新生儿轮状病毒肠炎及继发乳糖酶缺陷临床分析

为探讨新生儿腹泻中轮状病毒性肠炎及继发性乳糖酶缺陷的发病情况及临床特点.采用EILASA快速轮状病毒抗原检测方法及醋酸铅法,对38例确诊为轮状病毒性肠炎的病例进行总结分析.51例新生儿腹泻,轮状病毒抗原检测阳性38例(74.51%),而在确诊为轮状病毒性肠炎38例中,大便乳糖阳性37例(97.37%).结果提示,在秋冬季节,轮状病毒是新生儿腹泻的首位病原,而新生儿轮状病毒肠炎绝大多数有继发性乳糖酶缺陷.     

新生儿轮状病毒肠炎临床特征分析

我科 2 0 0 1年 1月～ 4月共收治新生儿轮状病毒 (ＲＶ)肠炎患儿 35例 ,其发病集中病例数之多是几年来罕见的 ,现对该组病例进行临床特征分析 ,以提高对该病的早期诊断能力 ,避免其在新生儿室流行。资料及方法1 一般资料 :本组病例均系住院治疗有腹泻症状的新生儿 ,共 4 8例 ,男 2 8例 ,女 2 0例。日龄 <3天 1例 (2 0 8% ) ,～ 7天 3例(6 2 5 % ) ,～ 14天 18例 (37 5 % ) ,>14天 2 6例 (5 4 17% ) ,均为足月儿 ,出生体重均 >2 5 0 0ｇ。 2 临床资料 :以腹泻发热住院的仅12例 ,余 36例是以新生儿肺炎 ,新生儿高胆红素血症 ,脐炎等疾病收…     

抗氧化剂治疗新生儿轮状病毒肠炎的探讨

应用抗氧化剂维生素Ｅ，维生素Ｃ和复方丹参治疗新生儿轮状病毒３４例，并与同期住院之常规治疗的３２例患儿比较，发现其平均退热时间，止泻时间，脱水纠正时间及总病程均明显短于对照组（Ｐ均〈０．０１），治疗组１日止泻率明显大于对照组（Ｐ〈０．０５）；营养不良并发症明显低于对照组（Ｐ〈０．０５），提示抗氧化剂治疗有助于提高机体抗 氧化能力，缩短病程，减少营养不良并发症的发生。     

26例新生儿轮状病毒性肠炎患儿心肌酶谱的变化

本文观察２６例新生儿轮状病毒性肠炎必心肌酶谱（ＣＰＫ、ＡＳＴ、ＬＤＨ、ＨＢＤＨ、ＣＰＫ－ＭＢ）活性变化，与下沉对照组比较差异非常显著，表明患儿伴有心肌损害，且脱水酸中毒症状愈重，心肌酶活性升高愈显著，肠炎痊愈，心电图恢复正常，心肌酶活也下降。因此，心肌酶活中作为观察新生儿轮状病毒性肠炎病情和转归重要指标，研究结果亦表明，抗氧化剂治疗有助于心肌酶活性较快下降，有利于疾病愈愈。     

继发性双糖酶缺乏症与轮状病毒肠炎的关系

目的　探讨继发性双糖酶缺乏症与轮状病毒 (RV)肠炎病程的相关性。方法　 85例RV肠炎按有无继发双糖酶缺乏症分成A、B组 ,接受相同治疗 ,观察病程长短及急性期临床表现 ,并行统计学处理。结果　A、B组平均病程差别有显著意义 (t=4 .0 9　P <0 .0 1) ,而发热、腹泻、脱水、肠外表现均无显著差别 (χ2 =0 .2 85、1.4 10、0 .5 72、0 .0 5 1　P均 >0 .0 5 )。结论　继发性双糖酶缺乏症明显延长RV肠炎病程 ,但对急性期临床症状的轻重无明显影响     

