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M A Dommergues

Publications and source records attributed to M A Dommergues.

10 recordsLinked to original sources
PubMed2005

[Hyaline membrane disease in full-term neonates].

OBJECTIVES: Evaluation of the consequences of preplanned delivery near term on the neonatal respiratory distress syndrome and its mechanism of occurrence. PATIENTS AND METHODS: During five years, full-term infants (> or =37 weeks gestational age) admitted in the Institut de Puericulture de Paris, with a well characterized hyaline membrane disease, were included in a retrospective study. RESULTS: During this period, 97 full-term neonates with respiratory distress syndrome were hospitalized in the neonatal intensive care unit. The diagnosis of hyaline membrane disease was made in view of clinical and radiological criteria. The study of mode of delivery has shown a high frequency of pre-planned delivery: 54% caesarean and 24% vaginal delivery. A high-risk of occurrence of hyaline membrane disease was identified around 37 weeks gestational age in the case of preplanned delivery. CONCLUSION: Preplanned delivery near 37 weeks gestational age may increase the risk of occurrence of hyaline membrane disease in full-term neonates.

Adult↗
PubMed2004

[Erythropoietin administration to preterm infants: comparison between subcutaneous and intravenous route].

OBJECTIVE: Our aim was to compare the effectiveness of a one-month treatment with recombinant human erythropoietine (rHuEpo) according to the administration route. METHODS: Retrospective study based on the data collection from medical files of 64 preterm infant hospitalized in the "institut de puériculture et de périnatalogie" (Paris) between January 13th, 2002 and April 13th, 2002. The first group (N =33) was treated by subcutaneous rHuEpo 750 IU/kg per week, in three injections by week, for one month. The second group (N =15) was treated by continuous infusion of rHuEpo in total parenteral nutrition 1050 IU/kg per week (30% augmentation to compensate the amount absorbed by the filter). The third group (N =16) received 750 IU/kg per week of rHuEpo in three direct intravenous injections. The effectiveness of rHuEpo was evaluated by the absolute reticulocyte count, the level of hemoglobin and the incidence of blood transfusion (multiple logistic analysis of variant and regression). RESULTS: The absolute reticulocyte count and hemoglobin level were significantly reduced after one month of treatment by continuous infusion of rHuEpo in total parenteral nutrition and direct intravenous injections compared with a one-month treatment by subcutaneous rHuEpo. Hemoglobine level were at 8.8 and 9.6 g/dl vs 10.3 g/dl (P =0.02) and absolute reticulocyte count at 123,000/mm3 and 190,000/mm3 vs 216,000/mm3 (p =0.001). The number of transfused infants was significantly increased with utilization of continuous (40%) and direct intravenous (75%) compared with those treated by subcutaneous route (21.2%) while the ferritin level and phlebotomy losses were not significantly different in the three groups. The number of blood transfusion was significantly linked to phlebotomy losses and administration route of rHuEpo. CONCLUSION: Our study tends to demonstrate that rHuEpo administered subcutaneously reduces significantly the number of transfusion in contrary to intravenous routes. Waiting for pilot study and new molecules, we recommend subcutaneous administration of rHuEpo to preterm infants 250 IU/kg three times weekly in the treatment of anemia of prematurity.

Anemia↗
PubMed2003

[Acute neonatal appendicitis in an inguinal hernia].

UNLABELLED: Acute neonatal appendicitis is a rare surgical emergency. Prognosis depends on early diagnosis and management. CASE REPORT: A three and a half-month-old premature infant needed an urgent laparotomy because of an occlusive syndrome and sepsis with an inflammatory skin reaction. The per-operative diagnosis was suppurative acute appendicitis with local peritonitis, the appendix being strangulated into the inguinal hernia. DISCUSSION: Neonatal appendicitis represents 0.1% of all infantile appendicitis. Fifty percent of such cases occur in premature infants. Two clinical presentations exist, whose diagnosis is often made during surgery. The abdominal presentation (2/3 of the cases) can mimic necrotizing enterocolitis; the diagnosis is often late and evolution leads to diffuse peritonitis in the majority of the cases, while the mortality rate is higher than 50%. The intra-hernial presentation (1/3 of the cases), instead, is usually diagnosed and managed early due to the inguino-scrotal induration, while mortality rate is near zero. CONCLUSION: The high frequency of inguinal hernia in premature infants should not mask the risk for intra-hernial appendicitis. Inguino-scrotal inflammation should evoke the diagnosis. Prognosis depends on early and urgent surgical management.

Acute Disease↗
PubMed2002

[Neonatal enterovirus myocarditis].

UNLABELLED: Enterovirus infections in neonates are difficult to diagnose. Diphasic pattern and possibly fatal myocarditis must be anticipated. CASE REPORT: A 14-day-old girl had presented a heart failure after an initial episode of gastroenteritis and supraventricular tachycardia. Investigation demonstrated global myocardial dysfunction. Diagnosis of neonatal enterovirus myocarditis was made by polymerase chain reaction detection of viral genome. Heart failure was controlled with medical treatment. CONCLUSION: Enterovirus myocarditis is typically a biphasic illness. Rapid diagnosis of enteroviral infection in neonatal period may be made by polymerase chain reaction detection of viral genome. There is anecdoctal evidence that immunoglobulin infusions may improve outcome.

