Figure 1.

doi: 10.3346/jkms.2020.35.e213.Deftereos SG, Giannopoulos G, Vrachatis DA, Siasos GD, Giotaki SG, Gargalianos P, Metallidis S, Sianos G, Baltagiannis S, Panagopoulos P, Dolianitis K, Randou E, Syrigos K, Kotanidou A, Koulouris NG, Milionis H, Sipsas N, Gogos C, Tsoukalas G, Olympios CD, Tsagalou E, Migdalis I, Gerakari S, Angelidis C, Alexopoulos D, Davlouros P, Hahalis G, Kanonidis I, Katritsis D, Kolettis T, Manolis AS, Michalis L, Naka KK, Pyrgakis VN, Toutouzas KP, Triposkiadis F, Tsioufis K, Vavouranakis E, Martinèz-Dolz L, Reimers B, Stefanini GG, Cleman M, Goudevenos J, Tsiodras S, Tousoulis D, Iliodromitis E, Mehran R, Dangas G, Stefanadis C; GRECCO-19 investigators.JAMA Netw Open. This leads to subsequent down regulation of multiple inflammatory pathways and modulation of innate immunity. Name must be less than 100 characters Its clinical use may grow to include this indication.Deaths – both accidental and intentional – have resulted from overdose of colchicine.According to one review, colchicine poisoning by overdose (range of acute doses of 7 to 26 mg) begins with a gastrointestinal phase occurring 10–24 hours after ingestion, followed by multiple organ dysfunction occurring 24 hours to 7 days after ingestion, after which the affected person either declines into multi-organ failure or recovers over several weeks.Colchicine can be toxic when ingested, inhaled, or absorbed in the eyes.If the affected person survives the gastrointestinal phase of toxicity, they may experience multiple organ failure and critical illness.

Colchicine interferes with several inflammatory pathways including adhesion and recruitment of neutrophils, superoxide … Similar binding was demonstrated in vitro and was confined to a component of the soluble fraction. Borisy GG, Taylor EW. Colchicine is an alkaloid isolated from Colchicum autumnale with anti-gout and anti-inflammatory activities.

Curr Rheumatol Rep. 2008 Jul;10(3):218-27. Two proteins, P-glycoprotein (P-gp) and CYP3A4 seem to play a pivotal role, governing its pharmacokinetic. In patients with recent myocardial infarction (recent heart attack), it has been found to reduce risk of future cardiovascular events. This site needs JavaScript to work properly.

There is no conflict of interest in regard to the content of the manuscript. COVID-19 is an emerging, rapidly evolving situation. 2016 Jun;45(6):e25. Colchicine binds to tubulin, thereby interfering with the polymerization of tubulin, interrupting microtubule dynamics, and disrupting mitosis. 2020 Jul 21;7:100045. doi: 10.1016/j.metop.2020.100045. doi: 10.1001/jamanetworkopen.2020.13136.Cureus.

eCollection 2020 Sep.Di Gregorio SE, Volkening K, Strong MJ, Duennwald ML.Int J Mol Sci. The right arm depicts the effect of higher concentrations of colchicine through microtubules depolymerization and mass reduction. CASPASE= cysteine-dependent aspartate-directed proteases, CCF= crystal-derived chemotactic factor, MSU=monosodium urate (gout) crystals, MICL= myeloid inhibitory C-type lectin-like receptor, NALP3=NACHT-LRRPYD-containing protein 3, TLR=toll-like receptors, MyD88= myeloid differentiation primary response gene 88, VEGF= vascular endothelial growth factor.Dashed lines refer to inhibitory activities and continuous lines to stimulatory activities of colchicine. Colchicine also has anti-fibrotic activities and various effects on endothelial function.

The FDA reviewed approved colchicine for gout flares, awarding Colcrys a three-year term of market exclusivity, prohibiting generic sales, and increasing the price of the drug from $0.09 to $4.85 per tablet.Numerous consensus guidelines, and previous randomized controlled trials, had concluded that colchicine is effective for acute flares of gouty arthritis. 1998 May;15(5):712-8. doi: 10.1023/a:1011914902121.Consult Pharm. Binding of colchincine-3H to cellular protein.

Colchicine’s effectiveness as a treatment for gout has been postulated to be due to its ability to block neutrophil-mediated inflammatory responses induced by monosodium urate crystals in synovial fluid. Newly described mechanisms include various inhibitory effects on macrophages including the inhibition of the NACHT-LRRPYD-containing protein 3 (NALP3) inflammasome, … Many of these cases are intentional overdoses, but others were accidental; for example, if the drug was not dosed appropriately for kidney function. [PMC free article] Borisy GG, Taylor EW. Nuki G(1). Epub 2014 Aug 21.Curr Pharm Des. COLCRYS potentially interferes with the inflammasome complex, which mediates IL-1β activation1 Prevents the activation, degranulation, and migration of neutrophils thought to mediate gout pain The effects described below have been proposed as the potential mechanism of action for colchicine in gout. Epub 2015 Oct 22.Semin Arthritis Rheum.

doi: 10.2174/1381612824666180123110042.

Epub 2016 Mar 2.Clin Ther.