Abstract
We developed and validated an analytical method based on microextraction packed sorbent (MEPS) and high-performance liquid chromatography (HPLC) coupled to photodiode array (PDA) detector to simultaneously quantify multiple nonsteroidal anti-inflammatory drugs (NSAIDs) and fluoroquinolones (FLQs), which may provide as combination several adverse reactions in nephrology and neurology. The linearity range from LOQs (0.1 μg/mL) to 10 μg/mL, and LODs values were 0.03 μg/mL for both NSAIDs and FLQs. The validation was performed according to international guidelines and the accuracy was tested measuring the precision, intermediate precision and trueness. The drugs stability was tested under different storage conditions (+4 °C and −20 °C) and after three different cycles of freezing and thawing. The method can be a suitable tool to simultaneously detect a possible association of drugs in human biological samples and provide several potentialities for clinical applications, bioequivalence studies, pharmacodynamics and toxicodynamics of different pharmaceutical dosage forms showing NSAIDs and FLQs.
Highlights
NSAIDs is the acronym of nonsteroidal anti-inflammatory drugs, which are used to treat from acute to moderate painful occurrences, and are often ‘‘abused’’ in the treatment of an inflammatory pain
We developed and validated an analytical method based on microextraction packed sorbent (MEPS) and high-performance liquid chromatography (HPLC) coupled to photodiode array (PDA) detector to simultaneously quantify multiple nonsteroidal anti-inflammatory drugs (NSAIDs) and fluoroquinolones (FLQs), which may provide as combination several adverse reactions in nephrology and neurology
The COX-2 is expressed in the kidney, gastrointestinal tract and central nervous system (CNS)[1], and its expression depends on the inflammation process and leads mainly to the production of prostaglandin E2 (PGE2) or other prostaglandins that increase the pathological occurrence[2]
Summary
NSAIDs is the acronym of nonsteroidal anti-inflammatory drugs, which are used to treat from acute to moderate painful occurrences, and are often ‘‘abused’’ in the treatment of an inflammatory pain. The NSAIDs inhibit the phospholipase A2 and cyclooxygenase, decreasing the biosynthesis of prostanoids. The first is constitutive of gastrointestinal tract tissues and inhibits the synthesis of prostanoids. The COX-2 is expressed in the kidney, gastrointestinal tract and central nervous system (CNS)[1], and its expression depends on the inflammation process and leads mainly to the production of prostaglandin E2 (PGE2) or other prostaglandins that increase the pathological occurrence[2]. The antiinflammatory effect of NSAIDs depends on the inhibition of COX-2 isoform, while the inhibition of COX-1 can provide several side effects, at the gastrointestinal tract[2]. The abuse of anti-inflammatory drugs suppresses this protective function, producing a renal ischemia[1,2,3,4]. Some COX inhibitors can act on other biological targets, such as celecoxib that shows inhibition activity on carbonic anhydrase[5]
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