Enterovirus B, Human↗
PubMed2001

Central role of microglia in neonatal excitotoxic lesions of the murine periventricular white matter.

Periventricular leukomalacia (PVL) is the main cause of neurologic handicap in pre-term infants. The understanding of cellular and molecular mechanisms leading to white matter damage is critical for development of innovative therapeutic strategies for PVL. The pathogenesis of PVL remains unclear but possibly involves glutamate excitotoxicity as an important molecular pathway. We previously described a neonatal mouse model of excitotoxic white matter lesion mimicking human PVL. In the present study, we used this experimental tool to investigate the cellular populations and the glutamate receptor subtypes involved in excitotoxic white matter lesions. Combined immunohistochemical, electron microscopic, and cell death detection data revealed that microglial activation and astrocytic death were the primary responses of white matter to excitotoxic insult. In vitro experiments suggested that microglia activated by ibotenate released soluble factors that kill astrocytes. The use of selective agonists and antagonists of glutamate receptors revealed that N-methyl-D-aspartate (NMDA) receptor activation was essential and sufficient to produce cystic white matter lesions. NMDA receptor immunohistochemistry labeled microglial cells in the neonatal periventricular white matter. The developing white matter displayed a window of sensitivity to excitotoxic damage that was paralleled by the transient presence of NMDA receptor-expressing white matter cells. Assuming that similar pathophysiologic mechanisms are present in human pre- term infants, microglia and NMDA receptors could represent key targets for treatment of PVL.

Animals↗
PubMed2001

Deleterious effects of IL-9-activated mast cells and neuroprotection by antihistamine drugs in the developing mouse brain.

Elevated mean IL-9 serum levels have been observed in human neonates who will later develop cerebral palsy. In earlier studies, using a newborn mouse model of excitotoxic lesions mimicking those described in human cerebral palsy, we found that IL-9 pretreatment exacerbated brain damage produced by intracerebral injections of the glutamatergic analog ibotenate. Among its different cell targets, the Th2 cytokine IL-9 is a mast cell growth and differentiation factor that can cause mast cells to release various substances including histamine. In the present study, we sought to determine whether the deleterious effects of IL-9 in our mouse model were mediated by mast cells through histamine release. All mouse pups were pretreated with intraperitoneal injections of IL-9 or saline between postnatal days (P) P1 and P5. Immunohistochemistry for murine mast cell protease-1 performed on P5 showed an increased density of labeled cells in the neopallium of IL-9-treated Swiss pups as compared with controls. Western blot analysis confirmed the increased murine mast cell protease-1 brain content of IL-9-treated Swiss mice. IL-9 pretreatment had no significant effect on ibotenate-induced excitotoxic brain lesions in mast cell-deficient P5 pups (WBB6F1/J kit(W/W-v)), whereas IL-9 exacerbated these lesions in the control littermates with normal mast cell populations. Finally, cromoglycate or antihistamine drugs significantly reduced ibotenate-induced brain lesions in IL-9-treated Swiss pups. Taken together, these data suggest that recruitment of cerebral mast cells with histamine release may contribute to the exacerbation of neonatal excitotoxic brain lesions produced by IL-9. Neuroprotective strategies targeting mast cells may be useful in some neonates at risk for cerebral palsy.

Animals↗
PubMed2000

Proinflammatory cytokines and interleukin-9 exacerbate excitotoxic lesions of the newborn murine neopallium.

Many prenatal and perinatal factors are hypothesized to play a role in the cause of cerebral palsy (CP). Epidemiological data implicate maternal-fetal infection and associated increase in circulating cytokines. Murine model data suggest that excitotoxic damage can produce pathological change in brain tissue consistent with lesions observed in CP. Specifically, on day 5 after birth, mouse pups injected with ibotenate, a glutamatergic analogue, develop transcortical necrosis and white matter cysts mimicking some human perinatal lesions associated with CP. The present study builds on this murine model to assess the modulating role of several cytokines on the development of excitotoxic lesions. Pups pretreated with interleukin (IL)-1beta, IL-6, IL-9, or tumor necrosis factor-alpha developed significantly larger ibotenate-induced cortical and white matter damage than controls; IL-4 did not produce such an effect. In a similar manner, IL-9-overexpressing transgenic pups developed ibotenate-induced brain lesions, which were significantly larger than those induced in nontransgenic control pups. Pretreatment with proinflammatory cytokines significantly increased neopallial microglial density without affecting astrocytic density; IL-9 or IL-4 did not produce a similar effect. To our knowledge, this is the first in vivo study to demonstrate that systemically administered proinflammatory cytokines and IL-9 exacerbate brain lesions that are similar to those found in human infants with CP.

Animals↗
PubMed1998

Iron supplementation aggravates periventricular cystic white matter lesions in newborn mice.

Periventricular leukomalacia (PVL) is the main cause of neurological impairment in premature newborns. The pathogenesis of PVL remains unclear but may involve glutamate excitotoxicity and free radical production. Oxygen and iron, which are widely used in premature newborns, are oxidizing agents with a potential for promoting free radical production. We previously described a mouse model of excitotoxic neonatal white matter lesions mimicking several aspects of human PVL. In the present study, we used this mouse model to investigate whether iron pretreatment or 100% oxygen exposure worsened excitotoxic lesions. We found that iron pretreatment but not hyperoxia significantly increased white matter lesions, suggesting that high doses of iron may aggravate PVL in premature newborns.

Animals↗