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Colchicine-responsive protracted gouty arthritis with systemic inflammatory reactions.

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Acute gouty arthritis is a severe but self-limiting arthritis caused by inflammatory responses to urate crystals. Oral colchicines are effective for initial stages or prophylaxis, but generally, colchicines are ineffective for established gouty arthritis. We describe an unusual case of gouty

Colchicine and post-inflammatory adhesions in a rabbit model: a dose-response study.

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OBJECTIVE To determine the dose-response relationship of colchicine in reducing inflammatory adhesive disease secondary to Neisseria gonorrhoeae in the rabbit. METHODS Following intrauterine inoculation of a suspension of N gonorrhoeae, the rabbits were divided into five groups of 11 rabbits each.

Etoricoxib inhibits peripheral inflammation and alters immune responses in intracerebroventricular colchicine injected rats.

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The present study was designed to investigate the effectiveness of etoricoxib induced inhibition of neuroinflammation by studying the peripheral inflammatory markers and select immune parameters in intracerebroventricular colchicine injected rats (ICIR). Results showed time dependent upregulation of

Colchicine in the treatment of the inflammatory phase of Graves' ophthalmopathy: a prospective and randomized trial with prednisone.

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OBJECTIVE To investigate if colchicine is valuable in the treatment of Graves' ophthalmopathy (GO), we compared its effect with prednisone in 22 patients during the inflammatory phase of GO. METHODS All patients, similar in age, sex and smoking habits, were euthyroid for at least 3 months and

Colchicine modulates expression of pro-inflammatory genes in neutrophils from patients with familial Mediterranean fever and healthy subjects.

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Colchicine (Col) is a microtubule depolymerizing drug, widely used for treatment of familial Mediterranean fever (FMF). Mechanisms by which Col exerts its beneficial effects are not yet completely understood, especially with respect to gene expression in polymorphonuclear neutrophils (PMNs), the

Colchicine suppression of local inflammation due to calcinosis in dermatomyositis and progressive systemic sclerosis.

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Two girls, one with progressive systemic sclerosis and a second with dermatomyositis, developed calcinosis in the skin of the prepatellar area. Calcinosis was accompanied by local inflammation and skin ulceration. Oral colchicine therapy in a dosage of 1 mg per day was followed within two months by

Colchicine effectiveness in symptom and inflammation modification in knee osteoarthritis (COLKOA): study protocol for a randomized controlled trial.

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BACKGROUND Despite the high prevalence and global impact of knee osteoarthritis (KOA), current treatments are palliative. No disease modifying anti-osteoarthritic drug (DMOAD) has been approved. We recently demonstrated significant involvement of uric acid and activation of the innate immune

Lithium + Colchicine: A Potential Strategy to Reduce Pro-inflammatory Effects of Lithium Treatment.

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OBJECTIVE Rosenblat and McIntyre (Acta Psychiatr Scand. 2015;132: 180-191) propose that immune disorders are important mediators between bipolar disorders and medical comorbidities. Rosenblat et al (Bipolar Disord. 2016;18:89-101) present a meta-analysis showing that adjunctive anti-inflammatory

Design and Biological Evaluation of Colchicine-CD44-Targeted Peptide Conjugate in an In Vitro Model of Crystal Induced Inflammation.

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Gout is an inflammatory arthritis due to the joint deposition of monosodium urate (MSU) crystals. Phagocytosis of MSU crystals by tissue macrophages results in the generation of reactive oxygen species (ROS) and production of inflammatory cytokines and chemokines. Colchicine use in gout is limited

A comparison of the anti-inflammatory activity of selective 5-lipoxygenase inhibitors with dexamethasone and colchicine in a model of zymosan induced inflammation in the rat knee joint and peritoneal cavity.

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Intraperitoneal and intra-articular (knee joint) injection of zymosan in the rat caused two phases of increased vascular permeability, a rapid increase (0.25-0.5 h) and a secondary increase (2-3 h) which was temporally associated with the onset of leukocyte infiltration. Intraperitoneal injection of

[Good response to colchicine in amyloidosis secondary to inflammatory bowel disease].

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Acquired systemic amyloidosis may develop during the course of a number of chronic inflammatory diseases, including inflammatory bowel disease. Amyloidosis, although rare, is life-threatening, especially when it involves the kidneys. It is important to recognize this complication, especially since

Effect of colchicine on experimental amyloidosis in two CBA/J mouse models. Chronic inflammatory stimulation and administration of amyloid-enhancing factor during acute inflammation.

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To investigate the mechanism of action of colchicine in blocking amyloid deposition, two model systems of amyloidosis in CBA/J mice were studied. In experimental chronic inflammation, daily injection of silver nitrate (AgNO3) resulted in the deposition of 667 +/- 68 ng of amyloid A protein (AA)/mg

Colchicine increases intestinal permeability, suppresses inflammatory responses, and alters gut microbiota in mice

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Although colchicine (COL) has been used to treat gout for more than a thousand years, it has been shrouded in a dark history for a long time due to its high toxicity, especially for the gastrointestinal tract. With the widespread clinical application of COL, COL's toxicity to the gastrointestinal

Inflammatory reaction in familial Mediterranean fever (FMF) before and with colchicine therapy.

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The familial mediterranean fever (FMF) is an inherited, autosomal, recessive disorder which occurs predominantly but not exclusively in Sephardic Jews. It is characterized by a total increase of blood complement components, particularly C4, without any molecular anomaly and associated with an

Misoprostol stimulates leukocyte cyclic adenosine 3',5' monophosphate production and synergizes with colchicine: novel combination of established drugs may boost anti-inflammatory potential.

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Elevation of intracellular cyclic adenosine 3',5' monophosphate (cAMP) inhibits various proinflammatory and immune responses of leukocytes. Among agents known to stimulate cAMP production in these cells, prostaglandins E (PGEs) have received particular attention as potential immunosuppressive and/or

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