Prognostic utility of serum neopterin in obstructive jaundice secondary to malignant lesions treated by percutaneous transhepatic biliary drainage.

PURPOSE: To perform biochemical profiles before and after percutaneous transhepatic biliary drainage (PTBD) and investigate the potential utility of measuring C-reactive protein (CRP), circulating cytokines, and neopterin, a marker of cell-mediated immunity, to predict outcomes of patients with obstructive jaundice. MATERIALS AND METHODS: In a prospective study, 47 patients with obstructive jaundice secondary to malignant lesions were evaluated before, at the fifth hour after, and on the fifth day after PTBD for neopterin, nitrate, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, CRP levels, and liver function. RESULTS: Neopterin levels on day 5 after PTBD were significantly higher than the levels before treatment and at the fifth hour. However, nitrate, cytokine, white blood cell, albumin, and creatinine levels were not significantly different. On the fifth day after PTBD, CRP levels were significantly higher and total bilirubin, direct bilirubin, alkaline phosphatase, aspartate transaminase, and alanine transaminase values were lower than the before-treatment values. Seven patients (15%) died within 30 days after drainage. On the fifth day after PTBD, neopterin, IL-6, IL-10, and creatinine levels were significantly higher and albumin levels were lower in the early mortality group. The performance characteristics of neopterin and creatinine were statistically significant in predicting mortality. CONCLUSIONS: Neopterin levels increased after PTBD, indicating cellular immune activation. The nonsignificant change in cytokine levels may be related to low enduring release in malignancy. The extremely elevated levels of neopterin and creatinine after PTBD might serve as harbingers of early death in patients with cholestasis secondary to malignant lesions.

Fibroblast growth factor-19 levels in type 2 diabetic patients with metabolic syndrome.

This study aimed to examine fibroblast growth factor-19 (FGF-19) in type 2 diabetic (T2DM) patients with metabolic syndrome (MetS) and to evaluate the relationship between FGF-19 and other cardiovascular risk factors, such as atherogenic index of plasma (AIP) and hsCRP. 26 T2DM patients with MetS and 12 healthy controls were enrolled in the study. Serum FGF-19 levels were measured by sandwich ELISA, and compared with other cardiovascular risk factors; lipid profile, AIP, glucose, HbA1c, and hsCRP. AIP was calculated as log (TG/HDL-c). The median (1-3.quartile) FGF-19 levels in T2DM patients with MetS and healthy controls were 122.90 (108.63-237.60) pg/ml and 293.45 (153.64-370.31) pg/ml, respectively (P=0.003). Patients were also grouped by body mass index (BMI) <30 kg/m(2) (n=13) and ≥30 kg/m(2) (n=13) with median (1-3.quartile) FGF-19 values 168.70 (113.54-275.77) pg/mL and 115.89 (97.94-200.40) pg/mL, respectively (P=0.007). Significant negative correlations were found between FGF-19 and BMI, triglyceride, log (TG/HDL-c), hsCRP, and HbA1c (r=-0.526, P=0.001; r=-0.327, P=0.05; r=-0.312, P=0.05; r=-0.435, P=0.006; r=-0.357, P=0.028, respectively). We showed that FGF-19 levels are low in T2DM patients with MetS. The negative relationship between FGF-19 and several known cardiovascular risk factors such as TG, log (TG/HDL-c), hsCRP and HbA1c in diabetic patients with MetS suggests that FGF-19 can be used as a contributing marker.

Effects of percutaneous transhepatic biliary drainage on renal function in patients with obstructive jaundice.

