Acta paediatrica Japonica : Overseas edition最新文献

{"title":"CD48 expression on leukocytes in infectious diseases: flow cytometric analysis of surface antigen.","authors":"M Katsuura,&nbsp;Y Shimizu,&nbsp;K Akiba,&nbsp;C Kanazawa,&nbsp;T Mitsui,&nbsp;D Sendo,&nbsp;T Kawakami,&nbsp;K Hayasaka,&nbsp;S Yokoyama","doi":"10.1111/j.1442-200x.1998.tb01994.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01994.x","url":null,"abstract":"<p><strong>Background: </strong>The function of CD48, one of the pan leukocyte cell surface antigens, is not yet well understood. CD48 was recently shown to enhance the CD40-mediated activating signal to B lymphocytes. As CD48 is one of the activation antigens of monocytes, neutrophils and lymphocytes, a change of its expression on the cells could be expected in infectious diseases.</p><p><strong>Methods and results: </strong>Leukocytes from 27 healthy controls and 97 patients with various infectious diseases were stained with anti CD48 antibody and analyzed by flow cytometry. On monocytes and neutrophils, the CD48 expression was increased in all of the patients with varicella, measles, rubella, infectious mononucleosis, streptococcus tonsillitis, sepsis and appendicitis. On lymphocytes, a significant increase of CD48 was also detected in the patients with the same diseases, except those with sepsis or appendicitis. The normalization of increased CD48 expression was confirmed on monocytes at the convalescent phase.</p><p><strong>Conclusion: </strong>These data suggest that CD48 expression on leukocytes reflects the disease activity of infectious diseases, especially of viral infections.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 6","pages":"580-5"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01994.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20799348","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}

{"title":"Immunoglobulin G subclasses in wheezing infants.","authors":"O Karaman,&nbsp;A Uğuz,&nbsp;N Uzuner","doi":"10.1111/j.1442-200x.1998.tb01991.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01991.x","url":null,"abstract":"<p><strong>Background: </strong>The wheezing infant is a common but difficult patient to approach diagnostically. The prevalence of immunoglobulin (Ig) G subclass deficiency in wheezing infants is still controversial.</p><p><strong>Methods: </strong>We studied the serum concentration of IgG subclasses in 38 wheezing infants (aged 6-24 months) who had not received systemic steroids before investigation and in 30 healthy age matched controls (aged 6-24 months).</p><p><strong>Results: </strong>The prevalence of one or more IgG subclass deficiencies was 31.6% in wheezing infants and 26.7% in controls. There was no significant difference in prevalence of IgG subclass deficiency between patients and controls (P > 0.05). The mean concentration of IgG subclasses in patients were compared with controls. There was no significant difference in mean serum concentration of IgG1, G2 and G3 subclasses. However, there was a trend towards higher concentrations of IgG4 in wheezing infants and this difference for IgG4 was significant (P < 0.01). Immunoglobulin G subclass deficiency was found in 25 and 36.4% of wheezing infants who had experienced from two to four and five or more wheezing episodes in 2 years, respectively (P > 0.05).</p><p><strong>Conclusion: </strong>Our findings suggest that wheezing in infancy is not associated with IgG subclass deficiency, and in wheezing infants low IgG subclasses levels do not increase the frequency of wheezing. However, there is a relationship between recurrent wheezing and serum IgG4 subclass concentration.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 6","pages":"564-6"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01991.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20799345","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}

{"title":"An infant with Costello syndrome complicated with fatal hypertrophic obstructive cardiomyopathy.","authors":"H Tomita,&nbsp;S Fuse,&nbsp;K Ikeda,&nbsp;K Matsuda,&nbsp;S Chiba","doi":"10.1111/j.1442-200x.1998.tb02000.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb02000.x","url":null,"abstract":"<p><p>We report a 3-month-old girl with Costello syndrome complicating fatal hypertrophic obstructive cardiomyopathy. She had typical findings of this syndrome, slight dyspnea and persistent wheezing. Doppler echocardiography revealed asymmetric septal hypertrophy and systolic anterior movement of the anterior mitral leaflet. There was grade 1 mitral regurgitation. Although once her heart failure had been controlled medically, she died suddenly following deterioration of her heart condition. Costello syndrome can complicate fatal hypertrophic obstructive cardiomyopathy.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 6","pages":"608-11"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb02000.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20799792","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}

