Estudo da coagulação em um caso de hepatite de lábrea

Paiva, M C; Prata, Áluízio; Moura, Rômulo César Sabóia; Pinto, Alexandre de Siqueira; Santos, Fernando Sérgio Dumas dos

doi:10.1590/s0037-86821984000100008

Cited by 1 publication

(1 citation statement)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although consumptive coagulopathy has been hypothesized to contribute to the hemorrhagic manifestations accompanying severe YF, historically there is limited data to support this idea ( 15 , 22 ). Despite all of the clinical studies of YF in humans over the past 100 y, elevated D-dimers are described in only a few case reports ( 44 , 45 ). The lack of data regarding the development of coagulopathy in human YF is relevant given the recent trend of treating severe YF with plasma exchange ( 24 ).…”

Section: Discussionmentioning

confidence: 99%

Consumptive coagulopathy of severe yellow fever occurs independently of hepatocellular tropism and massive hepatic injury

Bailey

Kang

Zanella

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Yellow fever (YF) is a mosquito-transmitted viral disease that causes tens of thousands of deaths each year despite the long-standing deployment of an effective vaccine. In its most severe form, YF manifests as a hemorrhagic fever that causes severe damage to visceral organs. Although coagulopathy is a defining feature of severe YF in humans, the mechanism by which it develops remains uncertain. Hepatocytes are a major target of yellow fever virus (YFV) infection, and the coagulopathy in severe YF has long been attributed to massive hepatocyte infection and destruction that results in a defect in clotting factor synthesis. However, when we analyzed blood from Brazilian patients with severe YF, we found high concentrations of plasma D-dimer, a fibrin split product, suggestive of a concurrent consumptive process. To define the relationship between coagulopathy and hepatocellular tropism, we compared infection and disease in Fah−/−, Rag2−/−, and Il2rɣ−/− mice engrafted with human hepatocytes (hFRG mice) and rhesus macaques using a highly pathogenic African YFV strain. YFV infection of macaques and hFRG mice caused substantial hepatocyte infection, liver damage, and coagulopathy as defined by virological, clinical, and pathological criteria. However, only macaques developed a consumptive coagulopathy whereas YFV-infected hFRG mice did not. Thus, infection of cell types other than hepatocytes likely contributes to the consumptive coagulopathy associated with severe YF in primates and humans. These findings expand our understanding of viral hemorrhagic disease and associated coagulopathy and suggest directions for clinical management of severe YF cases.

show abstract