Visfatin and retinol-binding protein 4 concentrations in lean, glucose-tolerant women with PCOS.

Since insulin resistance is accepted to be a common feature of polycystic ovary syndrome (PCOS), the exact molecular mechanism(s) involved in glucose and lipid metabolism have been under investigation in the syndrome. Recently, two novel adipokines, namely visfatin and retinol-binding protein 4 (RBP4), have been suggested to play a role in insulin resistance and diabetes. This study sought to determine whether plasma concentrations of visfatin and RBP4 are altered in PCOS by comparing a total of 27 lean, normal glucose-tolerant PCOS patients with 19 age- and body mass index-matched healthy controls. The mean plasma visfatin concentrations were higher in PCOS patients than those in healthy subjects (37.9+/-18.2 versus 19.8+/-17.5, P<0.01), while RBP4 concentrations were similar between the two. Both adipokines were correlated with each other in the whole (r=0.50, P<0.01) and in PCOS (r=0.52, P<0.01) groups but not in controls. The results suggest that lean, glucose-tolerant women with PCOS have increased circulating visfatin and unaltered RBP4 concentrations compared with healthy lean women. In order to clarify overlapping effects and their potential contribution to the pathophysiology of PCOS, further studies are needed.

The adhesion molecules of L-selectin and ICAM-1 in thrombocytosis and thrombocytopenia.

Thrombopoiesis is regulated by a variety of cytokines. Intracellular adhesion molecules are inducible cell-surface glycoproteins that belong to the immunoglobulin superfamily. Cytokines, endothelium and adhesive molecules represent the point of crosstalk in normal and pathological hematopoiesis. With the hypothesis that circulating intracellular adhesion molecule-1 (ICAM-1) and lymhocyte adhesion molecule-1 (L-selectin) concentrations could be changed based on pathological thrombopoiesis resulting in quantitative platelet disorders, we evaluated ICAM-1 and L-selectin levels in patients with thrombocytosis, thrombocytopenia and healthy controls. The L-selectin levels were found to be significantly higher in the thrombocytopenia group compared to the control group. ICAM-1 levels were found to be significantly higher in both thrombocytopenia and thrombocytosis groups compared to control group. Our study corroborates our original hypothesis implying the roles of adhesion molecules in the challenging status of pathological thrombopoiesis.

Thrombopoietic cytokines and platelet count in multiple myeloma.

Cytokines like interleukin (IL)-6 and IL-1beta are both implicated in multiple myeloma (MM) pathogenesis and megakaryopoiesis. The dynamic interaction between thrombopoiesis and thrombopoietic cytokines in MM may affect platelet (PLT) counts. Sixty-eight patients with MM (30 female, 38 male; median age 58 (40-79), 38 newly diagnosed, 15 in plateau, and 15 relapse and/or refractory patients) and 21 controls were included in the study. Plasma levels of thrombopoietin (TPO), IL-1beta, IL-11 and IL-6 were measured by ELISA. PLT counts were not different between the control group and MM patients with various disease stages and activity. IL-6 and TPO levels were higher in MM patients than healthy subjects (p < 0.001). PLT counts were inversely correlated with TPO (r = -0.566; p < 0.001) and positively correlated with IL-6 (r = 0.263; p = 0.04) levels in MM patients. TPO and IL-6 levels were significantly correlated (r = 0.305; p < 0.001). Disease activity has no effect on plasma cytokine levels. TPO levels were higher in stage III than stage I (p = 0.05) and stage II (p = 0.03) patients in newly diagnosed MM. High TPO levels induced by IL-6 may sustain normal PLT counts despite bone marrow infiltration by plasma cells and decreased PLT half-life.

Ultrastructural and morphological analyses of the in vitro and in vivo hemostatic effects of Ankaferd Blood Stopper.

