Therapeutic Use of Antithrombin III in Shock and Disseminated Intravascular Coagulation

Vinazzer, H

doi:10.1055/s-2007-1002727

Cited by 73 publications

(31 citation statements)

References 20 publications

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“…In patients with disseminated intravascular co agulation, adequate AT III substitution re duces the duration of symptoms and may even be life-saving [21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

In vitro Characterization of Antithrombin III Concentrates – A Single-Blind Study

Hellstern

Moberg²,

Ekblad³

et al. 1995

Pathophysiol Haemos Thromb

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Twenty-three lots of five antithrombin III (AT III) concentrates from four manufacturers were analyzed in a single-blind study. All the preparations had been virus-inactivated by pasteurization, and one concentrate had also been treated with solvent/detergent (S/D). AT III activities were determined using two thrombin-based and one factor Xa-based chromo-genic substrate assays. AT III antigen was measured by kinetic nephelometry. All AT III assays were tested against the first international reference preparation coded 72/1. In addition, AT III was characterized by crossed immunoelectrophoresis in the presence of heparin and by gel filtration. The following were quantified: heparin cofactor II activity and antigen content, heparin activity, thrombin-AT III complexes, AT III-protease complexes, total protein, albumin, immunoglobulins, glucose and pH. The AT III concentrates differed markedly in terms of their purity and potency. The specific activities of AT III and the ratios of AT III activity to antigen content ranged from 3.4 to 6.9 and from 0.63 to 0.84, respectively. The highest values were found in five lots of the concentrate that had been treated by both pasteurization and S/D. This preparation was the only one that was virtually free of denaturated AT III, as judged by crossed immunoelectrophoresis. Marked batch-to-batch variation in AT III potencies was found in two out of the five preparations analyzed. In two out of five lots from one manufacturer, the measured potencies were more than 10% lower than the declared potencies. None of the analyzed preparations contained heparin cofactor II, and heparin activities were very low in all lots.

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“…In patients with disseminated intravascular co agulation, adequate AT III substitution re duces the duration of symptoms and may even be life-saving [21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

In vitro Characterization of Antithrombin III Concentrates – A Single-Blind Study

Hellstern

Moberg²,

Ekblad³

et al. 1995

Pathophysiol Haemos Thromb

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“…AT-III is clinically used as a therapeutic for sepsis or septic shock with disseminated intravascular coagulation and plays a pivotal role in coagulation abnormality (3). In contrast to heparin, which prevents coagulopathy, but does not reduce overall mortality, AT-III significantly increases the survival of endotoxin-induced shock without improving coagulopathy (4,5). Accumulating evidence suggests that AT-III demonstrates not only an anticoagulant effect but also an antiinflammatory effect.…”

Section: Introductionmentioning

confidence: 99%

Antithrombin III reduces collagen-stimulated granule secretion of PDGF-AB and the release of soluble CD40 ligand from human platelets

Doi

Adachi²,

Matsushima‐Nishiwaki³

et al. 2010

Int J Mol Med

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Abstract. Although antithrombin-III (AT-III), an anticoagulant, has been shown to affect human platelet functions, the direct effect of AT-III on platelets is still unknown. We recently reported that the collagen-induced phosphorylation of the heat shock protein 27 (HSP27) via the p44/p42 mitogen-activated protein (MAP) kinase is sufficient for granule secretion and the release of soluble CD40 ligand (sCD40L) from platelets but not platelet aggregation. In the present study, we investigated whether AT-III affects the collagen-induced secretion of the platelet-derived growth factor (PDGF)-AB and sCD40L release. AT-III inhibited collagen-stimulated platelet aggregation. The collageninduced secretion of PDGF-AB was significantly suppressed by AT-III. AT-III also reduced sCD40L release. AT-III markedly attenuated the collagen-induced phosphorylated levels of p44/p42 MAP kinase. In addition, AT-III suppressed collagen-induced HSP27 phosphorylation. These results strongly suggest that AT-III reduced collagen-stimulated platelet granule secretion due to the inhibition of HSP27 phosphorylation via p44/p42 MAP kinase.

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“…ХХ в. появи-лись первые работы, в которых приводились данные результатов исследования АТ III при ДВС-синдроме [13][14][15]. В этих и последующих публикациях было подтверждено закономер-ное снижение активности АТ III в ходе разви-тия синдрома ДВС вследствие его потребления тромбином и другими плазменными серино-выми протеазами, что создает состояние гепа-ринорезистентности и способствует прогрес-сированию тромбинемии [16].…”

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“…Рандомизированное исследование сравни-тельной эффективности лечения ДВС-синдро-ма гепарином, концентратом АТ III или сочета-нием АТ III-гепарин показало, что у пациентов с ДВС-синдромом, имевших уровень АТ III 52,6 ± 9,7% от нормы, введение концентратов АТ III до восстановления нормального уровня инги-битора было значительно более эффективным, чем лечение только одним гепарином [14,15]. Однако следует отметить, что у пациентов с массивными травмами сочетание концентрата АТ III с гепарином не только не дало дополни-тельных преимуществ по сравнению с АТ III, но и потребовало достоверно большего объема переливания крови, что объясняется повышен-ной кровоточивостью при комбинированной терапии [23].…”

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“…В дальнейшем этим же автором было продолжено изучение влияния введения концентрата АТ III на смерт-ность у пациентов с ДВС крови. В рандомизи-рованном контролируемом исследовании на 170 пациентах (85 пациентов -введение кон-центрата АТ III при его исходной активности ниже 80%, 85 пациентов -введение гепарина по 300 МЕ/час при постоянной его инфузии) было показано снижение смертности в группе АТ III (13%) против контроля (31%, р < 0,005) [14,15,23].…”

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ROLE OF ANTITHROMBIN IN DIAGNOSTICS AND INTENSIVE THERAPY OF ACUTE DIC-SYNDROME (review of literature and evidence of actual clinical practice)

Воробьева¹

2017

Aterotromboz

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Одним из самых тяжелых и серьезных ди-сбалансов системы гемостаза в практи-ке критической медицины является ост-рый ДВС-синдром. Искусство врача-интенси-виста, реаниматолога, хирурга, акушера часто определяется именно успехами в интенсивной терапии данного состояния.Как известно, ДВС-синдром является неспе-цифическим универсальным клинико-патоло-гическим процессом, осложняющим течение самых многочисленных заболеваний, а также причиной высокой летальности, что опреде-ляет междисциплинарность и актуальность данной проблемы для врачей всех специально-стей. Многочисленные фундаментальные ра-боты отечественных и зарубежных авторов по-священы вопросам этиологии, патогенеза, ди-агностики и интенсивной терапии острого ДВС-синдрома. Немаловажно отметить, что ДВС-синдром осложняет и предопределяет АНТИТРОМБОТИЧЕСКАЯ ТЕРАПИЯ

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Therapeutic Use of Antithrombin III in Shock and Disseminated Intravascular Coagulation

Cited by 73 publications

References 20 publications

In vitro Characterization of Antithrombin III Concentrates – A Single-Blind Study

In vitro Characterization of Antithrombin III Concentrates – A Single-Blind Study

Antithrombin III reduces collagen-stimulated granule secretion of PDGF-AB and the release of soluble CD40 ligand from human platelets

ROLE OF ANTITHROMBIN IN DIAGNOSTICS AND INTENSIVE THERAPY OF ACUTE DIC-SYNDROME (review of literature and evidence of actual clinical practice)

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