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PubMedDate not supplied

Multiple organ failure in a kidney transplant patient receiving both colchicine and cyclosporine.

Colchicine is a relatively safe and effective medication when given at appropriate doses to patients with normal kidney and liver function. A clinical picture of multiple organ failure has been described in cases of colchicine poisoning and in kidney graft recipients treated with usual doses of colchicine during cyclosporine therapy. We report a case of multiple organ failure in a renal transplant patient who received appropriate doses of colchicine in combination with cyclosporine therapy. Interaction between colchicine and cyclosporine is postulated but boosting of CSA toxicity was excluded because of the low CSA blood through levels before and throughout the episode, in the presence of relatively stable renal function and for the prompt CSA withdrawal. Mechanism of toxicity and modulation of the P-glycoprotein by cyclosporine are reviewed. Although the proscription of the drug in cyclosporine-treated patients is not justified, caution is recommended in prescribing colchicine to patients receiving cyclosporine therapy, particularly in the presence of suboptimal kidney graft function.

Colchicine↗

PubMed2003

Safety of colchicine therapy during pregnancy.

QUESTION: A 27-year-old patient in our clinic with familial Mediterranean fever (FMF) has been treated with colchicine for the last decade. She is planning her first pregnancy. What recommendations should we give her regarding use of colchicine before and during pregnancy, bearing in mind that discontinuation of colchicine could lead to complications from amyloidosis? ANSWER: Colchicine passes through the placenta in humans, is teratogenic in animals, and raises rates of male and female infertility. Based on several patients with chromosomal anomalies, some authorities recommend that patients who require colchicine therapy during pregnancy undergo amniocentesis with karyotyping. In contrast, an increasing body of evidence suggests that colchicine use throughout pregnancy carries no substantial teratogenic or mutagenic risk when used at recommended doses. Its use prevents febrile attacks of FMF and reduces the frequency of renal complications.

Amyloidosis, Familial↗

PubMedDate not supplied

The efficacy of continuous interferon alpha administration as an adjunctive agent to colchicine-resistant familial Mediterranean fever patients.

OBJECTIVE: About 10-20% of familial Mediterranean fever (FMF) patients are resistant to regular colchicine treatment and have painful recurrent attacks due to polyserositis. In clinical practice there is no alternative drug for such patients. In a previous pilot study on a small number of colchicine-resistant patients, interferon-alpha (IFN-alpha) was administered when painful attacks were about to occur. METHODS: In this study we gave IFN-alpha continuously to 8 colchicine-resistant FMF patients in a schedule while the colchicine therapy had been continued. All those patients were complicated with vasculitis or arthritis or together during the FMF course. Those complications were treated with the other immunosuppressive drugs. While they were under intense immunosuppressive therapy, the abdominal and the other serosal attacks remained to continue. RESULTS: After the administration of IFN-alpha therapy only one out of eight patients had abdominal painful attacks in twice, and one patient had arthritis in knees and ankles, the others responded well. Observed side effects were generally mild and acceptable. CONCLUSION: Continuous IFN administration in addition to the regular colchicine treatment may be useful for the colchicine-resistant attacks in FMF patients.

Adjuvants, Immunologic↗

PubMed1992

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

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 and TNF in 28 PBC patients before and during treatment with either colchicine or placebo. Compared with normal controls, untreated PBC patients had increased serum IL-2 (39 +/- 13 U/ml vs. 0.8 +/- 0.5) and TNF (549 +/- 162 pg/ml vs. nondetectable). During colchicine treatment, both IL-2 and TNF levels decreased significantly (57 +/- 24 to 40 +/- 22, p less than 0.04; 586 +/- 295 to 445 +/- 295, p less than 0.02). No significant changes in IL-2 or TNF levels occurred in the placebo-treated patients. DR4-positive patients had elevated levels of IL-2 at entry, compared with DR4-negative patients (67 +/- 26 vs. 14 +/- 5, p less than 0.04). The effect of colchicine in PBC may be due, in part, to modulation of IL-2 and TNF levels. Alternatively, the changes in IL-2 and TNF may simply reflect the overall improvement in biochemical tests of liver function related to colchicine therapy. DR4 appears to relate to serum levels of these cytokines in PBC and, possibly, also to the response to colchicine.

Biological Assay↗

PubMed2005

[A case report of acute neuromyopathy induced by concomitant use of colchicine and bezafibrate].

