Thrombotic microangiopathy following <i>Bothrops jararaca</i> snakebite: case report

Bucaretchi, Fábio; Pimenta, Maira M. Branco; Borrasca-Fernandes, Carla Fernanda; Prado, Camila Carbone; Capitani, Eduardo Mello De; Hyslop, Stephen

doi:10.1080/15563650.2018.1514621

Cited by 23 publications

(33 citation statements)

References 28 publications

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“…Although many studies have reported the relationship between TMA and the venom-induced consumption coagulopathy (VICC), TMA in snakebite may occur without VICC 10,11 . VICC is characterized by prolonged clotting times caused by activation of the coagulation cascade by prothrombin, thrombin-like enzymes and factor X activators present in the venom 2,12 , which resolves after the toxins neutralization. There are controversies about the treatment of TMA associated with snakebite envenoming.…”

Section: Discussionmentioning

confidence: 99%

Thrombotic microangiopathy due to Bothrops erythromelas: a case report in Northeast Brazil

Mota

Albuquerque

Júnior

et al. 2020

Rev. Inst. Med. trop. S. Paulo

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Section: Discussionmentioning

confidence: 99%

Thrombotic microangiopathy due to Bothrops erythromelas: a case report in Northeast Brazil

Mota

Albuquerque

Júnior

et al. 2020

Rev. Inst. Med. trop. S. Paulo

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“…This is the most likely pathway in AKI due to Bothrops snakes: the association between AKI and abnormal coagulation, including abnormal aPTT, hypofibrinogenemia and hemorrhagic symptoms, as soon as the increase of LDH is reported [ 5 , 14 , 66 ]. Snakebite induces thrombotic microangiopathy, characterized by the triad of AKI, thrombocytopenia, microangiopathic and haemolytic anaemia, which could lead to renal cortical necrosis [ 103 - 105 ]. Hemorrhagins contained in venoms of some snakes such as Bothrops spp.…”

Section: Methodsmentioning

confidence: 99%

“…These studies reported the abnormal activated partial thromboplastin time (aPTT), bleeding symptoms and abnormal LDH level which are factors associated with AKI development [5,14,66]. The increase of LDH levels was observed in recent case reports about thrombotic microangiopathy in Bothrops envenoming and expressed the high cellular turnover and necrosis following the increase of creatinine levels [90,91].…”

Section: Main Pathwaysmentioning

confidence: 98%

Clinical assessment and pathophysiology of Bothrops venom-related acute kidney injury: a scoping review

Albuquerque

Paiva

Martins

et al. 2020

J. Venom. Anim. Toxins incl. Trop. Dis

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Bothrops are one of the most common medically important snakes found in Latin America. Its venom is predominantly hemotoxic and proteolytic, which means that local lesion (edema and redness) and hemorrhagic symptoms are recurrent in envenoming by this snake. Although hemorrhage is usually the major cause of death, snakebite-related acute kidney injury is another potentially fatal clinical complication that may lead to chronic kidney disease. The present review highlights the main studies on Bothrops venom-related acute kidney injury, including observational, cross-sectional, case-control and cohort human studies available up to December 2019. The following descriptors were used according to Medical Subject Headings (MeSH): on Medline/Pubmed and Google Scholar "acute kidney injury" or "kidney disease" and "Bothrops"; on Lilacs and SciELO "kidney disease" or "acute kidney injury" and "Bothrops". Newcastle-Ottawa quality assessment scale was used to appraise the quality of the cross-sectional and cohort studies included. The selection of more severe patients who looked for health care units and tertiary centers is a risk of bias. Due to the methodological heterogeneity of the studies, a critical analysis of the results was performed based on the hypothesis that the design of the included studies influences the incidence of acute kidney injury. Fifteen human studies (total participants 4624) were included according to stablished criteria. The coagulation abnormalities (hemorrhagic symptoms, abnormal fibrinogen and activated partial thromboplastin time) were associated with acute kidney injury in

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“…Hemostatic abnormalities evoked by B. jararaca snakebites include direct proteolytic activity of snake venom enzymes on fibrinogen, prothrombin, and factors X, VIII and V, in a mechanistic process that is distinct from the extrinsic and intrinsic coagulation pathways, and by a feedback mechanism of these activated factors, especially meizothrombin or thrombin, which ultimately leads to activation and consumption of coagulation factors in circulation, as well as exacerbated secondary fibrinolysis [12,[20][21][22][23]. Thrombocytopenia and platelet dysfunction are also observed during B. jararaca envenomation [16,22,24], but they are independent of coagulation activation [21,25]. Gradual fibrinogen consumption during snakebite envenomation causes hypofibrinogenemia or afibrinogenemia, leading to a prolongation of whole blood coagulation time (WBCT)-which is a sign of snake envenomation [26].…”

Section: Introductionmentioning

confidence: 99%

“…Gradual fibrinogen consumption during snakebite envenomation causes hypofibrinogenemia or afibrinogenemia, leading to a prolongation of whole blood coagulation time (WBCT)-which is a sign of snake envenomation [26]. In health centers that treat snakebites, the modified WBCT is the most frequently used laboratory test to evaluate how intensely snake venoms have impaired the blood coagulation cascade [24,26,27].…”

Section: Introductionmentioning

confidence: 99%

Liver gene regulation of hemostasis-related factors is altered by experimental snake envenomation in mice

2020

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Few studies have addressed gene expression of hemostasis-related factors during acute thrombo-hemorrhagic diseases. Bites by the lanced-headed viper Bothrops jaracaca induce rapid hemostatic disturbances in victims, leading to systemic bleedings, thrombocytopenia and consumption coagulopathy. Although circulating levels of coagulation factors recover rapidly after administration of specific antivenom therapy, it is unclear if B. jararaca venom (BjV) upregulates the mRNA synthesis of hepatic hemostasis-related factors, or if the recovery occurs under basal conditions after the neutralization of venom components by antivenom. Thus, we aimed to investigate if BjV regulates gene expression of important hemostasis-related factors synthetized by the liver. On that account, Swiss mice were injected with saline or BjV (1.6 mg/kg b.w, s.c.), and after 3, 6 and 24 h blood samples and liver fragments were collected to analyze mRNA expression by real-time qPCR. Increased gene expression of fibrinogen chains, haptoglobin and STAT3 was observed during envenomation, particularly at 3 and 6 h. At 24h, mRNA levels of F10 were raised, while those of Serpinc1, Proc and Adamts13 were diminished. Surprisingly, F3 mRNA levels were steadily decreased at 3 h. Gene expression of Thpo, F7, F5 Tfpi, Mug1 was unaltered. mRNA levels of Vwf, P4hb, F8, F2, Plg, and Serpinf2 were minimally altered, but showed important associations with Nfkb1 gene expression. In conclusion, snakebite envenomation upregulates hepatic mRNA synthesis particularly of fibrinogen chains, and acute-phase markers. This response explains the fast recovery of fibrinogen levels after antivenom administration to patients bitten by B. jararaca snakes.

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Thrombotic microangiopathy following Bothrops jararaca snakebite: case report

Cited by 23 publications

References 28 publications

Thrombotic microangiopathy due to Bothrops erythromelas: a case report in Northeast Brazil

Thrombotic microangiopathy due to Bothrops erythromelas: a case report in Northeast Brazil

Clinical assessment and pathophysiology of Bothrops venom-related acute kidney injury: a scoping review

Liver gene regulation of hemostasis-related factors is altered by experimental snake envenomation in mice

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