The effect of mad honey on testosterone levels of male rats.

OBJECTIVE: We aimed to investigate the effect of mad honey on sexual performance. BACKGROUND: In traditional medicine in Turkey, mad honey is used to improve appetite, to heighten mental alertness, to reduce joint pain, to eliminate gastrointestinal system pains and to increase sexual performance. METHODS: In this experimental animal study eighteen Sprague Dawley male rats were randomized into three groups, a control group, a normal honey group and a mad honey group. Rats in the treatment groups were given a daily dose of 80 mg/kg normal honey or mad honey throughout the 30-day study period. Total testosterone, free testosterone, FSH, LH, estradiol, and progesterone levels were subsequently investigated from blood sera on day 30. RESULTS: Comparison of blood total testosterone levels among the groups revealed significantly higher levels in the mad honey group compared to the normal honey and control groups (p = 0.006, p = 0.00). Free testosterone levels were also significantly higher in the mad honey group than in the normal honey and control groups (p = 0.023, p = 0.01). No statistically significant differences were determined for other hormonal measurements. CONCLUSIONS: This study revealed a significant increase in both total and free testosterone levels in mad-honey group (Tab. 1, Fig. 2, Ref. 16).

Perspective on rhabdomyolysis-induced acute kidney injury and new treatment options.

AIM: The purpose of this study was to assess the role of caspase-dependent apoptosis, caspase 1, calpain 1, inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) and the protective effect of grape seed proanthocyanidin extract (GSPE) in the development of rhabdomyolysis-induced acute kidney injury (AKI). MATERIALS AND METHODS: Twenty-one rats were divided into 3 groups - control, rhabdomyolysis and rhabdomyolysis + GSPE. Rhabdomyolysis was induced in the rhabdomyolysis and rhabdomyolysis + GSPE groups with the injection into both hind limbs of 10 ml/kg hypertonic (50%) glycerol following 24-hour dehydration on the 6th day. The rhabdomyolysis + GSPE group was given GSPE at 100 mg/kg by gavage for 7 days. The experiment was concluded 48 h after glycerol injection. Blood specimens were collected, and kidney tissues were extracted for histopathological examination. RESULTS: We identified an increase in blood urea nitrogen, creatinine, histopathological score, iNOS, caspase 3, caspase 1 and calpain 1 expression in the rhabdomyolysis group compared to the controls and a decrease in eNOS expression. In the rhabdomyolysis + GSPE group, however, there was a decrease in these mediators, together with an increase in eNOS expression. CONCLUSION: This study shows for the first time in the literature that calpain 1 is involved in the pathogenesis of rhabdomyolysis-induced AKI, and that GSPE may have a renoprotective effect.

Lipoprotein-associated phospholipase A2 level in patients with Behçet's disease.

BACKGROUND: Behçet's disease (BD) is a chronic multisystem inflammatory disorder characterized by vasculitis. Vasculitis is thought to underlie many of the clinical manifestations of Behçet's disease. Lipoprotein-associated phospholipase A2 (Lp-PLA2 ) is a highly specific biomarker for vascular inflammation, and has low biological variability. Those features make it more attractive than other inflammatory markers including C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), which may reflect systemic inflammation non-specifically. OBJECTIVES: It was aimed to investigate circulating Lp-PLA2 levels and its relationship with CRP and ESR in patients with BD by considering disease activity. METHODS: Study group included 72 patients with BD (34 men and 38 women with a mean age of 35.3 years) and 30 sex- and age-matched healthy subjects (15 men and 15 women with a mean age 32.6 years). Patients group included 40 patients with active and 32 patients with inactive BD. RESULTS: Lp-PLA2 , CRP and ESR levels were found to be significantly higher in patient group than controls. In addition, those levels were also significantly higher in patients with active BD than in patients with inactive disease. Lp-PLA2 showed positive correlations with CRP and ESR (r = 0.63, P < 0.05 and r = 0.33, P < 0.05 respectively). Lp-PLA2 also showed significant important area under curve (AUC) value (0.779), besides CRP (0.941) and ESR (0.888). Optimum cut-off value was obtained as 218.5 ng/mL. CONCLUSIONS: It was concluded that Lp-PLA2 may be a new useful biomarker to evaluate clinical or subclinical activity of the disease besides CRP and ESR.

