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Piroxicam
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Piroxicam is an oxicam derivative with anti-inflammatory, antipyretic and analgesic properties. As a non-selective, nonsteroidal anti-inflammatory drug (NSAID), piroxicam binds and chelates both isoforms of cyclooxygenases (COX1 and COX2), thereby stalling phospholipase A2 activity and conversion of arachidonic acid into prostaglandin precursors. This results in inhibition of prostaglandin biosynthesis. As a second, independent effect, piroxicam inhibits the activation of neutrophils. Piroxicam is indicated for treatment of osteoarthritis and rheumatoid arthritis, musculoskeletal disorders, dysmenorrhea and postoperative pain. It is also used in topical formulations for treating pain and swelling due to strains, sprains, backache or arthritis (1).
Epidemiology of Severe Cutaneous Drug Reactions
Published in Kirsti Kauppinen, Kristiina Alanko, Matti Hannuksela, Howard Maibach, Skin Reactions to Drugs, 2020
Maja Mockenhaupt, Erwin Schöpf
A different method for risk evaluation of drugs is provided by the case-control design. An international case-control study on severe cutaneous adverse reactions (SCAR) has been performed in France, Germany, Italy, and Portugal between 1989 and 1995.42 To date, phase I of the SCAR study, comprising data until the middle of 1993, has been analyzed and published. Altogether, 245 hospitalized patients with SJS, SJS/TEN overlap, and TEN, as well as 1147 controls were compared in terms of their drug use prior to the onset of the disease.43 The controls used in mat study were hospitalized patients admitted for reasons other than severe skin reactions or conditions related to previous drug use, mainly patients with trauma or acute infections not based on a chronic condition.42 Drugs usually taken for a short time period, and those usually given for a longer time period, e.g., months or years, were analyzed separately. Concerning drugs usually taken for a short time, the risk was increased for co-trimoxazole and other anti-infective sulfonamides, aminopenicillins, quinolones, cephalosporines (Table 2), and chlormezanone. In terms of drugs with a longer period of intake, the crude relative risk was increased for carbamazepine, phenobarbital, phenytoin, valproic acid, oxicam-NSAIDS, allopurinol, and corticosteroids. For these drugs, the risk seems to be higher during the first two months of treatment.43
Acute generalized exanthematous pustulosis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
In at least 90% of the cases, AGEP is caused by drugs. As per the EuroSCAR study, drugs with high risk to trigger AGEP were identified as ampicillin/amoxicillin, pristinamycin, quinolones, chloroquine, sulfonamides, terbinafine, and diltiazem. Less strong association was recorded for corticosteroids, macrolides, nonsteroidal anti-inflammatory drugs of the oxicam type, and antiepileptics. The time of onset after drug intake could depend on the drug concerned and its mechanism of action, and is therefore variable. It could range from 24 hours to 1–2 weeks. Rapid onset following the intake of certain drugs could be due to rechallenge to the drug to which there has been a prior exposure, or due to some mechanism that has so far not been elucidated.
Managing the ADR of Stevens-Johnson syndrome/toxic epidermal necrolysis
Published in Expert Opinion on Drug Safety, 2022
Bertrand Sheng-Yang Lian, Haur Yueh Lee
Causality analysis poses a few pitfalls. Firstly, in at least 15% of SJS/TEN cases, no apparent drug trigger can be identified [15]. Although these non-drug cases are thought to be infection related, infectious triggers are rarely identified. Mycoplasma pneumoniae has been identified in less than 30% of idiopathic SJS/TEN cases and should be screened in patients without a clear drug causality [17]. Secondly, protopathic biases may occur in drug causality determination, particularly in idiopathic cases of SJS/TEN. Protopathic bias occurs when the drug, initiated in response to the prodromal symptoms such as fever and sore throat, is erroneously deemed as the culprit [1,18]. This commonly results in cold/flu medications being implicated as triggers of SJS/TEN [18]. Nonetheless, amongst the NSAIDS, Oxicam group is a high-risk drug particularly if initiated within the appropriate latency [12,13]. Similarly, the risk of acetaminophen remains uncertain in the pediatric age-group. As shown in the SCAR/EuroSCAR studies, the risk in children remains elevated despite adjusting for confounding by indication and other concomitant use of high-risk drug [19].
Synthesis of PEG-4000-co-poly (AMPS) nanogels by cross-linking polymerization as highly responsive networks for enhancement in meloxicam solubility
Published in Drug Development and Industrial Pharmacy, 2021
Kifayat Ullah Khan, Muhammad Usman Minhas, Muhammad Sohail, Syed Faisal Badshah, Orva Abdullah, Shahzeb Khan, Abubakar Munir, Muhammad Suhail
Meloxicam is a non-steroidal anti-inflammatory (NSAID) drug [10,11]. It is an oxicam derivative with long lasting analgesic, anti-pyretic, and anti-inflammatory activity used in the treatment of rheumatoid arthritis, osteoarthritis, and in other body pain [12,13]. MLX is also studied as a potential drug for Alzheimer’s disease as well as an effective adjuvant in the treatment of different types of cancer i.e. lung, prostate, urinary bladder, and colorectal cancer [14,15]. However, it is a poorly aqueous soluble (12 μg/mL) drug belonging to biopharmaceutical classification class II (BCS II) with elimination half-life of about 20 h [16–18]. Poor solubility issue of MLX leads to low dissolution and poor absorption from gastro-intestinal tract (GIT) at physiologic pH which limits its clinical efficacy [19–21]. Therefore, it is vital to develop an appropriate drug carrier system for efficient MLX delivery.
Synthesis and in‐vivo taste assessment of meloxicam pivalate
Published in Drug Development and Industrial Pharmacy, 2019
Bandoo C. Chatale, Mariam S. Degani
1H NMR of MXP was recorded in CDCl3 solvent. NMR also showed disappearance of –OH of MX (12.72 ppm, s, 1H) [38] and chemical shift δ (ppm), for pivalate group was found at 1.46 (s and 9H) which suggested the presence of pivalate group (OCO(CH3)3) (Figures 3a and 3b; Tables 3 and 4). The aromatic region of MXP was found at 7.95 (m, H), 7.67 (2H), 7.52 (m, 1H), and 7.18 (s, 1H), respectively. N methyl of oxicam derivative was found at 3.05 (s and 3H), the 5-methyl attached to thiazole of MXP was found at 2.43 (s, 3H) (Figures 3a and 5a; Table 3). MX was not practically insoluble in CDCl3 solvent hence 1H NMR of MX was recorded in DMSO-d [6] solvent in which MX was freely soluble. The aromatic region of MX was found at 7.98 (d and H), 7.81 (dd, 3H), and 7.26 (s, 1H), respectively. N-methyl of oxicam derivative was found at 2.82 (s and 3H), the 5-Methyl attached to thiazole of MXP was found at 2.29 (s, 3H) (Figures 3a, 3b and 5b; Table 4).