陳慧玲2006-07-262018-07-112006-07-262018-07-112005http://ntur.lib.ntu.edu.tw//handle/246246/22906為了解台灣全面施行B 型肝炎所造成之兒童猛暴性肝炎之現況，我們執行此一全 國性合作計畫，分析全台1985 至1999 年所有因猛暴性肝炎住院之1 個月至15 歲兒童(62 名男性及33 名女性)；並分析他們的B 型肝炎感染現狀(HBsAg and/or IgM-anti-HBc seropositive)，B 型肝炎感染占所有病患的45% (43/95)，猛暴性肝炎的平均年發生率在 1 至15 歲兒童為0.053/100,000 、在一歲以下嬰兒為1.29/100,000，猛暴性肝炎病患有 61%(58/95)為一歲一下之嬰兒。在0-1 歲嬰兒中B 型肝炎感染占猛暴性肝炎之57%, 而在 1 至15 歲的兒童B 型肝炎感染占27%，比例嬰兒為較低(0.004), 以B 型肝炎陽性的病例 分析，一歲以上比一歲以下的發生率比(rate ratio)為54.2，B 型肝炎陰性的病例，一歲 以上比一歲以下的發生率比為(rate ratio)15.2。在母親帶原方面，母親表面抗原的陽性 率在嬰兒並例為97%, 而這些病例中有84%母親之e 抗原均為陰性。所有B 型肝炎病例中 有74%病例曾經打過B 型肝炎疫苗、而81%之一歲以下嬰兒曾經接種過B 型肝炎疫苗。 在預後方面，所有病例的死亡率為75%, 死亡病例組年紀較高，總膽紅素較高，凝 血時間較長，而B 型肝炎帶原陽性率較低。B 型肝炎陽性組的死亡率有65%，陰性組死亡 率83% (p=0.05)；陽性組及陰性組的危險因子不同；以B 型肝炎陽性的病例來分析，死 亡組有較高的凝血時間(p=0.036); B 型肝炎陰性組的病例，年齡較大並有較高的總膽紅 素值 (P < 0.001 and P = 0.006)，多因子分析顯示總膽紅素值是唯一的影響因子。分析年 代的因素，發現B 型肝炎陽性組的死亡率在三個年代區間(91, 67 and 38%, P = 0.027 in year 1985–1989, 1990–1994, 1995–1999) 有逐漸下降的趨勢，而B 型肝炎陰性組的死亡率則在 三個年代沒有明顯變化。 分析八位嬰兒期的猛暴性B 型肝炎病例，病人的病毒濃度由1.8x 104 to 1.9 x 108 copies/ml; 母親的病毒濃度為2.3 x 103 to 8.7 x 107 copies/ml，母親均為e 抗原陰性 之B 型肝炎帶原者，病人的病毒量大多高於母親病毒量 (7/8)。病人的病毒量與預後沒有 明顯相關，基因型除了一位病人之外全部是B 型。 總結來說，在台灣實施B 型肝炎疫苗接種15 年內，B 型肝炎在一歲以上兒童已經 很少造成猛暴性肝炎，但仍然是一歲以下嬰兒之猛暴性肝炎之重要原因，B 型肝炎造成的 猛暴性肝炎容易在e 抗原陰性的表面抗原帶原母親所生的嬰兒發生，這些嬰兒在目前我國 的疫苗政策下並未接種B 型肝炎免疫球蛋白。B 型肝炎陽性的猛暴性肝炎患者有較低的死 亡率，而B 型肝炎陽性與陰性者，其預後因子不同。嬰兒期得到猛暴性B 型肝炎者通常有 高病毒量，傳染來源最可能來自母親的陽性病毒血液。To investigate the role of hepatitis B virus (HBV) infection in pediatric fulminant hepatic failure (FHF) following the launch of universal HBV vaccination, we analyzed the data from patients with FHF collected from a nationwide collaborative study group. Children from one month to 15 years old who were diagnosed with FHF (62 males and 33 females) from 1985 to 1999 were included. HBV infection (HBsAg and/or IgM-anti-HBc seropositive) accounted for 45% (43/95) of all the cases of FHF. The average annual incidence of FHF in the years 1985 to 1999 was 0.053/100,000 in the one to 15-year-old population, and 1.29/100,000 in those below one year of age. Sixty-one percent (58/95) of all FHF cases were infants. The percentage of HBV infection was higher in infants (57%) than in one to 15-year-old children (27%) (p=0.004). The incidence rate ratio of those below one year of age to those aged one to 15 years was 54.2 for HBV-positive FHF and 15.2 for HBV-negative FHF. Maternal HBsAg was positive in 97% of the infants with HBV-positive FHF, and HBeAg was negative in 84%. Seventy-four percent of all HBV-positive FHF cases and 81% infantile HBV-positive cases were vaccinated. The overall mortality rate was 75%. Patients in the mortality group were of an older age, had higher peak total bilirubin levels, a longer prothrombin time, and a lower percentage of HBV positivity (P < 0.001, P = 0.003, P = 0.0027 and P = 0.042, respectively). Mortality was 65% in the HBV positive (n = 42) and 83% in the HBV negative (n = 52) group (P = 0.05). In the HBV positive group, the prothrombin time was noted to be the single factor affecting outcome (P = 0.036). In the HBV negative group, older age and higher peak value of total serum bilirubin were suggestive of poor survival rate (P < 0.001 and P = 0.006, respectively). Multivariate analysis revealed that total bilirubin was the single factor affecting outcome in the HBV-negative group. The mortality rate of HBV positive children in three consecutive time periods without liver transplantation (1985–1989, 1990–1994, 1995–1999) decreased gradually (91, 67 and 38%, respectively, with P = 0.027). This change was not observed in HBV-negative cases. The viral load of patients ranged from 1.8x 104 to 1.9 x 108 copies/ml; the viral load of mothers ranged from 2.3 x 103 to 8.7 x 107 copies/ml. In all but one pair, patient’s viral load was higher than mother’s viral load. There was no correlation between patient’s viral load and prognosis. The genotype was all B except on patient who was mixed B and C type. In conclusion, within the first 15 years of universal vaccination, HBV rarely caused FHF in children above one year of age, but remained a significant cause of FHF in infants. HBV-positive FHF was prone to develop in infants born to HBeAg-negative, HBsAg-carrier mothers; these infants had not received HBIG according to our vaccination program. Hepatitis B virus positive FHF had a lower mortality rate than HBV negative FHF, with each group having different factors affecting mortality. Infants with fulminant hepatitis B had high viral load, likely to be transmitted from their HBsAg (+)/HBeAg(-) mothers with viremia.application/pdf97812 bytesapplication/pdfzh-TW國立臺灣大學醫學院小兒科肝衰竭B 型肝炎感染兒童疫苗接種發生率[SDGs]SDG3reporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/22906/1/932314B002046.pdf