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PubMed1983

Effects of cytochalasin D and colchicine on the uptake, translocation, and biliary secretion of horseradish peroxidase and [14C]sodium taurocholate in the rat.

The roles of microfilaments and microtubules in the hepatocellular uptake, translocation, and biliary excretion of horseradish peroxidase and [14C]sodium taurocholate were investigated using the microfilament inhibitor cytochalasin D and the microtubule inhibitor colchicine. In separate studies, horseradish peroxidase and [14C]taurocholate were injected separately as a bolus into rat portal veins after treatment with cytochalasin D or colchicine, and bile was collected and analyzed for the presence of horseradish peroxidase and [14C]taurocholate. Cytochalasin D treatment depressed bile flow by approximately 50% and decreased the biliary secretion of [14C]taurocholate in direct proportion to bile flow. Horseradish peroxidase secretion into bile was unaffected, and total biliary protein secretion was decreased only slightly. Because of the depression of bile secretion, concentrations in bile of horseradish peroxidase and total biliary protein increased significantly. Consistent with reported observations of cytochalasin D, decreases in microfilaments and dilated bile canaliculi were observed by electron microscopy; however, the vesicular transport of horseradish peroxidase as observed using electron microscopy cytochemistry appeared to be normal and unaffected by cytochalasin D treatment. Colchicine, in contrast, had minimal effect on bile flow and did not diminish the biliary secretion of [14C]taurocholate. Colchicine inhibited both the total amount of horseradish peroxidase secreted into bile as well as the rate of its secretion in comparison with control and cytochalasin D-treated animals. Cellular morphology was consistent with published observations for colchicine, which included a marked decrease in microtubules. In addition, after electron microscopy cytochemistry there was a paucity of horseradish peroxidase-containing vesicles within the hepatocytes, suggesting that colchicine interfered with the vesicular transport of horseradish peroxidase. Collectively, the data suggest that (a) the mechanism used by hepatocytes for the secretion of bile acids is independent of the vesicular transport of biliary proteins and is dependent upon intact microfilaments and (b) such vesicular transport of protein into bile requires an intact and functioning microtubular network.

Animals↗

PubMed1983

Effect of colchicine on heart lipoprotein lipase.

Changes in heart lipoprotein lipase (LPL) activity provoked by colchicine (0.5 mg/100 g body weight) and heparin (10 IU/100 g body weight) were studied in heart homogenates and serum from rats treated with both drugs or with heparin alone. In addition experiments were carried out in vitro in which the action of colchicine alone and colchicine plus heparin was compared with controls. In vivo experiments showed that colchicine decreased post-heparin release of the enzyme in fed animals, but was incapable of doing so in fasted animals. Accordingly, heart LPL activity, expressed in percentage of control values, did not change in fed animals, but significantly decreased (p less than 0.05) in fasted animals. In the in vitro experiments, colchicine significantly decreased heart LPL activity (p = 0.025) whether or not heparin was present and regardless of the nutritional state of the rats. Apparently, colchicine has two distinct actions on heart LPL activity: a direct one on the enzyme and another mediated by the nutritional state of the animal.

Animals↗

PubMed1981

[Mouse cell line with stable inheritance of colchicine resistance].

A new mouse cell line B-82CH(R)-9 is described, which is 25-fold more resistant to the cytotoxic action of colchicine than the known lines. The drug resistance of this cell line originates from the decreased plasmic membrane permeability. This follows from several facts: 1) 3H-colchicine uptake by intact resistant cells is decreased 5-10-fold; 2) the binding of labeled colchicine by extracts of resistant cells is unchanged; 3) colchicine resistant cells are cross-resistant to the drugs which are not active in binding the microtubular protein tubulin: the uptake of 3H-puromycin and 3H-cytochalasin B is decreased 2.1 and 2.5-fold, respectively. Unlike colchicine resistant mouse cell lines obtained earlier, the drug resistance of B-82CH(R)-9 cells is stable. After cultivation without a selective agent for 3 and 6 months the level of colchicine resistance remained unchanged.

Animals↗

PubMed1981

Colchicine in the treatment of Paget disease of bone: a new therapeutic approach.