PURPOSE: We assessed the effects of percutaneous transhepatic biliary drainage on renal function in patients with obstructive jaundice using the estimated glomerular filtration rate (eGFR) and evaluated the factors associated with renal dysfunction. MATERIALS AND METHODS: Between July 2007 and September 2009, 108 consecutive patients (69 men 39 women; median age, 59 years; range, 29-87 years) with obstructive jaundice (20 benign, 88 malignant) that were unsuitable for endoscopic retrograde cholangiopancreticography were evaluated at admission and at follow-up exams five and thirty days after percutaneous transhepatic biliary drainage. Two patients with suspected contrast-induced nephropathy were excluded. Renal function was assessed by measuring levels of urea, creatinine and electrolytes and evaluating the modification of diet in the renal disease formula for eGFR. RESULTS: eGFR was < 60 mL/min/1.73 m2 before percutaneous transhepatic biliary drainage in 27 patients (25%) and increased significantly 30 days after percutaneous transhepatic biliary drainage (P = 0.008). In the malignant external drainage subgroup, there was a significant increase in eGFR on the fifth day after percutaneous transhepatic biliary drainage (P = 0.038). The procedure-related mortality rate was zero. Nine malignant patients (8.49%) died within thirty days due to underlying diseases. On the fifth day, eGFR was significantly lower in these patients than in surviving patients (P = 0.049), and bilirubin levels were significantly higher before the intervention than in surviving patients (P = 0.04). Multiple logistic regression analysis showed that serum direct bilirubin is a significant predictor of renal function (P = 0.049). CONCLUSION: Obstructive jaundice is associated with renal dysfunction, and serum direct bilirubin is a significant predictor of renal function. Percutaneous transhepatic biliary drainage improves renal function and is crucial for prognosis of obstructive jaundice.

The detection of left ventricular diastolic dysfunction in hypertensive patients: Performance of N-terminal probrain natriuretic peptide.

AIM: Diastolic dysfunction (DD) results in increased cardiovascular risk in hypertensives. We studied the performance of N-terminal probrain natriuretic peptide (NT-proBNP) in detecting DD. MATERIALS AND METHODS: 241 hypertensive patients admitted to cardiology polyclinics were included in this study. They were grouped according to the presence of DD. Group 1: Essential hypertensive patients without DD (n= 119); group 2: essential hypertensive patients with DD (n= 122). All underwent trans-thoracic echocardiography for the evaluation of transvalvular flow, morphology, left ventricular wall motion abnormalities and ejection fraction. NT-proBNP levels were measured by an electrochemiluminescence immunoassay. RESULTS: The systolic blood pressure (BP) (mean+/-SD) was 140+/-12 mmHg in group 1 and 144+/-16 mmHg in group 2 (p=0.049), the diastolic BP (mean+/-SD) was 88+/-10 mmHg in group 1 and 90+/-14 mmHg in group 2 (p=0.043). The median (1st-3rd quartile) NT-proBNP level in group 2 was significantly higher than group 1 [121.05 (61.03-207.66) and 31.17 (17.07-54.09) pg/ml, respectively (p<0.001)]. In the receiver operating characteristics analysis, the area under the curve was 0.862 (95% CI 0.816-0.908). At the cut-off of 45 pg/ml, sensitivity was 86.9%, specificity was 62.4%, and at the cut-off 65 pg/ml, sensitivity was 74.6%, specificity was 83.8%. CONCLUSION: Plasma NT-proBNP levels may be useful for identifying patients with DD and it is conceivable to use a cut-off level 65 pg/ml as a "rule in" test.

Pleural fluid neopterin levels in tuberculous pleurisy.

OBJECTIVES: Neopterin is produced by stimulated macrophages under the influence of gamma interferon of lymphocyte origin. It is regarded as a biochemical marker of cell-mediated immune response. This study was designed to assess the diagnostic value of pleural fluid neopterin levels in tuberculous pleurisy in comparison with adenosine deaminase activity. DESIGN AND METHODS: Pleural fluid adenosine deaminase (ADA) activity and neopterin levels were measured in 16 patients with tuberculous pleurisy (TP) and 19 patients with malignant pleurisy (MP). ADA activity was determined by a colorimetric method, whereas neopterin levels were determined by a reversed-phase liquid chromatography technique. All values were given as median (min-max). RESULTS: The mean age was 45.43+/-20.39 years in the TP group and 60.42+/-11.02 years in the MP group (p=0.026). The median pleural fluid ADA activity was 51.75 U/L (3.50-62.40 U/L) in the TP group and was 2.30 U/L (1-8.20 U/L) in the MP group. The difference was statistically significant (p<0.001). The median pleural fluid neopterin levels were 13.15 nmol/L (1.86-59.50 nmol/L) and 2.44 nmol/L (0.92-27.60 nmol/L) in the TP group and the MP group, respectively (p=0.021). In order to evaluate the diagnostic value of pleural fluid neopterin concentrations, receiver-operating-characteristic curve analysis was performed. CONCLUSION: Pleural fluid neopterin concentration is significantly higher in TP when compared to MP, however when compared, its clinical use as a diagnostic marker is not valuable as ADA.

