Person: YEŞİLBURSA, DİLEK
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YEŞİLBURSA
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DİLEK
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Publication Serum cancer from lung-6: Promising biomarker to differentiate cpfe from ipf(Mattioli 1885, 2022-01-01) Uzaslan, Esra; DEMİRDÖĞEN, EZGİ; UZASLAN, AYŞE ESRA; GÖREK DİLEKTAŞLI, ASLI; ÖZKAYA, GÜVEN; Dilektaşlı, Aslı Görek; Öztürk, Nilüfer Aylin Acet; Karadağ, Mehmet; KARADAĞ, MEHMET; ACET ÖZTÜRK, NİLÜFER AYLİN; YEŞİLBURSA, DİLEK; Yeşilbursa, Dilek; Budak, Ferah; BUDAK, FERAH; Öztürk, Alper; Ursavaş, Ahmet; COŞKUN, NECMİYE FUNDA; URSAVAŞ, AHMET; Tıp Fakültesi; Kardiyoloji Ana Bilim Dalı; 0000-0002-7400-9089; 0000-0001-7099-9647; 0000-0002-6375-1472; 0000-0001-7625-9148; 0000-0003-3604-8826; 0000-0003-0297-846X; 0000-0002-9027-1132; AAD-1271-2019; JPK-7012-2023; IZP-9398-2023; A-4421-2016; F-4657-2014; AAI-3169-2021; AAG-8744-2021Background: Combined pulmonary fibrosis and emphysema (CPFE) has been recognised as a phe-notype of pulmonary fibrosis. We aimed to compare serum surfactant protein-A (SP-A), surfactant protein-D (SP-D) and Krebs von den Lungen-6 (KL-6) levels, functional parameters, in CPFE and IPF (idiopathic pul-monary fibrosis) patients. Methods: Patients diagnosed with ???CPFE??? and ???IPF??? were consecutively included in 6 months as two groups. The patients with connective tissue diseases are excluded. Results: In this study, 47 patients (41 males, 6 females) with CPFE (n = 21) and IPF (n = 26) with a mean age of 70.12 ?? 8.75 were evaluated. CPFE patients were older, had more intense smoking history, had lower DLCO/VA, lower FVC, and worse six-minute walking distance than the IPF group (p=0.005, p=0.027, p=0.02, p<0.001, p=0.001, respec-tively). Serum KL-6 levels were higher in CPFE group compared to IPF group [264.70 U/ml (228.90-786) vs 233.60 (101.8-425.4), p<0.001]. Serum KL-6 levels of 245.4 U/ml and higher have 81% sensitivity and 73% specificity for the discrimination of CPFE from IPF. Conclusions: Our study has shown that serum KL-6 level is a promising biomarker to differentiate CPFE from IPF. In CPFE cases respiratory and functional parameters are worse than those of pure fibrosis cases.Publication Approach to mitral valve diseases in the elderly(Aves, 2017-09-01) Yeşilbursa, Dilek; YEŞİLBURSA, DİLEK; Tıp Fakültesi; Kardiyoloji Ana Bilim DalıValvular disease continues to be an important cause of morbidity and mortality across the globe with an increasing number of elderly patients affected by degenerative valvular diseases. Mitral valve disease is the most common of the valvular heart disorders, particularly in ageing populations, with a prevalence of more than 10% in people aged older than 75 years. Mitral regurgitation (MR) is divided into either primary (or organic) or secondary (or functional) MR. It is necessary to distinguish primary from secondary MR because these diseases differ not only by their cause, but also by their prognosis and management. Mitral stenosis is usually due to rheumatic disease, but annular calcification might cause obstruction in mitral valve, particularly in the elderly population. Because of the accompanying risk factors and comorbidities with the increasing age, surgical interventions have been replaced by catheter based alternative treatment options.Publication The effect of fenofibrate on inflammatory markers and serum paraoxonase activity in patients with combined hyperlipidaemia(W B Saunders Co Ltd, 2004-08-01) Yesilbursa, Dilek; YEŞİLBURSA, DİLEK; Saltan, Yelda; Serdar, Osman Akın; Güçlü, S.; Serdar, Z; SERDAR, ZEHRA; Heper, Y; HEPER, YASEMİN; Cordan, J; SERDAR, OSMAN AKIN; Tıp Fakültesi; Biyokimya Ana Bilim Dalı; 0000-0003-1744-8883; AAH-6506-2021; AAF-5116-2019Publication Coronary risk factors and coronary angiography results of 12.257 patients(Elsevier, 2013-10-29) Günay, Şeyda; Serdar, Osman Akın; Özyılmaz, Sinem Özbay; Dereli, Seçkin; Aydınlar, Ali; Baran, İbrahim; Özdemir, Bülent; Yeşilbursa, Dilek; Güllülü, Sümeyye; GÜNAY POLATKAN, ŞEYDA; SERDAR, OSMAN AKIN; Özyılmaz, Sinem Özbay; Dereli, Seçkin; AYDINLAR, ALİ; Baran, İbrahim; ÖZDEMİR, BÜLENT; YEŞİLBURSA, DİLEK; GÜLLÜLÜ, NAZMİYE