Paget disease of the bone (PDB) has been treated effectively with various agents including calcitonins, diphosphonates, and mithramycin. Each agent has relatively serious toxic side effects or practical inconveniences associated with its use. An effective agent with fewer adverse reactions and a more convenient route of administration would be preferable. The purpose of this study was to evaluate the effect of colchicine for the treatment of PDB in five patients. All patients were symptomatic and had typical changes on roentgenograms and bone scans consistent with the disease. Serum alkaline phosphatase ranged from 408 to 1,311 mU/ml (normal, 30 to 115 mU/ml), and urinary excretion of total hydroxyproline ranged from 68 to 205 mg/24 hr (normal, 30 to 65 mg/24 hr). Colchicine, 0.6 mg, was given orally three times a day to each patient, who had subsequent follow-up with clinical and laboratory determinations evaluated at each visit. The duration of follow-up was eight to 28 weeks, with a mean of 20 weeks. Pain was relieved in all patients, and two became asymptomatic. Serum alkaline phosphatase decreased 18% to 38%, and urinary hydroxyproline decreased 26% to 53% from the pretreatment values. The biochemical values and and clinical symptoms changed markedly in two patients, correlating with withdrawal and reinstitution of colchicine. These results indicate that colchicine may be effective in the treatment of PDB. Although the mode of action and long-term efficacy of colchicine in this disorder remains to be evaluated, the antimitotic effect on osteoprogenitor cells, the adherence of colchicine to the microtubular structures in preexisting osteoblasts, and the nonspecific anti-inflammatory effect of this agent may explain the therapeutic response noted in this study.

Aged↗

PubMed1995

Characterization of the interaction of the marine cyanobacterial natural product curacin A with the colchicine site of tubulin and initial structure-activity studies with analogues.

Curacin A, the major lipid constituent of a strain of the marine cyanobacterium Lyngbya majuscula obtained off the coast of Curaçao, is a potent antimitotic agent that we have previously shown to inhibit microtubule assembly and colchicine binding to tubulin. In the present study, we report that curacin A probably binds in the colchicine site because it competitively inhibits the binding of [3H]colchicine to tubulin with an apparent Ki value of 0.6 microM and stimulates tubulin-dependent GTP hydrolysis, as do most other colchicine-site agents. The binding of curacin A to tubulin resembled the binding reactions of combretastatin A-4 and podophyllotoxin in contrast to that of colchicine in that it occurred as extensively on ice as at higher temperatures. However, once bound, the dissociation rate of curacin A from tubulin is very slow, more closely resembling that observed with colchicinoids (thiocolchicine was the drug examined) than the faster dissociation that occurs with combretastatin A-4 and podophyllotoxin. Because the molecular structure of curacin A is so different from that of previously described colchicine-site drugs (e.g., there is no aromatic moiety, and there are only two conjugated double bonds in its linear hydrocarbon chain), we have been examining the activities of natural isomers and synthetic derivatives. So far, only modest enhancement or reduction of activity has been observed with a variety of structural changes.

Animals↗

PubMed1995

Colchicine and cytochalasin B enhance cyclic AMP accumulation via postreceptor actions.

The role of cytoskeletal microtubules and microfilaments in modulating cAMP generation in S49 lymphoma cells was investigated using the agents colchicine and cytochalasin B, respectively, which are known to disrupt these structures. A 1-hr pretreatment of S49 cells with 10 microM colchicine typically enhanced maximal isoproterenol-(beta-adrenergic receptor) stimulated cAMP accumulation by 100%, whereas cytochalasin B increased isoproterenol-stimulated cAMP by 30%. The combination of colchicine and cytochalasin B synergistically enhanced agonist-stimulated cAMP to 225% over control values. A synergistic increase in cAMP accumulation was also observed in cells treated with the agonist prostaglandin E1 or cholera toxin (which activates the stimulatory guanine nucleotide regulatory (Gs) protein). Colchicine and cytochalasin B did not ablate the inhibitory effects of somatostatin or the stimulatory effect of pertussis toxin treatment on beta-receptor-stimulated cAMP accumulation, indicating that these cytoskeletal disrupting agents do not enhance responsiveness in S49 cells via alterations in the inhibitory guanine nucleotide regulatory protein pathway. Moreover, colchicine, but not cytochalasin B treatment, enhances expression of isoproterenol-promoted 3H-forskolin binding in intact cells (a measure of Gs/adenylyl cyclase coupling). Thus, colchicine and cytochalasin B appear to enhance signaling in the Gs/adenylyl cyclase pathway by alterations of components distal to hormone receptors, most likely at the Gs protein and/or via cAMP generation. These results imply that microtubules and microfilaments can interact in the regulation of this pathway and that increases in cellular cAMP may contribute to the action of drugs that alter function of these cytoskeletal elements.

