[Use of therapeutic hypothermia in sudden unexpected postnatal collapse]. / Malaise grave inopiné du nouveau-né à terme : une place possible pour l'hypothermie thérapeutique.

Sudden postnatal collapse of a full-term newborn is uncommon but may result in severe consequences: these include death; epilepsy; and motor, cognitive, or sensory impairment. Most authors suggest applying a therapeutic hypothermia approach when a previously healthy newborn develops moderate or severe encephalopathy after a sudden postnatal collapse occurring within the first hours or days after birth. However, this technique has still not been validated by randomized trials. Only a few cases have been reported in the literature. This article describes five apparently healthy newborns, born between 2007 and 2012, who suffered moderate to severe encephalopathy following a postnatal collapse on their first day of life. It describes their clinical history as well as their treatment and follow-up. The article focuses on the implementation of hypothermia in this indication and its limitations. Two newborns underwent classic therapeutic hypothermia, two others underwent temperature regulation (one at 34.5 °C, the other one for only 15 h because she quickly improved). One newborn, with severe pulmonary arterial hypertension, did not receive therapeutic hypothermia. Two newborns died (one had classic hypothermia and the other hypothermia at 34.5 °C), the outcome of the three survivors at three years, 18 months, and 15 months is good with only transient postural anomalies. Follow-up must be continued to assess their cognitive development and particularly their memorization processes. Additional research and centralization of the cases is required to evaluate the feasibility, safety, and benefits of therapeutic hypothermia in this situation.

[Implementation of the intestinal micro flora in the early stage and adequate immunity later on]. / Etablissement du microbiote intestinal en bas âge et qualité de l'immunité ultérieure.

The pre and postnatal development of human immunity are remarkably continuous. The feto-placental unit builds up to promote a climate of immune tolerance specifically driven in this way by the maternal immunity. The process of birth triggers the development of the infant's postnatal immunity, in first place through the bacterial colonisation of a sterile intestinal mucosa. The progressive immune response stabilisation at the sub-mucosa level during the first year of life will arise from the interface between the host and its microflora. It will take place progressively and will occur thanks to a variety of successive and complementary very complex immune mechanisms, under the influence of a rich and diversified intestinal microbiotia. Solid scientific arguments allow hypothesising that immune deviances later in life could be the consequence of an inadequate bacterial pressure on the intestinal mucosa at the early stage. A variety of epigenetic modifications taking place in this early stage could account for the deviant programming of later immunity. Each health care provider should acknowledge that some therapeutic and nutritional interventions during the first year of life may interfere with this complex immune development, giving rise to a risk of increasing immune deviancies later on.

[Chronic visceral leishmaniasis during chemotherapy for metastatic osteosarcoma]. / Leishmaniose viscérale chronique au cours d'une chimiothérapie pour ostéosarcome métastatique.

UNLABELLED: Leishmaniasis refers to a spectrum of diseases caused by Leishmania. Clinically, three types of leishmaniasis can be distinguished: the cutaneous, mucous and visceral leishmaniasis, the latter being caused by Leishmania donovani. CASE REPORT: An 11-year-old Thai, living in Belgium for 6 years, had surgery for a vertebral osteosarcoma with pulmonary metastases, followed by polychemotherapy, then pulmonary metastasectomy. During a post-chemotherapy bone marrow aplasia, febrile episode with a general condition impairment was noted and first treated by broad-spectrum antibiotherapy, then by amphotericin B, in the absence of any accurate etiology. The outcome first was favorable. Nevertheless, 7 months later, the visceral leishmaniasis diagnosis was made because of the recurrence of the same symptoms. Classical treatments by antimony derivatives (Glucantim), then liposomal amphotericin (Ambisome) proved to be inefficient. A liposomal amphotericin-gamma interferon association suppressed the symptoms without eradicating the parasite. The patient was given a maintenance therapy based on liposomal amphotericin. CONCLUSION: The stubborn and recurring nature of this chronic visceral leismaniosis can be due to the immune deficit inherent in the polychemotherapy performed in order to treat the metastatic osteosarcoma which currently is in first full remission.