SÜMEYYE; Tıp Fakültesi; Kardiyoloji Ana Bilim Dalı; 0000-0003-1744-8883; 0000-0002-7788-9739; 0000-0003-0090-3835; AAF-5116-2019; AAG-8709-2020; AAI-5350-2021; AAI-6632-2021; AAJ-3962-2020; AAB-5861-2021; CDA-1396-2022; JHE-3353-2023; EHA-0046-2022; JGR-6552-2023Publication Management of hyperkalemia in heart failure(Kare Publ, 2021-10-01) Altay, Hakan; Çavuşoğlu, Yüksel; Çelik, Ahmet; Demir, Şerafettin; Kılıçarslan, Barış; Nalbantgil, Sanem; Temizhan, Ahmet; Tokgöz, Bülent; Ural, Dilek; Yıldırımtürk, Özlem; Yılmaz, Mehmet Birhan; Yeşilbursa, Dilek; YEŞİLBURSA, DİLEK; Tıp Fakültesi; Kardiyoloji Ana Bilim DalıHyperkalemia is a common electrolyte abnormality in heart failure (HF) that can cause potentially life-threatening cardiac arrhythmias and sudden cardiac death. HF patients with diabetes, chronic kidney disease and older age are at higher risk of hyperkalemia. Moreover, hyperkalemia is also often associated with the use of renin-angiotensin-aldosterone system inhibitors (RAASi) including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists and sacubitril-valsartan. In clinical practice, the occurrence of hyperkalemia is a major concern among the clinicians and often limits RAASi use and/ or lead to dose reduction or discontinuation, thereby reducing their potential benefits for HF. Furthermore, recurrent hyperkalemia is frequent in the long-term and is associated with an increase in hyperkalemia-related hospitalizations. Therefore, management of hyperkalemia has a special importance in HF patients. However, treatment options in chronic management are currently limited. Dietary restriction of potassium is usually ineffective with variable adherence. Sodium polystyrene sulfonate is commonly used, but its effectiveness is uncertain and reported to be associated with intestinal toxicity. New therapeutic options such as potassium binders have been suggested as potentially beneficial agents in the management of hyperkalemia. This document discusses prevalence, predictors and management of hyperkalemia in HF, emphasizing the importance of careful patient selection for medical treatment, uptitration of the doses of RAASi, regular surveillance of potassium and treatment options of hyperkalemia.Publication Bilateral perirenal fluid accumulation associated with tetralogy of fallot(Modestum Ltd, 2017-01-01) Sağ, Saim; Nas, Ömer Fatih; Öztürk, Alper; Yeşilbursa, Dilek; Erdoğan, Cüneyt; Sağ, Saim; NAS, ÖMER FATİH; Öztürk, Alper; YEŞİLBURSA, DİLEK; Erdoğan, Cüneyt; Tıp Fakültesi; Radyoloji Ana Bilim Dalı; AAG-8561-2021; AAW-9185-2020; JKP-3323-2023; EHA-0046-2022; COE-1124-2022This report describes a case of spontaneously developing bilateral perirenal fluid accumulation in a patient under monitoring for tetralogy of Fallot. The causal pathophysiology of perirenal fluid accumulation in patients with tetralogy of Fallot is unidentified. As a result of comprehensive examinations we establish that perirenal fluid develops due to high hematocrit. Perirenal fluid did not relapse after repeated phlebotomy treatment. Our case is the first to describe the combination of tetralogy of Fallot and perirenal fluid accumulation in the literature.Publication Iron deficiency and anemia in heart failure(Türk Kardiyoloji, 2017-09-01) Çavuşoglu, Yüksel; Altay, Hakan; Çetiner, Mustafa; Güvenç, Tolga Sinan; Temizhan, Ahmet; Ural, Dilek; Yeşilbursa, Dilek; Yıldırım, Nesligül; Yılmaz, Mehmet Birhan; YEŞİLBURSA, DİLEK; Tıp Fakültesi; Kardiyoloji Ana Bilim Dalı; EHA-0046-2022Heart failure is an important community health problem. Prevalence and incidence of heart failure have continued to rise over the years. Despite recent advances in heart failure therapy, prognosis is still poor, rehospitalization rate is very high, and quality of life is worse. Co-morbidities in heart failure have negative impact on clinical course of the disease, further impair prognosis, and add difficulties to treatment of clinical picture. Therefore, successful management of co-morbidities is strongly recommended in addition to conventional therapy for heart failure. One of the most common co-morbidities in heart failure is presence of iron deficiency and anemia. Current