We report a patient of acute neuromyopathy induced by concomitant use of colchicine and bezafibrate. A 75-year-old man with chronic renal failure and hyperlipidemia treated with bezafibrate (400 mg/day) for 1.5 years had developed watery diarrhea followed by acute tetraparesis, 14 days after the administration of colchicine for recurrent gout. Neurological examination showed proximal muscle weakness with myalgia, distal mild numbness (dysesthesia) of four limbs and generalized decreased or absent reflexies. The findings including elevated serum muscle enzymes, myogenic patterns with widespread myotonic discharge on the electromyography and delayed latency of F-wave on nerve conduction study indicated that the patient's clinical features were consistent with neuromyopathy. Soon after both colchicine and bezafibrate were stopped, the patient's symptoms resolved rapidly, therefore we made a diagnosis of drug-induced neuromyopathy, although rhabdomyolysis with Guillain-Barré syndrome was initially suspected. Recently, there had been reported acute and severe neuromuscular disorder induced by combination therapy with colchicine and anti-hyperlipidemic drugs, and there were clinical similarities between the cases of these reports and our case. Co-administration of colchicine with bezafibrate might accelerate the onset of neuromyopathy in connection with chronic renal failure in this case. Extreme caution is warranted when the patient with renal insufficiency concomitant use of colchicine and bezafibrate.

Acute Disease↗

PubMed2005

Colchicine and benzathine penicillin in the treatment of Behçet disease: a case comparative study.

Behçet disease is a chronic relapsing disease characterized by multiple signs and symptoms such as recurrent orogenital ulceration, eye involvement, skin manifestations, and other systemic involvement. Multiple therapeutic modalities have been used to treat Behçet disease. These agents act through different mechanisms and are associated with a variety of side effects. We performed a case-comparative study to evaluate efficacy of combined colchicine and benzathine penicillin in the treatment and prophylaxis of Behçet disease. Sixty-six patients who fulfilled the international study group criteria for diagnosis of Behçet disease were included. The patients were divided into three groups: group 1 (20 patients) received 1.2 Mu benzathine penicillin injection monthly; group 2 (21 patients) received two tablets of colchicine daily (each tablet contained 0.5 mg); and group 3 (25 patients) received both 1.2 Mu benzathine penicillin injection monthly and two tablets of colchicine daily. Each patient was followed up monthly for 5 months, 4 months on treatment and 1 additional month followup. The clinical manifestation index (CMI), the numerical sum of the clinical features, was calculated for each patient initially and then monthly. Pathergy test was performed for each patient monthly. The CMI was reduced by colchicine and benzathine penicillin treatment, and the reduction was highly significant. The reduction in the CMI remains satisfactory and good for 1 month after stopping the treatment. When each colchicine and benzathine Penicillin are used alone the index is also reduced significantly, but this reduction is much less than when both drugs are used together and there is also rapid and earlier relapse. Based on our findings, the combination of colchicine and benzathine penicillin appears to be of greater efficacy in the treatment of Behçet disease than the use of either drug alone.

Adult↗

PubMed1991

Colchicine: a state-of-the-art review.

Colchicine is an ancient drug that is attracting renewed interest because of its actions at a subcellular level. Specifically, it interferes with microtubule growth and therefore affects mitosis and other microtubule-dependent functions. Various mechanisms have been proposed to account for the action of colchicine in acute gouty arthritis, its interaction with cellular membrane and cyclic 3',5'-adenosine monophosphate, and its action in amyloidosis. Pharmacokinetic studies have been relatively limited and their results somewhat contradictory, with mean terminal elimination half-lives of 19 minutes to 9 hours being reported. Some of these differences may be attributed to assay difficulties. Colchicine can cause gastrointestinal side effects and should be used with care to protect patients from toxic doses. Colchicine-induced myopathy and neuropathy may be more frequent than previously recognized, and therefore patients receiving long-term therapy should be monitored carefully. Bone marrow depression has been reported, primarily in cases of acute colchicine intoxication, and intravenous administration of the drug has been associated with severe pancytopenia and death. Colchicine intoxication causes multiple organ failure. Because of its cytogenic effects and reported association with Down's syndrome, the agent should not be used by pregnant women.

Amyloidosis↗

PubMed1978

The subcellular distribution of [3H]-colchicine-binding activity and tubulin in pig blood platelets.