轮状病毒肠炎引发抽搐22例临床分析

目的探讨轮状病毒肠炎引发抽搐的临床表现特点和可能发生的原因。方法收集近2年秋冬季轮状病毒肠炎及其发生抽搐的病历,进行分析。结果发病年龄为4月～2岁婴幼儿,既往健康。抽搐形式为大发作,无热惊厥,多为单次发作,发生于病程的1～4d,血清电解质、血糖、脑电图正常。预后良好。并发现2004年末～2005年初轮状病毒肠炎并发抽搐几率明显高于2005年末～2006年初。结论轮状病毒肠炎可引起抽搐,抽搐表现似良性婴幼儿惊厥。其原因不明,但不支持低钙惊厥及低血糖惊厥。在不同的年份发生几率不一致,可能与病毒变异,存在嗜神经性有关,且不能除外病毒进入脑脊液引发轻型脑炎的可能。     

无乳糖奶粉联合炎琥宁治疗轮状病毒性肠炎临床观察

目的探讨无乳糖奶粉联合炎琥宁治疗轮状病毒肠炎疗效。方法将90例年龄4～18个月、病程在1周内、以母乳或普通配方奶喂养为主的轮状病毒肠炎患儿随机分为3组,A组:补液及对症治疗;B组:A组治疗+炎琥宁;C组:B组治疗+去乳糖奶粉。A、B组继续母乳或普通配方奶喂养,C组改用无乳糖奶粉。观察疗效、退热时间、止泻时间。结果 B、C组患儿治疗总有效率优于A组(P均<0.05),B组与C组之间差异无统计学意义(P>0.05);止泻时间(指大便成形,每日<3次)三组患儿间差异有统计学意义(F=18.58,P<0.05),B、C组均短于A组(P均<0.05),C组短于B组(P<0.05);平均退热时间三组患儿间差异有统计学意义(F=5.233,P<0.05),B、C组均短于A组(P均<0.05),B组与C组差异无统计学意义(P>0.05)。结论无乳糖奶粉联合炎琥宁治疗婴幼儿轮状病毒肠炎可缩短腹泻病程,有效、安全。     

肠炎宁糖浆治疗婴幼儿轮状病毒肠炎28例临床观察

目的观察肠炎宁糖浆治疗轮状病毒肠炎的疗效。方法52例轮状病毒肠炎患儿随机分成两组，对照组24例给予液体治疗及利巴韦林静滴，治疗组28例在对照组基础上加用肠炎宁糖浆口服。结果治疗组与对照组的显效率差异有显著性（P〈0．05）。结论肠炎宁糖浆治疗轮状病毒肠炎有效。     

1024例小儿轮状病毒肠炎临床流行病学分析

轮状病毒肠炎 (ＲＶ)是小儿最常见的疾病之一 ,尤其在短期内发生大量流行 ,直接影响小儿健康。现将我院１９９８年１０月～２０００年１月诊治的１０２４例小儿轮状病毒肠炎的临床流行病学情况介绍如下。临床资料肠炎诊断依据《实用儿科学》标准 ,轮状病毒（ＲＶ）检测由中国珠江医院生物高科技中心提供试剂盒。阳性判断分 +— ++++４级 ,均在患儿第一次就诊时做粪常规检查及粪ＲＶ检查 ,住院病例在入院时查血生化。１０２４例中 ,年龄５０天～１２岁。其中～３月１４０例 ,占１３．７ % ;～３岁６４８例 ,占６３．３ %，～１２岁２３６例 ,…     

轮状病毒肠炎并心肌损害临床分析

近年来发现轮状病毒肠炎并心肌损害的病例渐增多，心肌损害发生机制及相关因素尚未明确，国内外有关报道也较少。现对1996年10月～1999年2月我院消化内科收治的171例病原学证实为轮状病毒的腹泻儿心脏受损情况进行总结，报告如下。资料及方法一、一般资料 男126例，女45例，发病年龄4个月～2 a。既往均未发现心脏病史。发病到入院时间为1～3 d。大便细菌培养均阴性，大便轮状病毒抗原阳性（ELISA法）。二、临床表现 发热147例，占86 %。呕吐129例，占75.4 %。并上呼吸道感染72例，占42.1 %。并脱水138例，占80.7 %。45例在安静、体温正常…     

