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Biomedical subjects

S Kirazli

Publications and source records attributed to S Kirazli.

At least 55 records · Page 3Linked to original sources
PubMed1998

In vivo platelet and T-lymphocyte activities during pulmonary tuberculosis.

Platelets have been suggested to play a role in the inflammatory response, including defence against bacteria. The aims of this study were to determine in vivo platelet activity during the clinical course of pulmonary tuberculosis and to investigate whether or not there is a correlation between the magnitude of platelet activation and the extent of the pulmonary disease. T-lymphocyte activity was also analysed in the patients. Platelet factor-4 (PF4) and soluble interleukin-2 receptor-alpha (sIL-2Ralpha) concentrations were used as markers of platelet and T-lymphocyte activation, respectively. Twenty-five patients with pulmonary tuberculosis were studied. Fifteen healthy subjects served as a control group. The levels of both sIL-2Ralpha (3,000+/-1,948 pg x mL(-1)) and PF4 (103.1+/-6.7 IU x mL(-1)) were significantly higher in the patients with tuberculosis than in the control group (984+/-360 pg x mL(-1) and 78.2+/-23.9 IU x mL(-1), respectively) (Mann-Whitney U-test, p<0.001 for both comparisons). The plasma PF4 levels were found to be well correlated with the extent of pulmonary lesions on chest radiography (the Spearman's bivariate correlation analysis, r=0.65, p<0.001). However, sIL-2Ralpha concentrations did not correlate with the extent of disease. In conclusion, it has been suggested that platelet and T-lymphocyte activation occurs during pulmonary tuberculosis. The good correlation between platelet activation and the extent of pulmonary tuberculosis might be ascribed to a pathophysiological role of platelets in pulmonary tuberculosis.

Adolescent↗
PubMed1998

Soluble L-selectin increases in the cerebrospinal fluid prior to meningeal involvement in children with acute lymphoblastic leukemia.

Soluble L-selectin was determined in the CSF samples of 20 children with CNS leukemia at the time they had blasts in CSF and/or clinical findings of CNS involvement; 17 CSF fluid samples were obtained from 17 of these 20 children, 29-91 days before the appearance of CSF cytological and/or clinical findings of CNS involvement; while 15 CSF samples were withdrawn from among the same group of children, after treatment of meningeal leukemia. In addition, CSF sL-selectin was also assayed in 17 children with ALL, who remained in complete remission at least for a year and, as controls, in 12 children without malignant or meningeal disorders. There was no significant difference in CSF sL-selectin levels between the children with ALL without evidence of meningeal involvement and the controls (1.34 +/- 0.21 ng/ml, 1.46 +/- 0.18 ng/ml respectively, p > 0.05). However, in children with CNS leukemia, not only at the time CNS involvement was diagnosed, but also 29-91 days before the diagnosis of CNS leukemia, the concentrations of the CSF sL-selectin (12.41 +/- 2.14 ng/ml, 7.70 +/- 1.60 ng/ml respectively) were significantly higher than those in controls (p < 0.001 and p < 0.01 respectively). After treatment and disappearance of the blasts in CSF, sL-selectin was found to be decreased and even normalized in the majority of children who had meningeal involvement (2.87 +/- 2.14 ng/ml). In 5 children, the CSF sL-selectin remained high, after the blasts in CSF had disappeared and CNS leukemia recurred within 3 months in 4 of these 5 children. In conclusion, assay of sL-selectin in CSF seems to be a good diagnostic tool in the detection of CNS involvement in children with ALL. This method may also be used as an indicator, in prediction of the CNS leukemia, which is going to develop.

Adolescent↗
PubMed1998

P-selectin as a circulating molecular marker in rheumatoid arthritis with thrombocytosis.

