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水果梨

这个贴子 不错   牛哥就是牛！  我顶......

买平安的

早上上班头件事，顶牛哥的贴

加油寳

放牛哥哥

Tenofovir, an acyclic nucleotide analog with a molecular structure related to that of
adefovir, is currently approved bothonly for the treatment of HIV infection and for HBV
infection, but it also has been shown to haveand was known prior to licensure for the treatment
of CHB to have potent activity against HBV.96,97 Data from several small studies suggest that
tenofovir may be more potent than adefovir in inducing the early and rapid suppression of HBV
DNA in both HBeAg-positive and -negative patients.96,97,116 Limited clinical data suggest its
efficacy in treating lamivudine-resistant patients.96,97,116 In a small study that compared the
antiviral activity of tenofovir with that of adefovir in lamivudine-resistant patients, the tenofovir
group achieved potent and rapid suppression of HBV DNA within weeks of treatment initiation
as compared with a less-consistent pattern of suppression in patients treated with adefovir.97 At
48 weeks, significantly more patients treated with tenofovir had a reduction of HBV DNA levels
to <105 copies/mL than did patients treated with adefovir (100% vs. 44%). A follow-up study
confirmed the superiority of tenofovir over adefovir in this setting.96
Preliminary results from a multicenter, randomized, phase III trial comparing the safety and
efficacy of tenofovir and adefovir in patients with HBeAg-positive CHB have been reported
(Table 5).98 A total of 266 patients were randomized in a 2:1 ratio to receive tenofovir 300 mg or
adefovir 10 mg for 48 weeks. The primary end point of this study was complete response at week
48, defined as HBV DNA levels of <400 copies/mL and histologic improvement, defined as a
≥2-point reduction in Knodell inflammatory score without worsening of fibrosis. At 48 weeks,
67% of patients in the tenofovir arm achieved a complete response compared with 12% of
patients in the adefovir arm (P <0.001). A higher proportion of patients in the tenofovir arm than
in the adefovir arm achieved undetectable HBV DNA levels at week 48 (<400 copies/mL: 76%
vs. 13%). The respective rates for ALT normalization were 69% vs. 54% and for HBeAg
seroconversion were 21% vs. 18%. A higher proportion of patients treated with tenofovir had
HBsAg loss (3.2% vs. 0%) and HBsAg seroconversion (1.3% vs. 0%). The incidence of grade 2
to 4 adverse events was similar in the tenofovir and adefovir arms. No patients taking tenofovir
experienced a 0.5-mg increase in serum creatinine levels or creatinine clearance of <50 mL/min
(possible indicators of renal toxicity, which has been associated with tenofovir in some studies of
patients with HIV infection) compared with 1% of patients taking adefovir. As with adefovir
therapy, new onset or worsening renal impairment may occur, and it is recommended that
baseline calculated creatinine clearance be obtained and creatinine clearance and serum
phosphorus be monitored in patients at risk during therapy. The incidence of grade 3 or 4 ALT
flares 2 × the baseline values were greater in the tenofovir arm than in the adefovir arm (11% vs.
4%). All patients taking tenofovir who did not achieve HBV DNA levels of <400 copies/mL by
week 48 or who experienced viral breakthrough while receiving treatment underwent genotypic
resistance testing. The clinical benefits of tenofovir with respect to suppression of serum HBV
DNA levels below the level of detection (79%) and ALT normalization (77%) were maintained
through 72 weeks of treatment.117 The rate of HBsAg loss and seroconversion increased from 3%
to 5% and from 1% to 2%, respectively, at weeks 48 and 64 in patients in the tenofovir arm
whereas no increase in HBsAg loss was observed among patients in the adefovir arm. No
mutations associated with tenofovir resistance were identified at weeks 48 or 72.

放牛哥哥

Tenofovir. Preliminary data are available from a randomized phase III study comparing tenofovir
and adefovir in patients with HBeAg-negative CHB.99 The primary end point of this study was
complete response at week 48, defined as HBV DNA levels <400 copies/mL and histologic
improvement (defined as a ≥2-point reduction in Knodell inflammatory score without worsening
of fibrosis). For this study, 375 patients were randomized in a 2:1 ratio to receive tenofovir 300
mg (n = 250) or adefovir 10 mg (n = 125) for 48 weeks. At week 48, a significantly higher
proportion of patients treated with tenofovir achieved the primary end point compared with
patients treated with adefovir (71% vs. 49%) (Table 6). At the end of treatment, 93% of the
patients in the tenofovir group had HBV DNA levels of <400 copies/mL, compared with 63% of
patients in the adefovir group. The rates of ALT normalization were similar in both treatment
groups (Table 6). No patients treated with tenofovir had a confirmed 0.5-mg increase in serum
creatinine level or creatinine clearance of <50 mL/min. The incidence of ALT flare (>10 × ULN
and 2 × baseline) was low and similar in the two treatment groups (1.2% vs. 0.8%). The clinical
benefit of tenofovir with respect to the achievement of HBV DNA levels of <400 copies/mL
(98%) and ALT normalization (79%) was maintained through week 72 with continuous tenofovir
therapy.120 The resistance rate was 0% for tenofovir at weeks 48 and 72.