Ultrastructural and morphological analyses of a novel hemostatic agent, Ankaferd Blood Stopper (ABS), in comparison to its in vitro and in vivo hemostatic effects were investigated. High-resolution scanning electron microscopy (SEM) images accompanied with morphological analysis after topical application of ABS revealed a very rapid (<1 second) protein network formation within concurrent vital erythroid aggregation covering the classical coagulation cascade. Histopathological examination revealed similar in vivo ABS-induced hemostatic network at the porcine hepatic tissue injury model. Instantaneous control of bleeding was achieved in human surgery-induced dental tissue injury associated with primary and secondary hemostatic abnormalities. Ankaferd Blood Stopper could hold a great premise for clinical management of surgery bleedings as well as immediate cessation of bleeding on external injuries based on upcoming clinical trials.

Increased circulating soluble P-selectin in polycystic ovary syndrome.

OBJECTIVE: To determine whether the P-selectin-von Willebrand factor (vWF) pathway is altered in patients with polycystic ovary syndrome (PCOS). DESIGN: Case-control study. SETTING(S): Tertiary care academic medical center. PATIENT(S): Thirty-two normal glucose-tolerant patients with PCOS and 21 age- and body mass index-matched healthy women were prospectively enrolled. All the patients with PCOS had clinical and/or biochemical hyperandrogenism and chronic oligoanovulation, and 89% had polycystic ovaries on ultrasound. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Soluble P-selectin (sP-selectin), vWF, total T, sex hormone-binding globulin, total cholesterol, high-density lipoprotein cholesterol, triglycerides, fasting glucose and insulin, 2-hour glucose, and homeostatic model assessment-insulin resistance. RESULT(S): Soluble P-selectin levels were significantly higher in patients with PCOS compared with controls (58.7 +/- 19.0 vs. 45.3 +/- 15.0 ng/mL), whereas PCOS and control groups had similar vWF levels (46.7 +/- 24.2 vs. 39.5 +/- 22.3, respectively). There was no correlation between sP-selectin and anthropometric measurements or any of the androgen, lipid, or insulin resistance parameters. CONCLUSION(S): Our results suggest increments in the circulating sP-selectin concentrations associated with unaltered vWF levels in PCOS. Increased sP-selectin might potentially contribute to the future risk of cardiovascular disease in patients with PCOS.

The efficacy of Ankaferd Blood Stopper in antithrombotic drug-induced primary and secondary hemostatic abnormalities of a rat-bleeding model.

Ankaferd comprises a standardized mixture of plants Thymus vulgaris, Glycyrrhiza glabra, Vitis vinifera, Alpinia officinarum and Urtica dioica. Ankaferd Blood Stopper (ABS) as a medicinal product has been approved in the management of external hemorrhage and dental surgery bleedings in Turkey. This study aimed to evaluate the in-vivo hemostatic effect of ABS in rats pretreated with acetylsalicylic acid or enoxaparin. Wistar rats (210-270 g) of both sexes were used in this study. The animals were pretreated with acetylsalicylic acid (10 mg/kg) orally for 4 days or enoxaparin sodium (8 mg/kg) subcutaneously for 3 days or did not receive any anticoagulant before tail cut at 4th day. ABS was administered topically [a total of 4 ml (1 ml/puff x 4)] to the cut tail in the studied animals. The duration of bleeding and the amount of bleeding were measured in order to evaluate the hemostatic effect of ABS. In acetylsalicylic acid-treated animals, topical ABS reduced both the duration and also the amount of bleeding volume by 68.4 and 54.6%, respectively. It was also effective in shortening the duration of bleeding (30.6%) and decreasing the amount of bleeding (32.8%) in enoxaparin-treated animals. ABS, a traditional folkloric medicinal plant extract, has in-vivo hemostatic actions, which may provide a therapeutic potential for the management of patients with deficient hemostasis in the clinical medicine.

Association among serum fetuin-A level, coronary artery calcification, and bone mineral densitometry in maintenance hemodialysis patients.

