Preexisting renal failure diminishes the excretion of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP), therefore limits the diagnostic value of this peptide for concomitant heart failure. The aim of this study was to evaluate the association between NT-proBNP and the stages of renal dysfunction in a typical population attended to emergency department with acute dyspnea.In this cross-sectional study, all consecutive patients with acute dyspnea underwent clinical evaluation, laboratory assessment of NT-proBNP, and echocardiographic examinations. Among subjects, 54.5% were diagnosed as heart failure. Grouping variables according to renal function capacity and ejection fraction, independent variables were compared with Kruskal-Wallis or ANOVA with posthoc tests. Correlation and linear regression analysis were done to analyze the variables associated with NT-proBNP. The diagnostic performance of NT-proBNP was evaluated by receiver-operating characteristic (ROC) curve.Serum median NT-proBNP level in patients with severe renal impairment was significantly higher than moderate and mildly decreased renal functions (p=0.001). In patients with moderate and severe left ventricular failure, NT-proBNP was significantly higher compared with normal subjects (LVEF>50%) (p=0.040, and 0.017, respectively). Renal dysfunction was associated in 56% of patients with heart failure. The area under the ROC curve of NT-proBNP for identifying left ventricular failure in patients with renal failure (eGFR<90 mL/min/1.73 m2) was 0.649 and reached significant difference (95% CI:0.548-0.749, p=0.005).In addition to NT-proBNP measurement in clinical judgement of heart failure, renal functions have to be taken into consideration to avoid misdiagnosis.
It is well known that necrotizing enterocolitis (NEC) is less frequent in newborns being fed human breast milk. Since recent studies indicated that platelet-activating factor (PAF) plays an important role in pathogenesis of NEC, this study was conducted to investigate the PAF levels in human milk. Colostrum and mature human milk (samples obtained in the third week) of three groups of mothers were investigated. The first group had given birth within less than 32 weeks, the second between 33-37 weeks and the third group after 38 weeks of gestation. The PAF levels in colostrum of all three groups were similar (0.95 +/- 0.57, 1.05 +/- 0.52 and 1.19 +/- 0.64 ng/ml, respectively). Mature human milk in groups I and II had similar PAF levels (1.16 +/- 0.54 and 1.21 +/- 0.60 ng/ml, respectively), however, mature human milk in group III had a significantly higher PAF concentration (2.04 +/- 0.59 ng/ml) than both groups' levels. However, this phenomenon by itself does not explain the protective effect of human milk against NEC.
The aim was to reveal the mechanism of hemolysis-induced acute pancreatitis and to evaluate the role of heme and heme oxygenase activity in inducing pancreatic inflammation in an experimental hemolysis model.Hemolytic anemia was induced in rats by intraperitoneal injection of 60 mg/kg acetylphenylhydrazine (APH). To evaluate the toxic effect of free heme after hemolysis, heme oxygenase inhibitor (HOI) was used to inhibit the enzyme which decreases the free heme concentration after hemolysis. One hundred and fifty rats were divided into two treatment and three control groups. Rats in the hemolysis group were given APH intraperitoneally. Rats in the HOI+hemolysis group were given Cr(III)mesoporphyrin IX chloride as HOI and then APH intraperitoneally. Serum amylase and lipase levels as well as pancreatic tissue cytokine content were determined and histological examination performed.No hemolysis or pancreatitis was seen in the control groups. Massive hemolysis was seen in 22 of the 30 rats of the hemolysis group and 20 of the 30 rats of the HOI+hemolysis group. The total pancreatitis rates were 60% and 76.6% in the hemolysis and HOI+hemolysis groups, respectively (p<0.05). Pancreatic cytokine levels were significantly higher in the HOI+hemolysis and hemolysis groups than in all control groups. The highest ICAM-1 and MCP-1 levels were in the HOI+hemolysis group. Histological signs of acute pancreatitis were also more severe in this group.Acute massive hemolysis can induce acute pancreatitis. Excess of free vascular heme seems to be an inducer of inflammation by modulating ICAM-1 and MCP-1.