Serum N-terminal-pro-B-type natriuretic peptide (NT-pro-BNP) levels in hyperthyroidism and hypothyroidism.

E Natriuretic peptides represent a novel diagnostic tool in the assessment of heart failure. N-terminal-pro-B-type natriuretic peptide (NT-proBNP), a member of the natriuretic peptid family, is produced and released from cardiac ventricles. Changes in cardiac functions are observed in thyroid dysfunctions. The aim of this study was to assess the changes in serum NT-proBNP levels and to evaluate impact of thyroid hormones on serum NT-proBNP in patients with hyperthyroidism and hypothyroidism. Serum NT-proBNP levels were measured in 21 patients with hyperthyroidism and in 24 patients with hypothyroidism and compared with 20 healthy control subjects. Patients without cardiac disease were included into the study as well. Serum NT-proBNP levels were measured by electrochemiluminescence immunoassay. Serum NT-proBNP levels were higher in hyperthyroid patients than in hypothyroid patients and in control subjects, with mean values of 239.03 +/- 47.33, 45.97 +/- 13.48, 55.57 +/- 13.01 pg/ml, respectively (p < 0.0001). Serum NT-proBNP and thyroid hormones were correlated in all patients. Moreover, there was a significant positive correlation between serum NT-proBNP and serum free T4 (FT4) levels (r = 0.549, p = 0.012) in hyperthyroidic patients. Multiple regression analyses demonstrated that increasing FT4 was independently associated with a high serum NT-proBNP levels, whereas heart rate was not in hyperthyroid patients. Serum NT-proBNP levels are higher in the hyperthyroid state as compared with the hypothyroid and euthyroid state. Thyroid dysfunction affects serum NT-proBNP levels, possibly influencing the secretion of the peptide. Therefore, thyroid function has to be considered when evaluating high serum NT-proBNP levels in patients without cardiac dysfunction.

Increased serum neopterin levels in women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) occurs in 5-10% of premenopausal women. Studies suggest that PCOS is associated with increased risk of coronary heart disease (CHD). To investigate this relationship, 15 PCOS women (group 1) and 10 healthy women (group 2) were studied. Blood leukocyte counts (white blood cells, WBC) and serum levels of total cholesterol, HDL-cholesterol, LDL-cholesterol, sensitive C-reactive protein (sCRP), and neopterin were measured in the 2 groups. There were no significant differences in serum total cholesterol, HDL-cholesterol, or LDL-cholesterol concentrations between groups 1 and 2. Blood WBC counts and serum levels of neopterin and sCRP were significantly higher in group 1 than group 2. The median (min-max) levels were: WBC, group 1: 8.05 (5.10-9.70) cells x 10(9)/L, group 2: 6.25 (4.70-9.70) cells x 10(9)/L (p <0.01); neopterin, group 1: 10.6 (7.5-49.5) nmol/L, group 2: 9.6 (6.5-12.9) nmol/L (p < 0.05); and sCRP, group 1: 7.0 (1.2-12.0) mg/L, group 2: 2.0 (0.1-12.0) mg/L (p <0.01). This study shows that blood WBC counts and serum sCRP and neopterin levels are significantly elevated in women with PCOS. These findings support an increased risk for early-onset cardiovascular disease in women with PCOS. This is the first report that women with PCOS have higher serum neopterin levels than healthy women with regular menstrual cycles.

Impact of renal function or folate status on altered plasma homocysteine levels in hypothyroidism.

