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Items 1 - 14 of 14
One page.
1: Arch Dermatol. 2004 Oct;140(10):1289-90. Related Articles, Links
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Analysis of risk factors in psoriatic patients with methotrexate-induced increases in transaminase levels.

Heydendael VM, Spuls PI, Bossuyt PM, Bos JD, de Rie MA.

Publication Types:
  • Letter

PMID: 15492205 [PubMed - indexed for MEDLINE]


2: J Hepatol. 2004 Mar;40(3):446-53. Related Articles, Links
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Induction of Mx-2 in rat liver by toxic injury.

Batusic DS, Armbrust T, Saile B, Ramadori G.

Division of Gastroenterology and Endocrinology, Department of Medicine, Georg-August-University Gottingen, Robert-Koch-Strasse 40, Gottingen 37075, Germany.

BACKGROUND/AIMS: Mx proteins are supposed to be strictly regulated by viruses or interferon-alpha (IFN-alpha). We used a non-viral model of acute liver injury to study Mx expression. METHODS: We induced toxic liver injury by CCl(4), and studied the expression of IFN-alpha, IFN-gamma, and IFN-inducible antiviral genes (Mx-2; 2'-5' oligoadenylate synthetase, 2-5 A; double-stranded RNA-activated protein kinase, PKR). RESULTS: Similar to 2-5 A and PKR, Mx-2 gene expression was biphasically induced after CCl(4) administration with a maximum at 24 h, and a second peak at 72 h. On protein level, Mx-2 only was up-regulated. IFN-alpha remained constant for the first 24 h while IFN-gamma peaked at 6 h. Thereafter, IFN-alpha increased to a maximum at 72 h while IFN-gamma decreased to 77+/-4%. Small monocyte-like liver macrophages, but not large macrophages, expressed Mx-2 constitutively. In vitro, IFN-alpha but not IFN-gamma induced Mx-2 in different liver cell populations. IFN-gamma, instead, reduced the susceptibility of liver macrophages to the actions of IFN-alpha. CONCLUSIONS: Our data suggest that Mx expression does not invariably result from the presence of a viral particle or IFN-alpha synthesis but may represent an innate defensive armamentarium that may be up-regulated without antigen specificity upon liver injury.

PMID: 15123359 [PubMed - indexed for MEDLINE]


3: J Toxicol Clin Toxicol. 2004;42(6):927-32. Related Articles, Links

Acute endosulfan poisoning with cerebral edema and cardiac failure.

Eyer F, Felgenhauer N, Jetzinger E, Pfab R, Zilker TR.

Department of Toxicology, Klinikum rechts der Isar, Technical University Munich, Munich, Germany. Florian.Eyer@t-online.de

BACKGROUND: Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide with several deaths. Despite their widespread use in agriculture during the 1940s to 1960s and the well-known signs and symptoms of intoxication, the clinical picture in case of poisoning varies. We report two cases of acute intentional endosulfan intoxication with cerebral edema and cardiac failure. CASE REPORTS: Both cases developed life-threatening signs like epileptic state, respiratory insufficiency and hemodynamic instability soon after ingestion. The survivor developed severe myocardial insufficiency and pulmonary edema documented by echocardiography and x-ray of the chest. The deceased patient developed severe cerebral edema and multiorgan failure ten days after ingestion of Thiodan 35. The peak serum concentration of endosulfan in the survivor was 0.12 mg/L approximately 23 hours after ingestion, whereas the peak blood concentration in the fatal case was 0.86 mg/L approximately 25 hours post-ingestion. Post-mortem endosulfan levels in different organs were determined. CONCLUSION: Endosulfan is a highly toxic organochlorine insecticide that produces well-known neurological symptoms of tonic-clonic convulsions, headache, dizziness and ataxia but also can cause gastrointestinal symptoms and metabolic disturbances. Life-threatening cerebral edema and hemodynamic instability may occur. Treatment is symptomatic and supportive.

PMID: 15533034 [PubMed - in process]


4: J Toxicol Clin Toxicol. 2004;42(6):917-9. Related Articles, Links

Lack of toxic effects following acute overdose of cellcept (mycophenolate mofetil).

Bebarta VS, Heard K, Nadelson C.

Rocky Mountain Poison and Drug Center-Denver Health, Division of Emergency Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.

Mycophenolate mofetil is an immunosuppressive drug used for prevention of graft rejection following solid organ transplant and for treatment of autoimmune disorders. We report a case of a 24-year-old female with lupus nephritis that presented following ingestion of 10 grams of mycophenolate in a suicide gesture. Serum levels confirmed ingestion. The patient was treated with decontamination and supportive care and recovered with no adverse effect.

