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The induction of DNA fragmentation by cytosine arabinoside (araC) and 2',2'-difluorodeoxycytidine (dFdC, gemcitabine) was compared in human leukemic cell lines. For both araC and dFdC this process was time- and concentration-dependent and resulted in loss of clonogenic survival of HL-60 myeloid leukemic cells. There was a marked difference in the potency between these two analogs in inducing apoptosis. A 6 h exposure to 5 microM araC was required to produce DNA laddering in HL-60 cells, whereas dFdC at a concentration 100-fold less (0.05 microM) was sufficient to produce similar results. Pre-incubation of HL-60 cells with staurosporine, a non-specific protein kinase C inhibitor, increased the level of apoptosis induced by a 3 h exposure to araC or dFdC, suggesting the possible involvement of this family of enzymes in this process. Also, dFdC was able to increase the expression of both c-jun and c-fos in Molt-3 leukemic cells with a concentration known to induce apoptosis in this cell line.

Early somatosensory (SEP) and auditory (BAEP) evoked potentials, when recorded within the first seven days of the course of anoxic coma, appear to be reliable to evaluate anoxic ischemic cortical or under-cortical lesions. Prognosis depends especially on cortical SEP (N20-P25): the lack of SEP is a good outcome predictor of death (abnormal BAEP) or of vegetative status (normal BAEP); the presence of normal and bilateral cortical SEP (with normal BAEP) allows to predict awakening, without prejudging of neurologic sequelae, even if they are severe.

Measurement of the nutrient oxidation rate with 13C as a tracer requires knowledge of the value of its coefficient of fractional recovery in the expired gas (FR). We measured FR in nine intensive care patients who were mechanically ventilated and received total parenteral nutrition. NaH13CO3 was administered at a priming dose (3.75 mumol.kg-1.min-1) followed by a continuous infusion (0.05 mumol.kg-1.min-1). Metabolic rate and pulmonary carbon dioxide elimination (VCO2) were measured by using a mass-spectrometer system. The 13C-12C ratio was measured in the expired gas with an isotopic-ratio mass spectrometer and FR was calculated by using standard equations. The average value of FR was 0.899 +/- 0.026 (means +/- SE) and remained stable for each patient on 2 consecutive days. Between patients, the coefficient of variation of FR was 8.6%. Metabolic rate was the only physiological factor found to affect the FR value.

Introduction En post-operatoire precoce de transplantation hepatique (TH), le risque infectieux est majore, notamment en raison de l’immunosuppression medicamenteuse. La procalcitonine (PCT) est un biomarqueur utilise pour le diagnostic precoce d’infection bacterienne. Neanmoins, de nombreuses causes non infectieuses d’elevation de la PCT sont egalement rapportees : polytraumatisme, brulure severe, pathologies inflammatoires, causes medicamenteuses (Ig anti-thymocyte) ainsi que le syndrome de reperfusion (PRS) [1] . L’objectif de cette etude etait de mettre en evidence une association entre la survenue d’un PRS lors d’une chirurgie de TH et l’elevation de la PCT a j1 postoperatoire. Patients et methodes Il s’agit d’une etude de cohorte retrospective evaluant l’ensemble des patients ayant beneficie d’une TH entre janvier 2004 et decembre 2010. La survenue d’un syndrome de reperfusion, les valeurs de PCT a j1 ainsi que la survenue d’une infection a j1 ou pre-existante a la transplantation ont ete recueillies. Les analyses statistiques ont ete realisees avec le test de Mann-Whitney. Un syndrome de reperfusion etait defini par la survenue d’une chute de la pression arterielle moyenne de 30 % ou plus pendant au moins une minute au cours des 5 minutes suivant le declampage vasculaire [2] , ou par la necessite d’introduire des amines vasoactives, ou de doubler la dose d’amines. Resultats Deux cent quatorze patients ont ete inclus dans l’etude. Cent seize patients (54,2%) ont presente un syndrome de reperfusion, avec une valeur mediane de PCT de 13 μg/L a j1 ( Tableau 1 , Fig. 1 ). Les valeurs de PCT a j1 etaient statistiquement plus elevees (p Fig. 1 ). Quatre patients (1,9 %) ont presente une infection a j1 ou pre-existante a la transplantation. On ne retrouvait pas de difference significative des valeurs de PCT a j1, que les patients soient infectes ou non (p = 0,49). Discussion La survenue d’un PRS lors d’une TH est associee a une franche elevation des valeurs de PCT a j1, que les patients soient infectes ou non. Ces resultats suggerent que les lesions d’ischemie-reperfusion survenant lors d’une TH sont responsables d’une elevation de PCT. La physiopathologie de ce phenomene reste mal connue.