Increased ischemia-modified albumin levels in patients with gastric cancer.

Reactive oxygen species (ROS) are found in the development stages of carcinogenesis. Fifty two patients with gastric cancer and 35 controls were enrolled in this trial. IMA, MDA, Total Oxidant Status (TOS), Total Antioxidant Status (TAS) and Oxidative Stress Index (OSI) were evaluated. There was a significant increase in IMA and MDA levels in the patient group (0.405±0.111, 0.271±0.066; p= 0.0001 and 0.207±0.251, 0.077±0.103; p= 0.004 respectively). TOS was also higher in the patient group but it was not statistically different. TAS was statistically lower and there was significant difference in OSI (0.621±0.394, 0.996±0.37; p=0.0001 and 9.68±18.2, 2.9±3.85; p=0.001 respectively). The areas under receiver operating characteristics curves for the determination of gastric cancer were 0.842 for IMA and 0.708 for MDA. Increased levels of IMA, MDA and oxidative stress index were detected and this condition is associated with the impairment of oxidant-antioxidant balance.

Course of serum lipoprotein(a) and acute phase protein levels in patients undergoing open heart surgery.

BACKGROUND: Lipoprotein(a) [Lp(a)] is an important risk factor in the pathogenesis of coronary artery disease because of its thrombogenic and atherogenic properties. Lp(a) also displays another property by acting as an acute phase reactant. METHODS: In this work, the study group consisted of 20 male patients having coronary artery bypass under cardiopulmonary bypass (CPB). Preoperative and postoperative levels of plasma total cholesterol, triglyceride, apolipoprotein A1 (Apo A1), apolipoprotein B (Apo B), alpha-1 antitrypsin (a1-AT), alpha-2 macroglobulin (alpha 2-MG), alpha-1 acid glycoprotein (alpha 1-AG), Lp(a) were measured in all patients one day before and after the 1st, 2nd, 4th, and 10th days of CPB. RESULTS: It was observed that the levels of Lp(a) levels gradually reached the preoperative levels at the 10th postoperative day period. Observed change of the Lp(a) levels was similar to that of the other acute phase proteins which are synthesized and released from liver. In contrast, alpha 2-MG has shown different behaviour in terms of operative values. The changes observed for all these 3 parameters were found to be statistically significant (p<0.01). CONCLUSIONS: The data has indicated that Lp(a) levels show similar progress with alpha 2-MG levels. It can be concluded that serum levels of Lp(a) after coronary arterial bypass decrease depending upon several factors and reach basal levels at the end of a 10 day-period of postoperation. The main cause for this decrease might result from the contact of blood with foreign surfaces of the heart-lung machine.

Iron status and its relationship with lipid peroxidation in patients with acute myocardial infarction.

AIM: The aim of this study was to investigate iron status and its relationships with lipid peroxidation in patients with acute myocardial infarction (MI). METHODS: The study included 30 male patients aged between 32 and 73 years (mean 55 +/- 6) with acute MI. We measured the levels of plasma iron, transferrin (TF), ferritin (FER), ceruloplasmin (CER), cardiac enzymes, and erythrocyte malondialdehyde (e-MDA) in patients with acute MI on the admission and 1st, 3rd, 5th, 7th, 15th, 45th post MI day and investigated the variations of these parameters in acute MI. RESULTS: The e-MDA level started to increase on the admission day and showed a peak value on the post MI 1st day (88 +/- 23 and 98 +/- 26 nmol/g Hb, respectively). Afterwards, the e-MDA level minimally changed until post Ml 45th day, which showed a minimum level (57 +/- 13 nmol/g Hb) (p < 0.05). In addition, the iron concentration of serum reached its maximum level on the 1st post Ml day (99 +/- 30 mg/dl, p < 0.05) and relatively decreased after the 3rd day. Courses of MDA and iron levels were similar. The FER level started to increase from the admission day of the patients (230 +/- 375 mg/dl), showed a mean peak value on the 3rd day (296 +/- 568 mg/dl) and decreased to a minimum level on the 45th day (121 +/- 85 mg/dl) (p < 0.05). Contrarily, the TF level started to decrease on the 1st day (221 +/- 44 mg/dl), decreased minimum level on the 3rd day (211 +/- 37 mg/dl) and continued approximately the same level until the 45th day (244 +/- 45 mg/dl) (p < 0.05). The CER level started to increase from the first day of admission of the patients (43 +/- 12 mg/dl), reached a maximum level on the 7th day (59 +/- 12 mg/dl) and similar levels were observed until the 15th day. On the 45th day, the CER level was higher than on the first day (52 +/- 13 mg/dl) (p < 0.05). CONCLUSION: There was an association of higher iron status with increased lipid peroxidation in patients with myocardial infarction.

