Human Plasma Kallikrein-Kinin System: Physiological and Biochemical Parameters

Bryant, JW; Shariat‐Madar, Zia

doi:10.2174/187152509789105444

Cited by 118 publications

(101 citation statements)

References 192 publications

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“…The demonstrated data show significantly higher values in both scoring systems comparing the survival to the non-survival group, according to the severity of tissue destruction. Tissue destruction leads to the set free of the Kininogene and Kallikrein leading to the activation of the factor XII (Hageman-factor) [20]. Systemic spread of Kininogene and Kallikrein may activate systemically the factor XII leading to a consumptive coagulopathy.…”

Section: Iss and Niss: Tissue Destruction Bleedsmentioning

confidence: 99%

Independent Predictors of Early Death of Polytrauma Patients: An Analysis of 696 Patients

Mica

Albrecht²,

Keel³

et al. 2012

J Trauma Treatment

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Polytrauma patients are at high risk to die due to acute physiological deterioration after a high injury load within the first hours. Trauma scores such as ISS, NISS and APACHE II and laboratory parameters were collected at admission. The aim of this study was to evaluate the independent predictors of early death of the polytrauma patient. A total of 696 patients (age 40.8 ± 15.5 years) who had an ISS 17 and were admitted to a trauma center within the first 24 hours after trauma were included into this retrospective study. The patients were subdivided into survivors and those who died within the first 72 hours. ISS, NISS and APACHE II score, and laboratory parameters such as lactate, prothrombin time, pH-value, hematocrite, middle arterial pressure and platelets were collected at admission time. Data were compared with Mann-Whitney test and 2-test for proportions. The data were considered as significant if p < 0.05. Predictive ability was evaluated by using receiver operating characteristic curves. Independent predictors were analyzed by logistic regression analysis. Significantly increased values of ISS, NISS, APACHE II and serum lactate, and significantly decreased values of prothrombin time, middle arterial pressure, hematocrite, Platelets and pH-value were found in the non-survivor group (p < 0.001). APACHE II, NISS, ISS score and the prothrombin time were found to be independent predictive values of death. Early recognition of the risk of death followed by multidisciplinary resuscitation efforts could lead to a better survival rate in the population of polytrauma patients.

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Section: Iss and Niss: Tissue Destruction Bleedsmentioning

confidence: 99%

Independent Predictors of Early Death of Polytrauma Patients: An Analysis of 696 Patients

Mica

Albrecht²,

Keel³

et al. 2012

J Trauma Treatment

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“…ACE plays an important role in RAS and angiotensin II conversion, directly increases vascular smooth muscle cell contraction, and affects smooth muscle proliferation, monocyte adhesion, platelet adhesion, and aggregation (Coates, 2003;Bryant and Shariat-Madar, 2009). The ACE I/D polymorphism accounts for 47% of the variation in ACE plasma activity (Rigat et al, 1990); therefore, the source of most variation remains unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II and inactivates bradykinin via the kallikrein-kininogen system (Coates, 2003;Bryant and Shariat-Madar, 2009). Angiotensin II, a potent vasoconstrictor, is the main effector molecule of the renin-angiotensin-system (RAS).…”

Section: Introductionmentioning

confidence: 99%

“…Dysregulation of this system can contribute to the development of essential hypertension. Furthermore, angiotensin II is a potent proinflammatory modulator that augments immune responses (Kranzhofer et al, 1999;Nataraj et al, 1999;Marchesi et al, 2008;Bryant and Shariat-Madar, 2009). The ACE gene, located on chromosome 17q23, contains an insertion (I)/deletion (D) polymorphism within intron 16 that may contain or lack a 250-287 base pair (bp) repeat sequence (Rigat et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin-converting enzyme insertion/deletion polymorphism and susceptibility to systemic sclerosis: a meta-analysis

Song¹,

Lee²

2014

Genet. Mol. Res.

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ABSTRACT. The purpose of this study was to examine whether the insertion (I) or deletion (D) polymorphism of the angiotensin-converting enzyme gene (ACE) is associated with susceptibility to systemic sclerosis (SSc). A meta-analysis examining the associations between the ACE I/D polymorphism and SSc was conducted in overall and European populations using 1) allelic contrast (D vs I); 2) recessive (DD vs ID + II); 3) dominant (DD + ID vs II); and 4) additive (DD vs ID vs II) models. A total of 7 studies consisting of 837 cases and 754 controls were available for meta-analysis. The meta-analysis revealed no association between the D allele and SSc in any study subjects [odds ratio (OR) = 0.956, 95% confidence interval (CI) = 0.733-1.246, P = 0.737]. Stratification by ethnicity indicated no association between the D allele of the ACE I/D polymorphism and SSc in Europeans (OR = 1.117, 95%CI = 0.776-1.607, P = 0.551). Meta-analysis using all other genetic models showed the same D allele pattern in the overall and European groups. This metaanalysis showed that the ACE I/D polymorphism was not associated with susceptibility to SSc in the study subjects and in Europeans.

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“…As shown in Figure 1, firstly, in a reciprocal feedback mechanism, kallikrein accelerates not only FXII activation but also PK activation. Secondly, cleavage of HK by kallikrein results in liberation of the angiogenic and inflammatory mediator Bradykinin (BK) and cleaved high molecular weight kininogen (HKa, anti-angiogenic and anti-infection properties), each of which have evolved to occupy a unique physiological niche [16]. Both BK and HKa protect injured/dysfunctional tissues in a cooperative manner but they exert opposite effects [17,18].…”

Section: Introductionmentioning

confidence: 99%

Physiological Effects of the Plasma Kallikrein-Kinin System: Roles of the Blood Coagulation Factor XII (Hageman Factor)

Lynch¹,

Shariat‐Madar²

2012

J Clin Toxicol

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For many decades the intrinsic coagulation research has focused on factor XII (Hageman factor; FXII) and its significant role as a sole instigating factor driving the stabilization of thrombotic clotting. FXII is a relatively weak risk factor for thrombosis although its amidolytic and proteolytic function renders its presence important. Accumulating evidence suggests that FXII is pivotally involved in pathologic coagulation. In particular, the role of FXII in initiation and propagation of the blood coagulation and fibrinolytic systems has impeccable scientific support to the extent of which the existence of a "FXII-dependent pathway of thrombosis" is now generally accepted. The concept, although not a new one to scientists in the field of coagulation, is a caveat to the pathologic clot forming FXII concept in that it appears to cause a conceptual shift in de-emphasizing the inherent complexity of FXII activation representing a spectrum of responses. For instance, FXII contributes to the activation of inflammation and complement systems and influences catecholamine release from the adrenal system, suggesting that FXII can trigger multiple signaling pathways upon activation. The nature and duration of each of the FXII-dependent pathways may depend not only on the kind of stimulus, but also it may have distinct response pattern under normal and pathophysiologic conditions.Because a plethora of pathophysiological pathways are influenced by FXII, additional studies into its role as an important first step behind regulating common daily stresses may promise to provide new insight to better understand the unique and subtle biology behind FXII.

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Human Plasma Kallikrein-Kinin System: Physiological and Biochemical Parameters

Cited by 118 publications

References 192 publications

Independent Predictors of Early Death of Polytrauma Patients: An Analysis of 696 Patients

Independent Predictors of Early Death of Polytrauma Patients: An Analysis of 696 Patients

Angiotensin-converting enzyme insertion/deletion polymorphism and susceptibility to systemic sclerosis: a meta-analysis

Physiological Effects of the Plasma Kallikrein-Kinin System: Roles of the Blood Coagulation Factor XII (Hageman Factor)

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