Adenylyl Cyclases↗

PubMed1994

Interaction of desacetamidocolchicine, a fast binding analogue of colchicine with isotypically pure tubulin dimers alpha beta II, alpha beta III, and alpha beta IV.

Desacetamidocolchicine (DAAC) is a colchicine analogue that lacks the acetamido side chain in the ring-B of colchicine. Unlike colchicine, it binds to tubulin very quickly, and yet it has powerful antimitotic properties. It has been demonstrated that the beta-tubulin isoforms differ significantly in their interactions with colchicine. In an effort to understand the role of the ring-B of colchicine, we have studied the interaction of DAAC with purified beta-tubulin isoforms. The association was studied fluorometrically using a stopped-flow instrument under pseudo-first-order conditions in the presence of a large excess of drug. The observed pseudo-first-order rate constants increased in a nonlinear way with the drug concentration, indicating that the binding of DAAC to tubulin isoforms occur in two steps as is true for the binding of colchicine to tubulin (Garland, D.L. (1978) Biochemistry 17, 4266-4272), [formula: see text] where the first step is a fast reversible binding and the second step is a slow conformational change leading to the formation of the stable complex (T.DAAC)*. Kinetic analysis shows that the tubulin isoforms exhibit very little differences in their K1 values, which are 5794 +/- 670, 7109 +/- 1800, and 8993 +/- 1780 M-1 for alpha beta II, alpha beta III, and alpha beta IV, respectively. The k2 values for alpha beta II, alpha beta III, and alpha beta IV are 0.67 +/- 0.05, 0.05 +/- 0.006, and 0.59 +/- 0.07 s-1, respectively. The apparent on-rate constants (k(on,app) = K1k2) for alpha beta II, alpha beta III, and alpha beta IV are 3907 +/- 530, 376 +/- 80, and 5305 +/- 1200 M-1 s-1, respectively. The off-rate constants as measured by the loss of fluorescence of drug-tubulin complexes in the presence of a large excess of podophyllotoxin are 6.3 x 10(-4), 5.2 x 10(-4), and 5.7 x 10(-4) s-1, respectively, for alpha beta II, alpha beta III, and alpha beta IV. The affinity constants as determined by Scatchard analyses are 2.5 x 10(6), 1.5 x 10(6), and 4 x 10(6) M-1 for alpha beta II, alpha beta III, and alpha beta IV, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

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

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. The control group received no medications. The remaining four groups received 0.1, 0.5, 1, and 2 mg, respectively, of colchicine intramuscularly daily for 14 days. The day after the last injection of colchicine, the peritoneal cavity was explored and assessed for the presence, number, and grade of adhesions. RESULTS: With increasing doses of colchicine, the incidence of adhesions decreased. A linear model (log [dose + 0.5]) showed, however, that as the dose of colchicine increased, the response tended to plateau (P < .05). CONCLUSION: In this model, colchicine was effective in preventing inflammatory adhesions in the rabbit. Increasing doses produced a greater effect in reducing adhesion formation. However, there was a plateau of the response at the 1-mg dose.

Animals↗

PubMed1993

Evidence for an alternative pathway for colchicine binding to tubulin, based on the binding kinetics of the constituent rings.

The kinetics of tropolone methyl ether binding to tubulin were measured by following the loss of colchicine binding capacity upon preincubation of tubulin with tropolone methyl ether. At 25 degrees C a bimolecular association rate constant of 2.7 (+/- 0.2) M-1 min-1 was determined, and from the temperature dependence an activation energy of 37 (+/- 8) kJ.mol-1 was calculated. By displacement experiments a dissociation rate constant of 2.9 (+/- 0.6) x 10(-2) min-1 was determined at 25 degrees C. The effect of 3',4',5'-trimethoxyacetophenone (TMA) is 2-fold. TMA reduces the apparent association rate constant of colchicine, indicating that it equilibrates very rapidly and reversibly with the colchicine binding site. From this reduction the binding constant for TMA can be obtained. At 25 degrees C a value of 112 (+/- 13) M-1 is estimated. The binding of TMA is practically thermoneutral. Preincubation of tubulin with TMA over 30 min not only reduces the subsequent binding rate constant of colchicine but also the amplitude. This indicates that TMA also binds slowly in a second mode or site. Stopped-flow kinetic studies reveal that fast TMA binding competes for the initial binding of colchicine. From these results it is concluded that colchicine binds initially with its trimethoxybenzene ring and in a subsequent step with the tropolone ring.

