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Acute Phase Reactants (acute + phase_reactant)

Distribution by Scientific Domains

Medical Sciences	87%

Selected Abstracts

Type 2 diabetes mellitus: a disease of the innate immune system?

DIABETIC MEDICINE, Issue 3 2004
An update
Abstract A few years ago a hypothesis was proposed suggesting that elements of the innate immune system, such as acute phase reactants, contribute to the development of Type 2 diabetes mellitus. Acute phase reactants such as C-reactive protein and sialic acid may thus predict risk of developing Type 2 diabetes mellitus, as well as being markers of diabetes microvascular and macrovascular complications. This article discusses these issues. [source]

Is procalcitonin a reliable marker for the diagnosis of infected pancreatic necrosis?

ANZ JOURNAL OF SURGERY, Issue 7 2004
Nadir Yonetci
Background: Infected necrosis in acute pancreatitis is the main factor in determining the prognosis of the disease. Early and accurate diagnosis of infected pancreatic necrosis might decrease mortality. The aim of the present study is to identify a reliable marker for the onset infection in three different experimentally induced pancreatitis models. Methods: Ninety female Wistar albino rats were randomly divided into nine groups. In three different experimental models, including cerulein induced acute oedematous pancreatitis (AEP), sterile pancreatic necrosis due to taurocholate-induced acute pancreatitis (SPN) and infected pancreatic necrosis taurocholate-induced acute pancreatitis (IPN). Serum levels of procalcitonin (PCT), C-reactive protein (CRP), tumour necrosis factor a (TNF-,), interleukin 6 (IL-6) and interleukin 8 (IL-8), amylase were measured. The degree of pancreatic damage also evaluated pathologically. Results: Procalcitonin levels were increased significantly in AEP, SPN and IPN compared to control groups (P < 0.05). PCT and IL-6 level were the highest in the IPN group (P < 0.05). Serum amylase, CRP, TNF-,, IL-2, and IL-8 levels were similar between IPN and SPN groups (P > 0.05), but higher than in other groups. The results of histological evaluation also correlated with the advent of the disease. Conclusion: Procalcitonin and IL-6 acts as reliable acute phase reactant in an experimental model of AEP, SPN and IPN in the rat. PCT and IL-6 combination might be surrogate marker of infected pancreatic necrosis and should be preferred to other markers assay especially in severe pancreatitis. [source]

Type 2 diabetes mellitus: a disease of the innate immune system?

The PPAR, agonist GW501516 suppresses interleukin-6-mediated hepatocyte acute phase reaction via STAT3 inhibition

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2007
T. Kino
Abstract Background, Interleukin-6 and downstream liver effectors acute phase reactants are implicated in the systemic inflammatory reaction. Peroxisome proliferator-activated receptor , (PPAR,), which binds to and is activated by a variety of fatty acids, was recently shown to have anti-inflammatory actions. Materials and methods, We examined the ability of the synthetic PPAR, agonist GW501516 to suppress interleukin-6-induced expression of acute phase proteins in human hepatoma HepG2 cells and rat primary hepatocytes. Results, GW501516 dose-dependently suppressed interleukin-6-induced mRNA expression of the acute phase protein ,1-antichymotrypsin in HepG2 cells. The compound also suppressed interleukin-6-induced mRNA expression of ,2-acid glycoprotein, ,-fibrinogen and ,2-macroglobulin in and the secretion of C-reactive protein by rat primary hepatocytes. Depletion of the PPAR, receptor, but not of PPAR, or ,, attenuated the suppressive effect of GW501516 on interleukin-6-induced ,1-antichymotrypsin mRNA expression, indicating that PPAR, specifically mediated this effect. Since interleukin-6 stimulates the transcriptional activity of the ,1-antichymotrypsin promoter by activating the signal transducer and activator of transcription (STAT) 3, we examined functional interaction of this transcription factor and PPAR, on this promoter. Overexpression of PPAR, enhanced the suppressive effect of GW501516 on STAT3-activated transcriptional activity of the ,1-antichymotrypsin promoter, while GW501516 suppressed interleukin-6-induced binding of this transcription factor to this promoter. Conclusions, These findings indicate that agonist-activated PPAR, interferes with interleukin-6-induced acute phase reaction in the liver by inhibiting the transcriptional activity of STAT3. PPAR, agonists might be useful for the suppression of systemic inflammatory reactions in which IL-6 plays a central role. [source]

