Hereditary Cerebral Hemorrhage with Amyloidosis -Dutch Type: A Study of Fibrinolysis

1992 ◽  
Vol 67 (01) ◽  
pp. 016-018 ◽  
Author(s):  
J Haan ◽  
C Kluft ◽  
F W G Leebeek ◽  
A C W de Bart ◽  
O J S Buruma ◽  
...  

SummaryIn view of reported associations between increased bleeding tendency and systemically decreased α2-antiplasmin in patients with systemic amyloid deposition we studied α2-antiplasmin, fibrinogen, C-reactive protein and blood levels of locally produced endothelial hemostasis factors in the acute and quiescent phase in 16 patients with hereditary cerebral hemorrhage with amyloidosis - Dutch type (HCHWA-D).None of the factors measured in the quiescent phase of the disease was abnormal. In the acute phase, shortly after a stroke, only factor VIII: Ag was evidently elevated. We concluded that systemic abnormalities in the part of the fibrinolysis system studied are not likely to be responsible for multifocal and recurrent cerebral hemorrhages in HCHWA-D. The role of an elevated factor VIII: Ag level in the acute phase is unclear.

2020 ◽  
Vol 134 (13) ◽  
pp. 1613-1629 ◽  
Author(s):  
Fangfang Qiu ◽  
Xiang Ma ◽  
Young-Hwa Shin ◽  
Jianglei Chen ◽  
Qian Chen ◽  
...  

Abstract Purpose: Elevated blood levels of C-reactive protein (CRP) are associated with both type 1 and type 2 diabetes and diabetic complications, such as diabetic retinopathy (DR). However, its pathogenic role in DR remains unknown. The present study aims to investigate the potential role of CRP in DR pathogenesis and explore its underlying mechanism. Materials and methods: Human CRP transgenic (hCRP-Tg) rats were employed for streptozotocin (STZ)-induced diabetic and oxygen-induced retinopathy (OIR) models. The retina function was monitored by electroretinography (ERG) and retinal thickness was measured by optical coherence tomography (OCT). TUNEL and cell death ELISA were performed to measure the apoptosis. Oxidative stress was detected by the measurement of reactive oxygen species (ROS) in cells and 3-Nitrotyrosine staining in tissue sections. Results: In non-diabetic condition, hCRP-Tg with elevated hCRP levels in the retinas demonstrated declined ERG responses and decreased retinal thickness. In STZ-induced diabetic condition, overexpression of hCRP deteriorated retinal neurodegeneration as shown by ERG and apoptosis assays. hCRP also exacerbated retinal leukostasis and acellular capillary formation induced by diabetes. In the OIR model, overexpression of hCRP exacerbated retinal neovascularization (NV). In retinal cell lines, hCRP treatment induced cell death and over-production of ROS. Furthermore, hCRP-induced overexpression of pro-inflammatory, pro-oxidative, and pro-angiogenic factors was associated with up-regulation of CD32 and the NF-κB signaling in the retinas. Conclusions: Elevated hCRP levels play a pathogenic role in DR. Targeting the hCRP-CD32-NF-κB pathway may represent a novel therapeutic strategy for DR.


2019 ◽  
Vol 10 (01) ◽  
pp. 20684-20690
Author(s):  
Shamim Shaikh Mohiuddin ◽  
Syed Rehan Hafiz Daimi

Diabetes Mellitus is one of the most common major public health problems having worldwide distribution. Depending on the etiology of diabetes mellitus, factors contributing to hyperglycemia may include; reduced insulin secretion, decreased glucose usage and increased glucose production. Recently, there in increasing evidence that an ongoing cytokine induced acute phase response which is sometimes called low grade inflammation, but part of a widespread activation of the innate immune system, is closely involved in the pathogenesis of type 2 diabetes mellitus and associated complications such as dyslipidemia and atherosclerosis. Elevated circulatory inflammatory markers such as C-reactive protein and interleukin-6 predict the development of type 2 Diabetes mellitus and several drugs with anti-inflammatory properties both lower both acute phase reactants and glycemia and possible decrease the risk of developing type 2 diabetes mellitus. In this mini review article, we aimed to systematically review the role of C-reactive protein (CRP) as inflammatory marker with increased risk of type 2 diabetes as well the relation with type 1 diabetes


2020 ◽  
Vol 11 ◽  
Author(s):  
Peter C. Hart ◽  
Ibraheem M. Rajab ◽  
May Alebraheem ◽  
Lawrence A. Potempa

Cancer disease describes any pathology involving uncontrolled cell growth. As cells duplicate, they can remain localized in defined tissues, forming tumor masses and altering their microenvironmental niche, or they can disseminate throughout the body in a metastatic process affecting multiple tissues and organs. As tumors grow and metastasize, they affect normal tissue integrity and homeostasis which signals the body to trigger the acute phase inflammatory response. C-reactive protein (CRP) is a predominant protein of the acute phase response; its blood levels have long been used as a minimally invasive index of any ongoing inflammatory response, including that occurring in cancer. Its diagnostic significance in assessing disease progression or remission, however, remains undefined. By considering the recent understanding that CRP exists in multiple isoforms with distinct biological activities, a unified model is advanced that describes the relevance of CRP as a mediator of host defense responses in cancer. CRP in its monomeric, modified isoform (mCRP) modulates inflammatory responses by inserting into activated cell membranes and stimulating platelet and leukocyte responses associated with acute phase responses to tumor growth. It also binds components of the extracellular matrix in involved tissues. Conversely, CRP in its pentameric isoform (pCRP), which is the form quantified in diagnostic measurements of CRP, is notably less bioactive with weak anti-inflammatory bioactivity. Its accumulation in blood is associated with a continuous, low-level inflammatory response and is indicative of unresolved and advancing disease, as occurs in cancer. Herein, a novel interpretation of the diagnostic utility of CRP is presented accounting for the unique properties of the CRP isoforms in the context of the developing pro-metastatic tumor microenvironment.


