Les infections fongiques représentent une complication fréquente chez les enfants prématurés pesant moins de 1500 g à la naissance. Il s'agit d'une source importante de mortalité et de morbidité. Nous avons repris les données de la littérature, afin de mieux connaître les mécanismes et les conséquences cliniques de ces infections. L'utilisation des antibiotiques a large spectre et le recours fréquent à l'alimentation parentérale sont les principaux facteurs de risque d'infection fongique chez les prématurés séjournant en service de soins intensifs. La majorité des infections fongiques néonatales est due à Candida, un faible nombre d'infections est lié à Malassezia. La prépondérance de Candida sp. est liée à ses propriétés d'adhérence sur les muqueuses et la peau ainsi que les cathéters. C. albicans représente 50 % des cas d'infections fongiques invasives du prématuré, cependant la place de C. parapsilosis tend à croître ces dernières années. Les facteurs de risque de colonisation par les levures du genre Candida sont: un poids de naissance inférieur à 1000 g, l'utilisation d'antibiotiques large spectre, le recours aux corticoïdes et l'alimentation parentérale. L'infection est précédée par une colonisation initiale de la peau, des muqueuses et des cathéters. La clinique est souvent fruste et la majorité des enfants porteurs d'une infection fongique présentent des signes non spécifiques comme une thrombopénie et une fièvre. L'évaluation des enfants atteints de telles infections nécessitent une évaluation rigoureuse, incluant un examen du liquide céphalorachidien, une culture des urines et la recherche d'une endocardite et d'une endophtalmie. La mortalité des infections invasives chez le nouveau-né reste élevée et atteint 30 % chez les enfants de poids extrêmement bas.Fungal infections were frequent in premature baby (<1500 g) and were associated with significant morbidity and mortality. In this paper we review the risk factors for invasive fungal infections and clinical settings. A better understanding of the mechanism of fungal infection in preterm infants is important in treatment and prevention. The early neonatal intensive care unit course favours colonization and proliferation of fungi since many preterm infants have central catheters and are exposed to broad spectrum antibiotics and parenteral nutrition. The majority of fungal infections in preterm neonates are due to Candida, with a small number due to other yeasts such as Malassezia. Candida is an opportunistic pathogen, which adheres to the skin, mucosal, and catheter surface. C. albicans account for 50% of cases of fungal sepsis. C. parapsilosis is the second most prevalent species in very low birth weight children; its frequency increased from 1995 to 2000. Risk factors for fungal colonization are: very low birth weight, exposure to broad spectrum antibiotics, parenteral nutrition and use of corticosteroids. Colonization of the skin, gastro-intestinal tract and respiratory tract and central vascular catheter precede infection. The majority of preterm infants with fungal infections develop thrombocytopenia, but this is a common feature shared with other sepsis. The evaluation of infants with fungal sepsis should include cerebrospinal fluid examination and culture of urine with surveillance for endocarditis, renal, liver and brain abscesses and endophthalmitis. The mortality rate can reach 30%, and is higher in very low birth weight infants.

Antiphospholipid antibody (aPL) is associated with thromboembolism. There is scant evidence of a relationship between the aPL profile and serious adverse pregnancy outcome. The aim of this study was to assess whether aPL measurements during early pregnancy were useful in predicting a serious adverse pregnancy outcome. In this prospective study, we measured aPLs, including lupus anticoagulant (LA), IgG, IgM, IgA anticardiolipin antibody (aCL), IgG, IgM phosphatidylserine-dependent antiprothrombin antibody, and IgG kininogen-dependent antiphosphatidylethanolamine antibody (aPE) during the first trimester in a consecutive series of 1155 women. The 99th percentile cut-off values in each aPL were determined using samples from 105 women who did not exhibit any pregnancy morbidity. We assessed the predictive risk of a serious adverse pregnancy outcome adjusted for confounding factors. We found that IgG aCL was asssociated with developing pregnancy-induced hypertension (PIH) (odds ratio 11.4, 95% CI 2.7–48); IgG aPE with PIH (8.3, 2.4–29), severe PIH (20.4, 4.5–91), and premature delivery (PD) (12.7, 3.1–50); and LA with PD (11.0, 2.8–44) and low birth weight (8.0, 2.1–31). The combinations of IgG aPE plus IgG aCL (17.5, 4.7–66.7) or IgG aPE plus LA (22.2, 5.4–909) measurements predicted severe PIH with 30.8% sensitivity and 99.2% specificity. We conclude that aPL measurements during early pregnancy may be useful in predicting adverse pregnancy outcome.

INTRODUCTION:Equivalence trials are actually frequently used to prove non-inferiority in anticoagulant therapy. Equivalence trials consist to demonstrate that two treatments are not too much different. This difference has to be under a margin previously determined. The margin corresponds to an efficacy loss that is defined to be acceptable, in accordance to the advantages due to the new treatment. The aim of this work is to explore the equivalence trial published in the thromboembolic disease by focus on the non-inferiority margin used.METHODS:We identified published equivalence trials in the venous thromboembolic disease, by a systematic search in Medline. We calculated the efficacy loss by reference with the value of the smallest effect size of the standard treatment compared to placebo.RESULTS:We found 9 equivalence trials used in venous thromboembolic disease. The mean value of the efficacy loss was 434%, and the median value was 357%. Eighty-five percent of the values of the efficacy loss were above 100%.DISCUSSION:Eighty-five percent of the equivalence trials conclude to equivalence despite a complete efficacy loss of the effect of the standard treatment compared to placebo. The results of equivalence trials should be interpreted warily. The corresponding non-inferiority margin should be chosen more rigorously and by reference with the value of the smallest effect size of the standard treatment compared to placebo.

