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Am J Gastroenterol 2002 Aug;97(8):2156-7
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PMID: 12190207, UI: 22177489
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Am J Gastroenterol 2002 Aug;97(8):2154-5
PMID: 12190205, UI: 22177487
Am J Gastroenterol 2002 Jul;97(7):1854-5
PMID: 12135061, UI: 22130084
Am J Gastroenterol 2002 Jul;97(7):1853-4
PMID: 12135060, UI: 22130083
Am J Gastroenterol 2002 Jul;97(7):1598-606
Division of Infectious and Tropical Disease, IRCCS S. Matteo Hospital, University of Pavia, Italy.
HIV-hepatitis C virus (HCV) coinfection is common and affects more than one-third of all HIV infected persons worldwide. Prevalence among risk categories varies according to shared risk factors for transmission, mainly intravenous drug use (IDU) and hemophiliacs. Chronic HCV infection seems to accelerate the course of HIV disease, resulting in a worsened clinical and immunological progression. At the same time, several studies suggest that HIV disease modifies the natural history of HCV infection, leading to a faster course of progression from active hepatitis to cirrhosis, to end stage liver disease and death. HCV infection mimics opportunistic diseases because its natural history is significantly accelerated in HIV patients. Since highly active antiretroviral therapy (HAART) has slowed the progression of HIV disease and decreased the rate of HIV associated mortality, the prognosis of HIV disease has been modified, and the need to treat HCV coinfection become a significant issue. Because of the poor response rate obtained by either interferon alone or interferon thrice weekly plus ribavirin, the combination of pegylated interferon and ribavirin will probably become the standard of care, although the clinicians should be aware of the overlapping toxicity of nucleoside analogues and ribavirin. Many selected categories of patients pose particular challenges to physicians treating HCV infection: nonresponders to interferon, cirrhotic patients, and patients infected with both HCV and HBV. Liver transplantation in HIV patients is currently under evaluation, but should become the rescue therapy for HIV patients with end stage liver disease.
PMID: 12135007, UI: 22130030
Ann Emerg Med 2002 Oct;40(4):420-4
Israel Naval Medical Institute, IDF Medical Corps, Haifa. yanir192@netvision.net.il
We report the cases of 2 previously healthy young patients with acute carbon monoxide intoxication who deteriorated to cardiogenic shock in the face of apparent metabolic and neurologic recovery. Prolonged exposure to sublethal levels of carbon monoxide (>24 hours, carboxyhemoglobin level of 20.4% and 22.6%) and massive binding of the toxin to myocardial myoglobin and mitochondrial cytochrome chain enzymes might explain their protracted cardiac failure. The good response to inotropic agents and the findings of repeated echocardiographic studies support the probable diagnosis of myocardial stunning. Complete cardiac recovery was observed in both patients.
PMID: 12239499, UI: 22224334
Arch Pediatr 2002 Jul;9(7):694-6
Service de pediatrie-neonatologie, centre hospitalier sud-francilien, 91014 Evry, France. antoine.leblanc@easynet.fr
Methadone is a synthetic narcotic used in opioid dependent situations. Child intoxications are harmful, sometimes responsible for death. CASE REPORT: An one-year-old infant was seen in the emergency room, two hours after accidental methadone ingestion. He presented with coma, myosis and respiratory depression. After intubation, symptoms disappeared with naloxone injection. For maintaining this child safe, naloxone was given by continuous infusion during 48 hours. CONCLUSION: Patients, families and professionals should be informed of the risks of methadone intoxication. Owing to methadone long duration of action, initial injection of naloxone, the specific opioid antagonist, must be followed by continuous infusion.
PMID: 12162157, UI: 22152676
Br J Dermatol 2002 Jul;147(1):188-9
PMID: 12154773, UI: 22149432
Gastroenterol Clin Biol 2001 Dec;25(12):1115-6
PMID: 11910997, UI: 21909015
Int J Dermatol 2002 Jun;41(6):362-4
Department of Dermatology, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India.
PMID: 12100694, UI: 22095420
J Neurol 2002 Jun;249(6):780-1
PMID: 12173578, UI: 22162197
J Toxicol Clin Toxicol 2002;40(4):527-8; discussion 529-30
PMID: 12217011, UI: 22205168
J Toxicol Clin Toxicol 2002;40(4):523-4
PMID: 12217009, UI: 22205166
J Toxicol Clin Toxicol 2002;40(4):519-20
PMID: 12217007, UI: 22205164
J Toxicol Clin Toxicol 2002;40(4):517-8
PMID: 12217006, UI: 22205163
J Toxicol Clin Toxicol 2002;40(5):573-4
PMID: 12215054, UI: 22203399
MMWR Morb Mortal Wkly Rep 2002 Aug 9;51(31):684-6
Lead poisoning affects children adversely worldwide. In the United States, elevated blood lead levels (BLLs) (>10 microg/dL) result primarily from exposure to lead-based paint or from associated lead-contaminated dust and soil; however, other sources of lead exposure, including folk remedies, Mexican terra cotta pottery, and certain imported candies, also have been associated with elevated BLLs in children. This report describes five cases in California of lead poisoning from atypical sources. Health-care providers should be aware of the potential hazards of certain food products, and community members should be educated about potential sources of lead poisoning for children.
PMID: 12233910, UI: 22218931
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