Platelet activating factor (PAF) is synthesized and secreted by glomerular mesangial and endothelial cells. It increases glomerular basement membrane permeability and induces proteinuria. Leukotrienes (LT) are mediators released by either leukocytes or glomerular cells under the PAF effect. The possible role of PAF in steroid sensitive nephrotic syndrome (SSNS) of childhood was studied in 8 children with SSNS in the acute stage, 5 children in remission and 8 healthy controls. The PAF concentrations in urine and plasma were determined. Leukocytes were stimulated in vitro and the LT release in response to stimulation was determined. The urinary and plasma concentrations of PAF were significantly higher in the acute phase than in remission and in control patients. Children with SSNS were found to have peripheral leukocytes with increased LT releasing activity in vitro. These results are in accordance with clinical and experimental observations indicating that PAF originates in the kidney and plays a role in normal kidney physiology. Urinary PAF concentrations may be related to proteinuria because they were strongly correlated in the present study. Elevated plasma PAF concentrations in the acute stage of SSNS could result from either its secretion from the circulating leukocytes or decreased acetyl hidrolase activity needed for its hydrolysis in plasma. The increased LT release in vitro suggests that these cells might have been activated by PAF secreted from glomeruli. It is proposed that PAF and different LT in systemic and glomerular circulation are important mediators in childhood SSNS.
Platelet-activating factor, is a unique phospholipid with a broad range of biological activities that may be relevant in the development of inflammatory reactions. Platelet-activating factor has been suspected to play an important role in liver pathophysiology. The cultured Kupffer and endothelial cells produce and release platelet-activating factor in order to facilitate communication between hepatic sinusoidal and parenchymal cells. In this study, in the experimental jaundice model, platelet-activating factor levels were measured in liver tissue and plasma and the possible effects of mannitol on this mediator were assessed.The experimental model consisted of 7 rats in the control group (CG), 7 rats in the sham operation group (ShG), and 7 rats in the obstructive jaundice group (JG) created by ligating the common bile duct. The last group was the mannitol-treated jaundiced group (MJG) and all animals in this group received 20% mannitol in doses of 2 mL/day, intraperitoneally, following common bile duct ligation. A week later all animals were sacrificed and plasma and liver tissue samples were collected. Platelet-activating factor levels were measured by radioimmunoassay technique.Liver tissue platelet activating factor levels (pg/mg tissue protein) were 72 +/- 18 in the CG, 183 +/- 51 in the JG, 84 +/- 17 in ShG, and 124 +/- 36 in MJG. Plasma levels were 460 +/- 13, 1600 +/- 40, 560 +/- 19, and 1200 +/- 23, respectively. In both sample types, MJG and JG values were significantly different from CG and ShG as well. MJG levels were also different from JG.These results showed that plasma and liver tissue platelet-activating factor levels are increased in experimental obstructive jaundice; and activation of this mediator contributes to the ongoing liver injury. Mannitol may improve or lessen this damage.
Myocardial carnitine levels were measured in three groups of young mice. Group I (control group) consisted of 5 mice whose hearts were removed by a median thoracotomy without any previous asphyxia with a free carnitine levels of 15.4±0.89 µmol/mg heart tissue. Free carnitine level of Group II (5 mice subjected to asphyxia in airtight jars without any resuscitation later on and hearts were removed after death) was 6.8±1.48 µmol/mg heart tissue. Group III (7 mice recovered from asphyxia with resusciation) was found to a free carinitine level of 8.28±1.25 µmol/mg heart tissue. The statistical analysis revealed that Group II and Group III had similar values but both groups had lower levels of myocardial carnitine comparing to the control group (p
In this present study, we aimed: (i) To clarify if prediabetes is associated with subclinical inflammation independent of underlying obesity, and (ii) to evaluate the effect of postload glucose concentration on subclinical inflammation markers in a group of patients with elevated fasting glucose.In a cohort of 165 patients with newly detected fasting hyperglycemia, according to 75 g oral glucose tolerance test (OGTT), subjects were classified either as newly diagnosed type 2 diabetes (diabetes group, n = 40), impaired fasting glucose (IFG) plus impaired glucose tolerance (IGT) (IFG/IGT group, n = 42) or IFG only (IFG group, n = 83). A control group (n = 47) consisted of age- and body mass index (BMI)-matched healthy subjects with a normal OGTT. Circulating concentrations of lipids, insulin, interleukin-6 (IL-6), interleukin-8 (IL-8) and high sensitive C-reactive protein (hsCRP) were measured. HOMA index was calculated.Subclinical inflammation markers were elevated in patients with diabetes and IFG/IGT compared to healthy controls and also IFG patients (diabetes vs. control: p < 0.05 for hsCRP, IL-8, and IL-6; IFG/IGT vs. control: p < 0.05 for hsCRP, and IL-6; diabetes vs. IFG: p < 0.05 for hsCRP, and IL-6; IFG/IGT vs. IFG: p < 0.05 for hsCRP, and IL-6). In multiple regression analysis, postload glucose concentration was independently associated with circulating hsCRP and IL-6 concentrations when the data was controlled for age, gender, BMI and lipid concentrations (p < 0.05 for hsCRP, and IL-6).Our results suggest that patients with prediabetes, independent of underlying obesity, have increased concentrations of subclinical inflammation which is mostly driven by postload glucose concentrations.
