including refugees. After the death of a Sudanese refugee child from lead poisoning in New Hampshire in 2000, the New Hampshire Department of Health and Human Services (NHDHHS) developed lead testing guidelines to screen and monitor refugee children. These guidelines recommend 1) capillary blood lead testing for refugee children aged 6 months-15 years within 3 months after arrival in New Hampshire, 2) follow-up venous testing of children aged <6 years within 3-6 months after initial screening, and 3) notation of refugee status on laboratory slips for first tests. In 2004, routine laboratory telephone reports of elevated BLLs to the New Hampshire Childhood Lead Poisoning Prevention Program (NHCLPPP) called attention to a pattern of elevated BLLs among refugee children. To develop prevention strategies, NHDHHS analyzed NHCLPPP and Manchester Health Department (MHD) data, focusing on the 37 African refugee children with elevated BLLs on follow-up for whom complete data were available. This report describes the results of that analysis, which indicated that 1) follow-up blood lead testing is useful to identify lead exposure that occurs after resettlement and 2) refugee children in New Hampshire older than those routinely tested might have elevated BLLs. Refugee children in all states should be tested for lead poisoning on arrival and several months after initial screening to assess exposure after resettlement.
PMID: 15660019 [PubMed - indexed for MEDLINE]
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Escherichia coli O157:H7 infections associated with ground beef from a U.S. military installation--Okinawa, Japan, February 2004.
Centers for Disease Control and Prevention (CDC).
In February 2004, the Okinawa Prefectural Chubu Health Center (OCHC) and the Okinawa Prefectural Institute of Health and Environment (OIHE), Japan, investigated three cases of Escherichia coli O157:H7 infection in a Japanese family associated with eating ground beef. Public health officials from multiple agencies in Japan and the United States collaborated on this investigation, which resulted in a voluntary recall of approximately 90,000 pounds of frozen ground beef in the United States and at U.S. military bases in the Far East. This was the first reported instance in which Japanese public health officials identified contaminated, commercially distributed ground beef that was produced in the United States. This report summarizes epidemiologic and laboratory investigations conducted by OCHC and OIHE. The results underscore the importance of using standardized molecular subtyping methods throughout the world to facilitate international public health communication and intervention.
PMID: 15660018 [PubMed - indexed for MEDLINE]
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Unintentional non-fire-related carbon monoxide exposures--United States, 2001-2003.
Centers for Disease Control and Prevention (CDC).
Carbon monoxide (CO) is a colorless, odorless, poisonous gas that results from incomplete combustion of fuels (e.g., natural or liquefied petroleum gas, oil, wood, coal, or other fuels). CO sources (e.g., furnaces, generators, gas heaters, and motor vehicles) are common in homes or work environments and can put persons at risk for CO exposure and poisoning. Most signs and symptoms of CO exposure are nonspecific (e.g., headache or nausea) and can be mistakenly attributed to other causes, such as viral illnesses. Undetected or unsuspected CO exposure can result in death. To examine fatal and nonfatal unintentional, non-fire-related CO exposures, CDC analyzed 2001-2003 data on emergency department (ED) visits from the National Electronic Injury Surveillance System All Injury Program (NEISS-AIP) and 2001-2002 death certificate data from the National Vital Statistics System (NVSS). During 2001-2003, an estimated 15,200 persons with confirmed or possible non-fire-related CO exposure were treated annually in hospital EDs. In addition, during 2001-2002, an average of 480 persons died annually from non-fire-related CO poisoning. Although males and females were equally likely to visit an ED for CO exposure, males were 2.3 times more likely to die from CO poisoning. Most (64%) of the nonfatal CO exposures occurred in homes. Efforts are needed to educate the public about preventing CO exposure.
PMID: 15660017 [PubMed - indexed for MEDLINE]
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Tularemia associated with a hamster bite--Colorado, 2004.
Centers for Disease Control and Prevention (CDC).
