Faculty of Medicine
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Item type:Publication, Drug Induced Acute Pancreatitis(SHMSHM - AAMD, 2016); ; ; Mikjunovikj, LjubicaAcute pancreatitis is a severe disease with considerable morbidity and mortality. Drug-induced acute pancreatitis is rare, with an estimated incidence of 0.1-2%. More than 100 drugs have been implicated in causing the disease: acetaminophen has been associated with acute pancreatitis in cases where there has been an overdose of drugs; however, the frequency is rare. Based on analysis of the level of evidence, 4 classes of drugs could be identified. We report the case of a 28-year-old man who presented abdominal pain and elevated pancreatic enzymes suggesting acute pancreatitis, severe metabolic acidosis and systemic inflammatory response syndrome after overdosing on a drug containing acetaminophen. He was taking acetaminophen more than 5 g every day two weeks.Workup including an ultrasound,CT scan, microbiological and serological analysis failed to reveal any obvious etiology for the pancreatitis. The possibility of drug-induced pancreatitis was considered and acetaminophen was thought to be the probable etiologic agent and discontinued. A review of the relevant literature is also presented. Drug-induced acute pancreatitis is challenging for clinicians and a detailed mechanism is unknown. It is very important to rule out drug-induced pancreatitis when treating pancreatitis with an unknown etiology. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Some Aspects Of Nephrotoxicity Of Most Used Nonsteroidal Anti Inflammatory Drugs In Patients With Degenerative Spondyloarthropathy(2020); ; Objectives: To determine the effect of initial therapy with Acetaminophen and Ketoprofen on glomerular and tubular integrity in degenerative spondyloarthropaty (DSA), to quantify nephrotoxicity of these two drugs by measurement of enzymuria, which correlates with the damage of tubular epithelium. Microalbuminuria is used as a marker for glomerular damage, and urine excretion of N-Acetyl-−D-glucosaminidase (NAG) as an indicator of proximal tubular damage. Material and Methods: Using colorimetric method for determination of NAG, and immunoturbidimetric method for microalbuminuria, samples of 70 participants were examined (35 DSA patients treated with Acetaminophen only, 35 DSA pa - tients treated with Ketoprofen). The follow up was in 5 time-intervals in the course of 24 weeks. Results: There was a moderate correlation between NAG and microalbuminuria (r=0,16) in the group of patients treated with Acetaminophen only, and a moderate correlation (r=0,28) in the group of patients treated with Ketoprofen. NAG enzymuria in size, number of patients registered, and time of appearance, were greater and appeared earlier in the Ketoprofen group compared to the Acetaminophen group. Conclusion: Ketoprofen is more potent NAG inductor and provokes greater tubular enzymuriathan Acetaminophen. Results from our study confirm safety in use of Acetaminophen and Ketoprofen in everyday clinical practice.