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Items 1 - 14 of 14 |
One page. |
Comment on:
Systemic effects of crotalid envenomation mislabeled as anaphylaxis.
German BT.
Publication Types:
PMID: 15635328 [PubMed - indexed for MEDLINE]
Comment on:
Whole bowel irrigation and the capsule summary.
Tenenbein M.
Publication Types:
PMID: 15580715 [PubMed - indexed for MEDLINE]
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Loxoscelism: old obstacles, new directions.
Hogan CJ, Barbaro KC, Winkel K.
Department of Emergency Medicine, Medical College of Virginia/Virginia Commonwealth University Medical Center Hospital, Richmond, VA 23298-0401, USA. chogan@mcvh-vcu.edu
Loxosceles spiders have a worldwide distribution and are considered one of the most medically important groups of spiders. Envenomation (loxoscelism) can result in dermonecrosis and, less commonly, a systemic illness that can be fatal. The mechanism of venom action is multifactorial and incompletely understood. The characteristic dermonecrotic lesion results from the direct effects of the venom on the cellular and basal membrane components, as well as the extracellular matrix. The initial interaction between the venom and tissues causes complement activation, migration of polymorphic neutrophils, liberation of proteolytic enzymes, cytokine and chemokine release, platelet aggregation, and blood flow alterations that result in edema and ischemia, with development of necrosis. There is no definitive treatment for loxoscelism. However, animal model studies suggest the potential value of specific antivenom to decrease lesion size and limit systemic illness even when such administration is delayed.
Publication Types:
PMID: 15573037 [PubMed - indexed for MEDLINE]
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Do hobo spider bites cause dermonecrotic injuries?
Vetter RS, Isbister GK.
Publication Types:
PMID: 15573036 [PubMed - indexed for MEDLINE]
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Pressure immobilization delays mortality and increases intracompartmental pressure after artificial intramuscular rattlesnake envenomation in a porcine model.
Bush SP, Green SM, Laack TA, Hayes WK, Cardwell MD, Tanen DA.
Department of Emergency Medicine (Laack), Loma Linda University School of Medicine, Medical Center and Children's Hospital, Loma Linda, CA, USA. sbush@ahs.llumc.edu
STUDY OBJECTIVES: We determine the effect of pressure immobilization on mortality and intracompartmental pressure after artificial intramuscular Crotalus atrox envenomation in a porcine model. METHODS: We prospectively studied 20 pigs using a randomized, controlled design. After anesthesia, C atrox venom (20 mg/kg) was injected with a 22-gauge needle 10 mm deep into the tibialis anterior muscle of the hind leg. Pigs were randomized to receive either pressure immobilization (applied 1 minute after envenomation and maintained throughout the duration of the experiment) or no pressure immobilization. We measured time to death, intracompartmental pressure before venom injection and at 2 hours after injection, and leg circumference at a standardized location before injection and immediately postmortem. Duration of survival was compared using Kaplan-Meier survival analysis. RESULTS: The dose of venom resulted in 100% mortality. The median survival was longer in the pressure immobilization group (191 minutes, range 140 to 240 minutes) than in the control group (median 155 minutes, range 119 to 187 minutes). The difference between the groups was 36 minutes (95% confidence interval [CI] 2 to 64 minutes; P =.0122). The mean intracompartmental pressures were 67+/-13 mm Hg+/-SD with pressure immobilization and 24+/-5 mm Hg without pressure immobilization. The difference between groups was 43 mm Hg (95% CI 32 to 53 mm Hg). The mean circumferences were 14.3 cm in the pressure immobilization group and 19.1 cm in the control group. The difference between groups was -4.8 cm (95% CI -5.7 to -3.9 cm). CONCLUSION: Compared with control animals without treatment, the pressure immobilization group had longer survival, less swelling, and higher intracompartmental pressures after artificial, intramuscular C atrox envenomation in our porcine model.
Publication Types:
PMID: 15573035 [PubMed - indexed for MEDLINE]
Comment on:
Not enough relief from too much acetaminophen.
Brooks DE, Yealy DM.
Publication Types:
PMID: 15459623 [PubMed - indexed for MEDLINE]
Comment in:
Prospective evaluation of repeated supratherapeutic acetaminophen (paracetamol) ingestion.
Daly FF, O'Malley GF, Heard K, Bogdan GM, Dart RC.
Rocky Mountain Poison and Drug Center-Denver Health Authority, Denver, CO, USA.