Clinical features of renal cell carcinoma less than 25 millimeters in diameter

INTERNATIONAL JOURNAL OF UROLOGY, Issue 12 2002
YOSHIAKI YAMADA
Abstract Background: We retrospectively investigated the clinicopathological features and prognosis of patients who underwent surgical treatment at our department for renal cell carcinoma (RCC) less than 25 mm in diameter. Methods: Of the 158 patients who underwent surgical treatment between April 1975 and April 1998, 16 (17 kidney, 10.1%) were included in this study. The study included 11 men and 5 women (ratio: 2.2). The age range was 35,76 years (average: age 53). The right kidney was involved in 9, left kidney in 6 and bilateral kidneys in 1 patient. The follow-up period was 26,157 months (mean: 86 months). Results: Thirteen tumors (81.2%) were incidental carcinomas. No patients had a tumor of rapid growing type. Radical nephrectomy was performed for 12 kidneys (70.6%), simple nephrectomy for 2 (11.8%) and partial nephrectomy for 3 (17.8%). Seven patients (43.7%) received interferon-, as postoperative adjuvant therapy. All tumors were pathologically classified as expansive type; 11 (64.8%) as clear cell carcinoma; 3 (17.6%) cyst-associated, and 3 (17.6%) papillary. Nine (52.9%) tumors were grade 1, and 8 (47.1%) were grade 2. Fourteen patients were pNo and V(,). The 5- and 10-year survival rates were excellent (100%). Conclusion: The features of small RCCs less than 25 mm were as follows: many tumors were incidental to clear cell carcinomas; all tumors were low grade, low stage and expansive type; no tumors showed acute phase reactants; and few tumors were of the solid type. Thus, the prognosis seemed to be excellent. [source]

Serum YKL-40 as a marker of disease activity and stricture formation in patients with Crohn's disease

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8pt2 2008
Yusuf Erzin
Abstract Background and Aim:, YKL-40 is secreted by macrophages and neutrophils and is a growth factor for vascular endothelial cells and fibroblasts. Elevated serum levels of YKL-40 have been reported in patients with various inflammatory conditions and ongoing fibrosis. The aim of this study was to investigate the relationship between serum concentrations of YKL-40 and disease activity, acute phase reactants, and the presence of strictures in patients with Crohn's disease (CD). Methods:, We studied the serum concentrations of YKL-40 in 41 patients with CD, in which 12 had an endoscopically- or radiologically-proven stricture formation. Forty-six age- and sex-matched healthy volunteers served as controls and a multivariate regression analysis was performed to find out the independent predictors of intestinal strictures and clinical activity. Results:, The serum YKL-40 concentrations in the patients were significantly higher than that in the healthy controls (105.69 ± 88.08 ng/mL [range 20.23,333.57]vs 44.92 ± 24.89 ng/mL [range 18.31,113.43], P = 0.000) and patients with a stricture formation had significantly higher YKL-40 levels than those without strictures (167.50 ± 119.30 ng/mL [range 23.62,333.57]vs 80.12 ± 56.38 ng/mL [range 20.23,259.19], P = 0.003). Significant correlations were noted between YKL-40 levels and clinical activity (r = 0.681; P = 0.000) and the presence of intestinal strictures (r = 0.457; P = 0.003). The multivariate regression analysis found the serum YKL-40 levels to be an independent predictor of intestinal strictures (P = 0.001) and clinical activity (P = 0.001). Conclusion:, Patients with CD, particularly those with a stricture formation, have significantly higher levels of YKL-40. YKL-40 seems to be a useful marker of disease activity as well as stricture formation in patients with CD. [source]