NEONATAL ACIDOSIS ASSOCIATED WITH TRANSIENT METHYLMALONICACIDURIA AND VITAMIN B12 DEFICIENCY

Abstract Investigation of a neonate presenting with a metabolic acidosis, vomiting and an apnoeic attack revealed abnormal urinary excretion of methylmalonic acid (MMA) associated with a low serum vitamin B12. Restriction of dietary protein was followed by normalisation of acid-base balance. Reintroduction of normal daily protein intake did not precipitate further acidosis or increased excretion of MMA. The transient methylmalonicaciduria was probably due to deficiency of vitamin B12.     

STRUCTURAL AND FUNCTIONAL ABNORMALITIES OF THE SMALL INTESTINE IN INFANTS AND YOUNG CHILDREN WITH ROTAVIRUS ENTERITIS

Abstract. Structural and functional alterations in duodenal mucosa from 17 children with rotavirus enteritis were assessed. Structural changes were found in specimens from all patients. Patients with the most severe mucosal damage were more likely to require intravenous therapy to correct dehydration. Depression of one or more mucosal disaccharidases was found in 14 of 16 patients. Repeat duodenal biopsy three to eight weeks later in six patients showed marked improvement. The study clearly shows that rotavirus can cause a marked structural and functional lesion in the upper small intestine which is rapidly reversible.     

NATURAL HISTORY OF CHILDREN WITH ALPHA1-ANTITRYPSIN DEFICIENCY AND NEONATAL CHOLESTASIS

ABSTRACT. Ten children with α₁-antitrypsin deficiency, phenotype PiZ, and neonatal cholestasis were followed to the ages of 4-20 years. Standard liver function tests, urinary bile acid excretion and liver morphology were investigated within one week and the results were compared. Three patients had morphological signs of liver cirrhosis and one of these had clinical signs as well. Compared to healthy children of the same age urinary bile acid excretion was increased only in those with morphologically confirmed liver cirrhosis. Although most of the other patients had some minor histological changes in the liver biopsies, the normal urinary bile acid excretion was in accordance with their excellent general clinical state and is interpreted as a short-term favourable prognostic sign.     

CLINICAL FINDINGS AND INTESTINAL IMMUNOGLOBULINS IN CHILDREN WITH PARTIAL IgA DEFICIENCY

Abstract. We studied the intestinal morphology, and the jejunal and rectal immunoglobulins of 16 children with partial IgA deficiency, defined as serum IgA concentration more than two standard deviations below the mean for age, but higher than the lower limit of sensitivity of single radial immunodiffusion (0.02 g/l). Five of the patients had been treated with phenytoin, 2 had juvenile rheumatoid arthritis, 2 had ulcerative colitis and 5 had recurrent upper respiratory tract infections. The jejunal morphology was normal in every case. In 6 cases normalization of serum IgA occurred during the follow-up, while in one patient with ulcerative colitis the concentration fell below 0.02 g/l. In patients with recurrent infections, there was a decreased frequency of infections when the level of serum igA increased. In 4 patients, IgM-containing cells predominated in both the jejunal and rectal mucosa, and IgM was increased in the intestinal juice. In 6 patients a significant increase in IgM-containing cells or a decrease in IgA-containing cells or both were seen in either the rectal or jejunal mucosa. There was no correlation between the number of IgA-containing cells in the intestinal mucosa and the serum level of IgA.     