{"title":"Constructing the human cerebral cortex during infancy and childhood: types and numbers of cortical columns and numbers of neurons in such columns at different age-points.","authors":"B H Landing,&nbsp;W R Shankle,&nbsp;J Hara","doi":"10.1111/j.1442-200x.1998.tb01986.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01986.x","url":null,"abstract":"<p><p>This study examines JL Conel's data on neuron numbers in 35 human cortical areas for eight age points from 0 (birth) to 72 months, to analyze cortical columns, the presumed functional units of the cortex. For each cortical area at each age point, cortical surface divided by the square root of the area's neuron number gives cross-sectional areas with radii ranging from 180 microns at birth to 250 microns at 72 months. For the prefrontal cortex at birth and 48 months, these radii are approximately 2.10 and 1.19 times the longest radial basal dendrites, suggesting similar dimensions between these two measures of column radius. The logarithm of neuron number per cortical area and age point was examined in relation to the Weber-Fechner law governing the relationship between stimulus intensity and perception. A mechanism for this law consistent with the cortical model of Douglas et al. illustrates the importance of local circuit neurons. The cross-sectional areas of hexagonal columns for prefrontal cortex, using as radius, the longest radial extent of layer 5 pyramidal neuron basal dendrites, ranging from 0.013 mm2 at birth to 0.064 mm2 at 48 months, suggests that functional cortical columns increase cross-sectional area during development. These cross-sectional areas are 55-100-fold larger at birth, and 229-277-fold larger at 48 months, than those computed from somal width in prefrontal, layer 5 pyramidal neurons. Comparison of radial extent of pyramidal basal dendrites to their soma-to-soma distances shows that layer 3 pyramidal basal dendrites reach 1.5 and 4.0 other pyramidal neurons at 15 and 60 months, respectively, while layer 5, extra-large pyramidal basal dendrites reach 1.14 and 1.72 other such neurons at birth and 48 months, respectively. If such a relationship holds for other cortical areas, then the Conel data can be used to estimate basal dendrite extent, for which there currently is a paucity of data.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 6","pages":"530-43"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01986.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20798870","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}

{"title":"Hereditary pancreatitis: report of a family from Turkey.","authors":"A Kansu,&nbsp;N Girgin,&nbsp;C Yurdaydin,&nbsp;H Cetinkaya,&nbsp;O Uzunalimoglu","doi":"10.1111/j.1442-200x.1998.tb02001.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb02001.x","url":null,"abstract":"<p><p>Chronic pancreatitis is a rare disease in children and is usually secondary to underlying diseases such as hereditary pancreatitis, cystic fibrosis, hyperlipidemia, prolonged malnutrition, gallstones or anomalies of the biliary-pancreatic duct system. Hereditary pancreatitis is a common cause of chronic pancreatitis in children but is often unrecognized until months or years later. We report here a family with hereditary pancreatitis in which four members are affected.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 6","pages":"612-5"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb02001.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20799793","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}

{"title":"Pseudosarcomatous myofibroblastic tumor of the urinary bladder with massive intraperitoneal hemorrhage in a child.","authors":"K Okada,&nbsp;Y Fujii,&nbsp;K Uema,&nbsp;T Yoshimoto,&nbsp;T Nakatsu,&nbsp;T Yoshida,&nbsp;T Hasegawa","doi":"10.1111/j.1442-200x.1998.tb01971.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01971.x","url":null,"abstract":"<p><p>A 3-year-old boy presented with persistent abdominal pain, hematuria and facial pallor with progressive anemia. A computed tomography scan showed a massive intraperitoneal hemorrhage and tumor mass in the bladder. Histological examinations of the resected tumor revealed findings of pseudosarcomatous myofibroblastic tumor (PMT). The clinico-pathological features of this case warn us that PMT can cause acute abdomen syndrome with massive intraperitoneal hemorrhage.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 5","pages":"470-3"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01971.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20732686","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}

{"title":"Human parvovirus B19-associated thrombocytopenic purpura.","authors":"S Kido,&nbsp;Y Ito,&nbsp;N Nishimura,&nbsp;Y Kajita,&nbsp;T Ozaki","doi":"10.1111/j.1442-200x.1998.tb01975.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01975.x","url":null,"abstract":"<p><p>We report two patients who presented with thrombocytopenic purpura (TP) associated with primary human parvovirus B19 (B19) infection. One patient also had transient liver dysfunction. In both cases, B19-DNA was detected in serum and bone marrow by polymerase chain reaction. Six months after the illness in patient 1 and 8 months after the illness in patient 2, B19-DNA disappeared from the serum. Serum immunoglobulin (Ig)G antibody to B19 remained positive in both cases, but B19 IgM antibody became negative 3 months after the onset in case 1 and 4 months after the onset in case 2. The mechanism of TP by B19 infection is unknown.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 5","pages":"486-8"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01975.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20732690","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}