Decreased nitric oxide end-products and its relationship with high density lipoprotein and oxidative stress in people with type 2 diabetes without complications.

Diabetes mellitus is associated with hyperglycaemia, hyperlipoproteinaemia, increased oxidative stress and decreased nitric oxide production from endothelial cells. In the present study the aim was to determine the relationships between serum lipids, lipoproteins, erythrocyte malondialdehyde (eMDA), as a marker for oxidative stress, and serum nitrite and nitrate levels, as degradation products of nitric oxide in type 2 diabetic patients without complications. The study group included 30 patients and 30 sex- and age-matched healthy volunteers. Total cholesterol, triacylglycerol, LDL cholesterol, apo B, HbA(1c) and glucose levels in patients were significantly higher than in controls, and HDL cholesterol levels lower. Increased eMDA levels and decreased nitrate and nitrite+nitrate levels (+/-SD) were observed in patients compared to controls (87+/-22 vs 59+/-17 nmol/g-Hb (P<0.01); 11.8+/-8.6 vs 22.8+/-10.8 micromol/l (P<0.01); and 16.8+/-11.0 vs 28.8+/-11.3 micromol/l (P<0.01), respectively). When the patients were divided into two groups according to HDL cholesterol levels (< or =0.91 and >0.91 mmol/l), total plasma nitric oxide end-products were found to be decreased in patients with low HDL levels compared to those patients with high HDL levels [men, 11.7+/-6.4 vs 24.6+/-14.9 micromol/l (P<0.01); women, 12.5+/-6.6 vs 21.4+/-6.6 micromol/l (P<0.01]. Nitrite and nitrate levels were correlated with HDL cholesterol (r=0.50, P<0.05) and eMDA (r=-0.52, P<0.05). It was concluded that the patients with unregulated blood glucose levels have abnormal lipid and lipoprotein metabolism and decreased nitric oxide end-products, with relationships between nitric oxide products and dyslipidaemia, especially between low HDL cholesterol levels and increased oxidative stress.

C-Reactive protein as a risk factor for left ventricular thrombus in patients with acute myocardial infarction.

BACKGROUND: Elevated C-reactive protein (CRP) has been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that CRP may be involved in initiation process of coagulation; however, the role of CRP level in the formation of left ventricular (LV) thrombus has not been studied. HYPOTHESIS: This study investigated whether CRP is a risk factor for LV thrombus in patients with AMI. METHODS: Clinical, echocardiographic, and biochemical data were analyzed in 141 consecutive patients (aged 57 +/- 13 years; 33 women) with first anterior AMI. Two-dimensional and Doppler echocardiographic examinations were performed on Days 1, 3, 7, 15, and 30. Blood samples were obtained every day during hospitalization. Serum CRP concentrations were measured by an ultrasensitive immunonephelometry method. RESULTS: Left ventricular thrombus was detected in 33 (23.4%) patients. Univariate analysis showed that patients with LV thrombus had a higher peak creatine kinase (CK) level (2,879 +/- 742 vs. 1,693 +/- 1,210 I/U, p = 0.001), higher peak CRP level (14.9 +/- 7.1 vs. 9.2 +/- 6.8 mg/dl, p = 0.001), higher wall motion score index (1.8 +/- 0.2 vs. 1.5 +/- 0.3, p = 0.002), higher apical wall motion score index (2.35 +/- 0.72 vs. 2.07 +/- 0.70, p = 0.001), larger end-diastolic volume (145.2 +/- 43.7 vs. 116.5 +/- 44.2 ml, p = 0.002), larger end-systolic volume (85.4 +/- 37.2 vs. 62.9 +/- 31.6 ml, p = 0.003), and lower ejection fraction (42.1 +/- 12 vs. 47.3 +/- 13, p = 0.04). In multivariate analyses, only peak CK level (p = 0.0001), LV apical wall motion score index (p = 0.001), and CRP levels (p = 0.001) were independent predictors of LV thrombus formation. CONCLUSIONS: These results suggest that CRP is a risk factor for LV thrombus in patients with AMI.