1997 ◽  
Vol 77 (05) ◽  
pp. 0825-0828 ◽  
Author(s):  
J O’Donnell ◽  
E G D Tuddenham ◽  
R Manning ◽  
G Kemball-Cook ◽  
D Johnson ◽  
...  

SummaryA recent report from the Leiden Thrombophilia Survey identified high factor VIII activity levels as an independent risk factor for venous thromboembolism in a population survey. As the study measure for factor VIII was a one-stage coagulation assay, and since markers for the acute phase reaction were not assessed, it remained uncertain whether the increase was due to a constitutional increased rate of synthesis, to circulating activated factor VIII, or to an acute phase response.We added factor VIII activity assay (FVIII:C), factor VIII antigen (FVIILAg), vWF antigen (vWF:Ag), ABO blood group, fibrinogen and C-reactive protein to our routine thrombophilia screen of patients referred because of unexplained thromboembolism.Elevated FVIILC (>1.5 iu/ml) emerged as the single commonest abnormality detected in 25.4% of a group of 260 such patients.FVIILC and FVIILAg were highly correlated (p = 0.003), showing that this represented a true increase in FVIII. In 4 of 46 patients this was clearly attributable to an acute phase reaction. Eleven others showed minor elevation of ESR and one of CRP. Neither FVIILC or FVIII:Ag showed significant correlation with fibrinogen, ESR or C-reactive protein by non parametric analysis.Although there was an excess of patients with B blood group (known to be associated with FVIILC levels which are -15% higher than those in blood group 0), this could not account for the marked elevation of factor VIII observed in these patients.We conclude that factor VIII activity assay should be a routine part of thrombophilia screening. We are investigating the cause of the increased synthesis, initially by means of family studies and linkage analysis with polymorphic markers of the FVIII locus. We postulate that it may be constitutive in some cases and in others an abnormal or exaggerated response to inflammatory stimuli.


2009 ◽  
Vol 55 (2) ◽  
pp. 322-335 ◽  
Author(s):  
Regina Rückerl ◽  
Annette Peters ◽  
Natalie Khuseyinova ◽  
Mariarita Andreani ◽  
Wolfgang Koenig ◽  
...  

Abstract Background: C-reactive protein (CRP), a sensitive marker of the acute-phase response, has been associated with future cardiovascular endpoints independently of other risk factors. A joint analysis of the role of risk factors in predicting mean concentrations and variation of high-sensitivity CRP (hsCRP) in serum has not been carried out previously. Methods: We used data from 1003 myocardial infarction (MI) survivors who had hsCRP measured monthly up to 8 times and multivariate mixed effects statistical models to study the role of time-variant and -invariant factors on the geometric mean of and the intraindividual variation in hsCRP concentrations. Results: Patients with ≥6.5% glycosylated hemoglobin (HbA1c) had 26.2% higher hsCRP concentrations (95% CI, 7.2%–48.6%) and 20.7% greater variation in hsCRP values (P = 0.0034) than patients with lower baseline Hb A1c values (<6.5%). Similar but less pronounced differences were seen in patients with a self-reported diagnosis of type 2 diabetes. hsCRP concentrations showed less variation in patients who reported angina pectoris, congestive heart failure, or emphysema (−11.0%, −24.9%, and −41.6%, respectively, vs patients without these conditions) but greater variation in males and smokers (+24.8% and +27.3%, respectively, vs females and nonsmokers). Exposures in the 24 h before blood sampling, including exposure to environmental tobacco smoke, alcohol consumption, and extreme stress, did not have a major impact. Conclusions: One or 2 hsCRP measurements may not be sufficient to adequately characterize different patient groups after MI with similar precisions. We found hsCRP concentrations to be especially variable in males, smokers, and patients with increased Hb A1c values.


Author(s):  
Markus Rothenburger ◽  
Andreas Markewitz ◽  
Thomas Lenz ◽  
Hans-Georg Kaulbach ◽  
Klaus Marohl ◽  
...  

2017 ◽  
Vol 86 (2) ◽  
pp. 79-83
Author(s):  
E. Segers ◽  
V. Martlé ◽  
S. Piepers ◽  
L. Van Ham ◽  
S. F. M. Bhatti

Inflammatory reactions in dogs are associated with systemic changes in serum, called the acute phase response; changes in the concentration of acute phase proteins in the serum take place. C-reactive protein (CRP) is a positive acute phase protein, which increases during inflammation. The role of inflammation in epilepsy remains unclear. In this study, the inflammatory response in dogs with idiopathic epilepsy (IE) was investigated. The aims of the study were: 1. to measure serum CRP concentrations in dogs with IE and in healthy dogs, 2. to measure serum CRP concentrations in dogs with acute cluster seizures and in dogs with isolated seizures and 3. to observe the evolution of serum CRP concentrations in time after the last seizure. This study showed no significant differences in serum CRP concentrations between dogs with IE (7.8 mg/l) and dogs of the control group (8.3 mg/l). Furthermore, the results showed higher mean serum CRP concentrations in dogs with IE exhibiting cluster seizures (11,8 mg/l) than in dogs with isolated seizures (5.7 mg/l). However, these results were not statistically significant (P = 0,077). Finally, no statistically significant decrease in serum CRP concentrations was seen with time after the last epileptic seizure in dogs with IE (P = 0,077).


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