放牛哥哥

刚才打电话到同济，报了ID号，居然说我的dna复检的单子还没出来。
我都要吐血。

加油寳

顶一下
顶一下
顶一下

转阴就好

牛哥我的甲功结果：TSH   FT3  FT4    T3都正常    但是T4比标准值高5。9个单位 是怎么回事啊

会不会是甲亢啊？？？？？？？？？

转阴就好

牛牛      你去那里了？

放牛哥哥

http://blog.sina.com.cn/s/blog_5 ... el=rela_nextarticle
一、总三碘甲状腺原氨酸（TT3）和总甲状腺素（TT4）的测定
1．原理：全部甲状腺素（T4）和20%的三碘甲状腺原氨酸（T3）由甲状腺滤泡上皮直接合成和分泌，80% 的T3由T4在外周组织脱碘而来，血液中大部分甲状腺激素与甲状腺激素结合球蛋白（TBG）呈可逆性结合，T3和T4与蛋白结合的量分别为99.7%和99.97%，测定TT3和TT4分别代表结合与游离T3和T4的总量。甲状腺激素的分泌是受下丘脑－垂体－甲状腺轴的负反馈机制调节的。
2．采血方法：不抗凝静脉血1－2ml。
3．正常参考值（化学发光免疫分析法）:
TT3 0.60－1.81μg / L
TT4 45.0－109μg/ L
4．注意事项和影响因素：
⑴ 受TBG的影响，雌激素（如妊娠、避孕药）可使TBG升高，雄激素、水杨酸、皮质醇、严重肝肾疾病和低蛋白血症时TBG下降。
⑵ 血中存在的抗T3、抗T4 抗体可以干扰化验结果，使之出现假性增高或降低（根据试验方法）。
⑶ 采血时病人刚服用含T3的甲状腺激素，可使T3的水平升高。
⑷ 服用抑制T4转化为T3的药物如丙基硫氧嘧啶、普萘洛尔、地塞米松、胺碘酮可影响T3值，使T3减少。
5．临床应用和分析：
⑴ 甲亢时多数情况TT3和TT4平行增高，甲减时平行下降，但在甲亢初期和复发早期TT3较TT4上升明显（在甲亢时T3以更大的比例直接从甲状腺分泌），故更敏感，甲减时TT4较TT3更敏感。
⑵ 在T3型甲亢时TT3和FT3增高，TT4和FT4正常，见于甲亢初期、复发早期和缺碘等情况。在T4型甲亢时TT4和FT4升高，TT3和FT3正常，多见于甲亢伴有严重疾病或碘甲亢。
⑶ 低T3综合征是由非甲状腺疾病引起的TT3 和FT3降低，如肾衰竭、肝硬化、心肌梗死、严重的糖尿病、恶性肿瘤、结缔组织病等。如疾病进一步加重，TT4和FT4也可降低。

二、游离T3（FT3）和游离T4（FT4）测定
1．原理：FT3和FT4不受TBG的影响，是甲状腺激素中具有代谢活性的部分，能更直接反应甲状腺的功能。
2．标本采集：不抗凝静脉血2ml。
3．正常参考值（化学发光免疫分析法）：
FT3 1.81－4.31 ng/ L
FT4 7.4－19.5 ng / L
4．注意事项和影响因素：个别人体内存在抗T3和抗T4抗体，可以干扰FT3、FT4的化验结果，在分析时要结合病人情况以及TSH结果来判断病人的甲状腺功能情况。
5．临床应用和分析：FT3和FT4较TT3和TT4敏感，在甲亢初期或复发早期FT3和FT4升高可先于TT3 和TT4。