The subcellular distribution of the [3H]-colchicine-binding protein, believed to be tubulin, the subunit protein of microtubules, has been investigated in mammalian blood platelets. Studies on a soluble extract from pig platelets and two particulate fractions (viz. membrane-rich and granule-rich fractions) have shown that about 98% of the colchicine-binding activity in a platelet homogenate is located in the soluble phase. This result is in agreement with polyacrylamide gel electrophoresis experiments which show that the soluble fraction contains a substantial amount of 55,000 MW tubulin, whereas the membrane and granule-rich fractions contain very little of this component. The [3H]-colchicine-binding activity of the platelet soluble phase is largely precipitated by 40-50% ammonium sulphate and also by vinblastine sulphate in millimolar concentrations. Moreover the colchicine-binding protein in the platelet soluble fraction has a sedimentation coefficient of 5.9 S, is eluted in the void volume of a Sephadex G-100 column, and binds to DEAE-Sephadex at low ionic strength and is eluted from this ion-exchanger at an ionic strength of 0.47 M-KCl. In addition, most of the colchicine-binding activity of the platelet soluble phase is associated with protein which will undergo temperature-dependent polymerization in vitro and which has a molecular weight on SDS-polyacrylamide gels of 55,000. All these experimental findings suggest that the colchicine-binding activity of pig platelet homogenates is due to the presence of the microtubule protein, tubulin, which is largely found in the soluble compartment of the cells.

Actins↗

PubMedDate not supplied

Fatal i.v. colchicine injection in a 60-year-old woman.

Colchicine is a rather benign drug when used appropriately and with an understanding of its potential side effects and toxicity. However, colchicine toxicity, though uncommon, is life-threatening. It is especially devastating to geriatric or debilitated patients because of its cumulative effects. There are no toxicology tests that can detect specific blood levels of colchicine and there is no specific antidote for colchicine toxicity. Oral colchicine is administered until GI symptoms such as diarrhea occur. But when colchicine is administered intravenously, as in this patient, GI symptoms may not occur until it is too late and irreversible multiorgan system failure occurs. Careful consideration of dosage and route of administration of this drug can be crucial.

Colchicine↗

PubMed1989

[Value of colchicine in treating acquired epidermolysis bullosa].

In July 1986, a 46-year old male patient was admitted for a bullous skin disease of 4 years' duration. The disease fulfilled all the criteria of epidermolysis bullosa acquisita (EBA), as laid down by Roenigk and Pearson. Despite a guided investigation, none of the diseases classically associated with EBA could be found, but it must be noted that immunological stigmata of an old hepatitis B were present. After failures or partial results with prednisone alone (1 mg/kg/day from August to October 1986), then methotrexate (30 mg/week) combined with prednisone (20 mg/day), the patient was treated with colchicine in doses of 2 mg per day, and within a fortnight a dramatic improvement of buccal mucosal lesions and cutaneous fragility was observed. Colchicine was withdrawn, but 5 days later bullae and erosions of the mucosa reappeared. The reintroduction of colchicine in the same doses (2 mg/day) resulted in remission of the lesions. The disease has now remained stable for one year under colchicine 1 mg/day. Four attempts at reducing this dosage to 1 mg every other day brought about the recurrence of a few bullae and of cutaneous fragility. To our knowledge, colchicine has not yet been reported to be effective in the treatment of EBA. Its effectiveness may be due, to a great extent, to its immunomodulating properties, notably on some functions of neutrophils the role of which in the pathogenesis of bullous lesions seems to have been established. By modulating collagen synthesis and collagenase activity colchicine might induce structural modifications of the EBA antigen, identified as the carboxyterminal group of type VII collagen, and inhibit its recognition by autoantibodies.

Colchicine↗

PubMed1988

Review: systemic toxicity associated with the intravenous administration of colchicine--guidelines for use.

Published experiences with severe toxicity with intravenous colchicine have been reviewed. All reported cases reflect inappropriate use of the drug. Therapeutic rules for colchicine have been derived from this information: (1) Single intravenous doses should not exceed 2-3 mg, and cumulative total doses for an attack should not be more than 4-5 mg. (2) Patients should receive no more colchicine by any route for 7 days. (3) Colchicine doses must be reduced in the presence of renal or hepatic disease, and in the older patient with apparently normal renal function. (4) Intravenous colchicine doses should be half the size of oral ones. (5) Absolute contraindications to intravenous colchicine therapy for acute gout include combined renal and hepatic disease, creatinine clearances below 10 cc/min, and extrahepatic biliary obstruction.