Patients with end-stage renal disease have a very high prevalence and extent of arterial calcification. A number of studies suggest that similar pathophysiologic mechanisms are responsible for development and progression of calcification of atherosclerotic plaque and bone formation. Fetuin-A is a potent calcification inhibitor and is expressed in bone, with not-yet well-defined functions. The aim of this study was to investigate the relation between bone mineral densitometry parameters, coronary artery calcification, and serum fetuin-A levels. In a cross-sectional design, we included 72 maintenance hemodialysis (HD) patients and 30 age- and gender-matched healthy controls. Serum fetuin-A levels were studied both in maintenance HD patients and healthy controls. Maintenance HD patients had radius, hip, and lumbar spine bone mineral density (BMD) assessed by dual-energy X-ray absorptiometry and coronary artery calcification score (CACS) measured by electron-beam computed tomography. The associations between site-specific BMD parameters, CACS, and serum fetuin-A levels were studied in maintenance HD patients. CACS, mass, and volume of plaques in coronary arteries were significantly higher in patients with a T-score below -2.5 than above in the proximal region of the radius, neck and trochanter of the femur, and the lumbar spine. Mean serum fetuin-A concentration was 0.636 +/- 0.118 g/L in maintenance HD patients and it was less than healthy controls (0.829 +/- 0.100 g/L, P < 0.0001). CACS, mass, and volume of plaques in coronary arteries correlated significantly with the serum fetuin-A levels. Moreover, significant positive correlations were shown between the serum fetuin-A levels, BMD values, and T-scores of proximal radius, neck, and trochanter of the femur, but not with the lumbar spine. The present study demonstrates an association between serum fetuin-A levels, coronary artery calcification, and bone mineral densities--except for the lumbar spine, in maintenance HD patients. However, the results should be interpreted with caution because of the cross-sectional design of the study.

Hemostatic efficacy of Ankaferd Blood Stopper in a swine bleeding model.

OBJECTIVE: The purpose of this study was to show the hemostatic effect of spray, solution and tampon forms of Ankaferd Blood Stopper (ABS), a unique medicinal plant extract historically used as a hemostatic agent in Turkish folklore medicine, in a porcine bleeding model. MATERIALS AND METHODS: Two 1-year-old pigs were used as bleeding models for superficial and deep skin lacerations, grade II liver and spleen injuries, grade II saphenous vein injury and grade IV saphenous artery injury. Spray, solution or tampon forms of ABS were applied after continuing bleeding was confirmed. The primary outcome was time to hemostasis. Volume of blood loss was not measured. The pigs were euthanized at the end of the experiment. RESULTS: Spray or direct application of ABS solution resulted in instant control of bleeding in superficial and deep skin lacerations as well as puncture wounds of the liver. A 40-second application of ABS tampon was sufficient to stop bleeding of skin lacerations, while 1.5- and 3.5-min applications were used to control hemorrhage from the saphenous vein and artery, respectively. No rebleeding was observed once hemostasis was achieved. However, repeated applications of ABS solution and tampon were only temporarily effective in the hemostasis of spleen injury. CONCLUSIONS: The data showed that ABS was an effective hemostatic agent for superficial and deep skin lacerations and minor/moderate trauma injuries in a porcine bleeding model.

In vivo hemostatic effect of the medicinal plant extract Ankaferd Blood Stopper in rats pretreated with warfarin.

AIM: Ankaferd comprises a mixture of Thymus vulgaris, Glycyrrhiza glabra, Vitis vinifera, Alpinia officinarum and Urtica dioica. Ankaferd Blood Stopper (ABS) has been approved in the management of bleedings. This study aimed to evaluate in vivo hemostatic effect of ABS in rats pretreated with warfarin. MATERIALS AND METHODS: Wistar rats (210-270 g) were treated either with warfarin (2 mg/kg) or vehicle (0.9% NaCl) orally before bilateral hind leg amputation. ABS was administered topically to one of the amputed legs. The duration of bleeding and the amount of bleeding were measured to evaluate the hemostatic effect of ABS. RESULTS: Topical ABS administration to amputed leg shortened the duration of bleeding markedly in both untreated and warfarin-treated rats by 31.9% [1.42 min (95% CI: 0.35-2.49)] and 43.5% [5.12 min (95% CI: 2.16-8.07)] respectively. The amount of bleeding in ABS-administered amputed leg showed a decrease by 53.8% in warfarin-treated group. CONCLUSIONS: ABS has in vivo hemostatic actions that may provide a therapeutic potential for the management of patients with deficient primary hemostasis in clinical medicine.