Effect of Antiepileptic drugs on plasma lipoprotein (a) and other lipid levels in childhood.

Antiepileptic drugs may alter plasma lipid status in epileptic patients. We conducted a study to assess the effect of phenobarbital, carbamazepine, and valproate on plasma levels of lipoprotein (a), total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein A, and apolipoprotein B in 22 epileptic children. The children were separated as group 1, seven children, mean age 1.6+/-0.2 years, treated with phenobarbital, 5 mg/kg/day, twice daily; group 2, seven children, mean age 9.8+/-1.2 years, treated with carbamazepine, 20 mg/kg/day, twice daily; and group 3, eight children, mean age 6.8+/-0.6 years, treated with valproate, 20 mg/kg/day, twice daily. Plasma lipoprotein (a) and other lipid levels were studied before (pretreatment) and at 3 and 6 months of treatment. Friedman two-way analysis of variance and Wilcoxon's signed-rank test were used for statistical analysis, and the results were expressed as the mean and standard error of the mean. The mean age of children in group 1 was significantly low, compared with groups 2 and, 3 (P < .001). The mean pretreatment lipid levels between the groups were not significant. The increase in lipoprotein (a) at 3 and 6 months and high-density lipoprotein cholesterol at 6 months was statistically significant in group 1 (P < .025). We suggest a careful monitoring of plasma levels of lipoprotein (a) and other lipids in epileptic children treated with antiepileptic drugs.

The effects of impaired trace element status on polymorphonuclear leukocyte activation in the development of vascular complications in type 2 diabetes mellitus.

Impaired trace element metabolism may be involved in some of the metabolic dysfunctions, and contribute to the development of vascular complications in diabetic patients. In order to investigate the relationships among diabetes mellitus, trace element status, leukocyte activation and vascular complications, 55 type 2 diabetic patients (34 with vascular complications and 21 without vascular complications) and 50 non-diabetic control subjects were studied. The mean leukocyte count (p<0.001), polymorphonuclear elastase (p<0.001), erythrocyte malondialdehyde (p<0.001), and glycated haemoglobin (p<0.001) levels, and copper/ zinc ratio (p<0.001) were found to be higher in diabetic patients than in the control group, but serum zinc levels (p<0.001) and erythrocyte superoxide dismutase activities (p<0.001) were lower, and serum copper levels showed no differences. In patients with vascular complications, the mean leukocyte count (p<0.05), zinc (p<0.05), polymorphonuclear elastase (p<0.05), erythrocyte malondialdehyde (p<0.001) and glycated haemoglobin (p<0.05) levels, and copper/zinc ratio (p<0.001) were significantly different from those patients without complications. Closer correlations between the copper/zinc ratio and polymorphonuclear elastase (r=0.82, p<0.01), erythrocyte malondialdehyde (r=0.46, p<0.05) or erythrocyte superoxide dismutase (r= -0.85, p<0.01) were found in patients with vascular complications compared to those without, and all of those showed significant relationships with poor glycaemic metabolic control. We conclude that zinc deficiency may provoke polymorphonuclear leukocyte activation, and contributes to the development of vascular complications in type 2 diabetic patients. Furthermore, copper/zinc ratio and polymorphonuclear elastase may be used as important markers to evaluate the presence of vascular complications.

Effect of coronary angiography on plasma endothelin-1 and nitric oxide concentrations.

