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RISS 인기검색어
- 검색키워드
- 저자 : ( Yasin Yuksel ) (검색결과 2 건)
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( Feray Akbas ),( Hanife Usta Atmaca ),( Berrin Inal ),( Yasin Yuksel ),( Emin Piskinpasa ),( Mustafa Boz ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Recent studies have shown that microalbuminuria (MAU) refl ected in a higher probability of cardiovascular disease for cardiovascular risk assessment. We aimed to question the availability of microalbuminuria in metabolically healthy obese patients as a predictor of diastolic dysfunction to assess the cardiovascular risk. Methods: 100 obese patients without accompanying diseases were included in the study. They were screened for any signs of acute/chronic inflammation and those having any were excluded. None of the patients were on any medications infl uencing diastolic dysfunction. Blood glucose, HbA1c, urea, creatinine, total cholesterol, LDL, HDL, triglyceride and 24-hour-urine microalbuminuria and creatinine clearance (GFR) levels were studied. Two-dimensional doppler echocardiography was performed. Data was statistically analyzed using SPSS Windows 11.5. Results: Statistical analysis showed that there was no signifi cant difference between patients with diastolic dysfunction and normal echocardiograpghy fi ndings when compared for MAU and also for BMI. In all groups, there was no relation between MAU and BMI according to correlation analysis. There was statistically significant difference for age (p<0,0001), glucose (p=0,019), total cholesterol (p=0,009) and LDL (p=0,019) and no difference for gender, smoking, HbA1c, HDL, systolic and diastolic blood pressure, creatinine, GFR and triglyceride (p>0,05) between groups. Conclusions: Microalbuminuria found in obese patients can be related with diastolic dysfunction which might refl ect subclinical cardiac damage with a simple method and in advance. The lack of demonstration of this relationship in our study might be due to limited number of patients included and especially low percentage of patients with microalbuminuria. But the relationship found for blood glucose and lipid parameters still can show metabolic tendency. If an approval of this relationship can be achieved by studies with a higher number of patients, an easy and non-invasive method to predict obesity cardiomyopathy might be possible.
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( Betul Borku Uysal ),( Feray Akbas ),( Esma Altunoglu ),( Gulhan Ipek Deniz ),( Duygu Uysal ),( Harun Uysal ),( Hanife Usta Atmaca ),( Yasin Yuksel ),( Hale Aral ),( Guven Cetin ),( M Cem Ar ),( Must 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Anemia is an accelerating problem among patients with heart failure. In this study, we investigated whether anemia in heart failure was related to hepcidin level. Methods: Totally 70 patients; 50 patients with heart failure and 20 otherwise healthy subjects with no history of a chronic illness including heart failure as control group, were included in the study. Heart failure was verifi ed by echocardiography in each subject and patients were defi ned as ones with reduced ejection fraction (HFrEF) if EF = 40% and with preserved ejection fraction (HFpEF) if EF 40-50%. Exclusion criteria included presence of kidney failure (serum creatinine level>1.4), history of hemorrhage (gastrointestinal or severe menstrual bleeding), chronic liver disease (ALT>2 folds), hematologic disease, iron replacement therapy or blood transfusion in the past six months, hypothyroidism, autoimmune disease and manifest infection. Results: There was no correlation between hepcidin concentration and age, weight, creatinine, iron, vitamin B12, folate, white blood cell (WBC), platetelet, mean corpuscular volume, ESR, ejection fraction (EF) (p > 0,05). There was a positive correlation between hepcidin level and urea, ferritin, hemoglobin, hematocrite, C-reactive protein (p < 0,05). Hepcidin levels of anemic heart failure patients were signifi cantly lower than the non-anemic heart failure patients (p < 0,05). Conclusions: We found that serum hepcidin level in anemic patients with heart failure was lower than in heart failure patients without anemia. Previously, progression of heart failure was found to be associated with decline in circulating hepcidin and the development of iron defi ciency and low hepcidin level was related to unfavorable out come. We believe that iron defi ency occurs as a result of infl ammatory process in heart failure and therefore hepcidin concentrations decrease as a response. However, long-term follow up studies are needed.
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