重组α-2b干扰素治疗儿童慢性乙型肝炎疗效观察

目的观察基因重组α-2b干扰素治疗儿童慢性乙型肝炎疗效.方法将108例慢性乙型肝炎患儿分为治疗组78例、对照组30例,治疗组给予α-2b干扰素治疗,疗程半年,治疗后观察肝功能及HBV标志.结果治疗组HBeAg及HBV-DNA转阴率分别为39.7%和38.5%,均显著高于对照组(P<0.01),丙氨酸转氨酶(ALT)复常率、HBsAg转阴率分别为96.2%、5.1%,与对照组无显著性差异(P>0.05).结论基因重组α-2b干扰素是治疗小儿慢性乙型肝炎的有效药物,其疗效与ALT水平、年龄等因素有关.     

氧化苦参碱联合干扰素治疗儿童慢性乙型肝炎

目的研究氧化苦参碱联合干扰素治疗儿童慢性乙型肝炎的效果。方法84例慢性乙型肝炎患儿随机分为二组。治疗组采用氧化苦参碱联合干扰素α-2b治疗,对照组予干扰素α-2b,治疗3、6个月后观察肝功能、HBV DNA及HBeAg转阴率变化。结果治疗3和6个月二组临床症状、肝功能均明显改善,治疗组优于对照组（P〈0.05,0.01）;治疗6个月HBeAg和HBV DNA转阴率治疗组高于对照组（P〈0.05,0.01）。结论氧化苦参碱和干扰素联用在改善慢性乙型肝炎患儿肝功能及HBeAg和HBV DNA转阴率方面具有协同作用。     

阿奇霉素、干扰素联合治疗脑弓形虫病34例分析

我科于1996年1月至1999年6月收治脑弓形虫病34例。男22例,女12例;3月～5岁12例,～10岁16例,～14岁6例。均有动物接触史。临床表现:脑性瘫痪12例,小头并小眼症(脑萎缩)2例,脑积水2例,抽动-秽语综合征6例,多动症9例,继发性癫癎10例,痉挛性斜颈1例。检验结果:Toxo-IgG、IgM、DNA阳性1例,Toxo-IgG、IgM阳性8例,     

三联疗法治疗乙型肝炎病毒携带者130例

目的　观察麻疹疫苗、双嘧达莫、左旋咪唑三联疗法治疗儿童乙型肝炎病毒 (HBV)携带者的临床疗效。方法　选择儿童HBV携带者 130例 ,随机分两组 ,对照组用双嘧达莫和左旋咪唑口服 ,观察组在此基础上加用麻疹疫苗肌注。结果　观察组治疗各阶段HBVDNA和HBeAg阴转率均显著高于对照组 (P均 <0 .0 1)。结论　麻疹疫苗、双嘧达莫、左旋咪唑三联疗法治疗儿童HBV携带者疗效可靠     

干扰素治疗慢性乙型肝炎43例

探讨干扰素治疗小儿慢性乙型肝炎（CHB）的疗效、安全性及其影响因素。方法用干扰素α－2b治疗43例小儿CHB患者,并以32例患儿做为对照。结果治疗组病毒复制标志的阴转率显著高于对照组;ALT复常率近期显著高子对照组,远期则无明显差别。治疗前ALT高值、血清HBV－DNA低水平及非母婴传播为干扰素治疗的有利因素。干扰素治疗组未见严重不良反应。结论干扰素可用于小儿CHB的治疗,疗效的高低取决于适当病例的选择。     

小儿慢性乙型肝炎干扰素治疗引起的抗纤维化效应

目的观察儿童慢性乙型肝炎(CHB)应用α-干扰素(IFN-α)治疗引起的抗纤维化效应。方法30例小儿CHB应用IFN-α治疗24周以上,且停药后随访36周,其中5例治疗前后均行肝活体组织检查。所有患儿均在治疗前、治疗后24周和36周,应用放射免疫法检测患儿血清肝纤维化标志物:透明质酸(HA)、层连蛋白(LN)、Ⅳ型胶原(Ⅳ-C)。结果应用IFN-α治疗前(0周)、治疗后24周和36周,小儿CHB血清肝纤维化标志物HA值分别为(243.6±70.5)ng/mL、(145.2±51.6)ng/mL、(85.1±40.3)ng/mL;LN值分别为(180.5±61.3)ng/mL、(102.7±40.6)ng/mL、(62.8±32.6)ng/mL;Ⅳ-C值分别为(137.1±48.6)ng/mL、(108.9±40.3)ng/mL、(70.5±30.7)ng/mL,治疗后血清肝纤维化标志物较治疗前显著下降(P<0.05)。肝活体组织病理检查显示,治疗后肝组织纤维化分期比治疗前有明显降低(P<0.01)。结论IFN-α在治疗小儿CHB时,不仅有抗病毒作用,在改善肝纤维化方面,也具有一定疗效。     