Endothelium takes part in the regulation of vascular tone through the production of endothelium-derived relaxing factor, nitric oxide (NO), and the contracting factor endothelin-(ET-1). Induction of ET-1 and NO is influenced by many stimuli including hypoxia and shear stress. Some of these stimuli may arise during coronary angiography (CAG). In this study, the authors aimed to show endothelial response in patients undergoing CAG by evaluating plasma ET-1 and NO end-products including nitrite and nitrate concentrations. Twenty-four male patients with a mean age of 54.3 years (age range: 37-70) were included in the study. The patients had no coronary atherosclerotic lesions established by CAG. The mean time of the CAG procedures was 24.8 minutes, with a range of 19-33 minutes. Immediately before blood sampling, systolic and diastolic blood pressures were recorded. The mean blood pressures before and after CAG were 140/90 and 150/95, respectively. End products of NO radical, nitrite and nitrate (NOx), in plasma were used as a marker for the production of NO radical. ET-1 concentrations were measured by ELISA method. Significant increases in ET-1 concentrations were observed during CAG while no change observed in NOx concentrations. Duration of the CAG procedure was found to be correlated with the percent increase of the plasma ET-1 concentrations during CAG (r = 0.45, p<0.05, Figure 1), but not with NOx concentrations. Plasma ET-1 concentrations in patients who were cigarette smoking were found higher than those of patients who were nonsmokers (1.26 +/- 0.38 and 2.97 +/- 0.87 fmol/L, respectively). It was concluded that endothelial cells show increased ET-1 production as a response of some mechanical or emotional stimuli during CAG procedure that may play an important role in the regulation of vascular tonicity and some pathological processes. The authors suggest that duration and manipulation of CAG may be an important factor in plasma ET-1 concentrations.

Serum lipoprotein(a) and its relation to left ventricular thrombus in patients with acute myocardial infarction.

It is well known that the incidence of left ventricular (LV) thrombosis is high in patients with acute myocardial infarction (AMI). Due to the high degree of structural homology with plasminogen, lipoprotein(a) may produce thrombogenic effects by modulating the fibrinolytic system. However, the role of Lp(a) level in the formation of LV thrombus has not been studied. This study sought to determine whether Lp(a) is a risk factor for LV thrombus in patients with AMI. We have analyzed clinical, echocardiographic and biochemical data in 102 consecutive patients (aged 58+/-12 years, 92 men / 10 women) with first anterior AMI. Two-dimensional examination was performed on days 1, 3, 7, 15, and 30. Blood samples were obtained within 12 h after the onset of symptoms and before beginning the therapy. Plasma levels of fibrinogen and Lp(a) were measured using enzyme-linked immunosorbent assay and immunonephelometric methods, respectively. LV thrombus was detected in 20 (20.3%) patients. No significant difference was found for admission Lp(a) levels between patients with or without thrombus (30.5+/-17.2 vs 32.3+/-22.4 mg/dl, p = 0.7). Univariate analysis showed that patients with LV thrombus had a higher wall motion score index (1.8+/-0.3 vs 1.4+/-0.3, p = 0.002), a higher peak creatine kinase level (2945+/-898 vs 1805+/-1336, I / U p = 0.004), a larger end-diastolic volume (139.7+/-38.6 vs 114.1+/-41.8 ml, p = 0.04), a larger end-systolic volume (83.1+/-34.3 vs 59.2+/-30.6 ml, p = 0.02 ), and a lower ejection fraction (38+/-12 vs 47+/-11, p = 0.04). In multivariate analyses, only peak creatine kinase level (p = 0.04) and LV wall motion score index (p = 0.002) were independent predictors of left ventricular thrombus formation. These results suggest that Lp (a) is not a risk factor for LV thrombus in patients with AMI. Our data demonstrate that the best predictors of LV thrombus formation after AMI are a high peak creatine kinase level and a high LV wall motion score index.

Effects of antidepressant treatments on polymorphonuclear elastase levels in patients with depression.

BACKGROUND: We have previously reported that severe depression is associated with immunological and inflammatory alterations and these alterations may be showed easily by polymorphonuclear elastase (PMNE) measurements. The purpose of the present study is to show how PMN elastase levels change before and after antidepressant treatment. METHODS: Fifty-five patients with depression (40 with major depression [MD], 15 with dysthymic disorder [DD]) were included in the study. Blood samples were drawn prior to drug treatment, and 3 months after the treatment. Severity of depression was measured by 24-item Hamilton depression rating scale (HDRS). RESULTS: There was a positive correlation between Delta PMNE levels and Delta HDRS in patients with MD, but not in patients with DD. Twenty-eight patients were given moclobemide, and 27 patients were given imipramine. It was seen that PMN elastase levels were significantly reduced after 3-month antidepressant treatment period only in patients with MD. CONCLUSION: These findings suggest that PMNE activity is a state dependent parameter and improvement of depressive symptoms due to antidepressant treatment may lead to decrement of PMNE levels. CLINICAL IMPLICATION AND LIMITATIONS: PMN elastase measurements may be used as a sensitive biological marker to follow the time-course of the disease activity in patients with major depression.