Hyperhomocysteinemia is an independent risk factor for coronary, peripheral and cerebrovascular diseases. Moderately elevated total homocysteine (tHcy) levels have been reported in patients with overt hypothyroidism. Plasma tHcy concentration is affected by several physiological factors and is elevated under conditions of impaired folate and cobalamin status and in renal failure. The aim of this study was to assess plasma tHcy concentrations and to evaluate the role of potential determinants of plasma tHcy levels in hypothyroid patients. Fasting plasma tHcy, serum homocysteine-related vitamins folate and vitamin B(12), serum cystatin C (CysC) and creatinine, were determined in 22 hypothyroid patients and compared with 25 healthy control subjects. Creatinine clearance (CCr) was calculated using the Cockroft-Gault formula. Plasma tHcy levels were determined by HPLC with fluorescence detection and serum CysC by automated particle enhanced immunoturbidimetry. Plasma tHcy, creatinine levels were significantly higher, and serum CysC levels, and creatinine clearance values were lower in hypothyroid patients than in control subjects. Folate levels were lower in hypothyroidic group compared to the control group. There were no differences in vitamin B(12) levels between hypothyroid and control groups. Positive correlation was noted between tHcy and creatinine levels in hypothyroid patients (r = 0.596); however, an inverse correlation was found between tHcy and folate levels (r = -0.705) in hypothyroid patients. In conclusion, tHcy was increased in hypothyroidism, and this increase was more strongly associated with changes in serum folate than in serum creatinine and CysC, suggesting an altered folate status.

Treatment and prophylaxis with sucralfate ameliorates hypoxia/reoxygenation-induced intestinal injury in pup rats.

BACKGROUND: Sucralfate is widely used as a cytoprotective agent in patients with peptic ulcer and other intestinal mucosal injury. The aim of this study is to investigate whether sucralfate has any effect on the prevention and treatment of hypoxia/reoxygenation-induced intestinal injury. MATERIAL/METHODS: Four groups of 10 1-day-old rat pups were studied. Hypoxia/reoxygenation (H/O)-induced intestinal injury was created. Group 1 was subjected to H/O just after birth and sacrificed at the end of the third day (Treatment Control). Group 2 was subjected to H/O just after birth and treated with sucralfate for 3 days. They were sacrificed at the end of the third day (Treatment). Group 3 was subjected to H/O on the third day after birth and then sacrificed (Prophylaxis Control). Group 4 was treated with sucralfate for the first 3 days, then H/O was created. Just after H/O, the pups were sacrificed (Prophylaxis). The intestinal tissues were harvested for histopathological investigation. Malondialdehyde (MDA) levels in the intestinal tissues were determined. RESULTS: The mucosal injury grades of the treatment and prophylaxis groups were significantly lower than those of control groups (p<0.05). The mean MDA level in the treatment and prophylaxis groups were 0.42+/-0.17 and 0.21+/-0.23 nmol/mg respectively. The MDA levels of both groups were significantly lower than in the control groups (p<0.05). CONCLUSIONS: The present study shows that sucralfate has beneficial effects in an experimental model of hypoxia/reoxygenation-induced intestinal injury.

Effects of L-arginine and L-carnitine in hypoxia/reoxygenation-induced intestinal injury.

BACKGROUND: This study was designed to show the role of oxidative stress, nitric oxide and glutathione-related antioxidant enzymes in hypoxia/reoxygenation (H/R)-induced intestinal injury model in mice and to evaluate the potential benefits of arginine and carnitine supplementation. METHODS: A total of 28 young Balb/c mice were divided into four groups: Group 1 (untreated) was given physiological saline before the experiment; group 2 H/R mice were supplemented with L-arginine; group 3 H/R mice were given L-carnitine for 7 days; and group 4 mice served as controls. At the end of day 7, H/R injury was induced and intestinal tissue malondialdehyde (MDA), nitrate levels and glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase (GST) activities were measured. RESULTS: MDA levels were higher in the untreated animals than in the other three groups. MDA levels were higher in the L-arginine-treated animals than in the L-carnitine-treated animals. Nitrate levels were found to be increased in the L-arginine-treated group when compared to the controls. GSH-Px and GR activities were increased in the untreated, the L-arginine and the L-carnitine-treated H/R groups when compared to the control group. GST activities were indifferent between the groups. CONCLUSIONS: Oxidative stress contributes to the pathogenesis of H/R-induced intestinal injury. The glutathione redox cycle may have a crucial role in the H/R-induced intestinal injury. L-arginine and L-carnitine supplementations ameliorate the histological evidence of H/R-induced intestinal injury and decrease lipid peroxidation but do not alter the glutathione-related antioxidant enzyme activities.

