https://gnews.org/articles/589333 莲花清瘟胶囊千万不要用, 因为它的肝毒性已经在上个星期的Natural杂志上发表了,它的急性肝损伤是很严重。也不要去弄中药,因为肝损伤。

北京疫情严峻,医院内部紧急会议录音信息量很大

北京瑞奇德医院内部紧急会议说会百分百感染,并让会员尽量不要到医院就诊,治疗用泰诺和克感敏和小剂量激素。录音信息量很大,有中共故意释放病毒有计划感染以及杀死老年人和嫁祸美国等诸多疑点。

https://gnews.org/articles/589333
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Lin 認為 含有錯誤訊息
引用自 Lin 查核回應
Nature 在2022年12月19日發表的文章提到的是部分中藥成分的肝毒性,但並沒有明確指出是莲花清瘟胶囊/蓮花清瘟膠囊,此外本產品查無我國藥品許可證字號,如未經核准擅自輸入者,核屬藥事法第22條第1項第2款之禁藥。
建議消費者若有相關健康問題,應循正規管道找合格專業醫師診治為妥,不宜購買來路不明的商品做為預防或治療疾病之用。

資料佐證

https://www.nature.com/articles/s41419-022-05444-x

https://dep.mohw.gov.tw/DOCMAP/cp-4137-53165-108.html
天边眼前 認為 含有個人意見
引用自 天边眼前 查核回應
⋯⋯的部分,社會尚無共識。
自然杂志前几周确实发表了中国医药研究人员的论文,谈到了一些中药所包含成分的肝毒性,以及同时服用某些药物可能造成的肝损伤,但并没有指明包括”莲花清瘟“或者莲花清瘟包含具有肝毒性的具体那些成分,这位女士的说法至少不够严谨,或者说有些夸大其词,最好具体说明究竟莲花清瘟中的那些成分是这篇文章中指明的具有肝毒性。

不同意見出處

全文链接,https://www.nature.com/articles/s41419-022-05444-x
文章摘要和部分有关段落:

Abstract
The conjugation of neural precursor cell expressed, developmentally downregulated 8 (NEDD8) to target proteins, termed neddylation, participates in many cellular processes and is aberrant in various pathological diseases. Its relevance to liver function and failure remains poorly understood. Herein, we show dysregulated expression of NAE1, a regulatory subunit of the only NEDD8 E1 enzyme, in human acute liver failure. Embryonic- and adult-onset deletion of NAE1 in hepatocytes causes hepatocyte death, inflammation, and fibrosis, culminating in fatal liver injury in mice. Hepatic neddylation deficiency triggers oxidative stress, mitochondrial dysfunction, and hepatocyte reprogramming, potentiating liver injury. Importantly, NF-κB-inducing kinase (NIK), a serine/Thr kinase, is a neddylation substrate. Neddylation of NIK promotes its ubiquitination and degradation. Inhibition of neddylation conversely causes aberrant NIK activation, accentuating hepatocyte damage and inflammation. Administration of N-acetylcysteine, a glutathione surrogate and antioxidant, mitigates liver failure caused by hepatic NAE1 deletion in adult male mice. Therefore, hepatic neddylation is important in maintaining postnatal and adult liver homeostasis, and the identified neddylation targets/pathways provide insights into therapeutically intervening acute liver failure.

Drug-induced liver injury
Drug-induced liver injury (DILI) refers to the direct or indirect damage caused by drugs or their metabolites to the liver. It is one of the major adverse reactions of drugs, and also an important factor limiting the development of new drugs. DILI has been reported frequently, but the most representative ones are still non-specific drugs that need to be taken for a long time, such as efavirenz (an antiviral drug used to treat AIDS), rifampicin (an antimicrobial drug used to treat tuberculosis) and the common and classic antipyretic analgesic acetaminophen.

A growing literature suggests that the non-nucleoside analog reverse transcriptase inhibitor efavirenz can induce significant upregulation of CHOP and GRP78 mRNA and protein levels, phosphorylation of eIF2α, production of XBP1s, and expansion of ER membrane in primary human hepatocytes [88, 89]. Besides, the anti-tuberculosis drug rifampicin can increase the mRNA and protein expression levels of GRP78, PERK, ATF4, and CHOP in LO2 and HepG2, resulting in apoptosis, suggesting that it may induce DILI through ERS pathway [90]. Acetaminophen, a classic antipyretic and analgesic drug, can also induce glutathione depletion in mouse hepatocytes, causing redox imbalance in the lumen, accelerating the phosphorylation of eIF2α, activation of ATF6 and CHOP, and ultimately inducing hepatocyte apoptosis and liver injury by ERS [91]. In addition, Kusama H et al. found that intraperitoneal injection of acetaminophen in mice can cause extensive apoptosis or necrosis of mouse hepatocytes and increased level of ATF6 mRNA, suggesting that acetaminophen-induced hepatotoxicity may also be related to the activation of the ATF6 pathway [92]. In addition to the drugs mentioned above, liver injury caused by traditional herbal medicines remains an important concern. Fructus Cnidium can induce apoptosis by activating ERS and inhibiting the proliferation of LO2 cells [93]. Oxymatrine in Sophora flavescens can also induce the occurrence of ERS and the phosphorylation of c-JNK through the excessive accumulation of reactive oxygen species, causing LO2 apoptosis, which can be alleviated by 4-PBA [94]. In vivo studies found that psoralen induces ERS in hepatocytes of female C57 mice, increases liver injury-related factors’ expression, and causes inflammatory infiltration and vacuolar degeneration in hepatocytes [95]. The mechanism of DILI is indeed very complex, involving various mechanisms such as protein dysfunction, inflammation, oxidative stress, mitochondrial damage, and autoimmune response. However, overwhelming evidence suggests that ERS is also an important mechanism causing DILI.
天边眼前 認為 含有錯誤訊息
引用自 天边眼前 查核回應
【一般来说65岁以上症状重的病人有一个药,这个是个特效药可以使用,是美国辉瑞的,美国辉瑞免费给中国使用,所以配方都给到了中国,免费让中国是去仿制。】【已经有呼吸困难,症状比较重的老人主张用这个药】

完全是在严重误导,这位听上去还是院长的女士显然连美国辉瑞公司专门治疗SARS-COVID-2感染病患的Paxlovid 的英文名字都念不出来,而且她肯定没有看懂这款药物的使用说明,辉瑞公司和大量美国媒体对此药的使用对象、方法都有详细、明确的说明。

首先,它针对的病人是Covid-19的轻症患者,是特别针对高龄或有基础疾病的高危人群感染后出现轻症的患者,绝不是【65岁以上症状重的病人】
第二,药品说明中特别指明要在感染后5天之内服药,如果超过7天或已经出现重症后再服用就基本无效了!

按照这位女士的用药指导原则,既浪费了对中国大陆来说非常宝贵的医药资源,也严重耽误了高危、重症患者的治疗。

資料佐證

下面是耶鲁医学院流行病学专家关于Paxlovid的问答, Scott Roberts, MD, a Yale Medicine infectious diseases specialist.
其中明确说明,Paxlovid是专为防止具有重症风险的高危人群转成重症的药物,共13个问题,非常全面、明确、详细。

https://www.yalemedicine.org/news/13-things-to-know-paxlovid-covid-19

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