Biomedical subjects
Eric Maury
Publications and source records attributed to Eric Maury.
Schizocytosis in pernicious anemia mimicking thrombotic thrombocytopenic purpura.
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Circulating endotoxin and antiendotoxin antibodies during severe sepsis and septic shock.
The presence of circulating endotoxin is common during sepsis but its prognostic value is poor. We hypothesized that this lack of correlation with outcome could be related in part to the presence of circulating antiendotoxin antibodies. In a 14-bed medical intensive care unit, in an 821-bed tertiary teaching hospital, we prospectively assessed endotoxin and antiendotoxin antibodies in patients with severe sepsis or septic shock. Blood samples for the determination of circulating endotoxin and antiendotoxin antibodies were drawn when severe sepsis or septic shock were diagnosed (day 0) and then on day 1, day 2, and day 4. Daily measurements of antiendotoxin antibodies did not discriminate survivors from nonsurvivors. No antibody depletion was observed. However, during follow-up, the antiendotoxin immunoglobulin (Ig)M antibody level increased among survivors but decreased among nonsurvivors (51.2 vs -44.8 MU/mL, P=007). Circulating endotoxin was detectable among 9 of 17 patients on inclusion but neither the basal value nor sequential measurements correlated with outcome. These results suggest that during severe sepsis and septic shock, circulating endotoxin is a poor prognostic marker whereas the detection of an increase in IgM antiendotoxin antibody levels could identify survivors. This increase in IgM antibody levels could be attributed to a reactivation of the immune system.
Hyponatremia after hip arthroplasty may be related to a translocational rather than to a dilutional mechanism.
OBJECTIVE: Postoperative hyponatremia is a frequent metabolic disturbance that may cause life-threatening complications. It results from both a positive electrolyte-free water (EFW) balance and an antidiuretic hormone release. During surgery, intracellular solutes may leak out of cells because of an increased membrane permeability leading to increased osmolality, cellular water shift, and redistribution hyponatremia, a concept coined the sick cell syndrome. Because of release of osmotically active solutes, plasma or urinary osmolar gap should increase. Therefore, we tested the hypothesis that postoperative hyponatremia may be related to a translocational mechanism evidenced by a postoperative increase of the osmolar gap rather than to a positive EFW balance. SETTING: An anesthesiology department in a 1,200-bed university hospital. DESIGN: A 5-month prospective observational study. SUBJECTS: Thirty-three consecutive patients undergoing elective hip arthroplasty under general anesthesia. They were divided into two groups whether the postoperative plasma sodium concentration decrease was > or = 2 mmol/L (group 1) or <2 mmol/L (group 2). MEASUREMENTS: Plasma sodium concentration ([Na+]p) and plasma osmolality were measured before induction of anesthesia and at skin closure. Osmolality was calculated at the same times. Plasma osmolar gap (OG(p)) was calculated as the difference between measured and calculated osmolality. Postoperative urinary osmolar gap (OG(u)) was calculated in the same way. EFW balance was calculated as the ratio of (infused EFW - excreted urinary EFW) to total body water. RESULTS: In 33 patients, a significant [Na+]p decrease of -2.0 was observed. No relationship was demonstrated between EFW balance and perioperative [Na+]p variation (r =.28; p=.12). A relationship was observed between perioperative OG(p) variation and perioperative [Na+]p variation (r =.74; p<.0001). In the 19 group 1 patients, [Na+]p decreased by -3.0 mmol/L. EFW balance did not differ between group 1 and group 2 patients. No statistical relationship was observed between EFW balance and perioperative [Na+]p variation in group 1 (r =.20; p=.40) and in group 2 (r =.43; p=.14). OG(p) increased only in group 1 but not in group 2 patients, and postoperative OG(u) was greater in group 1 than in group 2 patients. A relationship was observed between perioperative OG(p) variation and perioperative [Na+]p variation in group 1 (r =.53; p=.02) but not in group 2 (r =.32; p=.26). CONCLUSION: Hyponatremia after hip arthroplasty may not be related to a positive EFW balance. The postoperative increase of the OG(p) and the greater postoperative OG(u) in patients developing postoperative hyponatremia suggest the release of osmotically active solutes leading to cellular water shift from intracellular to extracellular spaces. These data may support the clinical relevance of the sick cell syndrome in the postoperative context.
Human epidermis is a novel site of phospholipase B expression.
Phospholipase B (PLB) is an enzyme that displays both phospholipase A(2) and lysophospholipase activities. Analysis of human epidermis homogenates indicated the presence of a 97 kDa PLB protein, as well as a phospholipase A(2) activity, both being enriched in the soluble fraction. Immunolabelling and in situ hybridization experiments showed that this enzyme is expressed in the different layers of epidermis with an accumulation at the dermo-epidermis junction. RT-PCR data indicated that PLB is specifically expressed in natural and reconstructed epidermis. By 3'-RACE-PCR and screening of human genome databases, we obtained a 3600 bp cDNA coding for human PLB highly homologous to already described intestinal brush border PLBs. These data led us to conclude that the soluble PLB corresponds to a proteolytic cleavage of the membrane anchored protein. Altogether, our results provide the first characterization of human PLB which should play an important role in epidermal barrier function.
Blood ferritin and isoferritins measurements may be helpful in acute respiratory distress syndrome patients.
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Herpes simplex esophagitis in patients with liver disease.
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Osmolar gap hyponatremia in critically ill patients: evidence for the sick cell syndrome?
OBJECTIVE: Accumulation of nondiffusible solutes in plasma leads to redistribution hyponatremia with an increased osmolar gap (i.e., the difference between measured and calculated osmolality). In critically ill patients, intracellular solutes may leak out of the cell because of an increased membrane permeability and may lead to redistribution hyponatremia with increased osmolar gap, a concept called the "sick cell syndrome." The aims of this prospective study were to determine whether an increased osmolar gap related to endogenous solutes accumulation was present in intensive care patients with true hyponatremia and to identify the solutes accounting for this increased osmolar gap. SETTING: A 14-bed medical intensive care unit in an 821-bed university hospital. DESIGN: A 20-wk prospective observational study. PATIENTS: Fifty-five consecutive patients with a measured plasma sodium concentration 10 mosm/kg. Total plasma amino acid concentration also was measured. Organ dysfunctions were assessed with the Sequential Organ Failure Assessment. Thirty of the 55 patients (54%) had an osmolar gap >10 mosm/kg (17.2 +/- 7.1 mosm/kg). Sequential Organ Failure Assessment score was significantly higher in the osmolar gap patients (6.4 +/- 3.2 vs. 4.5 +/- 2.0; p =.015). No difference of amino acids concentration was observed between osmolar gap and non-osmolar gap patients, and no correlation was observed between osmolar gap and amino acid concentration. Accumulation of ketone bodies and lactic acid was also unlikely. During correction of hyponatremia in osmolar gap patients, a significant decrease of plasma osmolar gap was observed and a statistically significant inverse relationship was demonstrated between osmolar gap decrease and plasma sodium concentration increase. CONCLUSION: Hyponatremia with increased osmolar gap related to endogenous solutes accumulation is observed frequently in hyponatremic intensive care patients, especially in patients with the most severe organ dysfunctions. The nature of the endogenous solutes accounting for the increased osmolar gap remains to be determined. Simultaneous correction of sodium and osmolar gap suggests a causal link between increased osmolar gap and hyponatremia and may support the concept of sick cell syndrome.