Amlodipine and glutathione cycle in hypercholesterolaemia.

OBJECTIVE: Effects of amlodipine on lipid peroxidation and alterations in glutathione and related enzymes in blood and aortic tissue were investigated in a cholesterol-induced atherosclerotic rabbit model. METHODS AND RESULTS: New Zealand white male rabbits were fed with regular chow (group I), chow supplemented with I% cholesterol (group II), regular chow plus amlodipine 5 mg/kg/day p.o. (group III) and I% cholesterol diet supplemented with amlodipine (group IV) for 8 weeks. Cholesterol, malondialdehyde (MDA), reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione peroxidase (GSH-PX) and glutathione reductase (GSH-Rd) were determined in blood samples drawn before and after the experimental period. Aortic tissue was examined morphologically for atherosclerotic changes and tissue cholesterol, MDA, GSSG, GSH-PX, GSH-Rd and glutathione-S-transferase (GST) were measured. After 8 weeks, blood cholesterol, MDA, GSSG and GSH-PX were elevated in groups II and IV; GSH was reduced in group IV; MDA levels were higher in group II than in group IV. Aortic tissue investigations revealed higher cholesterol and MDA concentrations in group II than in group IV. Morphological examination of aortic tissues exhibited endothelial disarrangement and lipid deposition in group II. Histopathological alterations related to atherogenesis were less in group IV than in group II. CONCLUSIONS: Amlodipine reduced the increase in oxidative stress by inhibiting excessive MDA production. Accelerated glutathione redox cycle activity of erythrocytes from animals supplemented with amlodipine suggests that this drug may reduce oxidative stress by enhancing the glutathione system. However, this drug does not seem to affect the glutathione redox cycle in the aortic tissue.

Association between serum paraoxonase activity and oxidative stress in acute coronary syndromes.

OBJECTIVE: The oxidation of low-density lipoprotein (LDL) is believed to have a central role in atherogenesis. Under oxidative stress not only LDL, but all other serum lipids are exposed to oxidation. High-density lipoprotein (HDL)-associated paraoxonase (PON1) was shown to inhibit LDL and HDL oxidation. We investigated the relationship between PON1 and oxidative stress in acute myocardial infarction and unstable angina in a comparative fashion. METHODS AND RESULTS: Activities of PON1, concentrations of malondialdehyde (MDA), lipids and lipoproteins were measured in patients (38 subjects with acute myocardial infarction and 33 subjects with unstable angina pectoris) and in age- and sex-matched controls (32 subjects). Serum PONI activity was significantly lower in patients than in controls (p < 0.001). Patients had significantly increased serum MDA concentrations (p < 0.001) and there were strong negative correlations (p < 0.001) between serum PON1 and MDA levels in the acute myocardial infarction group (r = -0.673), in the unstable angina pectoris group (r = -0.868) and in healthy controls (r = -0.778). Serum HDL-cholesterol (HDL-C) concentrations were lower in patients than controls (p < 0.05). No correlation was observed between PON1 and HDL-C levels in patients or controls. Apo A I concentrations were significantly lower in the patient groups (p < 0.01), but were insignificant between patients with AMI and UAP. Apo A-I and PON1 levels did not show any correlation. Apo B concentrations were lowest in the healthy controls, higher in the UAPgroup and highest in the AMI group (p < 0.001). In the acute myocardial infarction group LDL/apo B ratio was lower than in healthy controls and in the UAP group, suggesting smaller LDL particle size. CONCLUSIONS: Results of this study indicate that lower serum PON1 activity is associated with oxidative stress and the activity of PON1 is not related to HDL-cholesterol.

Serum and urinary nitric oxide in Type 2 diabetes with or without microalbuminuria: relation to glomerular hyperfiltration.