Increased plasma endothelin-1 levels in patients with intracerebral hemorrhage.

Endothelins (ETs) are discovered peptides that are widely distributed in neurons and nonneuronal cells of the human nervous system. Previous studies showed that ischemic stroke may be associated with increased plasma ET-1 levels. There are no studies to show plasma ET-1 levels in intracerebral hemorrhage. Plasma ET-1 levels in 30 patients with cerebral hemorrhage within 72 hours after the onset of focal neurological deficit were measured by a microplate enzyme immunoassay. Thirty sex- and age-matched healthy subjects were accepted as a control group. The clinical neurological status in the patients was evaluated according to the modified Matthew Scale. The mean plasma ET-1 level in hemorrhagic stroke patients was significantly higher than in control subjects (2.39±2.08 v 0.65±0.32 fmol/mL, (P < .05). There was a significant difference in ET levels between patients who died in the hospital and patients who survived (P < .05). The mean ET-1 concentration in patients with severe neurologic deficit was significantly higher than in patients with mild neurologic deficit (P < .05). There was a correlation between hematoma volumes and plasma ET-1 levels in the patients (r = 0.66, Pt < .001). The mean plasma ET-1 concentration was found to be significantly higher in patients with intraventricular hemorrhage than in patients without intraventricular hemorrhage (P < 0.05). There were no significant differences in ET-1 levels between supratentorial and infratentorial subgroups or among supratentorial subgroups (P > .05). It was concluded that plasma ET-1 levels were increased in the acute period of hemorrhagic stroke. Plasma ET-1 levels may be associated with hematoma volume, which is related to a poor prognosis of the cerebral hematoma. We suggest that increased plasma ET-1 levels may be a consequence of local cerebral hemorrhage or the acute stress condition of the disease.

Plasma lipoprotein (a) levels in Turkish NIDDM patients with and without vascular diabetic complications.

OBJECTIVE: Plasma concentrations of lipoprotein (a) [Lp(a)], an independent risk factor for atherosclerosis, were measured in 59 non-insulin-dependent diabetes mellitus (NIDDM) patients with and without vascular complications, and 21 non-diabetic healthy subjects. RESULTS: The plasma log Lp(a) levels were found to be significantly increased in the NIDDM patients (1.40 +/- 0.36) compared with the healthy subjects (1.02 +/- 0.53; p < 0.05). Plasma Lp(a) levels in NIDDM patients with diabetic vascular complications (1.51 +/- 0.27) were significantly higher than those of the NIDDM patients without diabetic vascular complications (1.23 +/- 0.43) and healthy subjects (p < 0.05). There were significant correlations between plasma log Lp(a) levels and apolipoprotein B (apo B) in all NIDDM patients (r: 0.68, p < 0.05). No correlation was observed between Lp(a) levels and age, sex, duration of diabetes, fasting blood glucose, haemoglobin Alc, the mode of treatment, triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and apolipoprotein Al levels in all patients. CONCLUSIONS: It was concluded that Lp(a) was a risk factor for angiopathy in NIDDM patients and the patients who have a high plasma Lp(a) concentration should be kept under strict glycaemic control.

The significance of autoantibodies against oxidatively modified low-density lipoprotein (LDL) in patients with psoriasis.