STUDY OBJECTIVE: Repeated supratherapeutic ingestion of acetaminophen is potentially lethal but poorly described. We provide the first prospective description of the characteristics, course, and outcome of patients with repeated supratherapeutic ingestion of acetaminophen. METHODS: This was a prospective case series of consecutive patients aged 12 years and older with acetaminophen dosage greater than 4 g per 24 hours referred to our poison center. Acetylcysteine was recommended if serum acetaminophen level exceeded 10 mg/L or aspartate aminotransferase exceeded 50 IU/L. Acetaminophen dosage, demographic factors, treatment, and outcome were recorded using standardized methods. Minimum follow-up was 72 hours. RESULTS: Of 277 patients eligible, 249 patients were enrolled. At presentation, serum aspartate aminotransferase levels less than 50 IU/L were found in 126 patients, aspartate aminotransferase levels of 50 to 1,000 IU/L were present in 47 patients, and aspartate aminotransferase levels were above 1,000 IU/L in 37 patients. No aspartate aminotransferase data were available for 39 patients. No patient with an aspartate aminotransferase level below 50 IU/L at presentation developed hepatotoxicity (aminotransferase >1,000 IU/L). Seven (15%) patients with aspartate aminotransferase levels of 50 to 1,000 IU/L at presentation subsequently developed hepatotoxicity; 1 patient died. Six (16%) patients with aspartate aminotransferase levels above 1,000 IU/L at presentation died or received liver transplants. Study limitations included recall bias, incomplete patient follow-up, and the assumption that absence of clinical signs indicated insignificant liver injury. CONCLUSION: Our results suggest that the injury caused by acetaminophen repeated supratherapeutic ingestion is apparent at presentation and related to dose magnitude and duration. All patients who developed hepatotoxicity presented with aspartate aminotransferase above 50 IU/L. Determination of serum aspartate aminotransferase and acetaminophen concentrations may allow early discharge from the emergency department.
PMID: 15459622 [PubMed - indexed for MEDLINE]
Two patients with acute liver injury associated with use of the herbal weight-loss supplement hydroxycut.
Stevens T, Qadri A, Zein NN.
Publication Types:
PMID: 15767636 [PubMed - indexed for MEDLINE]
Trichomegaly following treatment with gefitinib (ZD1839).
Pascual JC, Banuls J, Belinchon I, Blanes M, Massuti B.
Publication Types:
PMID: 15541102 [PubMed - indexed for MEDLINE]
[Acute necrotizing esophagitis and Wernicke's encephalopathy in an alcoholic/smoker discovered during alcohol withdrawal]
[Article in French]
Lanternier F, Somogyi A, Kahn JE, Leport J.
Publication Types:
PMID: 15671947 [PubMed - indexed for MEDLINE]
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[Liver injury due to potassium para-aminobenzoate (Potaba)]
[Article in French]
Mesnil A, Lewden B, Dumortier J, Cuche M, Euvrard P, Dorez D, Vial T.
Publication Types:
PMID: 15671944 [PubMed - indexed for MEDLINE]
A case of complex movement disorder induced by fluoxetine with management of dystonia by botulinum toxin type A.
Chen JJ, Swope DM.
Publication Types:
PMID: 15705018 [PubMed - indexed for MEDLINE]
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Historical comments on tardive dyskinesia: a neurologist's perspective.
Paulson GW.
Department of Neurology, The Ohio State University, Columbus, OH 43210, USA. paulson.2@osu.edu
This article was undertaken to review the history of professional awareness of tardive dyskinesia (TD) and to address reasons for the delay in such recognition. The literature was reviewed, and selections are included to highlight some of the major issues. Personal recollections are deliberately emphasized since they may reflect the phenomenon of personal discovery familiar to others and the now widespread professional awareness of TD. TD is indeed well recognized by psychiatrists and neurologists, and most general practitioners are also aware that the syndrome exists. Physicians were once unfamiliar with the concept of a drug reaction that was so long delayed as is possible with TD, nor did they know that a drug side effect could present in this manner. The historical delay in initial recognition of TD, and the reason for such delay, remain of interest. The lack of a perfect therapy and the uncertainty regarding the precise pathophysiologic basis of TD remain as challenges. Most psychiatrists, and many neurologists, probably have vivid memories of specific patients with TD. This author, a neurologist, was blessed to work with George Crane and other investigators in the early days of TD and was witness to some of the original uncertainty regarding what seemed to be a new phenomenon. TD has reshaped our concepts of disease and our awareness that diseases can originate from deleterious late effects of beneficial agents.
Publication Types:
- Historical Article
- Review
PMID: 15705014 [PubMed - indexed for MEDLINE]
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Neurotoxic marine poisoning.
Isbister GK, Kiernan MC.
Tropical Toxicology Unit, Menzies School of Health Research, Charles Darwin University, NT, and Department of Clinical Toxicology and Pharmacology, Newcastle Mater Misericordiae Hospital, NSW, Australia.
Marine poisoning results from the ingestion of marine animals that contain toxic substances and causes substantial illness in coastal regions. Three main clinical syndromes of marine poisoning have important neurological symptoms-ciguatera, tetrodotoxin poisoning, and paralytic shellfish poisoning. Ciguatera is the commonest syndrome of marine poisoning and is characterised by moderate to severe gastrointestinal effects (vomiting, diarrhoea, and abdominal cramps) and neurological effects (myalgia, paraesthesia, cold allodynia, and ataxia), but is rarely lethal. Tetrodotoxin poisoning and paralytic shellfish poisoning are less common but have a higher fatality rate than ciguatera. Mild gastrointestinal effects and a descending paralysis are characteristic of these types of poisoning. In severe poisoning, paralysis rapidly progresses to respiratory failure. Diagnosis of all types of marine poisoning is made from the circumstances of ingestion (type of fish and location) and the clinical effects. Because there are no antidotes, supportive care, including mechanical ventilation in patients with severe paralysis, is the mainstay of treatment.
PMID: 15778101 [PubMed - in process]
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