α-干扰素联合糖皮质激素序贯治疗儿童慢性乙型肝炎疗效的Meta分析

目的评价α-干扰素(alpa interferon,IFN-α)联合糖皮质激素序贯治疗与α-干扰素单独治疗HBeAg阳性慢性乙型肝炎儿童的疗效差异。方法检索PubMed和CHKD期刊全文数据库,并追查所有纳入研究的参考文献。检索年限均从建库检索到2006年10月。纳入用英文或中文发表的比较IFN-α联合糖皮质激素序贯治疗与IFN-α单独治疗HBeAg阳性慢性乙型肝炎儿童疗效的随机对照试验。由2名评价员独立筛查文献,评价质量和提取资料。结果共纳入4个随机对照试验,包括181个HBeAg阳性的慢性乙型肝炎患儿。Meta分析结果显示,随访9个月至2年后,IFN-α联用糖皮质激素序贯组治疗HBeAg转阴率稍低于IFN-α单独治疗组,HBV-DNA转阴率稍高于IFN-α单独治疗组,HBsAg转阴率稍低于IFN-α单独治疗组,丙氨酸转氨酶(ALT)复常率稍低于IFN-α单独治疗组,HBeAg血清转换率稍低于IFN-α单独治疗组,HBsAg血清转换率稍高于IFN-α单独治疗组,两组差异均无统计学意义。结论对HBeAg阳性的慢性乙型肝炎患儿,IFN-α联用糖皮质激素序贯治疗与IFN-α单独治疗对比,在HBeAg转阴、HBV-DNA转阴、HBsAg转阴、ALT复常、HBeAg及HBsAg血清转换等方面均无明显的效能。     

硫唑嘌呤、强的松和左旋咪唑联合治疗小儿难治性血小板减少性紫癜

观察硫唑嘌呤 强的松 左旋咪唑（IPL方案）联合治疗小儿难治性血小板减少性紫癜（ITP）的疗效，对16例先后接受了VP、ITIG、MP和a-IFN等方案治疗的难治性ITP患儿，试用IPL方案治疗，观察患者血小板恢复情况，评价其近期和远期疗效。结果显示：IPL方案治疗总有效率100%，其中显效率68.7%，远期疗效仅3例复发。因此，IPL方案是治疗小儿难治性ITP的有效方法之一。     

左旋咪唑、转移因子辅助治疗儿童肾病45例分析

为了解左旋咪唑,转移因子辅助治疗儿童肾病综合征（ＮＳ）时对减少疾病反复发作的疗效,现将使用该药治疗的４５例为治疗组,未用该药的３８例为对照组,观察两组疾病反复次数以及完成整个疗程所需时间和免疫功能。结果显示,治疗组反复次数明显较对照组少;疗程时间也明显缩短;ＩｇＧ、ＩｇＡ恢复均民对照组比较有显著性差异。提示左旋咪唑、转移因子辅助治疗ＮＳ有一定的临床效果。     

Interferon treatment for chronic hepatitis B: enhanced response in children 5 years old or younger

OBJECTIVE: To test the hypothesis that there is an improved response to interferon in children with chronic hepatitis B (HBV) who are < or =5 years of age. STUDY DESIGN: Retrospective chart review of 22 consecutive children with chronic HBV (ages 17 months to 17 years; median, 83.9 months; 14 male, 8 female) treated with interferon-alpha2b. RESULTS: Ten patients (48%) responded to treatment [HBeAg (-), Anti-HBe (+), HBV DNA (-), HBsAg (+) and normal alanine aminotransferase/aspartate aminotransferase (ALT/AST) at 6 months after treatment], and 5 seroconverted HBsAg [above plus HBsAg negative and anti-HBs (+)]. Seven of 9 patients (78%) < or =5 years of age responded (5 cleared HBsAg). Three of 13 patients (23%) >5 years of age responded. Patient age at treatment was significantly lower in responders (63 +/- 70 months) versus nonresponders (104 +/- 55 months, P =.005). AST, ALT, and HBV DNA at the start of treatment were not different between responders and nonresponders or between patients < or =5 and >5 years old. CONCLUSIONS: Interferon treatment may be more effective in younger children with chronic hepatitis B.     