In April 2004, the Colorado Department of Public Health and Environment (CDPHE) was notified about a boy aged 3 years with diagnosed tularemia associated with a hamster bite. Tularemia has not been associated previously with pet hamsters. CDPHE conducted an investigation to determine whether other owners of hamsters were at risk. Clinicians and public health officials should be aware that pet hamsters are a potential source of tularemia.
Publication Types:
PMID: 15635290 [PubMed - indexed for MEDLINE]
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Fatal rat-bite fever--Florida and Washington, 2003.
Centers for Disease Control and Prevention (CDC).
Rat-bite fever (RBF) is a rare, systemic illness caused by infection with Streptobacillus moniliformis. RBF has a case-fatality rate of 7%-10% among untreated patients. S. moniliformis is commonly found in the nasal and oropharyngeal flora of rats. Human infection can result from a bite or scratch from an infected or colonized rat, handling of an infected rat, or ingestion of food or water contaminated with infected rat excreta. An abrupt onset of fever, myalgias, arthralgias, vomiting, and headache typically occurs within 2-10 days of exposure and is usually followed by a maculopapular rash on the extremities. This report summarizes the clinical course and exposure history of two rapidly fatal cases of RBF identified by the CDC Unexplained Deaths and Critical Illnesses (UNEX) Project in 2003. These cases underscore the importance of 1) including RBF in the differential diagnoses of acutely ill patients with reported rat exposures and 2) preventing zoonotic infections among persons with occupational or recreational exposure to rats.
Publication Types:
PMID: 15635289 [PubMed - indexed for MEDLINE]
Developmental neurotoxicity of ketamine: morphometric confirmation, exposure parameters, and multiple fluorescent labeling of apoptotic neurons.
Scallet AC, Schmued LC, Slikker W Jr, Grunberg N, Faustino PJ, Davis H, Lester D, Pine PS, Sistare F, Hanig JP.
Division of Neurotoxicology, NCTR/FDA, Jefferson, Arkansas 72079, USA. AScallet@nctr.fda.gov
Ketamine is a widely used pediatric anesthetic recently reported (C. Ikonomidou et al., 1999, Science 283, 70-74) to enhance neuronal death in neonatal rats. To confirm and extend these results, we treated four groups of PND 7 rats with seven sc doses, one every 90 min, of either saline, 10 mg/kg ketamine, 20 mg/kg ketamine, or a single dose of 20 mg/kg ketamine. The repeated doses of 20 mg/kg ketamine increased the number of silver-positive (degenerating) neurons in the dorsolateral thalamus to a degree comparable to previous results (Ikonomidou et al., 1999, Science 283, 70-74), i.e., 28-fold vs. 31-fold respectively. However, blood levels of ketamine immediately after the repeated 20 mg/kg doses were about 14 micrograms/ml, about seven-fold greater than anesthetic blood levels in humans (J. M. Malinovsky et al., 1996, Br. J. Anaesth. 77, 203-207; R. A. Mueller and R. Hunt, 1998, Pharmacol. Biochem. Behav. 60, 15-22). Levels of ketamine in blood following exposure to the multiple 10 mg/kg doses of ketamine or to a single 20 mg/kg dose ranged around 2-5 micrograms/ml; although these blood levels are close to an anesthetic level in humans, they failed to produce neurodegeneration. To investigate the mode of ketamine-induced neuronal death, coronal sections were stained with both Fluoro-Jade B (a green fluorescent stain selective for neurodegeneration) and DAPI (a blue DNA stain), as well as for caspase-3 (using an antisera labeled red with rhodamine). These histochemical results confirmed the developmental neurotoxicity of ketamine, demonstrated that Fluoro-Jade B (FJ-B), like silver methods, successfully stained degenerating neurons in neonatal rats, and indicated that ketamine acts by increasing the rate of neuronal apoptosis.
PMID: 15254342 [PubMed - indexed for MEDLINE]
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Chronic low-level mercury exposure, BDNF polymorphism, and associations with self-reported symptoms and mood.