Between 1977 and 1982, fifty cases of post-traumatic fat embolism were treated in a general intensive care unit. Average age of patients was 25.5 ± 13 years; there was no male majority. Mean free interval was 39 ± 27 h. 12 cases (24%) had single fractures and 38 (76%) multiple fractures. Forty-four patients had a fractured femur. Thirty-two patients presented the complete clinical syndrome with general, respiratory, neurological and cutaneous signs. Thrombocytopaenia and hypocholesterolaemia were the biological signs most often seen. In forty-four patients, orthopaedic treatment consisted of immediate immobilization, usually with traction. Twenty-six patients were reoperated on : intramedullary nail for twenty patients, plate for the other six. Fat embolism appeared in spite of surgery in six cases; it worsened after surgery in six others. Seven patients had per- or postanaesthetic problems. Fourteen per cent of patients died. The decrease in mortality was mainly due to an improvement in mechanical ventilation techniques. Early surgical fixation remained the rule if there was no serious respiratory distress or haemodynamic instability, although it did not seem to change the mortality rate in this group of patients.

The neurological signs, the cerebral CAT scan aspects and the ocular problems seen in five cases of acute methanol poisoning are reported; these were, respectively, a) coma requiring assisted ventilation, convulsions, hypotonicity, b) hypodensity of the putamen, and c) amaurosis and papillary œdema. The simplified acute physiologic score varied from 11 to 26; the value of 26 was observed in the only death of the series. Pathogenesis of the metabolic acidosis, as well as the different parts played by formic acid, lactic acid and ketone bodies are discussed. A normal or lowered serum potassium in a case of unexplained metabolic acidosis associated with an osmotic gap should make one think of the diagnosis. Macrocytosis, an indirect sign of folic acid deficiency, was in favour of a poor prognosis. The treatment included early gastric lavage, alkalinization, blocking of the metabolism of methanol by ethanol and haemodialysis with a bicarbonate dialysate enriched in ethanol; this corrected the acidosis and permitted the elimination of the toxic metabolites (clearance of methanol : 159 ml · min−1; half-life of methanol during purification : 3.46±1.32 h; quantity extracted : 246 g). The possible advantages of 4-methyl-pyrazol and alkyldiol derivatives need further confirmation.

A new case of oxytocin-induced water intoxication is reported in a 30 year old gravid woman. The severe symptoms of this uncommon complication are principally neurological; biological signs are a hyponatraemia with low plasma osmolality. Usually, biological and clinical signs are rapidly cleared up by treatment, but maternal death or neonatal water intoxication may occur. Such accidents must be prevented by clinical monitoring, watching out for alarm signals (oliguria is always found, resulting from the effect of oxytocin on the kidney), minimum fluid and proportional salt intakes, careful monitoring of oxytocin infusion rates, facilitated by the use of a constant flow-rate pump.

A case of postoperative myocardial infarction is reported. It occurred seven days after intra-abdominal surgery (left hemicolectomy), in a patient with coronary heart disease. Diagnosis was delayed because of lack of pain; it was suggested by cardiogenic shock occurring 48 h after the initial phase. The patient had been receiving postoperative epidural analgesia with an opioid (pethidine); this may explain the pain was missing, so delaying the diagnosis.