BACKGROUND: Glomerular hyperfiltration is considered as one of the pathophysiological mechanisms for the development of diabetic nephropathy. Oxidative stress is enhanced in patients with diabetes mellitus. Reportedly, nitric oxide (NO) might be involved in the pathogenesis of hyperfiltration. We investigated the relationship between hyperfiltration and NO system, and malondialdehyde (MDA) levels in Type 2 diabetics with/without microalbuminuria. METHODS: In 39 microalbuminuric, 29 normoalbuminuric Type 2 diabetic patients and 32 healthy controls, serum creatinine, nitrite, nitrate, urinary microalbumin, nitrite, nitrate, plasma MDA and estimated glomerular filtration rate (EGFR) values, calculated according to the Cockcroft and Gault formula, were recorded. RESULTS: Serum and urine NO levels were higher in both microalbuminurics and normoalbuminurics than controls. There were no significant differences in EGFR between groups. However, hyperfiltration was determined in 31% of normoalbuminurics and 20% of microalbuminurics. Serum and urine NO levels were higher in patients with hyperfiltration. Plasma MDA levels were significantly elevated in both microalbuminurics and normoalbuminurics when compared with controls. Serum glucose and microalbuminuria were positively correlated in microalbuminuric diabetics. Serum NO levels were also positively correlated with EGFR in both normoalbuminurics and microalbuminurics. HbA1c levels were positively correlated with both urinary albumin excretion and plasma MDA levels in normoalbuminuric diabetics. CONCLUSIONS: Hyperglycemia is associated with an increased NO biosynthesis and lipid peroxidation. Increased oxidative stress may contribute to the high NO levels in Type 2 diabetes. Furthermore, the high NO levels may lead to hyperfiltration and hyperperfusion, which in turn leads to an increase in urinary albumin excretion and thus causes progression of nephropathy in early Type 2 diabetes.

Increased excretions of glycosaminoglycans and heparan sulfate in lupus nephritis and rheumatoid arthritis.

Urinary glycosaminoglycans (GAG) and heparan sulfate (HS) are considered to be markers of early renal involvement. This study was undertaken to demonstrate their excretion patterns in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) with and without arthritis. Serum creatinine and urinary GAG, HS, microalbumin, and creatinine measurements were made in 51 biopsy-proven lupus nephritis (LN) cases, 12 RA patients, and 21 healthy controls. Urinary GAG and HS levels were higher in the LN and RA groups than in controls. Heparan sulfate excretions and SLE disease activity index (SLEDAI) scores were no different between SLE patients with classes 1 and 2 (group A) and those with classes 3, 4, and 5 (group B) renal involvement. However, GAG and microalbumin excretions were significantly high in the latter. There were no differences in GAG and HS excretions between normoalbuminuric, microalbuminuric, and macroproteinuric SLE patients or between those with and without arthritis. In conclusion, urinary GAG and HS, being unrelated to the presence of arthritis, are independent markers of LN. Extrarenal causes or subclinical renal involvement may be responsible in RA due to their increased excretion in these patients.

Nitric oxide and oxidative stress in atherosclerotic renovascular hypertension: effect of endovascular treatment.

PURPOSE: Because activation of the renin-angiotensin system leads to an increase in oxidative stress, the authors investigated nitric oxide (NO; nitrite + nitrate), superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) levels and the effect of endovascular treatment on these parameters in patients with atherosclerotic renovascular hypertension. The relationship of NO with blood pressure and renal functional indexes was also investigated. MATERIALS AND METHODS: In this prospective cohort study, serum creatinine, NO, SOD, catalase, plasma MDA, urinary microalbumin, and NO levels, and blood pressure were determined in 21 patients with hypertension and unilateral renal artery stenosis caused by atherosclerosis at entry and after 24 hours, 2 weeks, and 6 weeks of endovascular treatment. RESULTS: MDA concentrations decreased 24 hours after intervention and remained low 2 and 6 weeks later. In addition, serum SOD and NO and urine NO levels were increased significantly 24 hours after endovascular treatment and decreased after 2 and 6 weeks. However, serum catalase levels did not differ after the intervention. Blood pressures decreased after treatment. There were no significant differences in urinary microalbumin levels, estimated glomerular filtration rates, and creatinine levels after endovascular treatment. CONCLUSIONS: Endovascular treatment decreases oxidative stress and may offer new benefits in the treatment of patients with hypertension associated with renal artery stenosis. The decrease in oxidative stress and/or the upregulation of SOD may increase the bioavailability of NO, which in turn may lead to the rapid hypotensive response.