PMID: 15533032 [PubMed - in process]


5: J Toxicol Clin Toxicol. 2004;42(6):913-6. Related Articles, Links

Paradoxical cerebral cortical hyperexcitability following flupirtine overdose.

Hoffmann O, Gommert LR, Egert M.

Department of Neurology, Charite-Hochschulmedizin, Berlin, Germany. hoffmann@charite.de

We report the case of a patient with increased cerebral cortical excitability following intoxication with flupirtine, a centrally acting analgesic and antispastic drug. Typically, flupirtine exerts membrane stabilizing and hyperpolarizing effects through activation of neuronal G-protein regulated inwardly rectifying potassium channels (GIRK). Based on these properties, GIRK activators have been suggested as candidates for antiepileptic drug development. In contrast, our observation suggests that these substances may also display unexpected proconvulsant effects in vivo.

PMID: 15533031 [PubMed - in process]


6: J Toxicol Clin Toxicol. 2004;42(6):901-12. Related Articles, Links

Diagnostic accuracy of urinary amanitin in suspected mushroom poisoning: a pilot study.

Butera R, Locatelli C, Coccini T, Manzo L.

Pavia Poison Center and Toxicology Laboratory, IRCCS Maugeri Foundation and University of Pavia, Pavia, Italy. rbutera@fsm.it

BACKGROUND. Amatoxin-containing species are responsible for the most severe cases of mushroom poisoning, with high mortality rate. Therefore, this poisoning should be ruled out in all patients presenting gastrointestinal symptoms after wild mushroom ingestion. OBJECTIVE. To determine sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic efficacy (DE) of urinary amanitin analysis in cases of suspected mushroom poisoning. METHODS. All cases of mushroom ingestion referred to a Poison Center during a one-month period were analyzed. Amanitin measurements were performed by ELISA method (functional least detectable dose 1.5 ng/ml; cut-off value not clearly established). Gastrointestinal symptoms latency and initial clinical assessment were considered alternative diagnostic tools. Definitive diagnosis was used as the reference standard. RESULTS. Among 61 patients included in the study, amatoxin poisoning was diagnosed in 10 cases. Urine samples were collected 5.5 to 92 hours after mushroom ingestion. Urinary amanitin DE was 91.8%, 93.4%, and 80.3%, based on the cut-off value considered (1.5, 5.0, and 10.0 ng/ml, respectively). Symptoms latency longer than 6 hours and initial clinical assessment DE were 70.5% and 67.2%, respectively. To identify amatoxin poisoning, initial clinical assessment resulted more sensitive and urinary amanitin analysis more specific. CONCLUSIONS. Urinary amanitin analysis is a valuable diagnostic tool and may significantly contribute to the management of suspected mushroom poisoning. At present, the best diagnostic accuracy can be obtained taking advantage of both the high sensitivity and negative predictive value of the clinical assessment performed by an experienced toxicologist, and the high specificity and positive predictive value that characterize urinary amanitin analysis.

PMID: 15533030 [PubMed - in process]


7: J Toxicol Clin Toxicol. 2004;42(6):877-88. Related Articles, Links

A meta-analysis of prognostic indicators to predict seizures, arrhythmias or death after tricyclic antidepressant overdose.

Bailey B, Buckley NA, Amre DK.

Division of Emergency Medicine and Clinical Pharmacology, Department of Pediatrics, Hopital Ste-Justine, Universite de Montreal, Montreal, Canada. benoit.bailey@umontreal.ca

OBJECTIVES: To systematically review and summarize studies on the accuracy of ECG and tricyclic antidepressant (TCA) concentration as prognostic indicators of the risk of seizures, ventricular arrhythmia (VA) or death in patients with TCA overdose. METHODS: Articles were identified with MedLine and Cochrane register of controlled clinical trials searches and review of medical toxicology textbooks. Quality of the included studies was assessed. Pooled estimates of sensitivity, specificity, likelihood ratios and Summary Receiver Operating Characteristics (SROC) curves were generated. RESULTS: A total of 18 studies were included in the analysis. The pooled sensitivity (Se) and specificity (Sp) of the QRS for predicting seizures were 0.69 [95% CI 0.57-0.78] and 0.69 [95% CI 0.58-0.78] as compared to 0.75 [95% CI 0.61-0.85] and 0.72 [95% CI 0.61-0.81] for the TCA concentration. The Se and Sp of the QRS to predict VA were 0.79 [95% CI 0.58-0.91] and 0.46 [95% CI 0.35-0.59] compared to 0.78 [95% CI 0.56-0.90] and 0.57 [95% CI 0.46-0.67] for the TCA concentration. The Se and Sp of the QRS to predict death were 0.81 [95% CI 0.54-0.94] and 0.62 [95% CI 0.55-0.68] compared to 0.76 [95% CI 0.49-0.91] and 0.60 [95% CI 0.47-0.72] for the TCA concentration. Very few studies evaluated the accuracy of QTc, T 40 ms axis and the R/S ratio. CONCLUSIONS: Overall, the studies suggested that the ECG and TCA concentration have similar but relatively poor performance for predicting complications, such as seizures, VA or death, associated with TCA overdose.