Effect of interferon therapy on glucose metabolism in children with chronic hepatitis B

The aim of this study was to investigate the effect of interferon (IFN)-alpha treatment on glucose metabolism in children with chronic hepatitis B (CHB). Forty children with CHB received IFN 10 MU/m2 for six months. Oral glucose tolerance test, anti-insulin and anti-glutamic acid decarboxylase (GAD) antibody, fasting plasma C-peptide and insulin (FPI), postprandial insulin, homeostasis model assessment of insulin resistance (HOMA-IR), HOMA-cell, and glucose/insulin ratio (G/I) were measured before and after treatment. The last four parameters were also evaluated in healthy controls (n=42). In patients, fasting plasma glucose (FPG) and HOMA-IR levels were significantly lower than in controls (p = 0.001 and p = 0.020, respectively). There was a strong correlation between degree of liver disease and FPG. Two patients had hyperinsulinemia. HOMA-IR was suppressed in 7 patients enough to indicate increased sensitivity. FPI of 13 patients and HOMA-cell of 9 patients were lower than the minimum level of controls, features compatible with beta-cell hypofunction. Frequency of glucose metabolism abnormalities was not different before and after therapy. After therapy, only 1 patient developed anti-GAD antibody, and FPI of 8 children and HOMA-cell level of 9 children were lower than the minimum level of controls. Hyperinsulinemia was persistent in the same patients. We demonstrated that HBV-infected children had insulin sensitivity; however, no adverse effects of IFN on glucose homeostasis were seen.     

乙型肝炎病毒相关性肾炎患儿乙型肝炎病毒S基因突变分析

目的 探讨乙型肝炎病毒(HBV)S基因的突变在乙型肝炎病毒相关性肾炎(HBV-GN)发病中的意义.方法 从53例患儿(30例HBV-GN,5例肾病伴HBV携带者,18例HBV携带者)的血清中提取DNA,以聚合酶链反应技术对HBV-DNA的S基因进行扩增,然后对扩增产物进行测序.结果 (1)S3例患儿血清型中52例为adw,在HBV携带组中1例为adr.(2)HBV基因型分型:30例HBV-GN中29例为B型,1例为E型;5例肾病HBV携带患儿为B型;18例HBV携带患儿中17例为B型,1例为C型.(3)30例HBV-GN中21例(70%)有点突变,共计17种突变,11种为错义突变,6种同义突变.16例(16/21,76.2%)点突变导致S抗原中氨基酸取代,其中11例(11/16,68.8%)涉及丝氨酸、苏氨酸、酪氨酸等潜在促分裂素原活化蛋白激酶(MAPK)和蛋白酪氨酸激酶(PTK)的磷酸化位点.5例肾病伴HBV携带者中2例有同义突变,3例无任何突变;18例HBV携带者共有3例同义突变,无氨基酸改变.结论 HBV-GN患儿大多存在HBV S基因变异并导致S抗原中氨基酸取代,其中主要涉及丝氨酸、苏氨酸、酪氨酸等MAPK和PTK的磷酸化位点,这些重要位点氨基酸的取代可能在HBV-GN的发病中起作用.     

Acute hepatitis B in children with papular acrodermatitis

Thirteen children who had repeated liver biopsies over a period of 2-16 years after the onset of papular acrodermatitis (PAC) were studied retrospectively. Six patients, rebiopsied within 36 months after the onset of PAC, had histologic evidence of chronic periportal hepatitis. However, repeated biopsies in 3 of the patients revealed a normal liver or chronic portal hepatitis. Whereas all patients had at the end of the observation markers of hepatitis B virus infection, 8 of the 10 patients studied had HBs antigenemia. These data indicate that severe active liver disease may regress without treatment in patients who have had PAC. However, the high frequency of a chronic HBsAg-carrier state among these patients suggests either an inefficient clearance of the virus or an altered immune reaction.     