Comparison of the effects of dietary saturated, mono-, and n-6 polyunsaturated fatty acids on blood lipid profile, oxidant stress, prostanoid synthesis and aortic histology in rabbits.

BACKGROUND/AIMS: To compare the effects of saturated, monounsaturated and polyunsaturated n-6 fatty acid-enriched diets on the development of atherosclerosis and thrombosis in New Zealand white male rabbits, 3- to 6-month-old animals were supplemented daily (10 g/100 g diet) with butter (n = 8), olive oil (n = 8) or corn oil (n = 8) by oral administration for 7 weeks. METHODS: Total cholesterol (TC), HDL- (HDL-C) and LDL-cholesterol (LDL-C), triglycerides (TG), apolipoprotein A-1 (ApoA-1), apolipoprotein B (ApoB), lipid peroxides as thiobarbituric acid-reactive substances (TBARS), thromboxane B2 (TXB2) and 6-ketoprostaglandin F(1alpha) (6-ketoPGF(1alpha)) concentrations were determined in blood samples drawn before and after each group was fed the different dietary regimens. Histological examination was performed on the aortic tissues. RESULTS: After 7 weeks, TC, ApoB and TXB2 increased significantly (p < 0.05) in the butter-fed animals compared to pre-experimental concentrations. Olive oil administration lead to a significant (p < 0.05) decrease in TC and ApoB levels. The corn oil-enriched diet decreased TC, LDL-C concentrations, TC/HDL-C ratios and 6-ketoPGF(1alpha) (stable metabolite of prostacyclin-PGI2; p < 0.05 for all) but increased TBARS levels and TXB2/6-ketoPGF(1alpha) ratios. Light microscopic findings were in accordance with these biochemical alterations. CONCLUSION: Although effective in lipid lowering, corn oil increased oxidant stress as evidenced by increased TBARS and induced endothelial damage which lead to a reduction in PGI2 synthesis and consequently to an increase in the TXB2/6-ketoPGF(1alpha) ratio. Olive oil administration did not induce oxidant stress and it had no affect on PGI2 and TXB2 levels which are implicated in platelet aggregation. These findings suggest that oleic acid is more effective than linoleic acid in the protection of endothelial integrity.

Effect of endovascular treatment on nitric oxide and renal function in Takayasu's arteritis with renovascular hypertension.

BACKGROUND: Renal involvement in Takayasu's arteritis (TA) effects the disease outcome and endovascular treatment is an effective treatment of choice. We investigated nitric oxide (NO) levels and the effect of endovascular treatment in renovascular hypertensive TA patients. METHODS: In five hypertensive patients with renal artery stenosis due to TA, serum creatinine, nitrite, nitrate; urinary microalbumin, nitrite, nitrate measurements and blood pressures were recorded at entry and after 24 h and 6 weeks of endovascular treatment. RESULTS: Serum NO levels were higher in patients than controls (p = 0.008). Serum and urine NO levels increased 24 h after the treatment and decreased after 6 weeks (p = 0.015; p = 0.01, respectively). After the treatment blood pressures decreased. Urinary microalbumin excretions increased after the intervention (p = 0.02) and returned to normal in patients 1 and 4, and decreased in the others. There were no significant differences in estimated glomerular filtration rate (EGFR), serum creatinine, urinary sodium and potassium levels. CONCLUSION: Increased NO secretion in these patients may contribute to improve the prognosis of renal function through its vasodilator and antiproliferative activities possibly by counterbalancing the excessive vasoconstrictor actions. Endovascular treatment causes a dilatation-induced shear stress that may be responsible for the increased NO release, which in turn leads to the rapid hypotensive response.