Thrombomodulin and GFC levels in Legg-Calve-Perthes disease.

Legg-Calve-Perthes disease (LCPD) is a self-limited microvascular disorder leading to the occlusion of the femoral blood supply, which results in bone necrosis. Endothelial injury and hemostatic alterations may play a role in the microvascular compromise and decreased blood flow, which occur during the course of LCPD. Global fibrinolytic capacity (GFC) is a novel assay reflecting the overall fibrinolysis response resulting from the dynamic interactions of numerous stimulatory and inhibitory fibrinolytic molecules. Circulating soluble thrombomodulin (TM) reflects endothelial activation and/or injury. It is a cofactor in the clinically important protein C natural anticoagulant system. Beyond the coagulation pathway it is shown to have effects on biological events, especially inflammation. The aim of this study was to determine GFC and TM levels in LCPD patients. The study included 77 children in two groups. Group I consisted of 42 patients with LCPD and Group II (control) comprised 35 healthy children. Median (interquartile ratios) GFC and TM levels were significantly higher in the LCPD patients (Group I) (p<0.0001 and p=0.049, respectively). Circulating high levels of soluble TM may be associated with ongoing endothelial injury or ongoing inflammation during the disease course. Along with increased overall fibrinolytic response, increased TM may be a compensatory reaction to thrombosis. Further investigations are needed to elucidate the endothelial, anticoagulant, and fibrinolytic kinetics associated with the microvascular compromise and self-limiting nature of LCPD.

Statin potentiates human platelet eNOS activity without enhancing eNOS mRNA and protein levels.

BACKGROUND/AIMS: Experimental studies suggest an enhanced endothelial and platelet nitric oxide (NO) generation after statin treatment, possibly due to increased endothelial NO synthase (eNOS) activity and protein levels. In parallel with experimental research, statins were shown to increase the forearm blood flow independently of serum cholesterol in humans. However, it was not possible to correlate blood flow changes with eNOS levels in these studies due to limitations in obtaining arterial samples. Hence, we investigated changes in eNOS activity, mRNA and protein levels after statin treatment in human platelets, which are readily accessible unlike arteries. METHODS: In vitro bleeding times were measured in 22 patients by stimulating platelets with collagen-epinephrine or collagen-ADP. To assess platelet eNOS activity, the bleeding times were also determined after incubating platelets with L-arginine. The measurements were repeated following 14 days of pravastatin (40 mg/day) treatment. Platelet-rich plasma was collected before and after statin treatment to evaluate eNOS mRNA (semiquantitative RT-PCR) and protein levels (Western blotting). RESULTS: The basal bleeding time was prolonged by 24 +/- 3% (mean +/- SE) when the samples were incubated with 500 microM of L-arginine. The NOS inhibitor L-N(5)-(I-iminoethyl)ornithine reversed this effect, suggesting that it was mediated by NO. After statin treatment, the NO-mediated prolongation of the bleeding time with 500 microM of L-arginine was significantly potentiated (to 44 +/- 10%). Despite enhanced eNOS activity, there was no significant change in platelet eNOS mRNA and protein levels after statin treatment. CONCLUSION: These data demonstrate that platelet eNOS activity is potentiated after statin treatment in humans in parallel with experimental studies.

Thrombin activatable fibrinolysis inhibitor activity (TAFIa) levels in neonates with meconium-stained amniotic fluid.

OBJECTIVE: Meconium-stained amniotic fluid (MSAF) is thought to be a sign of fetal hypoxia, which causes activation of coagulation and inhibition of fibrinolysis. Inflammation is also seen in MSAF. On the other hand, thrombin activatable fibrinolysis inhibitor (TAFI) is an inhibitor of fibrinolysis and a regulator of vascular inflammation. For this reason, in this study we aimed to evaluate the relation between hypoxia, fibrinolysis, and inflammation by determining the levels of TAFI activity (TAFIa) in MSAF where inflammation was also thought to have a role in the pathogenesis. METHODS: The MSAF group consisted of 22 neonates; 20 neonates served as the control group. Plasma TAFIa levels were evaluated in all neonates in the first six hours of life. RESULTS: TAFIa levels were significantly higher in the MSAF group when compared with the control group and the levels correlated negatively with cord blood pH levels. CONCLUSIONS: Increased TAFIa levels in neonates with MSAF might be due to hypoxia. Inflammation observed in MSAF may also play an additional role in increased TAFIa expression. Although no clinical complication that can be attributed to this increase was seen, one should be alert to the complications of depressed fibrinolysis that might be observed in these neonates.

