我有不同的看法.
最不同意的是:抗毒后更纤维化更加加剧的.
你是对的, 在对抗病毒药物作出反应后,并非所有纤维化/肝硬化都可逆转. 我读过一个17%的数据表明纤维化仍在进展, 但是在Lancet 2013上发表的一项具有里程碑意义的研究, 在TDF 5年后,绝大多数患者的纤维化/肝硬化有所改善:
Regression of cirrhosis during treatment with tenofovir
disoproxil fumarate for chronic hepatitis B: a 5-year
open-label follow-up study
Patrick Marcellin, Edward Gane, Maria Buti, Nezam Afdhal, William Sievert, Ira M Jacobson, Mary Kay Washington, George Germanidis,
John F Flaherty, Raul Aguilar Schall, Jeff rey D Bornstein, Kathryn M Kitrinos, G Mani Subramanian, John G McHutchison, E Jenny Heathcote
这些并不重要,最重要的是找出你的纤维化似乎进展的原因. 较低的血小板计数与脾脏增加有关. 纤维化进展还有许多其他原因:
Coinfected patients with liver fibrosis progression had significantly higher levels of fasting glycaemia at the end of follow-up and those with regression had significantly lower levels of triglycerides at TDF-initiation – the median levels of both parameters were nonetheless borderline normal or slightly abnormal in these patient groups. Furthermore, patients progressing to severe fibrosis/cirrhosis had a higher, albeit non-significant, proportion with elevated liver enzymes at the end of follow-up, which has been associated with NASH, insulin resistance and liver fibrosis in HIV-mono-infected patients [32]. These results point to preliminary development of metabolic abnormalities as a possible underlying cause for some of the liver fibrosis progression observed here, yet would require further evaluation in other studies.
伴随肝纤维化进展的共同感染患者在随访结束时空腹血糖水平显着升高,并且在TDF开始时具有回归的患者甘油三酯水平显着降低 - 这两个参数的中位数水平仍然是临界正常或略有异常。 患者团体。 此外,进展为严重纤维化/肝硬化的患者在随访结束时肝酶升高的比例较高,尽管不显着,这与HIV单发感染患者的NASH,胰岛素抵抗和肝纤维化有关。[32]。 这些结果表明代谢异常的初步发展是这里观察到的一些肝纤维化进展的潜在原因,但是在其他研究中需要进一步评估。
那就是高血糖水平,高甘油三酯水平可以影响纤维化的退化/进展.
The host factors age and male gender have been traditionally strong determinants of liver fibrosis progression for a wide range of liver diseases
宿主因素年龄和男性性别传统上是肝纤维化进展的强烈决定因素,适用于广泛的肝脏疾病宿主因素年龄和男性性别传统上是肝纤维化进展的强烈决定因素,适用于广泛的肝脏疾病.