The need for hepatitis B immunoprevention in families with vertical hepatitis B infected children

We investigated the scope of hepatitis B infection in 11 families (family contacts: fathers, siblings) in which the mother transmitted (vertical) hepatitis B infection to the child. Results: The initial examination demonstrated an acute hepatitis B infection in one of the 11 fathers and former hepatitis B infection in 8 fathers. In 2 fathers no hepatitis B markers were found (susceptible for hepatitis B). In 3 of the 10 siblings examined an acute hepatitis B infection was demonstrated, one child showed signs of a former hepatitis B infection, and in 6 no hepatitis B markers were demonstrable. Current checks made in 5 families over a period of about 6.2 years showed another hepatitis B infection in one father and one child. These observations stress the importance of immunisation in such families.     

IgM antibody to hepatitis B core antigen in children with chronic type B hepatitis

IgM antibody to hepatitis B core antigen (anti-HBc IgM) was investigated by an antibody-capture radioimmunoassay (serum dilution 14000) in serum samples from 31 untreated children with chronic hepatitis B who were followed prospectively for 1–7 years. At the start, all patients were positive for hepatitis B e antigen (HBeAg), and anti-HBc IgM was detected in 23 cases, including 15 out of 16 with chronic active hepatitis and 7 out of 14 with chronic persistent hepatitis. A significant positive correlation was found between anti-HBc IgM levels and severity of liver damage (P<0.05), while an inverse relationship was found between anti-HBc IgM levels and distribution of hepatitis B core (HBcAg) antigen in the liver as detected by immunofluorescence. In fact 75% of anti-HBc IgM positive patients showed a focal HBcAg pattern (less than 40% positive nuclei), whereas 87% of antibody negative cases exhibited a diffuse HBcAg expression (more than 60% stained nuclei). During follow-up, seroconversion from HBeAg to anti-HBe with subsequent remission of liver disease occurred in 82% of patients presenting with detectable levels of anti-HBc, including three out of seven cases with chronic persistent hepatitis, but in none of the cases that were initially negative (P<0.01). These results indicate that during the natural course of chronic hepatitis B in children, anti-HBc IgM levels in serum reflect the degree of host immune response to infected hepatocytes. The close correlation between anti-HBc IgM seropositivity and seroconversion from HBeAg to anti-HBe suggests that anti HBc IgM may have a prognostic value during the follow-up of children with chronic HBeAg positive hepatitis B.Abbreviations anti-HBc IgM IgM antibody to hepatitis B core antigen - HBeAg hepatitis B antigen - HBcAg hepatitis B core antigen - HBV hepatitis B virus - ALT alanine aminotransferase - CAH chronic active hepatitis - CPH chronic persistent hepatitis     

Long-term evolution of chronic hepatitis B in children with antibody to hepatitis B e antigen

The aim of this study was to evaluate the long-term outcome of chronic hepatitis B in 27 children who had increased alanine aminotransferase activity and antibody to hepatitis B e antigen in serum from the time of their first clinical observation. Initial histologic changes were consistent with chronic active hepatitis in 13 cases (three with associated cirrhosis) and with persistent or lobular hepatitis in the remaining cases. On the basis of virologic testing, three groups of patients were identified: (1) two children had hepatitis delta antigen in the liver and anti-delta antibody in serum, and both had severe hepatitis; (2) 10 children had hepatitis B virus DNA in serum, and 60% of them had active hepatitis; (3) 15 patients had no hepatitis B virus DNA, and 33% of them had active hepatitis. During a follow-up period of 12 months to 12 years (mean +/- SD: 6.1 +/- 2.4 years), the disease remained active in both children with anti-delta antibody, but they had no major complaints. In all eight patients who could be followed in group 2, test results became negative for hepatitis B virus DNA and alanine aminotransferase activity normalized within 4 years; biochemical remission was delayed in three patients with higher hepatitis B virus DNA levels on entry, and one of these patients had a severe exacerbation of disease activity before remission. In group 3, a total of 10 patients (71%) achieved biochemical remission within 1 year, and two within 26 months; only two patients, who were transfused at birth, had long-lasting liver damage. These results indicate a trend to early remission of liver disease in children with chronic hepatitis B with antibody to hepatitis B e antigen without delta virus infection. Antiviral therapy aimed at accelerating the termination of hepatitis B virus replication may be indicated only in those with higher levels of hepatitis B virus DNA.