Administration, Oral↗

PubMed1986

[Colchicine therapy of fibrosing liver diseases--report of a randomized double-blind study].

It is reported on results of a double blind study of colchicine therapy in fibrotic liver diseases over a period of three years. The study includes 74 probands; 37 of them had been treated after randomization for five days a week with 4 X 0,25 mg/d colchicine, 37 with placebo. 53 probands attained the 12th month of treatment, 43 of them 24th, 24 probands were in the study for 36 months. 3 diagnoses groups had been formed with regard to the histological grades of fibrosis: chronic hepatitis (without structural transformation); structural liver transformation/moderate liver cirrhosis; severe liver cirrhosis. In 38 cases the disease was caused by alcohol. 45 data had been studied (clinical results, paraclinical data concerning hepatological diagnostic and connective tissue metabolism and morphologic data). The biometric evaluation was carried out with the stage variant analysis by Friedman. Rebiopsies have been carried out in 40 probands after 1 year, in 4 probands after 2 years. 4 data (Serumalbumine, Gamma-GT, ALAT, KP) showed significant changes in the colchicine-group as well as in the placebo-group. In both therapy groups the morphologic supervisions of the fibrosis grades (rebiopsies) showed improvements, no changes, and deterioration about in the same frequency. In this study there was no effectiveness of colchicine on the course of fibrotic liver diseases to be stated. Concerning the contradictions in the recent literature and probable the insufficient colchicine dose, the authors recommend further studies on colchicine therapy in liver diseases with incipient i.e. reversible fibrosis.

Clinical Trials as Topic↗

PubMed1986

[Experimental study of the use of colchicine in alcoholic liver diseases].

Rats kept on a standard diet were subdivided into several experimental groups: group 1, control; group 2, animals receiving ethyl alcohol for 10 days; group 3, animals receiving ethyl alcohol for 3 months; group 4, animals receiving colchicine; group 5, animals receiving alcohol in combination with colchicine; group 6, animals receiving alcohol in combination with carbon tetrachloride (CCl4); and group 7, animals receiving alcohol in combination with CCl4 and colchicine. Electron microscopy of the rat liver has shown that colchicine inhibited significantly the onset of hepatic fibrosis and degenerative changes in hepatocyte organells induced by hepatotoxins (alcohol alone or alcohol in combination with CCl4). Colchicine also inhibited monooxygenase activity in the liver homogenate of experimental rats. Possible mechanisms of hepatoprotective colchicine effect are discussed.

Animals↗

PubMed1985

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

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 of spleen after 25 days. Treatment with 10 micrograms of colchicine daily decreased AgNO3-induced AA deposition to 12 +/- 1 ng of AA/mg of spleen (p less than 0.001). Colchicine diminished the acute phase serum amyloid A protein (SAA) response after 24 hours. Over a 25-day period, SAA concentrations declined and approached baseline both in colchicine-treated and (unexpectedly) in control mice. This suggested that suppression of SAA levels was not the primary event inhibiting amyloid deposition. In a model of accelerated amyloid deposition, injection of preformed amyloid-enhancing factor along with AgNO3 induced the deposition of 974 +/- 46 ng of AA/mg of spleen 48 hours later. Colchicine only partially decreased amyloid-enhancing factor-induced amyloid deposition to 578 +/- 91 ng of AA/mg of spleen, while blunting the acute phase SAA response. These results suggest that colchicine inhibits amyloidosis in the predeposition phase, possibly by blocking formation of amyloid-enhancing factor.

Amyloid↗

PubMed1981

Effects of colchicine on myelination of rabbit optic nerve: a biochemical study.

The effects of intravitreous injections of colchicine on the myelination of the optic nerve were studied in rabbits at different times during development using biochemical and morphological techniques. Myelin basic protein concentrations and 2',3-cyclic nucleotide 3'-phosphodiesterase activities were affected in a similar way by colchicine treatment and reflected the degree of myelination of the tissue. During early development, colchicine produced axonal degeneration and secondary demyelination (Wallerian degeneration). Later, axonal and myelin abnormalities were more variable. Some demyelination was observed amd myelin formation also may have been inhibited. Thus, the effect of colchicine was proportional to the degree of optic nerve and retinal maturation (the youngest being the most sensitive) and, to a lesser extent, to the dosage, Under conditions used for this study, no remyelination was observed. In adult animals, no lesions could be detected histologically one to four months after injection of colchicine, Thus, intravitreous administration of colchicine is a useful chemical technique for producing Wallerian degeneration in optic nerves of young developing rabbits.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1982

[Amplification of genome regions in the somatic cells of mammals resistant to colchicine. III. Localization of the amplified genes in minute chromatin bodies].