ERYTHROCYTE GLUCOSE 6-PHOSPHATE DEHYDROGENASE DEFICIENCY (G6PD TYPE A-) AND NEONATAL JAUNDICE

ABSTRACT. The association of erythrocyte G6PD deficiency (type A-) and hyperbilirubinaemia in two groups of Nigerian male newborns has been examined. The results provide evidence that the enzyme deficiency is the single most important factor in the pathogenesis of severe neonatal jaundice in this West African population.     

GLUCOSE-6-PHOSPHATE DEHYDROGENASE AND RED CELL PYRUVATE KINASE DEFICIENCY IN NEONATAL JAUNDICE CASES IN EGYPT

Glucose-6-phosphate dehydrogenase (G6PD) deficiency can lead to acute hemolytic anemia, chronic nonspherocytic hemolytic anemia, and neonatal jaundice. Neonatal red cell pyruvate kinase (PK) deficiency may cause clinical patterns, ranging from extremely severe hemolytic anemia to moderate jaundice. The authors aimed at studying the prevalence of G6PD and PK deficiency among Egyptian neonates with pathological indirect hyperbilirubinemia in Cairo. This case-series study included 69 newborns with unconjugated hyperbilirubinemia. All were subjected to clinical history, laboratory investigations, e.g., complete blood counts, reticulocytic counts, direct and indirect serum bilirubin levels, Coombs tests, qualitative assay of G6PD activity by methemoglobin reduction test, and measurement of erythrocytic PK levels. The study detected 10 neonates with G6PD deficiency, which means that the prevalence of G6PD deficiency among Egyptian neonates with hyperbilirubinemia is 14.4% (21.2% of males). G6PD deficiency was significantly higher in males than females (P = .01). The authors detected 2 cases with PK deficiency, making the prevalence of its deficiency 2.8%. These data demonstrate that G6PD deficiency is an important cause for neonatal jaundice in Egyptians. Neonatal screening for its deficiency is recommended. PK deficiency is not a common cause of neonatal jaundice. However, this needs further investigation on a larger scale.     

新生儿化脓性脑膜炎及脑室炎治疗探讨

目的 探讨新生儿化脓性脑膜炎(新生儿化脑)及脑室炎的诊断及治疗。方法 回顾性分析1992年1月至2002年12月我科收治的新生儿化脑59例。结果 新生儿化脑缺乏特异性的症状和体征,临床表现复杂、多样化,一半以上表现为发热或体温不升,拒奶或吐奶,神萎及反应差,黄疸,前囟紧张和末梢白细胞增高等。血培养及脑脊液培养细菌阳性,大部份病人以青霉素/氨苄青霉素加头孢噻肟/头孢三嗪治疗有效,治愈率83.1％。脑室炎患儿还表现为:病程≥1周,发热>3天,频繁抽搐,前囟紧张及脑室扩大等。侧脑室穿刺注药治疗有效,治愈率66.6％。结论 新生儿化脑及脑室炎临床表现复杂、多样化,缺乏特异性,对出现上述临床表现的患儿要及时行腰穿及脑室穿刺,及时诊断治疗,大部分患儿以青霉素/氨苄青霉素加头孢噻肟/头孢三嗪治疗有效,合并脑室炎应侧脑室穿刺注药治疗。     

ERYTHROCYTE GLUCOSE 6-PHOSPHATE DEHYDROGENASE DEFICIENCY (G6PD TYPE A-) AND NEONATAL JAUNDICE

Abstract. The association of erythrocyte G6PD deficiency (type A^-) and hyperbilirubinaemia in two groups of Nigerian male newborns has been examined. The results provide evidence that the enzyme deficiency is the single most important factor in the pathogenesis of severe neonatal jaundice in this West African population.     

20例晚发性维生素K缺乏致颅内出血临床与CT分析

报告20例晚发性维生素K缺乏致颅内出血患儿，经CT检查证实蛛网膜下腔、硬膜下、脑室内及脑实质均可发生出血。其临床症状与出血部位及出血量有关。提示CT检查对明确诊断、估计预后，指导治疗均有较大帮助。