Soluble platelet glycoprotein V in distinct disease states of pathological thrombopoiesis.

Quantitative platelet disorders (i.e., thrombocytosis or thrombocytopenia) may also be associated with qualitative platelet alterations. Clonal thrombocythemia (CT), reactive thrombocytosis (RT), immune thrombocytopenic purpura (ITP), and thrombocytopenia of aplastic pancytopenia (AA) or infiltrative bone marrow disorders represent the major classes of pathological thrombopoiesis. Glycoprotein V may serve as an in vivo marker of platelet activation in thrombotic and hemorrhagic states. The aim of this study was to assess circulating plasma soluble platelet glycoprotein V (sGPV) concentrations in distinct disease states of pathological thrombopoiesis. The whole study group comprised 20 patients with thrombocytopenia, 32 patients with thrombocytosis and 14 healthy adults as the control group. sGPV was significantly increased in the group of thrombocytosis patients in comparison to the thrombocytopenic group and the healthy control groups. When sGPV levels were corrected according to platelet number (sGPV/tr), this ratio was very high in patients with thrombocytopenia compared to patients with thrombocytosis and the control group. Our results suggest that there is an ongoing platelet activation associated with thrombocytosis regardless of its origin is either CT or RT. Therefore, glycoprotein V system may serve to activate residual platelets in thrombocytopenia regardless of its origin is either ITP or AA.

Evaluation of serum granulocyte colony stimulating factor levels in infants of preeclamptic mothers.

In this study we aimed to evaluate the relationship between serum granulocyte colony stimulating factor (G-CSF) levels and absolute neutrophil counts (ANC) in infants of preeclamptic mothers. The study group consisted of 31 infants of preeclamptic mothers while the control group consisted of 24 gestational age-adjusted infants of normotensive mothers. G-CSF levels were determined by enzyme-linked immunosorbent assay (ELISA). The mean G-CSF level was 981.8 +/- 1682.5 (25.7-5924) pg/ml in the study group and 770.8 +/- 1779 (18-8526) pg/ml in control group (p > 0.05). There was no correlation between G-CSF levels and absolute or total neutrophil counts on the 1st, 2nd and 7th days in infants of preeclamptic mothers. There were positive correlations between G-CSF levels and ANC on the 1st and 7th days of life in infants of normotensive mothers. Neutropenia developed in 42.3% of the study group and in 21.7% of the control group on the 1st day of life (p > 0.05). On the 2nd day, neutropenia was observed in 61.5% of the study group and 26.1% of the control group (p = 0.013). Serum G-CSF levels were not low in neutropenic babies of preeclamptic mothers. In contrast, higher G-CSF levels in neutropenic infants suggest impaired G-CSF response in infants of preeclamptic mothers.

Stenotrophomonas maltophilia infection of the central venous catheter and lysis of an old thrombosis in a post-bone marrow transplantation child: implications in the fibrinolytic process.

In this report, we describe an 11-y-old girl who developed jugular venous thrombosis after allogeneic bone marrow transplantation for lymphoma and then experienced dissolution of the thrombosis following catheter-related Stenothrophomonas maltophilia bactearemia. The lysis of the old thrombosis around the central venous catheter suggested a local fibrinolytic activity of S. maltophilia. The global fibrinolytic capacity (GFC) was also tested in vitro by using S. maltophilia cultures obtained from the present patient; GFC of the patient was compared to that of another isolate of S. maltophilia, other bacteria (S. pyogenes and E. coli), and control plasma. The fibrinolytic capasity of S. maltophilia was significantly higher than that of the control plasma (p<0.05) and almost equal to that of S. pyogenes (p>0.05). Thus, if a potent local fibrinolytic activity of S. maltophilia is evident, the use of the fibrinolytic enzyme of S. maltophilia as a thrombolytic agent may be a useful therapeutic adjunct in the future. Further studies are needed to comfirm the results obtained in the present study.