Small chromatin bodies (SCB) were revealed in Djungarian hamster cells resistant to colchicine. They looked like single bodies or like clusters of small particles. SCB were localized both in nucleus and cytoplasm. Similar formations were earlier observed in oocytes of insects with amplified extrachromosomal rDNA genes. DNA in the SCB was able to replicate not only during the S phase but also during other phases of the cell cycle. The restriction analysis showed that in cells with SCB DNA amplified sequences were replicated autonomously too. These data indicate that SCB in colchicine-resistant cells contain amplified genes. Besides, SCB double-minute chromosomes (DMs) were observed in some resistant sublines. In one of them, DMs were the only karyotypic alteration. The relationship between SCB, chromosomal homogeneously staining regions (HSRs) and DMs was studied. Single SCB and DMs appeared at the early stage of the development of colchicine-resistance (the level of drug resistance is 16-22). Selection of variants 170-220-fold resistant to colchicine was usually accompanied by the decrease in the cell number with SCB and DMs and by the increase in the amount of cells containing the chromosomes with HSRs. During the further enhancement of drug resistance (700-750), some decrease in the number of cells with HSRs and the appearance of the great number of cells containing large groups of SCB were found. The loss of colchicine-resistance observed during cultivation in colchicine free medium was accompanied by the disappearance of HSRs, emergence of SCB and DMs and further elimination of SCB and DMs from cells. The quantity of autonomously replicating amplified DNA fragments after digestive by HindIII was increased with the enhancement of SCB number in cultures.

Animals↗

PubMed1984

Immobilization-dependent fluorescence of colchicine.

Colchicine fluoresces when bound to tubulin but not in water, dioxane, or benzene. The basis of the fluorescence has now been investigated. Colchicine fluoresces in higher alcohols and shows a blue shift as a function of chain length. Glycerol produces a higher fluorescence efficiency and a further blue shift. Plots of 1/fluorescence versus T/eta yield straight lines for both alcohols and glycerol/water mixtures. Fluorescence in glycerol/dimethyl sulfoxide mixtures, in which the dielectric constant remains unchanged, varies as a function of solvent viscosity. Even highly nonpolar solvents such as dioxane require a threshold viscosity for fluorescence to occur. When solvent polarity was decreased at constant viscosity, there was also an enhancement of colchicine fluorescence, but this effect appeared to be smaller than that obtained with increasing viscosity. Immobilization by covalent attachment of desacetylcolchicine to thyroglobulin, serum albumin, or lysozyme also promotes fluorescence from the drug. By contrast, the highly rigid analogue of colchicine, imerubine, fluoresces in water and is unaffected by viscosity changes. We concluded that a major contribution to colchicine fluorescence stems from immobilization of colchicine in the site and that this response to immobilization depends, in part, on the partially flexible nature of the drug. Since certain other flexible molecules such as auramine O, reduced flavines, and diarylalkanes also require increased viscosity or binding to macromolecules to fluoresce at room temperature, we propose that immobilization-enhanced fluorescence may be more common than heretofore believed.

Animals↗

PubMed1983

Inhibition of ovulation in the rabbit by the antimitotic agent, colchicine.

This study establishes the optimum time to administer colchicine to inhibit ovulation in the rabbit, and it examines the effect of colchicine on prostaglandin biosynthesis in ovulatory follicles. Colchicine (2 mg/kg) was given at intervals ranging from 50 hours to 2 hours before ovulation. The ovulation efficiency was significantly reduced when colchicine was administered between 30 hours and 9 hours before ovulation, with maximum inhibition occurring at 20 hours before ovulation. Normal elevation in prostaglandin biosynthesis at the time of ovulation was significantly reduced when colchicine was given at 20 hours before ovulation, but not when it was given at 9 hours or 2 hours before ovulation. The results suggest that the mechanism by which the antimitotic agent colchicine inhibits prostaglandin biosynthesis and ovulation may be different from that of the nonsteroidal antiinflammatory agent indomethacin.

Animals↗