OBJECTIVE: To compare plasma concentrations of soluble P-selectin (sP-selectin) in patients with rheumatoid arthritis (RA) and thrombocytosis with those with RA with normal platelet counts and healthy controls, and to explore the relationship between clinical and serological measures of disease activity. METHODS: Nineteen patients with RA with marked thrombocytosis, 20 with normal platelet counts, and 24 controls were enrolled. Ritchie articular index and morning stiffness were recorded as clinical markers of disease activity. Blood samples were collected for platelet count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and plasma sP-selectin determinations. Correlations between sP-selectin and clinical and serological markers of disease activity were noted. RESULTS: Patients with RA and thrombocytosis compared to patients with normal platelet counts showed evidence of more active disease when ESR, CRP, morning stiffness, and Ritchie articular index were considered. The thrombocyte count in patients with RA with marked thrombocytosis revealed a positive correlation with CRP and Ritchie articular score. Plasma sP-selectin levels were found to be significantly higher in patients with RA compared to controls. sP-selectin levels were significantly higher in patients with RA with thrombocytosis compared to those with normal platelet counts, and positive correlations were observed between plasma sP-selectin levels and Ritchie index, morning stiffness, and thrombocyte counts in those patients. CONCLUSION: Elevated plasma sP-selectin levels in RA could indicate the presence of a continuous underlying inflammatory stimulus. In addition, the augmented increase in patients with RA and thrombocytosis and its correlation with clinical activity may imply the cytokine-adhesion molecule interaction mediates the chronic inflammation of RA.

Adult↗
PubMed1997

Interleukin-1, -6, and -8 levels in juvenile chronic arthritis.

The immunoinflammatory pathogenesis of juvenile chronic arthritis (JCA) involves the activation of many pathways including various cytokines. We have evaluated the levels of interleukin(IL)-1, IL-6 and IL-8 in 29 JCA patients. The age range was 1-16 with a mean of 10.1. A disease activity score was developed on the basis of: 1. constitutional symptoms and/or morning stiffness, 2. presence of joint swelling, 3.warmth, 4.limited range of motion, and 5.joint pain. This score correlated very significantly with laboratory disease activity markers such as erythrocyte sedimentation rate (ESR) and CRP (both p = 0.006) and also correlated with IL-1 and IL-6 levels. The levels of IL-1 decreased in four of the five patients with improved disease activity. IL-6 but not IL-1 correlated significantly with the number of inflamed joints (p = 0.013); IL-6 also strongly correlated with rheumatoid factor supporting this cytokine's role in B cell induction (p = 0). Haemoglobin values correlated negatively with the activity index, ESR, CRP, IL-1 and IL-6. IL-8 did not correlate with disease activity markers. In the systemic patients all cytokines tended to be higher. Our data suggest that interleukins 1 and 6 are effective in the pathogenesis of JCA. Whether cytokines may be used for monitoring therapy may be clarified with further studies.

Adolescent↗
PubMed1997

Tissue factor pathway inhibitor concentrations in cirrhotic patients with and without portal vein thrombosis.

OBJECTIVES: Our aim was to determine whether tissue factor pathway inhibitor (TFPI), a physiologically important natural anticoagulant that acts by inhibiting the extrinsic pathway, concentrations decrease as liver disease progresses, and, second, whether TFPI has an etiologic role in portal vein thrombosis in cirrhotics. METHODS: After taking their informed consent, we determined TFPI concentrations in the plasma of healthy subjects (group I) (n = 15) (average age, 45.1 = 11.8 yr), cirrhotics (group II) (n = 16) (average age, 43.6 +/- 9.8 yr), and cirrhotics with portal vein thrombosis (group III) (n = 12) (average age, 42.6 +/- 10.7 yr). Mean and median TFPI values and interquartile ratios were determined for groups I, II, and III. Then group II and III were further divided according to the Child classes A, B, or C, and mean and median TFPI values and interquartile ratios were determined for these classes as well. Using the Man-Whitney U test, we compared the results. RESULTS: Statistically important differences were documented (p = 0.005) between the median TFPI levels of healthy adults and Child C cirrhotics (concentration lower in Child C) and between normal subjects and cirrhotics with portal vein thrombosis (p = 0.02) (TFPI concentration being lower in the latter group again). CONCLUSIONS: TFPI concentration decreases in advanced liver disease, and this may be a contributory factor for portal vein thrombosis in at least some cases of cirrhotics.

Adult↗
PubMed1996

Impaired haemostatic kinetics and endothelial function in Behçet's disease.

