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Monotorrent c-reactive protein

Опубликовано в Operation ivy energy tpb torrents | Октябрь 2, 2012

monotorrent c-reactive protein

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Subclinical inflammation during third trimester of pregnancy was not associated with markers of the metabolic syndrome in young adult offspring. Obesity Silver Spring. Dekker G. Deveci K. Pregnancy-associated plasma protein-A and C-reactive protein levels in pre-eclamptic and normotensive pregnant women at third trimester J. Obstetrics Gynaecology Research.

Du Clos T. Engin-Ustun Y. Biological markers of stress in pregnancy: associations with chronic placental inflammation at delivery. Am J Perinatol. Farzadnia M. Goldberger G. Gould Jane M. Grgic G. Imhof A. Irgens H. Kashanian M. Khan K. Kristensen K. Kumru S. Correlation of maternal serum high-sensitive C-reactive protein levels with biochemical and clinical parameters in preeclampsia.

Martinez J. Nazarov P. Nielsen F. Complement-dependent clearance of apoptotic cells by human macrophages. C-reactive protein does not opsonize early apoptotic human neutrophils, but binds only membrane-permeable late apoptotic cells and has no effect on their phagocytosis by macrophages.

C-reactive protein-mediated suppression of nephrotoxic nephritis: role of macrophages, complement, and Fcgamma receptors. Polymorphism at the C-reactive protein locus influences gene expression and predisposes to systemic lupus erythematosus.

Regulation of complement activation by C-reactive protein: targeting the complement inhibitory activity of factor H by an interaction with short consensus repeat domains 7 and C-reactive protein versus erythrocyte sedimentation rate, white blood cell count and alkaline phosphatase in diagnosing bacteraemia in bone and joint infections. C-reactive protein and atherothrombosis. Control of the acute phase response. Serum C-reactive protein kinetics after acute myocardial infarction.

Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction. Production of C-reactive protein and risk of coronary events in stable and unstable angina. Targeting C-reactive protein for the treatment of cardiovascular disease.

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Persistently elevated CRP levels can be seen in chronic inflammatory conditions such as chronic infections or inflammatory arthritides such as rheumatoid arthritis. There are numerous causes of an elevated C-reactive protein. These include acute and chronic conditions, and these can be infectious or non-infectious in etiology. However, markedly elevated levels of CRP are most often associated with an infectious cause [4] an example of pathogen-associated molecular pattern recognition.

Trauma can also cause elevations in CRP alarmin response. More modest elevations tend to be associated with a broader spectrum of etiologies, ranging from sleep disturbances to periodontal disease. A blood specimen is taken from a peripheral venous draw. A phlebotomist performs the procedure in most cases. The phlebotomist secures a snug, rubber band around the upper arm, and the patient pumps his or her fist several times.

The phlebotomist palpates the vein to confirm the location and cleanses the area with an alcohol prep pad. Once the area air dries, the practitioner introduces a needle into the vein and draws a vial of blood. He or she removes the band from the patient's arm, and then removes the needle and applies pressure to the venipuncture site until hemostasis occurs, usually within one minute. A bandage is applied over the site. The patient's medications should be reviewed, as these can affect the outcome of the test.

Fasting is not required before the blood draw. There are no special procedures required. Complications include oozing at the draw site, bruising or mild tenderness at the site, or very rarely, infection at the venipuncture site. Other bodily fluids, such as synovial fluid, can be tested for in this manner, but frequently are not. Immunoassays and laser nephelometry are the methods to quantify CRP levels and are cheap, accurate, and fast. To detect lower levels of CRP 0. High-sensitivity CRP only denotes the assay process used, allowing for detection of lower levels of CRP, and not a different, or more specific, differential diagnosis.

This test is performed when the physician suspects acute or chronic inflammation e. The utility of the hs-CRP for cardiac screening is debatable. There is some correlation between cardiovascular risk and elevated hs-CRP, but the application of this is still controversial especially given the poor specificity of this test, and it is currently undergoing more evaluation.

Lab values vary, and there is no standard at present. More than Statins, as well, have been known to reduce CRP levels falsely. Recent injury or illness can falsely elevate levels, particularly when using this test for cardiac risk stratification. Magnesium supplementation also can decrease CRP levels. As mentioned above, mild elevations in CRP can be seen without any systemic or inflammatory disease.

Females and elderly patients have higher levels of CRP. Obesity, insomnia, depression, smoking, and diabetes can all contribute to mild elevations in CRP, and the results shall be interpreted with caution in individuals with these comorbidities. The CRP gene is located on chromosome 1 1q It is a member of the small pentraxins family. The monomer has amino acids, [16] and molecular mass of 25, Da. The complete protein, composed of five monomers, has a total mass of approximately , Da.

In serum, it assembles into stable pentameric structure with a discoid shape. CRP binds to the phosphocholine expressed on the surface of bacterial cells such as pneumococcus bacteria. This activates the complement system , promoting phagocytosis by macrophages, which clears necrotic and apoptotic cells and bacteria.

