colchicine/nekros

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Colchicine prevents tumor necrosis factor-induced toxicity in vivo.

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Tumor necrosis factor (TNF) toxicity was induced in vivo by intravenous administration of 15 micrograms of recombinant murine TNF-alpha per kg to galactosamine-sensitized mice. Within 8 h, the animals developed a fulminant hepatitis. Intravenous administration of 0.5 mg of colchicine per kg at 19

Serum interleukin-2 and tumor necrosis factor-alpha in primary biliary cirrhosis: decrease by colchicine and relationship to HLA-DR4.

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Colchicine improves liver function tests and survival in primary biliary cirrhosis (PBC); however, its mechanism of action in PBC is unknown. Because elevated interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF) have been found in various inflammatory diseases, we measured serum levels of IL-2

Role of Colchicine Treatment in Tumor Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS): Real-Life Data from the AIDA Network

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Objective: To analyze the potential role of colchicine monotherapy in patients with tumor necrosis factor receptor associated periodic syndrome (TRAPS) in terms of control of clinical and laboratory manifestations.

Effects of anti-tumor necrosis factor agents for familial mediterranean fever patients with chronic arthritis and/or sacroiliitis who were resistant to colchicine treatment.

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BACKGROUND Effectiveness of anti-tumor necrosis factor (anti-TNF) agents in colchicine-resistant familial Mediterranean fever (FMF) patients has attracted attention in recent years. OBJECTIVE We analyzed the effect of anti-TNF agents on clinical findings of colchicine-resistant FMF patients with

Etanercept plus colchicine treatment in a child with tumour necrosis factor receptor-associated periodic syndrome abolishes auto-inflammatory episodes without normalising the subclinical acute phase response.

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We investigated the cause of hereditary periodic fever syndrome in a Spanish child with recurrent long episodes of fever, migratory skin rash, myalgia, arthralgia, conjunctivitis and abdominal pain. Infectious and autoimmune causes were ruled out. No familial history was reported. Analysis of the

Successful treatment with anti-tumor necrosis factor (anti-TNF)-alpha of proteinuria in a patient with familial mediterranean fever (FMF) resistant to colchicine: anti-TNF drugs and FMF.

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Familial mediterranean fever (FMF) is an autoinflammatory disease characterized by recurrent attacks of fever, peritonitis, pleuritis, and genetically by autosomal recessive inheritance. The major renal involvement in FMF is the occurrence of amyloidosis that can be prevented by a daily regimen of

Colchicine has opposite effects on interleukin-1 beta and tumor necrosis factor-alpha production.

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To study the role of microtubules in cytokine production, the effect of the microtubule depolymerizing agent colchicine on lipopolysaccharide endotoxin (LPS)-induced interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) release by blood monocytes and alveolar macrophages were

Idiopathic recurrent pericarditis refractory to colchicine treatment can reveal tumor necrosis factor receptor-associated periodic syndrome.

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Recurrences develop in up to 20-50% of patients with acute pericarditis. Although different causes of recurrent pericarditis have been identified, the etiology remains obscure in most cases which are therefore labelled as idiopathic. Autoinflammatory syndromes include familial Mediterranean fever

Novel analogue of colchicine induces selective pro-death autophagy and necrosis in human cancer cells.

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Colchicine, a natural product of Colchicum autumnae currently used for gout treatment, is a tubulin targeting compound which inhibits microtubule formation by targeting fast dividing cells. This tubulin-targeting property has lead researchers to investigate the potential of colchicine and analogs as

Inhibition of LPS-induced tumor necrosis factor-alpha production by colchicine and other microtubule disrupting drugs.

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Colchicine has been shown to act as an antiinflammatory agent. In this study, we examined whether colchicine and other microtubule-depolymerizing drugs affected the production of TNF-alpha. When rat peritoneal macrophages were stimulated by LPS, addition of colchicine, vincristine, vinblastine or

A position for tumor necrosis factor inhibitors in the management of colchicine-resistant familial Mediterranean fever?

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Fatal colchicine toxicity: report of a case.

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This report describes fatal colchicine toxicity occurring after a total dose of 9.3 mg. The reaction was characterized by leukopenia, thrombocytopenia, hypotension. disseminated intravascular coagulation and metabolic acidosis. Autopsy findings included a markedly hypocellular bone marrow,

Does colchicine really induce bone formation in the rodent bone marrow?

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Intravenous injection of a single dose of colchicine into inbred strains of BALB/c and CFW/L1 mice and into WAG rats did not effect rapid intramedullar bone formation and resorption, as has been claimed by the research group from Tokyo Medical and Dental University [14-17]. The applied doses of

Chemical bursectomy of chickens with colchicine applied to the anal lips.

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To induce chemical bursectomy, 30 microliter colchicine dissolved in saline solution (1 mg/ml) was applied on the anal lips of White Leghorn chickens once daily for four consecutive days after hatching. Histologic characteristics of the bursa of Fabricius, spleen, thymus, cecal tonsils, and rectal

Impact of Periprocedural Colchicine on Postprocedural Management in Patients Undergoing a Left Atrial Appendage Ligation Using LARIAT.

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BACKGROUND Left atrial appendage (LAA) can be effectively and safely excluded using a novel percutaneous LARIAT ligation system. However, due to pericardial catheter manipulation and LAA ligation and subsequent necrosis, postprocedural course is complicated by pericarditis. We intended to evaluate

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