Transfusions de plasma en réanimation pédiatrique

Whereas red blood cell transfusions have been used since the nineteenth century, plasma has only been available since 1941. It was originally mainly used as volume replacement, mostly during World War II and the Korean War. Over the years, its indication has shifted to correcting coagulation factors deficiencies or to preventing bleeding. Currently, it remains a frequent treatment in the intensive care unit, both for critically ill adults and children. However, observational studies have shown that plasma transfusion fail to correct mildly abnormal coagulation tests. Furthermore, recent epidemiological studies have shown that plasma transfusions are associated with an increased morbidity and mortality in critically ill patients. Therefore, plasma as any other treatment has to be used when the benefits outweigh the risks. Based on observational data, most experts suggest limiting its use either to massively bleeding patients, or bleeding patients who have documented abnormal coagulation tests, and refraining for transfusing plasma to non-bleeding patients whatever their coagulation tests. In this paper, we will review current evidence on plasma transfusions and discuss its indications.     

Marketing hospitals to physicians in the United States.

This paper discusses the application of multidimensional scaling (MDS) in formulating the strategies for marketing a hospital to physicians. An extensive hospital factor survey was used to provide information for interpreting the MDS results, and to formulate specific strategies to: attract new physicians to the hospital; and, to make the hospital attractive to affiliated physicians for patient referrals. We conclude that MDS provides a unique approach for formulating strategies for similar non-conventional situations.     

Increased platelet activation and fibrinogen in Asian Indians. Potential implications for coronary risk

Aims To determine whether Asian Indians (Indians), a group knownto have high rates of coronary heart disease, have increasedplatelet activation and fibrinogen levels relative to whiteAmericans of European origin (whites). Methods and Results Forty healthy, non-smoking Indians, aged 25–45, were matchedwith 40 healthy whites for age (within 3 years) and gender.Platelet activation was tested in blood exiting a bleeding timewound at 1 and 2min post-incision (wound-induced activation),as well as in venous blood stimulated in vitro with collagen,using whole blood flow cytometry. Other risk factors, includingfibrinogen levels, family history of diabetes or coronary heartdisease, fasting insulin and lipid levels, and Lp(a) were alsoassessed. Fibrinogen levels were higher among Indians than whites,even after adjustment for gender or family history of coronaryheart disease (P<0·05). Indians had higher levelsof wound-induced glycoprotein IIb/IIIa binding and plateletsecretion (P-selectin expression) than whites, with the greatestdifferences found when comparing the upper quintile of activationfor each group (Ps<0·05). Indians with a family historyof coronary heart disease (n=15) had higher levels of plateletsecretion (wound-induced and in vitro) than Indians withouta family history (Ps<0·05), while the relationshipwas reversed among whites. Platelet activation measures werenot consistently related to other coronary risk factors, whilefibrinogen was related to triglyceride and insulin levels amongIndians. Conclusion Indians have elevated fibrinogen and platelet activation levelsrelative to whites. These factors may contribute to the increasedcoronary risk observed in Indians.     

Increased detection by restaining of acid-fast bacilli in sputum samples transported in cetylpyridinium chloride solution.

SETTING: Seventeen health facilities in a Tuberculosis Unit, and the Tuberculosis Research Centre (TRC), Chennai, India. AIM: Evaluation of restaining by the auramine-phenol method for detection of acid-fast bacilli (AFB) in direct smears of samples transported in cetylpyridinium chloride (CPC) solution. METHODS: Among patients attending the above health facilities, 730 samples were collected in CPC and transported to the TRC. Two direct smears were prepared from each sample, one stained by the usual auraminephenol method (primary staining) and the other stained again by the same method (restaining) for examination by fluorescence microscopy. All the samples were processed for culture of Mycobacterium tuberculosis. RESULTS: A significantly higher proportion (49.6%) of samples were positive by restaining compared to primary staining (32.5%, P < 0.0001). Of 362 samples positive by restaining, 38.7% were negative by primary staining. The yield of different grades of smears was significantly higher with restaining than with primary staining (P < 0.0001). More smear-negative culture-positive smears were observed with the primary than with the restaining method (178/400 [44.5%] vs. 78/ 400 [19.5%], P < 0.001). CONCLUSION: The rate of detection of AFB in direct smears made from sputum samples transported in CPC was higher on restaining than on primary staining.     

Pharmacokinetic interactions of maraviroc with darunavir-ritonavir, etravirine, and etravirine-darunavir-ritonavir in healthy volunteers: results of two drug interaction trials

The effects of darunavir-ritonavir at 600 and 100 mg twice daily (b.i.d.) alone, 200 mg of etravirine b.i.d. alone, or 600 and 100 mg of darunavir-ritonavir b.i.d. with 200 mg etravirine b.i.d. at steady state on the steady-state pharmacokinetics of maraviroc, and vice versa, in healthy volunteers were investigated in two phase I, randomized, two-period crossover studies. Safety and tolerability were also assessed. Coadministration of 150 mg maraviroc b.i.d. with darunavir-ritonavir increased the area under the plasma concentration-time curve from 0 to 12 h (AUC12) for maraviroc 4.05-fold relative to 150 mg of maraviroc b.i.d. alone. Coadministration of 300 mg maraviroc b.i.d. with etravirine decreased the maraviroc AUC12 by 53% relative to 300 mg maraviroc b.i.d. alone. Coadministration of 150 mg maraviroc b.i.d. with etravirine-darunavir-ritonavir increased the maraviroc AUC12 3.10-fold relative to 150 mg maraviroc b.i.d. alone. Maraviroc did not significantly affect the pharmacokinetics of etravirine, darunavir, or ritonavir. Short-term coadministration of maraviroc with darunavir-ritonavir, etravirine, or both was generally well tolerated, with no safety issues reported in either trial. Maraviroc can be coadministered with darunavir-ritonavir, etravirine, or etravirine-darunavir-ritonavir. Maraviroc should be dosed at 600 mg b.i.d. with etravirine in the absence of a potent inhibitor of cytochrome P450 3A (CYP3A) (i.e., a boosted protease inhibitor) or at 150 mg b.i.d. when coadministered with darunavir-ritonavir with or without etravirine.