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关于乙肝的诊断,来自维基百科
关于乙肝的诊断,识别,来自维基百科综合各医学院、医疗杂志中的论文和资料,包括我前面提到的世界卫生组织WHO和斯坦福医学院亚裔肝病中心。
鉴定感染存在最常用的是乙肝表面抗原(HBsAg),在感染期,它是最早可测的显现的病毒抗原。然后在早期的感染期,在被宿主(寄生的主体)清除条件下,这个抗原可能不出现并在随后的感染中也可能不会监测到。这个传染的病毒包含一个内部带着病毒基因组的“核心粒子”,这个十二面体的核心粒子是由180或者240份核蛋白构成,或者被称作乙肝核心抗原,或者HBcAg。在这个时期宿主一直是感染的,但是正在成功的清除病毒。乙肝核心抗原IgM抗体(anti-HBc IgM)可能是唯一的疾病血清征兆。
紧随着HBsAg的出现,另一个被称作乙肝e抗原(HBeAg)的抗原将会出现。通常,HBeAg在一个宿主的血清的存在是同更高病毒复制比例相关联的,并且增强它的传染性,然而,乙肝病毒的变体并不出现这个"e"抗原,所以这个规则并不总是对。在这个感染的自然过程中,HBeAg可能会被清除,这个"e"抗原(anti-HBe)抗体将很快出现。这个转化过程经常同病毒复制的急速降低相联系的。
如果宿主能够清楚感染,在乙肝表面抗原和核心抗原的IgG抗体(anti-HBs and anti HBc IgG)出现后,最终会检测不到HBsAg。在HBsAg被清除和anti-HBs出现之间的这个时间被称作窗口期。一位HBsAg阴性同时anti-HBs阳性的人或者清除了感染,或者此前被种植过疫苗。
保持HBsAg阳性的至少6个月的个体被称作乙肝携带者。病毒携带者可能有慢性乙肝(隐性的,长期但很慢很慢),升高的血清谷丙转氨酶(ALT)和肝脏的感染,通过肝穿刺活组织检查(活体切片),可以反映这个慢性乙肝。HBeAg阴性的携带者,特别是那些在成年被感染的,存在微小的病毒复制,因此几乎没有远期并发症或者传染给别人的风险(此处是说,如果是成年以后感染成为包括乙肝小三阳在内的,HBeAg-阴性的携带者,自身和传染给别人的风险很小)。
PCR测试经常被用作测试和测量HBV DNA的数量,被称在临床样本中作病毒载量,这些测试被用作评估一个人的感染状况,以监测治疗处置。有高病毒载量的个体,特征(或者说通常)在活体检查中存在毛玻璃样细胞。
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注意: 我翻译了一下维基百科上面乙肝中“诊断”"Diagnosis"中的大部分内容(原文附后),没有进行校对,仅供参考。
The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen, or HBcAg. During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.
Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the 'e' antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.
If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG). The time between the removal of the HBsAg and the appearance of anti-HBs is called the window period. A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously.
Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers.Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status, particularly those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.
PCR tests have been developed to detect and measure the amount of HBV DNA, called the viral load, in clinical specimens. These tests are used to assess a person's infection status and to monitor treatment. Individuals with high viral loads, characteristically have ground glass hepatocytes on biopsy.
[ 本帖最后由 济南人 于 2010-4-11 10:20 编辑 ] |
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