Search PubMed⌕ Search

Biomedical subjects

L Argaud

Publications and source records attributed to L Argaud.

11 recordsLinked to original sources
PubMed2006

Loading dose of vancomycin in critically ill patients: 15 mg/kg is a better choice than 500 mg.

Delays in antimicrobial therapy in high-risk patients with infection may have deleterious effects on clinical outcomes. Therefore, appropriate treatment must be initiated promptly. The objective of this prospective study was to determine the better loading dose of vancomycin in critically ill patients with suspected Gram-positive infections. Two groups of patients were studied successively: Group A, loading dose of 500 mg; and Group B, loading dose of 15 mg/kg. The mean post-loading dose serum vancomycin concentration was significantly higher in Group B than in Group A (19.1 +/- 7.4 mg/L versus 10.4 +/- 2.7 mg/L; P < 0.001), without producing toxic peak levels. Clinical cure rates were significantly different for infected patients in Group B compared with Group A: 93% (14 of 15 patients) versus 56% (10 of 18 patients), respectively. However, the proportion of patients surviving to Intensive Care Unit discharge was similar. Because vancomycin is believed to achieve maximum killing at concentrations in serum of four to five times the minimum inhibitory concentration for the infecting organism, our results suggest that the 15 mg/kg loading dose should be preferred.

Aged↗
PubMed2006

Necrotizing gastritis due to Bacillus cereus in an immunocompromised patient.

Bacillus cereus is increasingly being acknowledged as a serious bacterial pathogen in immunocompromised patients. We present a case of acute necrotizing gastritis caused by B. cereus in a 37-year-old woman with acute myeloblastic leukemia, who recovered following total parenteral nutrition and treatment with imipenem and vancomycin. B. cereus was isolated from gastric mucosa and blood cultures. Up to now, no case of acute necrotizing gastritis due to this organism has been reported.

Adult↗
PubMed2005

Fas-independent mitochondrial damage triggers cardiomyocyte death after ischemia-reperfusion.

The Fas/Fas ligand and mitochondria pathways have been involved in cell death in several cell types. We combined the genetic inactivation of the Fas receptor (lpr mice), on the one hand, to the pharmacological inhibition of the mitochondrial permeability transition pore (mPTP), on the other hand, to investigate which of these pathways is predominantly activated during prolonged ischemia-reperfusion. Anesthetized C57BL/6JICO (control) and C57BL/6-lpr mice were pretreated with either saline or cyclosporin A (CsA; 40 mg/kg, 3 times a day), an inhibitor of the mPTP, and underwent 25 min of ischemia and 24 h of reperfusion. After 24 h of reperfusion, hearts were harvested: infarct size was assessed by 2,3,5-triphenyltetrazolium chloride staining, myocardial apoptosis by caspase 3 activity, and mitochondrial permeability transition by Ca2+-induced mPTP opening using a potentiometric approach. Infarct size was comparable in untreated control and lpr mice, ranging from 77 +/- 5% to 83 +/- 3% of the area at risk. CsA significantly reduced infarct size in control and lpr hearts. Control and lpr hearts exhibited comparable increase in caspase 3 activity that averaged 57 +/- 18 and 49 +/- 5 pmol x min(-1) x mg(-1), respectively. CsA treatment significantly reduced caspase 3 activity in control and lpr hearts. The Ca2+ overload required to open the mPTP was decreased to a similar extent in lpr and controls. CsA significantly attenuated Ca2+-induced mPTP opening in both groups. Our results suggest that the Fas pathway likely plays a minor role, whereas mitochondria are preferentially involved in mice cardiomyocyte death after a lethal ischemia-reperfusion injury.

Animals↗
PubMed2004

Fatal Microascus trigonosporus (anamorph Scopulariopsis) pneumonia in a bone marrow transplant recipient.

Over the past decade, an increasing number of opportunistic mycelial fungal infections have been reported in immunocompromised patients. Presented here is the first reported case of Microascus trigonosporus pneumonia, which occurred in a 24-year-old-man with a history of allogenic bone marrow transplantation with graft-versus-host disease. Despite the administration of effective antifungal treatment, the patient died after uncontrollable respiratory failure and multiorgan failure developed. This report confirms the results of previous studies that suggested a very poor outcome for bone marrow transplant recipients with non-Aspergillus mould infections.

Adult↗
PubMed2000

[Myocardial metabolism abnormalities during ischemia and reperfusion].

Normal cardiac function requires adequate oxygen and substrate (fatty acids, glucose lactate) supply for the energetic requirements of the myocardium. Ischaemia induces abnormalities in the production and excretion of products of myocardial metabolism. During ischaemia, the equilibrium which exists during aerobic respiration between the beta-oxidation of fatty acids and carbohydrates and which generates ATP is disturbed. Pyruvate oxidation and beta-oxidation of fatty acids decrease, and ATP is mainly produced by anaerobic glycolysis. Under these conditions, intracellular glycogen is mobilised, the lactate and protons accumulate in the cardiomyocyte. If reperfusion occurs before irreversible lesions are produced, then functional recovery is possible and is mostly dependant on the type of energetic substrate available. Circulating fatty acids are produced in large quantities after ischaemia: their beta-oxidation, which is then the principal source of ATP, may contribute to the aggravation of contractile dysfunction during reperfusion and accentuate or generate arrhythmias. The decoupling between acceleration of anaerobic glycolysis and the defect of pyruvirate oxidation (inhibition of pyruvirate dehydrogenase) participate in a significant fashion to the accumulation of protons. Rapid correction of intracellular acidosis during reperfusion by activation of the Na+/H+ exchanger, coupled with the accumulation of intracellular Na+ induces a deleterious calcium overload via the Na+/Ca++ exchanger. These different aspects of intracellular metabolism constitute pharmacological targets for the development of future cardio-protective agents.

Acidosis↗