Comparison of the effects of tibolone and estrogen therapy on hemostasis in surgical menopause: a randomized, double-blind, placebo-controlled study.

OBJECTIVE: To examine the effects of unopposed estrogen (E) and tibolone therapy on coagulation and natural anticoagulant systems in surgical menopause. DESIGN: A randomized, double-blind, placebo-controlled study. SETTING: University hospital clinic in Turkey. PATIENT(S): Ninety healthy surgically postmenopausal women. INTERVENTION(S): Ninety surgically postmenopausal women were randomized into three groups: unopposed conjugated ET (0.625 mg/d, group 1), tibolone (2.5 mg/d, group 2), and identical tablets of placebo (group 3). MAIN OUTCOME MEASURE(S): Effects on parameters in the clotting cascade at baseline and after 24 weeks of treatment. RESULT(S): After 6 months, fibrinogen, lipoprotein (a), and factor VIIa were decreased, and activated partial thromboplastin time was increased significantly in the ET group compared with in the placebo group. However, tibolone significantly decreased only the serum levels of factor VIIa and factor IX and prolonged the activated partial thromboplastin time, compared with placebo group. In addition, conjugated ET caused a significantly greater decrease in serum fibrinogen level than did tibolone. CONCLUSION(S): Neither E nor tibolone therapy led to activation of coagulation in the surgically menopausal women. Both preparations changed the overall hemostatic balance to a more fibrinolytic state.

Short-term hemostatic safety of strontium ranelate treatment in elderly women with osteoporosis.

BACKGROUND: Strontium ranelate offers significant clinical benefits in terms of efficacy, tolerability, and ease of administration in the treatment of postmenopausal osteoporosis. However, there are some data revealing an association between strontium ranelate treatment and increased incidence of venous thromboembolism (VTE), suggesting possible adverse prothrombotic effects of the drug. OBJECTIVE: To assess the effect of strontium ranelate treatment on primary hemostasis, secondary hemostasis, and the natural anticoagulant defense system, together with prothrombotic markers, in elderly women with osteoporosis. METHODS: This study was designed in a prospective manner. Thirty-five elderly women diagnosed with osteoporosis were included. During a 2 month treatment period, participants received strontium ranelate 2 g. Platelet Function Analyzer-100 (PFA-100) in vitro bleeding time was performed to depict primary hemostasis. Secondary hemostatic parameters including prothrombin time, international normalized ratio, activated partial thromboplastin time, anti-cardiolipine immunoglobulin (Ig) M and IgG, antiphospholipid IgM and IgG, protein C, protein S, antithrombin III, lupus anticoagulant, fibrinogen, thrombin, activated protein C resistance, and plasma levels of d-dimer were assessed. These parameters were tested before and after 2 month treatment with strontium ranelate. RESULTS: Mean +/- SD age of the patients was 72.82 +/- 5.69 years. After 60 days of treatment, there was no statistically significant prolongation in PFA-100 in vitro bleeding time and no statistically significant change in the critical hemostatic parameters in patients receiving strontium ranelate that led to discontinuation of the treatment. None of the subjects developed clinical VTE during the 2 month period of strontium ranelate treatment. CONCLUSIONS: The hemostatic safety of strontium ranelate in the elderly population with osteoporosis was shown over 2 months of treatment; however, its long-term hemostatic safety should be evaluated further.

Plasma osteopontin levels are elevated in non-ST-segment elevation acute coronary syndromes.

