9 citations found

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Links: Acad Emerg Med

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Acad Emerg Med 2002 Mar;9(3):179-85

Hypertonic sodium bicarbonate for Taxus media-induced cardiac toxicity in swine.

Ruha AM, Tanen DA, Graeme KA, Curry SC, Miller MB, Gerkin R, Reagan CG, Brandon TA

Department of Medical Toxicology, Good Samaritan Regional Medical Center, Phoenix, AZ 85006, USA. michelle.ruha@bannerhealth.com

OBJECTIVE: To determine whether intravenous (IV) hypertonic sodium bicarbonate is effective in the reversal of QRS widening associated with severe Taxus intoxication. METHODS: Seventeen anesthetized and instrumented swine were poisoned with an IV extract of Taxus media until doubling of the QRS interval on electrocardiography was achieved. After poisoning (time zero), the animals received either 4 mL/kg IV 8.4% sodium bicarbonate (experimental group; 6 animals), a similar volume of 0.7% NaCl in 10% mannitol (mannitol group; 6 animals), or nothing (control group; 5 animals). The main outcome parameter was QRS duration. Secondary outcome parameters were mean arterial pressure (MAP), heart rate (HR), and cardiac index (CI = cardiac output/kg). Additionally, arterial pH, partial pressure of carbon dioxide (pCO(2)), and plasma-ionized calcium, sodium, and potassium were monitored. RESULTS: Taxus toxicity, defined as a 100% increase in QRS duration, was produced in all animals. The animals were similar in regard to baseline and time 0 physiologic parameters as well as amount of Taxus media extract administered. From times 5 through 30 minutes, following assigned treatment, significant increases in QRS duration were detected in the experimental and mannitol groups compared with the control group. A significant lowering of MAP was found in the experimental group compared with the control group. No significant difference between groups was noted in HR or CI. The swine treated with hypertonic sodium bicarbonate had a statistically significant increase in pH, plasma sodium concentration, and base excess compared with the other groups. CONCLUSIONS: Hypertonic sodium bicarbonate was ineffective in reversing the widening of QRS interval associated with Taxus poisoning in this swine model.

PMID: 11874772, UI: 21863452


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Ann Intern Med 2002 Mar 19;136(6):I65

Summary for patients. Liver damage in a person taking the diabetes drug pioglitazone.

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PMID: 11900516, UI: 21897929


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Ann Intern Med 2002 Mar 19;136(6):480-3

"Did this drug cause my patient's hepatitis?" and related questions.

Nierenberg DW

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PMID: 11900502, UI: 21897915


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Ann Intern Med 2002 Mar 19;136(6):449-52

Mixed hepatocellular-cholestatic liver injury after pioglitazone therapy.

May LD, Lefkowitch JH, Kram MT, Rubin DE

Good Samaritan Hospital, Suffern, NY 10901, USA.

BACKGROUND: Pioglitazone is an oral hypoglycemic agent in the thiazolidinedione class. Only one case of hepatotoxicity related to this agent has previously been reported. OBJECTIVE: To report the clinical course of a patient with hepatitis after therapy with pioglitazone. DESIGN: Case report. SETTING: A community hospital. PATIENT: A 49-year-old diabetic man taking pioglitazone, 30 mg/d. INTERVENTION: Discontinuation of pioglitazone therapy. MEASUREMENTS: Serum aminotransferase and bilirubin levels, standard blood tests for causes of hepatitis and cirrhosis other than drug toxicity, and liver biopsy. RESULTS: After 6 months of pioglitazone therapy, significant hepatic dysfunction developed. Blood tests excluded viral, metabolic, and autoimmune disorders. Liver biopsy showed mixed hepatocellular-cholestatic injury compatible with drug toxicity. After treatment with pioglitazone was discontinued, liver enzyme values returned to normal. CONCLUSION: Patients receiving pioglitazone may develop serious liver injury and should be observed for evidence of hepatitis.

PMID: 11900497, UI: 21897910


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Br J Dermatol 2002 Feb;146(2):334-5

Dermatological complications of etanercept therapy for rheumatoid arthritis.

Misery L, Perrot JL, Gentil-Perret A, Pallot-Prades B, Cambazard F, Alexandre C

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PMID: 11903255, UI: 21900639


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Br J Dermatol 2002 Feb;146(2):320-4

Cutaneous sarcoidosis during interferon alfa and ribavirin treatment of hepatitis C virus infection: two cases.

Cogrel O, Doutre MS, Marliere V, Beylot-Barry M, Couzigou P, Beylot C

Departments of Dermatology and Gastroenterology, Haut-Leveque Hospital, CHU Bordeaux, avenue Magellan, 33604 Pessac cedex, France.

Interferon-induced sarcoidosis is well documented. We report two new cases of sarcoidosis in two patients with hepatitis C virus infection treated with interferon alfa and ribavirin. These patients developed cutaneous sarcoidosis about 3 months after the beginning of the combination therapy. Spontaneous regression of the lesions was noted after discontinuation of the treatment. There have been more than 20 observations of the appearance or aggravation of this granulomatosis with interferon alfa and more recently with the combination of interferon alfa plus ribavirin. Dermatological signs are found in 50% of cases, and are often diagnostic. Other clinical symptoms of sarcoidosis resemble side-effects of interferon. The evolution is fairly stereotypical and is marked by a regression of the lesions following a dose reduction or curtailment of interferon. Interferon alfa acts by stimulating the T-helper (Th) 1 immune response. In addition to its antiviral action, ribavirin also enhances the Th1 response. Indeed, the superiority of the combination of interferon alfa and ribavirin in terms of antiviral action is corroborated by the enhancement of a Th1-type immune reaction by this combination. At the same time, this immune cell reaction triggers a greater granulomatous reaction.

PMID: 11903249, UI: 21900633


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Lancet 2002 Apr 6;359(9313):1254

Avoiding unnecessary risks to our children.

Miro O, Nogue S, Burillo G

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PMID: 11955581, UI: 21953639


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Lancet 2002 Mar 30;359(9312):1127

Arsenic contamination affects millions in Bangladesh.

McLellan F

Publication Types:

PMID: 11943266, UI: 21941040


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Pediatr Emerg Care 2002 Feb;18(1):25-7

Suicidal psychosis secondary to isoniazid.

Iannaccone R, Sue YJ, Avner JR

Department of Emergency Medicine, Division of Pediatric Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, New York, USA.

PMID: 11862134, UI: 21851388


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