三、促甲状腺激素测定（TSH）
1．原理：TSH由腺垂体分泌，作用于甲状腺，促进甲状腺激素的合成和分泌，促甲状腺激素释放激素（TRH）可刺激TSH分泌，而甲状腺激素反馈抑制TSH分泌。
2．标本采集：空腹不抗凝静脉血2ml。
3．正常参考值（化学发光免疫分析法）：
TSH 0.20－6.20 mIU / L
4．注意事项和影响因素：
⑴ 不同化验方法，灵敏度不同，其意义有所不同，放射免疫法（RIA）不能区别正常人与甲亢病人，免疫放射法（IRMA）可区别绝大多数甲亢病人和正常人，称为高敏TSH（sTSH），免疫化学发光（ICMA）和时间分辨免疫荧光法（TRIFMA）为超敏TSH（uTSH）。
⑵ 多巴胺、皮质醇可显著减少TSH的释放，在使用这些药物时TSH水平可抑制到甲亢水平，生长抑素和5羟色胺也可使TSH分泌减少。
⑶ 在某些非甲状腺疾病和急性精神疾病，TSH水平急剧波动使结果难以分析，应待病情稳定后重新评价或连续观察TSH的动态变化。
5．临床应用和分析：用于了解下丘脑－垂体－甲状腺轴的功能。
⑴ 原发性甲亢时，sTSH和uTSH低于正常，较FT4和FT3更敏感，一般可替代TRH兴奋试验。亚临床甲亢时TSH降低， FT3和FT4在正常范围。服用过量甲状腺激素可使TSH降低。
⑵ 原发性甲减时各种方法测定的TSH均较灵敏的升高，亚临床甲减时，TSH升高，FT3和FT4在正常范围。下丘脑和垂体病变所致甲减时，根据其病变性质和程度，TSH降低或正常偏低。单测TSH不能区别下丘脑性还是垂体性甲减， TRH兴奋试验对鉴别两者有一定帮助。
⑶ 垂体TSH瘤、异源性肿瘤（分泌TSH）、甲状腺激素抵抗综合征（全身或垂体性抵抗）时，TSH升高或正常，同时有FT4 和或FT3增高。
⑷ 用sTSH或uTSH监测正在治疗中的甲亢或甲减，当甲功恢复到正常时，TSH水平恢复到正常需要更长时间。

四、促甲状腺激素受体抗体（TRAb）测定
1．原理：TRAb主要由甲状腺内的免疫活性淋巴细胞产生，作用于甲状腺TSH受体上，TRAb为多克隆抗体，其中包括甲状腺刺激抗体（TSAb），使甲状腺激素合成和分泌增加，导致Graves病，甲状腺刺激阻断抗体（TSBAb）使甲状腺激素分泌减少。
2．标本采集：不抗凝静脉血2ml
3．正常参考值（放射受体法）：正常人 ＜ 9U / L
4．注意事项和影响因素：试验方法不同其意义有所不同，放射受体法是依据患者抗体阻断同位素标记的TSH与TSH受体结合而测的TRAb，不能确定TRAb的性质，生物法可以测定兴奋性和阻断性TRAb。
5．临床意义和分析：
⑴ 用于Graves病的诊断、疗效观察、复发和停药的指标。Graves病患者TRAb阳性可达70-80%，Graves病经治疗（药物、手术、同位素）TRAb水平逐渐下降，提示治疗有效，如转为阴性并多次，则可考虑停用抗甲状腺药物。如TRAb持续阳性，即使甲功正常，停药后复发的可能性仍较大。治疗前TRAb水平很高且持续较长时间，则提示Graves病较难控制。
⑵ 甲亢病因的鉴别，亚甲炎、甲状腺功能自主性结节或腺瘤TRAb多为阴性，少数为阳性，可结合血沉、131碘摄取率和病理等结果明确诊断。
⑶ 孕妇及新生儿甲亢的诊断和预测，TRAb可经胎盘进入胎儿，引起新生儿甲亢。
⑷ 诊断甲功正常的Graves眼病，预测Graves病家属中可能发展为Graves病的可能。
⑸ 桥本氏甲状腺炎患者阳性较低约50%。

五、甲状腺球蛋白抗体（TGAb）测定
甲状腺过氧化物酶抗体（TPOAb）测定
1．原理：甲状腺球蛋白为甲状腺滤泡胶质的主要成份，甲状腺微粒体抗体（TMAb）其真正抗原成份为甲状腺过氧化物酶（TPO），TGAb和TPOAb经常存在于甲状腺自身免疫性疾病中，TPOAb与甲状腺淋巴细胞侵润关系密切。
2．标本采集：不抗凝静脉血2ml。
3．正常参考值：
放射免疫法 TGAb 结合率 ＜30 %
TMAb结合率 ＜15 %
化学发光免疫分析法 TGAb ＜40 Iu / ml
TPOAb ＜35 Iu / ml
4．注意事项和影响因素：大约10%的健康正常人有低水平的TGAb和TPOAb，影响TGAb和TPOAb的其他因素包括：
⑴ 用甲状腺激素替代治疗慢性淋巴细胞性甲状腺炎可使抗体滴度轻中度降低。
⑵ 甲状腺次全切或全切可使抗体滴度下降。
⑶ 131I治疗使抗体滴度升高，峰值在2－3个月。
⑷ 皮质醇和抗甲状腺药物治疗可降低抗体滴度。
⑸ 患慢性淋巴细胞性甲状腺炎的儿童和孕妇抗体滴度较低，孕妇产后升高。
⑹ 干扰素α可增加抗体的产生。
5．临床应用和分析：
⑴ 用于慢性淋巴细胞性甲状腺炎的诊断，在慢性淋巴细胞性甲状腺炎时TPOAb水平的升高较TGAb更明显和常见。在诊断时应结合病人的临床表现、甲状腺功能和其他实验室检查。
⑵ 约50-90%的Graves病患者有低水平的TGAb和TPOAb，具有较高水平TPOAb的Graves病患者，以后发生甲减的可能性较大。