evidence suggests that iron deficiency and anemia are more prevalent in patients with heart failure and reduced ejection fraction, as well as those with heart failure and preserved ejection fraction. Moreover, iron deficiency and anemia are referred to as independent predictors for poor prognosis in heart failure. There is strong relationship between iron deficiency or anemia and severity of clinical status of heart failure. Over the last two decades, many clinical investigations have been conducted on clinical effectiveness of treatment of iron deficiency or anemia with oral iron, intravenous iron, and erythropoietin therapies. Studies with oral iron and erythropoietin therapies did not provide any clinical benefit and, in fact, these therapies have been shown to be associated with increase in adverse clinical outcomes. However, clinical trials in patients with iron deficiency in the presence or absence of anemia have demonstrated considerable clinical benefits of intravenous iron therapy, and based on these positive outcomes, iron deficiency has become target of therapy in management of heart failure. The present report assesses current approaches to iron deficiency and anemia in heart failure in light of recent evidence.Publication Resolution of a giant atrial thrombus following anticoagulation therapy(Clinics Cardive Publ Pty Ltd, 2008-01-01) Şentürk, Tunay; ŞENTÜRK, TUNAY; Kaderli, Aysel Aydın; Yeşilbursa, Dilek; YEŞİLBURSA, DİLEK; Tıp Fakültesi; Kardiyoloji Ana Bilim Dalı; C-1517-2017We report on a patient in whom a giant thrombus in the left atrium was detected by transthoracic echocardiography. Anticoagulant theraphy was started. After two months of therapy, repeat echocardiography showed complete resolution of the thrombus. This case indicates that large and presumably organised thrombi may be treated with anticoagulant therapy.Publication The effects of fetuin-a levels on aortic stenosis(Derman Medical Publ, 2016-07-01) Tütüncü, Ahmet; Kustarcı, Taner; Özbek, Can; Aydınlar, Ali; AYDINLAR, ALİ; Yeşilbursa, Dilek; YEŞİLBURSA, DİLEK; Tıp Fakültesi; Kardiyoloji Ana Bilim Dalı; AAI-6632-2021; EHA-0046-2022Aim: We aimed to investigate the relation between fetuin-A and calcific aortic stenosis in non diabetic patients whose renal function were normal. Material and Method: 26 patients followed for aortic stenosis by our cardiology clinic for outpatients and 25 voluntary healthy subjects were included in the study. The fetuin-A levels were measured from the venous blood samples of the study population. All patients underwent transthorasic echocardiography, the aortic valvular area and left ventricular parameters of the patients were measured. Results: The average age of the patients in degenerative aortic stenosis group was significantly higher than the control group. The parameters related to aortic valve were naturally higher in patients with dejenerative aortic valve. There was no significant difference between two groups about fetuin-A levels. Further more there was no significant relation between fetuin-a levels and aortic stenosis severity. Discussion: In conclusion fetuin-A is a multifunctional glycoprotein that plays important role in systemic calcification inhibition and valvular calcification. Finally aortic stenosis is an active process and larger studies that investigate the relation between fetuin-a and the progression and prognosis of aortic stenosis are needed.Publication Coronary risk factors and coronary angiography results of 12.201 patients(Elsevier, 2015-07-01) Günay, Şeyda; Serdar, Osman Akın; Özyılmaz, Sinem; Dereli, Seçkin; Aydınlar, Ali; Baran, İbrahim; Özdemir, Burhan; Yeşilbursa, Dilek; Güllülü, Sumeyye; Kaderli, Aysel Aydın; Şentürk, Tunay; GÜNAY POLATKAN, ŞEYDA; SERDAR, OSMAN AKIN; Özyılmaz, Sinem; Dereli, Seçkin; AYDINLAR, ALİ; Baran, İbrahim; Özdemir, Burhan; YEŞİLBURSA, DİLEK; GÜLLÜLÜ, NAZMİYE SÜMEYYE; Kaderli, Aysel Aydın; ŞENTÜRK, TUNAY; Uludağ Üniversitesi; 0000-0003-1744-8883; 0000-0003-0090-3835; 0000-0002-8974-8837; 0000-0003-4829-8400; 0000-0003-0012-345X; AAI-5350-2021; AAI-6632-2021; AAG-8709-2020; AAB-5861-2021; AAJ-3962-2020; C-1517-2017; AAF-5116-2019; CDA-1396-2022; FRF-3343-2022