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Yarovaya, G. A.; Blokhina, T.; Neshkova, Elena

doi:10.1023/a:1013991828598

Cited by 39 publications

(15 citation statements)

References 72 publications

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“…Complement activation, inflammation and activation of the contact phase of blood coagulation are biologically related processes [3, 4]. C1 INH has a pivotal role in regulation of all these molecular pathways [5].…”

Section: Discussionmentioning

confidence: 99%

Hereditary Angioedema Associated with Heterozygous Factor V Leiden Mutation in a Patient with Purpura Fulminans

Çelikel

Büyükaşık²,

Karakaya³

et al. 2006

Int Arch Allergy Immunol

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Background: Hereditary angioedema (HAE) is an autosomal dominant, quantitative or functional defect of the C1 esterase inhibitor. The main role of the C1 esterase inhibitor is to regulate the activation of the complement system, the contact phase of the intrinsic coagulation system. On the other hand, factor V Leiden is the most common cause of primary and recurrent venous thromboembolism and displays a strong interaction with oral contraceptives. Here we report the case of a patient with HAE associated with the factor V Leiden mutation who had purpura fulminans when put on an oral contraceptive therapy. Case: A 42-year-old woman presented to the emergency room with a history of livid skin changes on her legs during a flight. On physical examination, the vital signs were normal, but there were edemas in her legs. The livid skin changes tended to increase, eventually leading to skin necrosis on the next day. She had a history of a similar episode two months before and experienced both episodes of necrotic skin lesions just after she had been put on a hormone replacement therapy due to irregular menstruations. She also had a history of recurrent angioedema attacks since her childhood, triggered by stress and physical stimulants such as pressure and heat. Subsequent investigations revealed heterozygous factor V mutation, activated protein C resistance and reduced C1 inhibitor levels. Conclusion: Thrombosis is a multifactorial disease. The coexistence of multiple hereditary and acquired factors eases its occurrence. Women with HAE should be screened for the factor V Leiden mutation before pregnancy or the start of a hormone replacement therapy.

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Section: Discussionmentioning

confidence: 99%

Hereditary Angioedema Associated with Heterozygous Factor V Leiden Mutation in a Patient with Purpura Fulminans

Çelikel

Büyükaşık²,

Karakaya³

et al. 2006

Int Arch Allergy Immunol

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“…Thus, the mechanisms of KKS activity regulation illustrated by Fig. 2 ensure the stability of the levels of all components of the system, including kinins [22][23][24][25][26][27], and thus provide for the implementation of physiological processes.…”

Section: The Current Concept Of Kks Structure and Functioningmentioning

confidence: 99%

Past and present research on the kallikrein-kinin system (on the 90th anniversary of the discovery of the system)

Yarovaya

Neshkova

2015

Russ J Bioorg Chem

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The kallikrein-kinin system (KKS) is the key proteolytic system participating in control of a wide spectrum of physiological functions and the development of many pathological conditions. This explains great interest in structures, functions and molecular biology of separate components of the system, molecular mechanisms of their interaction and relationship with other regulatory systems. The information in this field for the last two decades clarifies the role of KKS in morphogenesis of cells, regulation of smooth muscular contractility of some organs, decrease of blood pressure, increase of vascular permeability, the development of inflammation, transformation of cells and the other functions of both physiological and pathological processes. Essential progress in understanding of functions KKS was made by the discovery and study of bradykinin receptors, cloning of kininogen and kallikrein encoding genes, revealing of domain structure of kininogen, prekallikrein and some kininases and decoding of mechanisms of contact phase of proteolytic system activation in blood plasma.

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“…The intrinsic pathway: after contact with a negatively charged surface, a complex consisting of 4 proteins (hemocoagulation factors XII and XI, high-molecular-weight kininogen and prekallikrein) results in contact activation of factor XII, thus initiating the coagulation cascade through the intrinsic pathway (Yarovaya et al, 2002). The importance of the intrinsic pathway to the normal blood coagulation is not clear.…”

Section: Blood Constituentsmentioning

confidence: 99%

Drug-Induced Thrombosis—Experimental, Clinical, and Mechanistic Considerations

Ramot

Nyska²

2007

Toxicol Pathol

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Awareness of the dangers of drug-induced thrombosis has recently been heightened and led to demand for improved testing methodology. For example, reports indicating that some selective inhibitors of cyclooxygenase-2 (COX-2) increase the risk of myocardial infarction and atherothrombotic events caused the withdrawal of rofecoxib from global markets and the issuance of warnings concerning the usage of other COX-2 inhibitors. Drugs may exert a prothrombotic state by a variety of mechanisms-those affecting the vessel wall, the blood flow, and/or different blood constituents. Our review serves as an update to that of Gerhard Zbinden published in 1976 by presenting recently acquired data that more fully elucidate the different mechanisms by which drugs are believed to induce thrombogenic effects and discussing new methods used to detect these without losing sight of the classical pathology of thrombosis. We offer correlations between experimental findings and clinical data and conclude that, because drugs may induce a prothrombotic state by a variety of mechanisms, they should be tested for these using appropriate experimental methods and animal models.

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Untitled

Cited by 39 publications

References 72 publications

Hereditary Angioedema Associated with Heterozygous Factor V Leiden Mutation in a Patient with Purpura Fulminans

Hereditary Angioedema Associated with Heterozygous Factor V Leiden Mutation in a Patient with Purpura Fulminans

Past and present research on the kallikrein-kinin system (on the 90th anniversary of the discovery of the system)

Drug-Induced Thrombosis—Experimental, Clinical, and Mechanistic Considerations

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