{"title":"Clinical survey of congenital cytomegalovirus infection in Japan.","authors":"M Morita,&nbsp;T Morishima,&nbsp;T Yamazaki,&nbsp;S Chiba,&nbsp;T Kawana","doi":"10.1111/j.1442-200x.1998.tb01963.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01963.x","url":null,"abstract":"<p><strong>Background: </strong>The clinical features of congenital cytomegalovirus (CMV) infection in countries with a higher percentage of maternal seropositivity for CMV has rarely been reported. We conducted a national survey for the first time in Japan to investigate the prevalence of congenital CMV infection.</p><p><strong>Methods: </strong>Questionnaires were sent in 1994 to pediatricians and obstetricians of 3398 hospitals with either more than 100 beds or a neonatal intensive care unit (NICU). The questionnaire asked for the number of new cases in 1992 and 1993, maternal status of CMV infection, diagnostic methods, clinical manifestations at birth, sequelae and prognosis.</p><p><strong>Results: </strong>A total of 46 cases of CMV infection were reported for the years 1992 and 1993 by 1448 hospitals; of these 39 were symptomatic. The annual incidence of symptomatic disease was 1.6 cases/100,000 live births. Major clinical manifestations such as low birthweight, hepatosplenomegaly, petechiae and intracranial calcification were noted at birth in 38-50% of symptomatic neonates. Sequelae, such as hearing loss, mental retardation and motor disability developed in 71% of survivors. Thirty-five percent of the 49 infected infants had either died or had severe disability. Several clinical manifestations at birth, including petechiae/thrombocytopenia, were significantly associated with severe sequelae or a poor prognosis.</p><p><strong>Conclusion: </strong>The lower frequency of clinical findings at birth may be attributed to the higher seroprevalence of pregnant women in Japan than in Europe and the United States.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 5","pages":"432-6"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01963.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20732149","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}

{"title":"Yolk sac tumor with a unique uniform hepatoid pattern histology.","authors":"A Konno,&nbsp;M Kudo,&nbsp;T Ichihara,&nbsp;M Yamagami,&nbsp;S Horita,&nbsp;K Ohama,&nbsp;K Taketa,&nbsp;S Koizumi","doi":"10.1111/j.1442-200x.1998.tb01970.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01970.x","url":null,"abstract":"<p><strong>Background: </strong>Yolk sac tumors (YST) exhibit several different histological subtypes and the mechanisms of cellular differentiation and prognosis of each subtype remain unknown.</p><p><strong>Results: </strong>We report two infants with sacrococcygeal YST; one represented a typical histological subtype and the other showed a hepatoid subtype with uniform histology. The isoform of alpha-fetoprotein (AFP) in the patient with the hepatoid pattern was examined by lectin-affinity immunoelectrophoresis and represented as a YST, but not hepatocellular, subtype. The patient with typical YST responded well to VAB-6 combination chemotherapy. However, this regimen was only partially effective to the patient with the pure hepatoid histological subtype, and an etoposide with ifosfamide and cisplatin (VIP) regimen as a salvage chemotherapy combined with complete tumor resection was useful to achieve complete remission (CR). Both of the patients have been in CR for more than four years.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 5","pages":"466-9"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01970.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20732685","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}

{"title":"Henoch Schönlein purpura and amebiasis.","authors":"G Demircin,&nbsp;A Oner,&nbsp;O Erdoğan,&nbsp;M Bülbül,&nbsp;L Memiş","doi":"10.1111/j.1442-200x.1998.tb01976.x","DOIUrl":"https://doi.org/10.1111/j.1442-200x.1998.tb01976.x","url":null,"abstract":"<p><p>The pathogenesis of Henoch Schönlein purpura (HSP) is unknown but is believed to result from an immune complex reaction to various antigenic stimuli, such as infectious agents. However, its association with Entamoeba histolytica has not been reported before. We present an 11-year-old boy with HSP, confirmed by the demonstration of leukocytoclastic vasculitis from skin and diffuse endocapillary proliferative glomerulonephritis, together with immunoglobulin A and complement component C3 deposition from renal biopsies. Cysts and trophozoites of Entamoeba histolytica were detected from the stool of the patient at the same time and disappeared after the treatment with metranidasole. The temporal association of these two disorders is either coincidental or due to a causal relationship between them.</p>","PeriodicalId":76975,"journal":{"name":"Acta paediatrica Japonica : Overseas edition","volume":"40 5","pages":"489-91"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1442-200x.1998.tb01976.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20732691","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}