OBJECTIVES: This study was planned to explore the alterations of endothelial functions in the prethrombotic state of Behçet's disease (BD) patients. DESIGN: Plasma levels of endothelial secretory markers, in vivo molecular haemostatic and fibrinolytic parameters were cross-sectionally determined in the study group. SETTING AND SUBJECTS: In our tertiary referral centre, 30 (13 men, 17 women) BD patients, mean age 31 +/- 7 years, and 15 (eight men, seven women) healthy volunteers, mean age 26 +/- 9 years, were eligible for inclusion in the study after obtaining their written consents. INTERVENTIONS: All plasma samples for the assays of haemostatic parameters were obtained before and after an endothelial stimulant, desmopressin acetate (DDAVP). RESULTS: We have shown that in the procoagulant phase of BD patients: (1) basal thrombomodulin concentrations are increased and could not be provoked by DDAVP infusion; (2) both thromboxane B2 and 6-keto prostaglandin F1 alpha increments occur concurrently; (3) in vivo coagulation markers are elevated and raised plasmin-alpha 2 antiplasmin complex indicates a subclinical concomitant fibrinolysis; (4) the fibrinolytic process is conveyed in a somewhat complex manner in which plasminogen activator binding kinetics might be also altered. CONCLUSIONS: Endothelial cell injury, augmented thrombotic risk with compensatory excessive fibrinolysis and alterations in endothelial cell receptor-fibrinolytic marker relations might take place in the pathogenesis and thereby modulate the natural course of haemostatic processes of BD.

Adult↗
PubMed1996

Serum immunoglobulin E and soluble CD23 in patients with Graves' disease.

It is not clear whether the IgE system plays a role in the pathogenesis of Graves' disease which is an autoimmune disorder. The low-affinity receptor of IgE, which is known as CD23, is not simply a receptor, it has various functions related to immune cells. There is no information about its levels in Graves' disease. For these reasons, serum IgE and soluble CD23 levels were determined in 40 patients with thyroid disease, free from allergic disorders and/or parasitic infestations. Patients were divided into three groups: Group 1: Patients with Graves' disease (n = 15, age: 33.4 +/- 9.3, 9 women/6 men). Group 2: Patients with non-toxic diffuse or multinodular goitre (n = 15, age: 31.0 +/- 12.7, 13 women/2 men). Group 3: Patients with toxic nodular goitre (n = 10, age: 44.6 +/- 14.2, 9 women/1 men). There was no age or sex difference between the groups (p > 0.05). Serum IgE level was somewhat higher in group 1 as compared with the other two groups, but the difference was not statistically significant, the values showed great individual variations (Group 1: 99.60 +/- 105.10, Group 2: 47.89 +/- 53.42, Group 3: 46.48 +/- 35.90 IU/ml, p > 0.05). Serum sCD23 was detectable in 7 of 15 patients in group 1 (46.7%), 1 of 15 patients in group 2 (6.7%) and 1 of 10 patients in group 3 (10.0%). Serum sCD23 detectability ratio was found higher in patients with Graves' disease than in the other two groups (p < 0.02). Serum IgE levels were compared in sCD23 detectable and undetectable Graves' patients. The values were similar (sCD23 detectable group: 105.30 +/- 135.90, sCD23 undetectable group: 94.70 +/- 55.30 IU/ml, p > 0.05). These results suggest that increased detectability of sCD23 is associated with Graves' thyrotoxicosis. An underlying state of autoimmune thyroid disease may be a permissive factor for this phenomenon.

Adult↗
PubMed1996

Local fibrinolysis in native arteriovenous fistulas of haemodialysis patients.

This study was designed to evaluate local alterations of the fibrinolytic process in patent-functional native arteriovenous fistulas of patients on maintenance haemodialysis. For this aim, the concentrations of the main components of the fibrinolytic system were determined in plasma samples taken simultaneously from arteriovenous fistulas and contralateral upper extremity concurrent large veins of haemodialysis patients. Twelve patients (6 women and 6 men, age 36 +/- 8 years) with end-stage renal disease on maintenance haemodialysis and 15 non-smoker healthy volunteers (8 women and 7 men, age 31 +/- 10 years) with normal renal function were included in the study. The fibrinolytic parameters, except alpha 2-antiplasmin, were found to be elevated in arteriovenous fistulas of haemodialysis patients as compared with opposite upper extremity large veins of the same patients (p < 0.005). Increments in fibrinolytic parameters including tissue plasminogen activator antigen, urokinase-type plasminogen activator antigen and activity, and plasminogen activity together with lower alpha 2-antiplasmin levels favor activation of fibrinolysis, except for higher alpha 2-macroglobulin concentrations, in arteriovenous fistula. The study suggests that the fibrinolytic process is locally activated in arteriovenous fistulas of haemodialysis patients.

Adult↗