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Recent Developments in Therapies and Strategies Against COVID-19
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Misbah Hameed, M. Zia-Ul-Haq, Marius Moga
Indometacin is also one of the important NSAIDS which is usually recommended for the treatment of fever, pain, swelling, and inflammation and commonly prescribed in gout and arthritis. It inhibits the production of prostaglandins and also inhibits COX enzyme which is involved in the production of prostaglandins.
Analgesics during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Indomethacin is used for analgesic, and anti-inflammatory effects in the treatment of rheumatoid arthritis, osteoarthritis, bursitis, and tendonitis. Because of it prostaglandin inhibition, has been used to treat premature labor in the second and third trimesters of pregnancy (Niebyl et al., 1980; Sibony et al., 1994; Zuckerman et al., 1974, 1984). Intravenous indomethacin was used to close a hemodynamically significant patent ductus arteriosus in premature infants. It was also used treat symptomatic leiomyomata during pregnancy (Dildy et al., 1992).
Sonographic Assessment of Amniotic Fluid
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Tocolysis using indomethacin has been associated with decreased urine production in the fetus and has therefore been suggested as a therapeutic approach to treatment of polyhydramnios [76]. However, due to the increased risk for neonatal complications with use of this medication, such as necrotizing enterocolitis and intraventricular hemorrhage, current guidelines advise against the use of indomethacin as a treatment for polyhydramnios [74].
Tolerability of pharmacological agents in the treatment of headache following brain injury: a scoping review
Published in Brain Injury, 2023
Heather M. MacKenzie, Michael Robinson, Amanda McIntyre
Two case reports (level 5 evidence) and one case series (level 4 evidence) (13,15,16) (n = 6) described the use of indomethacin for PTH. One case report (16) focused on an individual with chronic paroxysmal hemicrania, whereas the other two articles (13,15) involved individuals with hemicrania continua. The treatment dose of indomethacin ranged from 100 mg to 300 mg daily. Five out of six of the subjects experienced gastrointestinal upset/nausea as a side effect of indomethacin, including one individual who developed colitis; two of these individuals discontinued indomethacin due to this side effect. Of these five subjects, three required the addition of another pharmacological agent to counteract the gastrointestinal upset, specifically a proton pump inhibitor, misoprostol or famotidine. Of note, the sixth subject, who did not specifically report any gastrointestinal symptoms, was simultaneously prescribed misoprostol, which counteracts gastrointestinal inflammation. The subjects (n = 4) described by Lay et al. (13) reported that their headaches were “significantly better” or “significantly lessened” with indomethacin treatment. Evans et al. (15) described a reduction in headache frequency from daily to every other day; of note, this individual was concurrently treated with amitriptyline 25 mg at bedtime, but no tolerability information was provided for this medication. The subject in the article by Jacob et al. (16) reported a complete resolution of his headaches.
Thymol Reduces Hepatorenal Oxidative Stress, Inflammation and Caspase-3#xd; Activation in Rats Exposed to Indomethacin
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Tijani Abiola Stephanie, Olori O. David, Ebenezer O. Farombi
Drug-induced multi-organ toxicities are common adverse reaction triggered by numerous drugs like indomethacin (IND). Indomethacin is one of the non-steroidal anti-inflammatory drugs used as analgesic and also has antipyretic property. However, its adverse side effects have raised a lot of concern for its continuous use in clinical settings. Indomethacin cause many organ toxicities including liver, kidney and gastrointestinal toxicities in humans and experimental animals [1,2]. In the liver, IND has been associated with hepatocellular enzymes elevation and cholestatic jaundice whereas in the kidney, IND caused acute interstitial nephritis typified by wide spread interstitial edema with infiltration of inflammatory cells [3,4]. The mechanisms by which IND causes its toxicities include prostaglandin synthesis inhibition, generation of reactive oxygen species (ROS) resulting to cellular oxidative stress, inflammation and apoptosis [5].
Indomethacin: an exploratory study of antiviral mechanism and host-pathogen interaction in COVID-19
Published in Expert Review of Anti-infective Therapy, 2022
Nishant Shekhar, Harpinder Kaur, Phulen Sarma, Ajay Prakash, Bikash Medhi
Indomethacin actively inhibits the expression of PTGES2 hence inhibiting the prostaglandin synthesis and reducing pain and inflammation significantly [30–32]. Gordon & Jang et al. (2020) have also highlighted indomethacin as a PTGES2 inhibitor in their work. The inhibition of ABCC1 transporter by indomethacin treatment alone is supported by in vitro studies like Matsunaga et al. (2006) and Leite et al. (2007), which report significant reversal of ABCC1 activity leading to reduced multi-drug resistance in the target cells [33,34]. The SARS-CoV-2 infection perturbed-consensome network suggests a 1.25 times geometric fold change (p = 0.0089) in ABCC1 expression in the human Calu-3 lung epithelial cells infected with SARS-CoV-2 with a multiplication of infection (MOI) equal to 5 [28,35]. This interaction clearly suggests that SARS-CoV-2 infection hampers the host’s drug efflux machinery. Marginally responsive action of indomethacin in clinical administration might be attributed to the increased susceptibility of the infected cell to the antiviral treatment due to ABCC1 inhibition. Furthermore, we studied old CoVs-human protein interactions and found that there was no interaction or effect of SARS and MERS protein with ABCC1 or any ABC transporter in general, suggesting SARS and MERS COVs to be comparatively more susceptible to antiviral treatment than SARS-CoV-2 [36]. A recent study from Ong EZ et al. (2021) also identifies indomethacin targeting PTGES2 and ABCC1 explaining the causative genes for respiratory dysfunction by the number of gene clusters indomethacin interacts with, which was 3 in their case [37].