EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.08.001
N Guiso , L Bassinet , P Reinert
{"title":"Coqueluche du nourrisson, de l’enfant et de l’adulte","authors":"N Guiso , L Bassinet , P Reinert","doi":"10.1016/j.emcped.2003.08.001","DOIUrl":"10.1016/j.emcped.2003.08.001","url":null,"abstract":"<div><p>Whooping cough is a human respiratory infection, dramatic for newborns. The first descriptions of this disease are recent, from the 16<sup>th</sup> century. Soon after the discovery of the causal agent of the disease, the bacterium <em>Bordetella pertussis</em>, whole cell vaccines, composed of bacterial suspensions inactivated by heat, were developed and their use generalized. These vaccines could be very efficacious but are very difficult to produce and not well tolerated. Because of the characterization of the bacterial proteins involved in the pathogenicity of <em>Bordetella pertussis</em>, an other type of vaccine was developped. This new type is called acellular vaccine because composed of purified bacterial proteins. The generalization of the vaccination with whole-cell vaccines conducted to an important decrease of mortality and morbidity. However, thirty years after the introduction of the vaccination, a resurgence is observed in vaccinated countries. This resurgence is principally due to the short duration of vaccinal immunity and the lack of vaccinal or natural boosters. The disease affects now adolescents and adults who present an atypical cough which difficult to diagnose. These adolescents and adults contaminate non vaccinated new borns. Vaccinal boosters are necessary and are now possible with acellular vaccines since 1998. France was the first country to introduce a booster for adolescents at 11-13 years of age and a booster for young adults is under discussion. Nevertheless, surveillance of the disease is of great importance and must continue to analyse the consequences of such boosters which are introduced to reduce the transmission of the disease to infants too young to be vaccinated</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 33-44"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.08.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87191025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.09.005
M.-F Gagnadoux (praticien hospitalier)
{"title":"Oxalose","authors":"M.-F Gagnadoux (praticien hospitalier)","doi":"10.1016/j.emcped.2003.09.005","DOIUrl":"https://doi.org/10.1016/j.emcped.2003.09.005","url":null,"abstract":"<div><p>Oxalosis is the systemic deposition of calcium oxalate crystals, caused by primary hyperoxaluria type 1 (PH1), the most frequent variety of primary hyperoxaluria. PH1 is an autosomal recessive disease due to an hepatic enzymatic defect <em>of alanine : glyoxylate aminotransferase</em> (AGT), resulting in oxalate overproduction. Because of the poor solubility of calcium oxalate in urine, the first symptom is usually a recurrent lithiasis, beginning in childhood. Associated nephrocalcinosis results almost always in terminal renal failure before the adult age, and oxalate crystals accumulate in many tissues, particularly bones. Liver transplantation, or more often combined liver-kidney transplantation, is the only curative treatment ; at an early stage, permanent urine dilution by hyperhydration may prevent nephrocalcinosis. Primary hyperoxaluria type 2, a much rarer disease due to a defect of <em>glyoxylate/hydroxypyruvate-reductase</em> (gr/HPR), is associated with L-glyceric aciduria. Its main manifestation is also recurrent lithiasis ; however renal failure is a rare occurrence.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 45-50"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.09.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137313228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.09.003
P Niaudet (Professeur des Universités, praticien hospitalier, chef de service)
{"title":"Syndromes néphrotiques congénitaux et infantiles","authors":"P Niaudet (Professeur des Universités, praticien hospitalier, chef de service)","doi":"10.1016/j.emcped.2003.09.003","DOIUrl":"https://doi.org/10.1016/j.emcped.2003.09.003","url":null,"abstract":"<div><p>Congenital nephrotic syndrome is present at birth or appears during the first three months of life and infantile nephrotic syndrome during the first year. Finnish type congenital nephrotic syndrome is an autosomal recessive disease. Nephrotic syndrome is present at birth, severe and does not respond to therapy. Infectious and nutritional complications are frequent. Renal function deteriorates necessitating a dialysis-transplantation program, between age 5 and 8. The disease does not recurr after transplantation. Diffuse mesangial sclerosis is the second cause of congenital and infantile nephrotic syndrome. It may be isolated or part of the Denys-Drash syndrome (association of the nephropathy with male pseudohermaphroditism and Wilm’s tumor). Nephrotic syndrom is resistant to therapy. Renal failure develops in early childhood. Therapy is aimed to prevent oedema, denutrition, infections and thrombosis. Proteinuria does not recurr after renal transplantation. Other causes of nephrotic syndrome are less frequent.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 89-96"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.09.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137313229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.06.004
F Freymuth (Professeur de virologie, biologiste des hôpitaux)
