Results 71 to 80 of about 141 (118)
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Cefazolin-induced hypoprothrombinemia
Baylor University Medical Center Proceedings, 2022Long-term antibiotic use can be associated with a myriad of side effects, ranging from relatively benign to life-threatening. The most common side effects of cephalosporins include dermatologic reactions and diarrhea. Here, we present a rarer side effect: a spontaneous retroperitoneal hematoma in the setting of cefazolin administration for vertebral ...
Mallory Smith +3 more
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Cefazolin-induced hypoprothrombinemia
American Journal of Health-System Pharmacy, 2008A case of cefazolin-induced hypoprothrombinemia in a patient with renal failure is reported.A 50-year-old African-American woman was transferred from the orthopedics service to the internal medicine service for management of acute renal failure. Before her transfer, she had spinal surgery and subsequently developed a wound infection complicated by ...
Amy H, Chung, Kristin, Watson
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Hypoprothrombinemia Associated with Cefmetazole
Annals of Pharmacotherapy, 1997Objective To report a case of hypoprothrombinemia associated with the use of cefmetazole sodium, define patients at risk for this adverse effect, and identify options to prevent this problem. Case Summary A malnourished patient with endstage renal disease received cefmetazole following a below-the-knee amputation of the right leg.
G A, Breen, W L, St Peter
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Hypoprothrombinemia Due to Cefamandole
Klinische Wochenschrift, 1988Two patients are described with severe coagulation disturbances, in one instance leading to extensive skin bleeding, secondary to the use of cefamandole. This cefalosporin antibiotic carries the same N-methylthiotetrazole side chain as moxalactam. Pathogenetic mechanisms leading to hypoprothrombinemia, its prevention and treatment are discussed.
V M, Conraads +3 more
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Hypoprothrombinemia in Naproxen Overdose
Drug Intelligence & Clinical Pharmacy, 1983Transient prolongation of the prothrombin time was observed in the setting of a 10-g overdose of naproxen. The patient reported was previously healthy, without chronic liver disease, bleeding disorders, or malnutrition. The most likely mechanism for this effect is direct inhibition of the synthesis of vitamin-K-dependent clotting factors, possibly via
P K, Waugh, D W, Keatinge
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