PMID: 15533027 [PubMed - in process]


8: J Toxicol Clin Toxicol. 2004;42(6):865-75. Related Articles, Links

Speed of initial atropinisation in significant organophosphorus pesticide poisoning--a systematic comparison of recommended regimens.

Eddleston M, Buckley NA, Checketts H, Senarathna L, Mohamed F, Sheriff MH, Dawson A.

South Asian Clinical Toxicology Research Collaboration, Department of Clinical Medicine, Faculty of Medicine, University of Colombo, Sri Lanka. eddlestonm@eureka.lk

OBJECTIVE: Early deaths from organophosphorus (OP) pesticide self-poisoning result from respiratory failure and cardiovascular collapse. Therapy requires the urgent use of atropine to reverse cholinergic excess, thereby improving respiratory function, heart rate, and blood pressure. We aimed to assess variation in textbook recommendations for early atropinisation and to see whether this variation affected time to stabilisation using model data from 22 severely poisoned patients seen in a Sri Lankan clinical trial. METHODS: We extracted prospectively recorded data on atropine requirements for 22 OP poisoned patients who required intubation but survived to discharge. We did a systematic search for textbook recommendations for initial atropinisation regimens. These regimens were then applied to data from the Sri Lankan patients. RESULTS: The patients required a mean of 23.4 mg (standard deviation 22.0, range 1-75 mg) atropine to clear the lungs, raise the pulse above 80 bpm, and restore systolic blood pressure to more than 80 mmHg. Textbook recommendations varied markedly--atropinisation of an average patient, requiring the mean dose of 23.4 mg, would have taken 8 to 1380 mins; atropinisation of a very ill patient, requiring 75 mg, would have taken 25 to 4440 mins. Atropinisation was attained most rapidly with a regimen of increasing bolus doses after failure to respond to the previous bolus. CONCLUSIONS: There is great variation in recommendations for atropinisation, with some regimens taking hours and even days to stabilise a patient. The guidelines are very flexible--possibly appropriate for experienced emergency physicians or clinical toxicologists, but completely inappropriate for the inexperienced junior doctors who see most cases worldwide. We recommend that a consensus guideline be developed by appropriate organisations to bring order to this important part of OP therapy, while acknowledging the paucity of data to drive the guidelines.

PMID: 15533026 [PubMed - in process]


9: J Toxicol Clin Toxicol. 2004;42(6):855-63. Related Articles, Links

Carbon monoxide and cyanide poisoning in fire related deaths in Victoria, Australia.

Yeoh MJ, Braitberg G.

Clinical Forensic Medicine, Victorian Institute of Forensic Medicine, Southbank, Victoria, Australia. Michael.YEOH@austin.org.au

OBJECTIVE: This study was undertaken to examine the association of hydrogen cyanide and carboxyhaemoglobin in victims of fire related deaths in Australia. The secondary aim was to document demographic data about Australian fire related deaths. METHODS: An observational retrospective study was undertaken of autopsy reports from the Victorian Institute of Forensic Medicine. Reports of fire related deaths were electronically searched using the terms burns, "smoke" or "fire" as a cause of death in the calender years 1992 to 1998. Data on the circumstances of the fire and results of toxicological screening were obtained on 178 persons. Additional whole blood cyanide levels were determined if blood samples were available in storage. Demographics of the victims were analysed, as well as the relationship between carboxyhaemoglobin and whole blood cyanide levels. RESULTS: Most (82%) of the victims died at the scene, whilst 32 victims died after a period of hospitalisation (hours to weeks). Suicide as a result of self-immolation was the reported cause of death in 32 cases. Most of the fires were in houses (114) and cars (29). The blood ethanol level was zero in 112 cases; the remaining cases (53) had a mean level of 0.17%. Other central nervous system (CNS) depressants were recorded in 49 of the 134 cases that received a complete toxicological screen. Carboxyhaemoglobin levels were measured in only 154 of 178 cases. The carboxyhaemoglobin level was zero in 43 cases. The remaining cases (111) had a mean level of 40%; with 44 cases having a level greater than 50%, a level considered to be potentially lethal. Whole blood hydrogen cyanide levels were measured in only 138 of 178 cases. The hydrogen cyanide level was zero in 52 cases. The remaining cases (86) had a mean level of 1.65 mg/L; with 11 cases having a level greater than 3.0 mg/L (potentially fatal). Blood ethanol levels were significantly correlated with both carboxyhaemoglobin (R = 0.22, P < 0.01) and cyanide (R = 0.36, P < 0.001). In addition, a significant correlation (r = 0.34) between carboxyhaemoglobin and hydrogen cyanide levels was noted. Conclusions: This study showed a correlation between elevated blood ethanol and whole blood cyanide levels (r = 0.36, p < 0.001) and between elevated carboxyhaemoglobin and hydrogen cyanide levels (r = 0.34). Although the mean cyanide level was 1.3 mg/L (above the level some consider potentially toxic) in those cases with a carboxyhaemoglobin level of greater than 10%, there is insufficient data to permit recommendations for clinical care. Further studies are required on those victims that reach hospital alive.