{"title":"Infections à virus respiratoire syncytial et virus para-influenza : prévention et traitement","authors":"F Freymuth (Professeur de virologie, biologiste des hôpitaux)","doi":"10.1016/j.emcped.2003.06.004","DOIUrl":"10.1016/j.emcped.2003.06.004","url":null,"abstract":"<div><p>Controlling the dissemination to children of the respiratory syncytial virus (RSV) and parainfluenzae virus (PIV) rests mainly on simple hygiene measures such as hand washing and contact precautions. In addition to the nonspecific treatment of bronchiolitis (chest physiotherapy), ribavirin, an antiviral agent active against the RSV and PIV in vitro, is used in clinical practice only by inhalation in severe forms of RSV infection. Anti-RSV immune globulins have been proved effective in preventing RSV infection or its severe forms. The humanized monoclonal antibody palivizumab is used in France in selected patients.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 28-32"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.06.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88850903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.09.001
P de Lagausie
{"title":"Pathologies acquises de l’œsophage chez l’enfant","authors":"P de Lagausie","doi":"10.1016/j.emcped.2003.09.001","DOIUrl":"10.1016/j.emcped.2003.09.001","url":null,"abstract":"<div><p>Main esophageal pathology in children include accidental ingestion of a foreign body, traumatic œsophageal perforation, infection and burn lesions. Accidental ingestion of foreign bodies are very frequent. In the majority of cases, natural elimination is the rule. In some cases, tear of the esophageal wall is induced by the size or the nature of the foreign body. In these cases, it is necessary to identify and treat the lesion. Esophageal perforation or rupture is rare in childhood and frequently iatrogenous. The prognosis depends mainly on early diagnosis. Treatment include gastric tube placement under endoscopy, saliva aspiration, antibiotic and sometimes surgical drainage. The accidental ingestion of corrosive agents is a major cause of œsophageal strictures in children. Althrough, The mainstay of treatment is repeated dilatations, significant number of patients still require œsophageal replacement.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 109-117"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.09.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"109869135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.06.005
M Broyer (Professeur des Universités)
{"title":"Tubulopathies congénitales","authors":"M Broyer (Professeur des Universités)","doi":"10.1016/j.emcped.2003.06.005","DOIUrl":"10.1016/j.emcped.2003.06.005","url":null,"abstract":"<div><p>Congenital tubular defects include a number of distinct entities sharing the same basis of a proximal and/or distal renal tube dysfunction, generally characterised by a reabsorptive defect of one or several elements. During the last years, the molecular basis of an increasing number of these entities was identified as one or several carriers or channels the mutations of which are responsible. An update of this lysinuria, Bartter and Gitelman syndrome, tubular acidosis, pseudohypoaldosteronisms, Liddle syndrome, and also cystinosis, other causes of inherited Fanconi syndrome and Lowe syndrome.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 59-72"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.06.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76253325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMC - PédiatriePub Date : 2004-02-01DOI: 10.1016/j.emcped.2003.09.002
B Blondel (Directeur de recherches), G Bréart (Professeur des Universités)
{"title":"Mortinatalité et mortalité néonatale","authors":"B Blondel (Directeur de recherches), G Bréart (Professeur des Universités)","doi":"10.1016/j.emcped.2003.09.002","DOIUrl":"10.1016/j.emcped.2003.09.002","url":null,"abstract":"<div><p>In France in 2000 the stillbirth rate was 4.6 per 1 000 births and the neonatal death rate was 3.0 per 1 000. France has an average position among European countries for neonatal mortality. The lowest level of mortality is observed in Finland and Sweden. According the International Classification of Diseases (ICD 9), the main causes of neonatal death in 1995 were congenital anomalies (27 % of deaths), and perinatal conditions (54 %), especially intrauterine hypoxia and birth asphyxia (10 %), respiratory distress syndrome (8 %), and fetal and neonatal haemorrhage (6 %). Mortality can be used to assess medical care during the perinatal period if the risk factors of mortality are collected and taken into account in the analysis. The main factors are : gestational age, birth weight, and the number of newborns (singletons, twins, triplets, …).The trend towards a more active approach of care during pregnancy, delivery and the first days of life has various consequences on mortality. Consequently it is necessary to follow some recommendations in medical assessment. Definitions of births and deaths should include very preterm births (≥ 22 weeks) and very small fetus or infants (≥ 500 grams), and rates of mortality should be measured for extended perinatal mortality or fetal and infant mortality, after excluding deaths attributed to congenital anomalies.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 97-108"},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.09.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86062530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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