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Acute coronary syndrome in patients with concomitant neoplastic disease and chemotherapy. Is clinical distinctness possible?

100%
Ciszewski A., Dąbrowski M., Bęćkowski M.
OncoReview
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2015
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vol. 5
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issue 3
A100-102
EN
We present 2 cases of acute coronary syndrome in patients with concomitant neoplastic disease during chemotherapy. In both patients, we found unusual angiographic image which showed that despite the presence of very large thrombi, there were no or hardly any atherosclerotic lesions in the vessel occlusion site. Aspiration thrombectomy was successfully performed in both cases to restore coronary flow and in the second patient, two bare metal stents were also implanted. After the patients were discharged from hospital, we decided to add enoxaparin to the routine dual antiplatelet therapy of both of them. So far, no guidelines have been developed on how to manage patients with acute coronary syndrome and concomitant neoplastic diseases while on chemotherapy.
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Aetiology, prophylaxis and management of preeclampsia

88%
Gronkowska K.
Acta Universitatis Lodziensis. Folia Biologica et Oecologica
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2021
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vol. 17
111-121
EN
Although preeclampsia affects approximately 3%–8% of pregnancies worldwide and is a major contributor to maternal and neonatal mortality and morbidity, the aetiology of preeclampsia is still not fully understood. This review presents the current knowledge on the aetiology of preeclampsia, with a special emphasis on risk factors and their role, and describes recommendations for the prevention and treatment of preeclampsia.
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Endothelial NADH/NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction.

75%
Kalinowski L., Malinski T.
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vol. 51
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issue 2
459-469
EN
There is growing evidence that endothelial dysfunction, which is often defined as the decreased endothelial-derived nitric oxide (NO) bioavailability, is a crucial factor leading to vascular disease states such as hypertension, diabetes, atherosclerosis, heart failure and cigarette smoking. This is due to the fact that the lack of NO in endothelium-dependent vascular disorders contributes to impaired vascular relaxation, platelet aggregation, increased vascular smooth muscle proliferation, and enhanced leukocyte adhesion to the endothelium. During the last several years, it has become clear that reduction of NO bioavailability in the endothelium-impaired function disorders is associated with an increase in endothelial production of superoxide (O2̇̄). Because O2̇̄ rapidly scavenges NO within the endothelium, a reduction of bioactive NO might occur despite an increased NO generation. Among many enzymatic systems that are capable of producing O2̇̄, NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O2̇̄ in the endothelial cells. It seems that O2̇̄ generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O2̇̄. That is maintained at diverse levels.
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