BACKGROUND: The regions of ruptured atherosclerotic plaques have numerous macrophages. Osteopontin that modulates macrophage function has been shown in atherosclerotic plaques. We aimed to study the plasma levels of osteopontin in patients with unstable angina or non-ST-seg ment elevation myocardial infarction (NSTEMI) and the rela tionship between osteopontin and the extent of the coronary artery disease (CAD). METHODS: We studied 65 patients with unstable angina or NSTEMI, 25 patients with stable angina and 18 patients as the control group. The extent of coronary artery stenosis was determined by the number of vessels with >50% stenosis. Plasma osteopontin concentrations were measured from the blood samples that were drawn immediately after admission to the emergency department in unstable angina/NSTEMI patients and before the coronary angiograph in the stable angina and control groups. RESULTS: The plasma osteopontin concentration was (495 118 ng/ml) significantly higher in the patients with unstable angina/NSTEMI compared to the stable angina group (319 106 ng/ml) and control group (125+/-54 ng/ml) (p=0.0001 The plasma osteopontin levels were lower in the patients with stable angina pectoris who had one-vessel disease compared to those with two-vessel disease (p=0.01). How ever, in the unstable angina/NSTEMI group, the plasma osteopontin levels were statistically not different among the patients with one-vessel, and two-vessel and three-vessel disease (p=NS). There was no correlation between the plasma osteopontin levels and the extent of coronary stenosis. CONCLUSIONS: The plasma osteopontin levels are elevatedin patients with unstable angina/NSTEMI, but there appears to be no correlation with the extent of CAD. These results ma suggest that osteopontin may have a role in the pathobiology of ACS.

The search for a common thrombophilic state during the active state of inflammatory bowel disease.

The clinical course of inflammatory bowel disease (IBD) is frequently associated with thromboembolic complications. The aim of this study was to investigate common thrombophilic markers in Turkish patients with active IBD. Twenty-seven consecutive patients with IBD who were followed-up at the Hacettepe University Hospital were recruited. All the patients were in the active disease state. International normalized ratio, activated partial thromboplastin time, lupus anticoagulant, anticardiolipin IgG, IgM antibodies, protein C, protein S, antithrombin-III, factor V, and factor II mutation of all the IBD patients and of a sex-matched and age-matched control group of non-IBD patients were measured. International normalized ratio, activated partial thromboplastin time, protein C, protein S, lupus anticoagulant, anticardiolipin IgG and IgM, and Proteins C and S mutations were comparable between the 2 groups, but antithrombin-III was significantly lower in the IBD group compared with healthy control group (P<0.0001). As a conclusion, it is reasonable to assume that there may be a subpopulation of the patients with IBD, in whom thrombophilic abnormalities might be important for either disease manifestation or for thrombotic complications. Those hemostatic abnormalities could be either inherited or secondary to the ongoing disease process. Routine screening for the common markers of thrombophilia does not seem to be warranted unless simultaneous arterial and venous thrombosis, major organ thrombosis, strong family history of thrombophilia, unusual and recurrent thrombosis resistant to standard anticoagulant therapy are present. Further studies are definitely required to clarify these complicated associations.

Plasma soluble osteopontin concentrations are increased in patients with rheumatic mitral stenosis and associated with the severity of mitral valve calcium.

Although the severity of valvular calcification is an important prognostic indicator, the cellular mechanisms of the calcification process are unknown. Osteopontin modulates inflammation and biomineralization, and increased osteopontin expression has been demonstrated in calcified degenerative or rheumatic cardiac valves. The present study evaluated soluble plasma osteopontin in 32 patients with echocardiographically determined rheumatic mitral stenosis and compared the results to those of a control group of 22 healthy patients. Patients were evaluated with routine echocardiographic techniques, Wilkins scoring, and 2-dimensional echocardiographic calcium scoring. Patients with rheumatic involvement other than in the mitral valve were excluded. Plasma osteopontin and high-sensitivity C-reactive protein levels in patients with mitral stenosis were significantly higher those of the control group (p = 0.006 and p = 0.0001, respectively). A significant correlation was found between plasma osteopontin levels and the severity of mitral valve calcification (p = 0.003) and also between high-sensitivity C-reactive protein levels and Wilkins score (p = 0.009). There was a stepwise and statistically significant increase in soluble plasma osteopontin levels in association with the severity of mitral valve calcification. In conclusion, increased osteopontin levels were correlated with the severity of mitral valve calcification in patients with rheumatic mitral stenosis, suggesting an important role of osteopontin in the modulation of valvular calcification. Elevated levels of high-sensitivity C-reactive protein concentrations suggest the presence of ongoing inflammation in those patients.