This so-called acute phase response occurs as a result of increasing concentrations of IL-6 , which is produced by macrophages [6] as well as adipocytes [7] in response to a wide range of acute and chronic inflammatory conditions such as bacterial , viral , or fungal infections; rheumatic and other inflammatory diseases ; malignancy; and tissue injury and necrosis. These conditions cause release of interleukin-6 and other cytokines that trigger the synthesis of CRP and fibrinogen by the liver.

CRP binds to phosphocholine on micro-organisms. It is thought to assist in complement binding to foreign and damaged cells and enhances phagocytosis by macrophages opsonin-mediated phagocytosis , which express a receptor for CRP. It plays a role in innate immunity as an early defense system against infections. In healthy adults, the normal concentrations of CRP varies between 0. CRP concentrations also increase with age, possibly due to subclinical conditions.

There is also no seasonal variations of CRP concentrations. Gene polymorphism of interleukin-1 family , interleukin 6 , and polymorphic GT repeat of the CRP gene do affect the usual CRP concentrations when a person does not have any medical illnesses. Therefore, the only factor that affects the blood CRP concentration is its production rate, which increases with inflammation, infection, trauma, necrosis, malignancy, and allergic reactions.

It can double every 8 hours and reaches its peak at 36 to 50 hours following injury or inflammation. Once inflammation subsides, CRP level falls quickly because of its relatively short half-life. CRP is used mainly as an inflammation marker.

Apart from liver failure , there are few known factors that interfere with CRP production. Measuring and charting CRP values can prove useful in determining disease progress or the effectiveness of treatments. ELISA , immunoturbidimetry , nephelometry , radial immunodiffusion [25] [21].

Normal levels increase with aging. CRP cut-off levels indicating bacterial from non-bacterial illness can vary due to co-morbidities such as malaria , HIV and malnutrition and the stage of disease presentation. Recent research suggests that patients with elevated basal levels of CRP are at an increased risk of diabetes , [30] [31] hypertension and cardiovascular disease.

It has been hypothesized that patients with high CRP levels might benefit from use of statins. Statins were selected because they have been proven to reduce levels of CRP. In a meta-analysis of 20 studies involving 1, patients with coronary artery disease , CRP levels were found to be reduced after exercise interventions. Among those studies, higher CRP concentrations or poorer lipid profiles before beginning exercise were associated with greater reductions in CRP.

To clarify whether CRP is a bystander or active participant in atherogenesis, a study compared people with various genetic CRP variants. Those with a high CRP due to genetic variation had no increased risk of cardiovascular disease compared to those with a normal or low CRP. Arterial damage results from white blood cell invasion and inflammation within the wall. CRP is a general marker for inflammation and infection, so it can be used as a very rough proxy for heart disease risk.

Since many things can cause elevated CRP, this is not a very specific prognostic indicator. Currently, C-reactive protein is not recommended as a cardiovascular disease screening test for average-risk adults without symptoms.

The American Heart Association and U. Centers for Disease Control and Prevention have defined risk groups as follows: [46] [21]. But hs-CRP is not to be used alone and should be combined with elevated levels of cholesterol, LDL-C, triglycerides , and glucose level. Smoking, hypertension and diabetes also increase the risk level of cardiovascular disease. Scleroderma , polymyositis , and dermatomyositis elicit little or no CRP response.

Elevations of CRP in the absence of clinically significant inflammation can occur in kidney failure. CRP level is an independent risk factor for atherosclerotic disease. Patients with high CRP concentrations are more likely to develop stroke , myocardial infarction , and severe peripheral vascular disease. High levels of CRP has been associated to point mutation CysArg in the APOE gene, coding for apolipoprotein E , establishing a link between lipid values and inflammatory markers modulation.

The role of inflammation in cancer is not well understood. Some organs of the body show greater risk of cancer when they are chronically inflamed. In a prospective cohort study on colon cancer risk associated with CRP levels, people with colon cancer had higher average CRP concentrations than people without colon cancer. However, these findings may suggest that low inflammation level can be associated with a lower risk of colon cancer, concurring with previous studies that indicate anti-inflammatory drugs could lower colon cancer risk.

Mechanistically, CRP also appears to influence osteoclast activity leading to bone resorption and also stimulates RANKL expression in peripheral blood monocytes. It has previously been speculated that single-nucleotide polymorphisms in the CRP gene may affect clinical decision-making based on CRP in rheumatoid arthritis, e. From Wikipedia, the free encyclopedia.

Mammalian protein found in Homo sapiens. Right lobe of liver islet of Langerhans gallbladder Body of pancreas pancreatic epithelial cell right coronary artery pancreatic ductal cell canal of the cervix right lung gastric mucosa. National Center for Biotechnology Information, U. National Library of Medicine. PMID The Journal of Clinical Investigation. PMC American Journal of Physiology. Heart and Circulatory Physiology. Journal of Clinical Immunology. S2CID The Journal of Experimental Medicine.

Harper's illustrated biochemistry. McGraw-Hill Medical. ISBN Henry's clinical diagnosis and management by laboratory methods. Saunders Elsevier. Philadelphia: Saunders. Entrez Gene. Protein Data Bank in Europe. Journal of Clinical Medicine. Lab Tests Online. Retrieved

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