PMID: 15533025 [PubMed - in process]


10: Med J Aust. 2004 Sep 20;181(6):343. Related Articles, Links
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Epidemic of gamma-hydroxybutyrate (GHB) ingestion.

Brown TC.

Publication Types:
  • Letter

PMID: 15377257 [PubMed - indexed for MEDLINE]


11: Med J Aust. 2004 Sep 20;181(6):310-3. Related Articles, Links
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Fatalities associated with the use of gamma-hydroxybutyrate and its analogues in Australasia.

Caldicott DG, Chow FY, Burns BJ, Felgate PD, Byard RW.

Department of Emergency Medicine and Trauma, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia. dcaldico@mail.rah.sa.gov.au

OBJECTIVE: To identify deaths in Australasia associated with overdose of gamma-hydroxybutyrate (GHB) and its precursors (gamma-butyrolactone and 1,4-butanediol). DESIGN: A retrospective search of medical and scientific information sources, as well as popular newsprint, for the period January 2000-August 2003, with formal clinical, toxicological and forensic evaluation of retrieved data. MAIN OUTCOME MEASURE: Death associated with forensic data implicating GHB or its analogues. RESULTS: Ten confirmed GHB-associated deaths were identified, with eight considered to be directly attributable to GHB. Only two of these eight cases were positive for ethanol toxicology. CONCLUSIONS: Our study supports the existing evidence that GHB overdose is associated with fatalities, and that fatal overdoses occur in the context of isolated use.

PMID: 15377240 [PubMed - indexed for MEDLINE]


12: MMWR Morb Mortal Wkly Rep. 2004 Nov 5;53(43):1018-20. Related Articles, Links
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Blood mercury levels in young children and childbearing-aged women--United States, 1999-2002.

Centers for Disease Control and Prevention (CDC).

Exposure to high levels of mercury (Hg) can cause neurologic and kidney disorders. Because methylated Hg (methyl-Hg) in the aquatic environment accumulates in animal tissues up the food chain, persons in the United States can be exposed by eating freshwater fish, seafood, and shellfish. Exposure of childbearing-aged women is of particular concern because of the potential adverse neurologic effects of Hg in fetuses. To determine levels of total blood Hg in childbearing-aged women and in children aged 1-5 years in the United States, CDC's National Health and Nutrition Examination Survey (NHANES) began measuring blood Hg levels in these populations in 1999. This report summarizes NHANES results for 1999-2002 and updates previously published information. The findings confirmed that blood Hg levels in young children and women of childbearing age usually are below levels of concern. However, approximately 6% of childbearing-aged women had levels at or above a reference dose, an estimated level assumed to be without appreciable harm (> or =5.8 microg/L). Women who are pregnant or who intend to become pregnant should follow federal and state advisories on consumption of fish.

PMID: 15525900 [PubMed - indexed for MEDLINE]


13: N Engl J Med. 2004 Nov 4;351(19):1996. Related Articles, Links
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Images in clinical medicine. Getting the lead out.

Shen J, Hirschtick R.

Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.

PMID: 15525725 [PubMed - indexed for MEDLINE]


14: N Engl J Med. 2004 Nov 4;351(19):1978-84. Related Articles, Links
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Clinical practice. Hypersensitivity to hymenoptera stings.

Freeman TM.

Department of Allergy and Immunology, Wilford Hall Medical Center, Lackland Air Force Base, San Antonio, TX 78023, USA. tfree95900@aol.com

Publication Types:
  • Review
  • Review, Tutorial

PMID: 15525723 [PubMed - indexed for MEDLINE]


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