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- 저자 : Mutlu Gungor (검색결과 2 건)
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Relationship Between Antimetabolite Toxicity and Pharmacogenetics in Turkish Cancer Patients
Dogan, Mutlu,Karabulut, Halil G.,Tukun, Ajlan,Demirkazik, Ahmet,Utkan, Gungor,Yalcin, Bulent,Dincol, Dilek,Akbulut, Hakan,Icli, Fikri Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.4
Introduction: Antimetabolites may cause severe toxicity and even toxic death in cancer patients. Our aim was to evaluate the relationship between antimetabolite toxicity and pharmacogenetics in patients with severe clinical toxicity or alanine transaminase (ALT) elevation after fluorouracil (5FU), capecitabine or methotrexate administration. Patients and Methods: Cancer patients with severe antimetabolite toxicity were evaluated for methylenetetrahydrofolate reductase (MTHFR) gene C667T, thymidilate synthase (TS) gene 5´UTR variable number of tandem repeats (VNTR), dihydroprymidine dehydrogenase (DPYD) gene IVS14+1G/A, Xeroderma pigmentosum (XPD) gene Lys751Gln and X-ray repair cross-complementing group 1 (XRCC1) gene Arg399Gln polymorphisms. Results: Eighteen patients were enrolled, with a male/female ratio of 0.8. They had osteosarcoma in methotrexate group (n=7), gastrointestinal malignancies in 5FU group (n=9) and breast cancer in the capecitabine group (n=2). Mucositis and dermatitis occurred in all groups, together with ALT elevation in the methotrexate group and 2 toxic deaths were encountered. DPYD, TS, MTHFR, XPD and XRCC1 gene polymorphism rare allele frequencies were observed to be higher than in the general population. Conclusion: Pharmacogenetics might contribute to tailored therapy.
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Erkan Yildirim,Murat Celik,Uygar Cagdas Yuksel,Mutlu Gungor,Baris Bugan,Deniz Dogan,Yalcin Gokoglan,Hasan Kutsi Kabul,Suat Gormel,Salim Yasar,Mustafa Koklu,Cem Barcin 대한심장학회 2017 Korean Circulation Journal Vol.47 No.6
Background and Objectives: Functional capacity varies significantly among patients with heart failure with reduced ejection fraction (HFrEF), and it remains unclear why functional capacity is severely compromised in some patients with HFrEF while it is preserved in others. In this study, we aimed to evaluate the role of pulmonary artery stiffness (PAS) in the functional status of patients with HFrEF. Methods: A total of 46 heart failure (HF) patients without overt pulmonary hypertension or right HF and 52 controls were enrolled in the study. PAS was assessed on parasternal short-axis view using pulsed-wave Doppler recording of pulmonary flow one centimeter distal to the pulmonic valve annulus at a speed of 100 mm/sec. PAS was calculated according to the following formula: the ratio of maximum flow velocity shift of pulmonary flow to pulmonary acceleration time. Results: PAS was significantly increased in the HFrEF group compared to the control group (10.53±2.40 vs. 7.41±1.32, p<0.001). In sub-group analysis of patients with HFrEF, PAS was significantly associated with the functional class of the patients. HFrEF patients with poor New York Heart Association (NYHA) functional capacity had higher PAS compared those with good functional capacity. In multivariate regression analysis, NYHA class was independently correlated with PAS. Conclusion: PAS is associated with functional status and should be taken into consideration as an underlying pathophysiological mechanism of dyspnea in patients with HFrEF.
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