Inflammatory lipid mediators, PAF and leukotrienes (LTs), are thought to have an important role in biocompatibility in hemodialysis. PAF, LTB4 and LTC4 were studied both in controls (n: 12) and in 11 children on regular hemodialysis (150 minutes) with cuprophane dialyzers. Blood samples were collected initially (0'-precapillary), at first minute (1'-postcapillary) and at one hour after the hemodialysis sessions (210'-venous). Presence of LTs and high levels of PAF in 0' samples compared to levels in controls and significant increases in 1' samples suggested the alterations in PAF and LTs likely originated from the peripheral leukocyte activation. In 210' samples, PAF and LTs levels were decreased but still higher than the levels in 0' samples. This study suggested that PAF and LTB4 may be the control elements in biocompatibility in hemodialysis with cuprophane membranes, and demonstrated that the effects of activation last until the following session.
Background: Leukotriene B 4 (LTB 4 ), a product of the lipoxygenase pathway of arachidonic acid metabolism, exhibits numerous activities that can account for most of the features of host responses seen in periodontal diseases. The aim of the present study was to examine the role of LTB 4 in the pathogenesis of specific periodontal diseases. Methods: LTB 4 levels were investigated in gingival crevicular fluid (GCF) and gingival tissue (GT) samples of 10 patients with chronic periodontitis (CP), 12 patients with generalized aggressive periodontitis (GAgP), 6 patients with localized aggressive periodontitis (LAgP), 6 patients with gingivitis (G), and 6 periodontally healthy subjects (H). Periodontal status was evaluated by measuring probing depth, gingival index, papillary bleeding index, and plaque index. LTB 4 was extracted from the samples by solid‐phase method using C 18 cartridge and was purified by high performance liquid chromatographic method and then analyzed by radioimmunoassay. Results: All patient groups had significantly higher levels of GCF and GT LTB 4 compared to the control group ( P <0.005). The CP patients had the highest LTB 4 levels compared to those in other patient groups ( P <0.005). GAgP, LAgP, and G groups had similar amounts of GCF and GT LTB 4 ( P >0.005). When the data were expressed as concentration, the CP group was found to have higher concentration of LTB 4 , compared to that of control group ( P <0.005). GAgP, LAgP, and G groups had similar LTB 4 concentration compared to that of control group ( P >0.005). No significant difference was found between GAgP, LAgP, and G groups ( P >0.005). The CP group had higher LTB 4 concentration compared to both GAgP and LAgP groups ( P <0.005). Although the CP group had a higher GCF LTB 4 concentration compared to G group, this difference did not reach significance ( P >0.005). No significant correlation was found between GCF and GT LTB 4 levels and clinical parameters. Conclusions: The results of the present study indicate that LTB 4 is likely to be an important mediator in regulating inflammatory responses in the human periodontal tissues. This lipid mediator may play an important role in the pathophysiology of periodontal disease. J Periodontol 2001;72:1025‐1031.