Heyer NJ, Echeverria D, Bittner AC Jr, Farin FM, Garabedian CC, Woods JS.
Battelle Centers for Public Health Research and Evaluation, Seattle, Washington, USA.
Recent reports have described neurobehavioral impairments in human subjects carrying a V66M polymorphism in the gene encoding brain-derived neurotrophic factor (BDNF). Inasmuch as ventral nervous system (CNS) deficits associated with this BDNF polymorphism are similar to those observed among subjects with chronic exposure to elemental mercury (Hg degrees ), we examined the potential effect of this BDNF polymorphism on symptoms and mood in an established cohort of dental practitioners with chronic low-level Hg degrees exposure. Self-reported symptoms and mood were obtained by computerized questionnaire from 193 male dentists (DTs) and 230 female dental assistants (DAs). Spot urine samples were analyzed for mercury concentrations to evaluate recent exposure. Detailed work histories were obtained to calculate chronic indices of Hg degrees exposure. Buccal cell samples were obtained to identify the V66M polymorphism of BDNF. Scores for 11 current and 12 recent and chronic symptom groups, along with six mood factors, were evaluated with respect to recent and chronic Hg degrees exposure and BDNF polymorphism. Multiple regression analysis controlled for age, race, socioeconomic status, tobacco and alcohol use, self-reported health problems, and medications. Separate evaluations were conducted for DTs and DAs. Twenty-three associations between recent or chronic Hg degrees exposure and BDNF status and self-reported symptoms were observed with p < 0.10. All but three were in the expected direction (symptom scores increasing with Hg degrees exposure or BDNF polymorphism), and all but six were among DAs. All eight correlations between chronic exposure indices and recent and chronic symptoms among DAs were in the expected direction. All seven associations between BDNF and symptoms were in the expected direction and split between DTs and DAs. All three associations with mood factors were among DAs and in the expected direction. These results indicate that among DAs very low levels of occupational Hg degrees exposure are associated with increased symptoms. The BDNF polymorphism is also associated with increased symptom and mood scores. Notably, Hg degrees and BDNF polymorphism were additive with respect to their associations with the same symptom group.
PMID: 15254338 [PubMed - indexed for MEDLINE]
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Investigations of strain and/or gender differences in developmental neurotoxic effects of polybrominated diphenyl ethers in mice.
Viberg H, Fredriksson A, Eriksson P.
Department of Environmental Toxicology, Uppsala University, Norbyvagen 18A, S-75236 Uppsala, Sweden. Henrik.Viberg@ebc.uu.se
Polybrominated diphenyl ethers (PBDEs), one class of flame retardants used to suppress or inhibit the risk of fire, are regularly found in the environment and in human milk. The present study shows that neonatal exposure to a widely, environmentally found PBDE, 2,2',4,4',5-pentaBDE (PBDE 99), can induce developmental neurotoxic effects, such as changes in spontaneous behavior (hyperactivity), effects that are dose-response related and worsen with age. These changes are seen in C57/Bl mice of both sexes. Neonatal C57/Bl male and female mice were orally exposed on day 10 to 0.4, 0.8, 4.0, 8.0, or 16 mg PBDE 99/kg body weight. Spontaneous behavior (locomotion, rearing, and total activity) was observed in two-, five-, and eight-month-old mice. The behavior tests showed that the effects were dose-response and time-response related for both male and female mice. The observed developmental neurotoxic effects seen for PBDE 99, in C57/Bl mice, are similar to effects seen for 2,2',4,4'-tetraBDE (PBDE 47), PBDE 99, 2,2',4,4',5,5'- hexaBDE (PBDE 153), 2,2',3,3',4,4',5,5',6,6'-decaBDE (PBDE 209) and for certain PCBs, in male NMRI mice. Furthermore, the effects of PBDEs appear to be as potent in female mice as in male mice, and as potent in C57/Bl mice as in NMRI mice, concerning developmental neurotoxicity.
PMID: 15240897 [PubMed - indexed for MEDLINE]
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