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Pseudohyperkalemia: in vitro phenomenon or misdiagnosis. A case report

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Struniawski K., Pogorzelski S., Wróblewski D., Kuźma Ł., Kobus G., Dobrzycki S.
Progress in Health Sciences
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2018
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vol. 8(2)
239-242
EN
Introduction: Hyperkalemia is a common electrolyte disturbance that occurs within many patients. The more often prevalence of cardiovascular or renal diseases is, the more frequent medical issue hyperkalemia will be. An increasing quantity of entities requires taking medications that affect electrolyte hemostasis. Therefore, reasons for hyperkalemia should be deeply reflected. One of them is pseudohyperkalemia. Purpose: In this study diagnostics and treatment of hypokalemia were presented based on the case report of a 56-year-old man. Case presentation: A 56-year-old man was admitted to the Department of Invasive Cardiology of Medical Hospital of Białystok for complaints of strong chest pain associated with palpitations, cold sweats, feelings of general weakness and anxiety. The patient had no medical history of chronic diseases and neglected to take any medications at length. The laboratory tests performed at admission showed an increased serum concentration of potassium. Through the whole hospitalization, many medications were implicated to overcome hyperkalemia (diuretics, calcium resonium, inhalation with beta2-adrenergic agonists, intravenous infusion of glucose with insulin) with no effect. Hormone test was performed, the results excluded Addison’s or pituitary disease. Differential diagnosis with arterial blood draw showed normal potassium serum concentration. Conclusions: Hyperkalemia is encountered in a broad spectrum of patients. The severely elevated level of potassium could lead to life-threating conditions. Therefore, proper diagnosis making process is a matter of great importance. As clinicians, we need to base not only on laboratory but also examine the whole picture of the patient. Misdiagnosing pseudohyperkalemia might result in unnecessary medical management.
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Obesity – is it really so bad for a patient with coronary heart disease?

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Pogorzelski S., Kuźma Ł., Struniawski K., Wróblewski D., Gajewska_Bachórzewska, H, Dobrzycki S.
Progress in Health Sciences
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2018
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vol. 8(2)
194-201
EN
According to American Obesity Medicine Association obesity is a chronic, relapsing, multifactorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences. Obesity has been renowned as a risk factor of cardiovascular, endocrinological, orthopedic and many other diseases. But for the last two decades, there have been many reports of beneficial influence of overweight or obesity on patients with coronary heart disease. This phenomenon got a name of obesity paradox. It’s existence is a matter of lively discussion in medical world, and even if true, the protecting mechanisms of obesity need much deeper understanding.
3
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Eptifibatide induced acute thrombocytopenia. Case report of 80- years old man with acute coronary syndrome

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Kuźma Ł., Pogorzelski S., Wróblewski D., Struniawski K., Róg-Makal M., Nowak K., Matys U., Gajewska-Bachórzewska H., Dobrzycki S.
Progress in Health Sciences
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2018
|
vol. 8(2)
234-238
EN
Introduction: Glycoprotein (Gp) IIb/IIIa is a platelet receptor participating in platelet aggregation. According to ESC guidelines, glycoprotein IIb/IIIa inhibitors might be considered during percutaneous coronary interventions in patients with the acute coronary syndrome. Purpose: A case study of profound thrombocytopenia in 80-year-old man with the acute coronary syndrome. Case presentation: An 80-year-old, medicationnaive man with acute coronary syndrome was admitted to the Department of Invasive Cardiology. Due to the unsuccessful invasive strategy, an intracoronary bolus of Gp IIb/IIIa inhibitor – eptifibatide - was administered. During the following intravenous infusion, large subcutaneous hematomas were observed. Eptifibatide infusion was discontinued. Drop in platelet count to 1 thou/μL without significant anemia was registered. A control sample in sodium citrate showed similarly low platelet count - 2 thou/uL. Acetylsalicylic acid and clopidogrel were discontinued, steroids were introduced. Neither PLT nor FFP transfusion were necessary. Consecutive lab tests showed the gradual increase of PLT up to 35 thou/μL at discharge. A week later, the patient did not complain of any cardiovascular or bleeding symptoms; hematomas resented significant involution. Laboratory findings were normal. During follow-up visit 30 days after the discharge, the patient presented no cardiovascular symptoms. Conclusions: There are patients at risk of druginduced thrombocytopenia, especially those with impaired kidney function and the elderly. In such cases, decisions concerning anti-platelet and antithrombotic therapy should be taken cautiously. Because of its rare occurrence, every case of severe thrombocytopenia in ACS patients should be reported. Moreover, such patients should be followed-up to minimalize risk of similar adverse events in the future.
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