Psoriasis is associated with changes in plasma lipid and lipoproteins, which may play a role in the development of occlusive vascular disease. The oxidation of low-density lipoprotein (LDL) is considered a key event in the development and progression of atherosclerosis. Autoantibodies against oxidized LDL (auAb-oxLDL) may contribute to understanding the relationship between oxidative processes and development of atherosclerosis. Thirty-three patients with psoriasis and 30 matched control subjects were investigated. LDL oxidation was evaluated as the presence of autoantibodies against LDL oxidatively modified with Cu++, by an ELISA system in the patients and control sera. AuAb-ox LDL levels of the patients were found to be significantly increased compared with a control group. 42% of the patients and 3.3% of the control subjects had higher auAb-ox LDL levels than the cut-off point (352 mU/ml). The levels of auAb-ox LDL were found to be correlated with PASI score (r = 0.67, p < 0.01). Also, The antibody level was found to be correlated with polymorphonuclear elastase and alpha-1 antitrypsin levels (r = 0.58, p < 0.05; r = 0.51, p < 0.05, respectively). It was concluded that increased levels of auAb-oxLDL in the psoriatic patients may be a consequence of the interaction between imbalance of oxidant-antioxidant system and lipoproteins, and the measurement of auAb-oxLDL in the patients may mirror in vivo occurrence of oxidative processes.

Autoantibodies against oxidatively modified low-density lipoprotein in patients with Behçet's disease.

BACKGROUND: Change of lipids and lipoprotein metabolism and an imbalance of the oxidant-antioxidant system related to the disease activity have been reported in Behçet's disease. Therefore, there is a tendency of oxidative modification of lipids and lipoproteins in patients with the disease. OBJECTIVE: To investigate serum autoantibodies against oxidatively modified low-density lipoprotein (oxLDL) as a marker for the degree of in vivo oxidation of lipoproteins in Behçet's disease. METHODS: Serum autoantibodies against oxLDL, total cholesterol, triacylglycerol, HDL cholesterol, LDL cholesterol, apolipoprotein (Apo) AI, Apo B, alpha1-antitrypsin, alpha2-macroglobulin and erythrocyte sedimentation rate were determined in 37 patients and 30 sex- and age-matched healthy volunteers. Autoantibodies against oxLDL were measured by a commercial enzyme-linked immunosorbent assay. RESULTS: Serum autoantibody levels against oxLDL were significantly higher in patients than in controls (425 +/- 365 and 187 +/- 132 mU/ml, respectively; p < 0.05). The levels of autoantibodies against oxLDL in the patients were found to correlate with total cholesterol, LDL cholesterol, HDL cholesterol and alpha1-antitrypsin levels (r = 0.38, p < 0.05; r = 0.42, p < 0.05; r = -0.38, p < 0.05; r = 0.42, p < 0. 05, respectively). CONCLUSION: It has been shown in previous studies that high autoantibody titers against oxLDL may be important in diseases with atherosclerosis as seen in systemic lupus erythematosus and rheumatoid arthritis. High autoantibody titers against oxLDL are not specific for Behçet's disease but probably important for pathologic processes in the disease. We suggest that increased levels of autoantibodies against oxLDL may be a factor responsible for endothelial dysfunction and development of vascular pathology in Behçet's disease.

Plasma lipoprotein (a) concentrations in hypothyroid, euthyroid and hyperthyroid subjects.

OBJECTIVE: Alterations of the lipid profile are a well known phenomenon in thyroid dysfunction. Thyroid hormones regulate lipid metabolism through various mechanisms, but a key role is played by the LDL receptor pathway. Thyroid hormone influence on lipoprotein (a) [Lp(a)] metabolism is known. METHODS AND RESULTS: Therefore we studied Lp(a) concentrations in a group of 16 hypothyroid patients and in a group of 22 hyperthyroid patients. Twenty-six euthyroid subjects were used as a control group. Plasma Lp(a) concentrations in hyperthyroid patients (23.2 +/- 28.1 mg/dl) were significantly lower than those of the hypothyroid patients (27.1 +/- 19.2, p < 0.05). There were negative correlations between plasma Lp(a) concentrations and total T4 levels in patients with hyperthyroidism and hypothyroidism (r: -0.49, p < 0.05; r: -0.40, p < 0.05, respectively). Also, decreased HDL-C levels, increased LDL-C, total cholesterol and apo B levels in the hypothyroid patients according to euthyroid subjects were observed (p < 0.05). Decreased LDL-C levels, increased HDL-C and apo Al levels in the hyperthyroid patients according to euthyroid subjects were determined (p < 0.05). CONCLUSIONS: It was concluded that plasma Lp(a) concentrations increase in hypothyroid patients and the observed relationships between thyroid status and Lp(a) levels can be explained by impaired catabolism of apo B and Lp(a) in hypothyroidism.