Kawasaki disease is an acute, self-limited vasculitis of unknown etiology that occurs predominantly in infants and children. If not treated early with high-dose intravenous immunoglobulin, 1 in 5 children develop coronary artery aneurysms; this risk is reduced 5-fold if intravenous immunoglobulin is administered within 10 days of fever onset. Coronary artery aneurysms evolve dynamically over time, usually reaching a peak dimension by 6 weeks after illness onset. Almost all the morbidity and mortality occur in patients with giant aneurysms. Risk of myocardial infarction from coronary artery thrombosis is greatest in the first 2 years after illness onset. However, stenosis and occlusion progress over years. Indeed, Kawasaki disease is no longer a rare cause of acute coronary syndrome presenting in young adults. Both coronary artery bypass surgery and percutaneous intervention have been used to treat Kawasaki disease patients who develop myocardial ischemia as a consequence of coronary artery aneurysms and stenosis.

Hemophagocytic lymphohistiocytosis occurring as a primary or acquired disorder is a condition of chaotic and uncontrolled immune system stimulation. Cytotoxic cells and macrophages cause multiorgan damage, hemophagocytosis, and severe systemic inflammation. Clinical manifestations include a fever, organ enlargement, and weight loss. Laboratory tests show bicytopenia or pancytopenia, cytolysis and cholestasis, serum ferritin elevation, and clotting disorders. The reference standard for the diagnosis remains the presence in histological specimens of hemophagocytic macrophages, which may be lacking early in the disease, leading to diagnostic challenges. Inherited forms produce symptoms in early childhood and are fatal in the absence of specific treatment. In adults, the clinical spectrum ranges from mild and self-limited hemophagocytic lymphohistiocytosis to rapidly fatal multiorgan failure. Many questions remain unresolved regarding the diagnosis and treatment in adults. This update is an attempt at providing answers.

Propos. – Après plusieurs décennies d'hégémonie du lymphocyte T, des travaux récents ont suggéré l'importance du lymphocyte B dans les maladies auto-immunes. C'est pour cette raison qu'émerge depuis peu l'idée d'utiliser des thérapeutiques antilymphocytaires B, en particulier le rituximab (un anticorps monoclonal chimérique anti-CD20).Actualités et points forts. – Cette revue a permis d'aborder différents points d'actualités : a) le rôle des lymphocytes B dans les maladies auto-immunes, en particulier leur capacité à être des cellules présentatrices d'antigènes et d'être activées par des systèmes originaux comme Blys/Baff ; b) le mécanisme d'action de rituximab (l'apoptose, la cytotoxicité complément–dépendante et la cytotoxicité cellulaire anticorps-dépendante) et les phénomènes expliquant les échecs et les échappements, en particulier dans les lymphoproliférations ; c) les résultats comprennent des données d'efficacité et de tolérance dans les principales affections auto-immunes. Pour celles-ci, les indications les plus prometteuses semblent être la polyarthrite rhumatoïde, le lupus systémique, mais quelques études ouvertes préliminaires suggèrent une efficacité dans le syndrome de Goujerot-Sjögren, les neuropathies, les cytopénies auto-immunes, le purpura thrombopénique idiopathique, les maladies des agglutinines froides, les affections cutanées bulleuses...Perspectives et projets. – Des études contrôlées s'imposent pour déterminer l'efficacité et la tolérance réelle de cette molécule, car il est impératif de valider ces nouvelles stratégies immunothérapiques surtout quand elles concernent des thérapeutiques innovantes et coûteuses. Néanmoins, ces différentes expériences suscitent un grand espoir mais également des questions passionnantes notamment sur le rôle des lymphocytes B dans les maladies auto-immunes.Subject. – After several decades of hegemony of the T lymphocyte, recent work has suggested the importance of the B lymphocyte in auto-immune diseases. As a consequence, there has emerged over the last few years the idea of using anti-B lymphocyte therapy, in particular rituximab (a chimeric anti-CD20 monoclonal antibody).Current topics and important results. – This review addresses various current topics: a) the role of B lymphocytes in auto-immune diseases, notably their capacity to be antigen presenting cells and to be activated by original systems like Blys/Baff; b) the mechanism of action of rituximab (apoptosis, complement-dependent cytotoxicity and antibody-dependent cell cytotoxicity) and the phenomena explaining failures and cases escaping treatment, in particular among lymphoproliferations; c) The results include efficacy and tolerance data for the principal auto-immune affections. Among these, the most promising indications would seem to be for rheumatoid polyarthritis and systemic lupus erythematosis, although some preliminary open studies point to an effect in Goujerot-Sjögren's syndrome, neuropathies, auto-immune cytopenia, idiopathic thrombocytopenic purpura, cryoagglutinins, blistering cutaneous affections...Perspectives and projects. – Controlled studies will be required to determine the true efficacy and tolerance of this molecule, as it is imperative to validate these new immunotherapeutic strategies, above all when they concern innovative and expensive therapy. Nevertheless, these different observations arouse great hopes and at the same time exciting questions, notably as to the role of B lymphocytes in auto-immune diseases.