Serum Amyloid A and Haptoglobin Concentrations and Liver Fat Percentage in Lactating Dairy Cows with Abomasal Displacement

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010
H. Guzelbektes
Background: There has been increased interest in measuring the serum concentration of acute phase reactants such as serum amyloid A [SAA] and haptoglobin [haptoglobin] in periparturient cattle in order to provide a method for detecting the presence of inflammation or bacterial infection. Objectives: To determine whether [SAA] and [haptoglobin] are increased in cows with displaced abomasum as compared with healthy dairy cows. Animals: Fifty-four adult dairy cows in early lactation that had left displaced abomasum (LDA, n = 34), right displaced abomasum or abomasal volvulus (RDA/AV, n = 11), or were healthy on physical examination (control, n = 9). Materials and Methods: Inflammatory diseases or bacterial infections such as mastitis, metritis, or pneumonia were not clinically apparent in any animal. Jugular venous blood was obtained from all cows and analyzed. Liver samples were obtained by biopsy in cattle with abomasal displacement. Results: [SAA] and [haptoglobin] concentrations were increased in cows with LDA or RDA/AV as compared with healthy controls. Cows with displaced abomasum had mild to moderate hepatic lipidosis, based on liver fat percentages of 9.3 ± 5.3% (mean ± SD, LDA) and 10.8 ± 7.7% (RDA/AV). [SAA] and [haptoglobin] were most strongly associated with liver fat percentage, rs=+0.55 (P < .0001) and rs=+0.42 (P= .0041), respectively. Conclusions and Clinical Importance: An increase in [SAA] or [haptoglobin] in postparturient dairy cows with LDA or RDA/AV is not specific for inflammation or bacterial infection. An increase in [SAA] or [haptoglobin] may indicate the presence of hepatic lipidosis in cattle with abomasal displacement. [source]

Primate models in women's health: inflammation and atherogenesis in female cynomolgus macaques (Macaca fascicularis)

AMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009
Thomas C. Register
Abstract Female cynomolgus monkeys are excellent models for understanding cardiovascular disease and the relationships between inflammatory processes and conditions such as atherogenesis. This review summarizes published research findings obtained through comprehensive, multidisciplinary, multi-investigator studies in nonhuman primates over the past two decades. These studies examined the effects of exogenous estrogens and dietary soy protein/isoflavones (IFs) on atherosclerosis, circulating biomarkers, and tissue inflammation in pre- and postmenopausal female cynomolgus monkeys. Inflammation may play a role in the initiation and progression of disease, be a consequence of the disease, or both. Circulating and tissue biomarkers with inflammatory and anti-inflammatory characteristics (including adhesion molecules such as e-selectin, VCAM-1, and ICAM-1, chemokines such as MCP-1, cytokines such as interleukins, and acute phase reactants such as CRP, and others) may be useful indicators of disease status. Treatment of postmenopausal subjects with estrogen resulted in significant reductions in several key inflammatory mediators as well as atherosclerosis, while dietary IF had a more limited effect on inflammation and atherogenesis. Circulating concentrations of key inflammatory proteins, including monocyte-chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6), were associated with atherosclerosis and lesion characteristics in these animals. In premenopausal female monkeys, a diet enriched in soy protein reduced arterial inflammation as well as atherogenesis in comparison to a diet enriched in casein-lactalbumin. Expression levels of arterial inflammation associated genes (MCP-1, ICAM-1) and markers for inflammatory cell types (macrophages and T cells) correlated with plaque size, were differentially influenced by treatments, and represent potential targets for interventions. Arterial expression of estrogen receptor ,, the key mediator of estrogenic effects, was inversely correlated with plaque size and indices of inflammation, suggestive of an atheroprotective role. The findings provide additional evidence that circulating inflammatory markers (particularly MCP-1) may be useful indicators of atherosclerotic disease progression and responses to treatment in female primates, and that estrogens and dietary soy may inhibit atherogenesis in part through anti-inflammatory mechanisms. Am. J. Primatol. 71:766,775, 2009. © 2009 Wiley-Liss, Inc. [source]