2012
DOI: 10.1007/s00392-012-0432-6
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Complement anaphylatoxin C3a as a novel independent prognostic marker in heart failure

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Cited by 29 publications
(32 citation statements)
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“…Moreover, complement inhibition consistently attenuated leukocyte recruitment following myocardial infarction highlighting the critical role of the complement cascade in triggering inflammation in the ischemic myocardium [25, 27]. Its role as a prognostic marker in heart failure was only addressed by a very limited number of investigations: Gombos et al recently presented data from 182 patients indicating an association between activated complement C3a and a combined endpoint consisting of all-cause mortality or rehospitalization due to progression of heart failure [28]. Aukrust et al found systemic complement activation in 39 patients with chronic heart failure; treatment with intravenous immunoglobulin reduced complement activation and increased left ventricular function during the 5-month follow-up period [29, 30].…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, complement inhibition consistently attenuated leukocyte recruitment following myocardial infarction highlighting the critical role of the complement cascade in triggering inflammation in the ischemic myocardium [25, 27]. Its role as a prognostic marker in heart failure was only addressed by a very limited number of investigations: Gombos et al recently presented data from 182 patients indicating an association between activated complement C3a and a combined endpoint consisting of all-cause mortality or rehospitalization due to progression of heart failure [28]. Aukrust et al found systemic complement activation in 39 patients with chronic heart failure; treatment with intravenous immunoglobulin reduced complement activation and increased left ventricular function during the 5-month follow-up period [29, 30].…”
Section: Discussionmentioning
confidence: 99%
“…Both C4a and C3a levels are predictive of the responses of esophageal cancer patients to chemoradiation (Maher et al, 2011). In more obviously inflammatory disorders, C3a (and to a lesser extent C4a) have been shown to be potentially useful markers in dermatomyositis (Campo et al, 2007), aneurysmal subarachnoid hemorrhage (Mack et al, 2007), acute Lyme disease in tick-bite patients (Shoemaker et al, 2008;Stricker et al, 2009) (Fassbender et al, 2009), adverse pregnancy outcomes (Lynch et al, 2011), chronic obstructive pulmonary disease (Marc et al, 2004;Zhang et al, 2011), cryptogenic and large-vessel disease subtypes of stroke (Stokowska et al, 2011), heart failure (Gombos et al, 2012), cerebral arteriovenous malformations (Haque et al, 2011), asthma (Joks et al, 2008), gestational diabetes mellitus (Lappas, 2011), SLE (Wild et al, 1990), acute relapses in multiple sclerosis (Ingram et al, 2010), IgA nephropathy/Henoch-Schonlein nephritis (Abou-Ragheb et al, 1992) and impaired renal function (Abou-Ragheb et al, 1991), atopic dermatitis (Sergeev Iu et al, 1989), psoriasis (Takematsu et al, 1986) and psoriatic arthritis (Muto et al, 1991), idiopathic pulmonary arterial hypertension (Abdul-Salam et al, 2006), postexercise malaise in myalgic encephalomyelitis/chronic fatigue syndrome (Nijs et al, 2010), AIDS-associated retinitis , and grafted corneas . In addition, C4a and C5a levels decrease after liver resection whereas C3a levels increase (Strey et al, 2009); and C3a and C4a are elevated in liver transplant recipients (Pfeifer et al, 2000).…”
Section: A Complement Peptides Are Important Biomarkers Of Diseasementioning
confidence: 99%
“…Complement activation occurs in CHF [4] and has been associated with adverse clinical events in patients with symptomatic heart failure [5,6]. Deposition of the terminal complement complex (TCC) has been observed in myocardial biopsies from patients with dilated cardiomyopathy [7], but its relation to disease severity in cardiomyopathy is debated [8].…”
Section: Introductionmentioning
confidence: 99%