Acetophenones↗

PubMed1997

C-anaphases (common variant) are unrelated to colchicine and phytohemagglutinin.

We evaluated the effect of different concentrations of colchicine (0.0, 0.1, 0.3, 0.5 microgram/ml) and phytohemagglutinin (PHA) (0.10, 0.15, 0.20 microgram/ml) on the rate of C-anaphases in lymphocyte cultures from five healthy individuals with the common variant of C-anaphases. For each of the 12 possible combinations, two subjects were randomly tested. The frequency of these variant figures was < 3%; a single-culture (out of six with the colchicine concentration of 0.1 microgram/ml) lacked C-anaphases. Multiple variance and Student's t tests revealed, as the only significant difference, a decrease with the colchicine concentration of 0.3 microgram/ml compared with the cultures without colchicine (p < 0.05), which exhibited the greatest ratio of C-anaphases. The PHA had no influence on the frequency of C-anaphases. We conclude that the common variant of C-anaphases is unrelated to the colchicine and PHA concentrations tested; moreover, our data confirm the occurrence of such a mitotic variant in colchicine-free cultures.

Adult↗

PubMed1998

Effects of colchicine and colchiceine in a biochemical model of liver injury and fibrosis.

BACKGROUND: The accumulation of collagen is a salient feature of chronic liver injury. The objective of this study was to investigate and compare the therapeutic effectiveness of colchicine and one of its metabolites, colchiceine, to protect rats from developing liver injury and fibrosis. METHODS: To accomplish this, the authors used a procedure developed by others to produce liver injury and fibrosis by chronic administration of CCl4 in rats. The effect of both compounds on collagen metabolism and liver injury was analyzed. RESULTS: Although both compounds prevented increase in collagen synthesis, animals treated with colchicine did not show a reduction in collagen content compared with animals treated with CCl4. On the other hand, the animals treated with colchiceine along with CCl4 showed a 50% reduction in hepatic collagen content as well as an improvement in histological architecture. Both compounds, colchicine and colchiceine, increased the intracellular degradation of collagen in addition to increasing collagenase activity as compared to non-treated rats. However, collagenase activity was lower in animals treated with colchicine and colchiceine than in the fibrotic livers treated with CCl4. The changes in collagen metabolism correlated with changes in parameters of liver injury. CONCLUSIONS: In conclusion, the compound colchiceine may be recommended in the treatment of chronic liver diseases rather than its precursor, colchicine, due to the fact that it showed a lower accumulation of collagen content and has a better anti-fibrogenic effect than does colchicine.

Animals↗

PubMedDate not supplied

Effects of colchicine on inflammatory cytokines and selectins in familial Mediterranean fever.

OBJECTIVE: To evaluate whether basal levels of circulating cytokines and selectins exhibit a distinct profile in attack-free, non-colchicine taking familial Mediterranean fever (FMF) patients compared to normal healthy controls, and to determine the effect of colchicine treatment on these parameters. METHODS: Serum levels of interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-alpha, and soluble P-, E-, and L-selectin in attack-free, asymptomatic, non-colchicine using FMF patients (n = 11) and in normal controls (n = 10) were studied. Following 2 months of colchicine treatment the same parameters were evaluated again in the FMF patients. RESULTS: Before colchicine treatment the serum levels of all parameters except soluble P-selectin were significantly higher in FMF patients than in controls. After two months of treatment statistically significant decreases were observed in these parameters (p < 0.05). CONCLUSION: A distinct profile of IL-6, IL-8, TNF-alpha, and soluble E- and L-selectin levels was observed in FMF patients, which could reflect the presence of sustained inflammation in attack-free FMF patients. The effect of colchicine on these parameters suggests its therapeutic potential.

Adult↗

PubMed1988

Energy-transfer studies of the distance between the high-affinity metal binding site and the colchicine and 8-anilino-1-naphthalenesulfonic acid binding sites on calf brain tubulin.

The high-affinity metal divalent cation Mg2+, associated with the exchangeable guanosine 5'-triphosphate (GTP) binding site (E site) on purified tubulin, has been replaced by the transition metal ion Co2+ on tubulin as well as on the tubulin-colchicine, tubulin-allocolchicine and tubulin-8-anilino-1-naphthalenesulfonic acid (tubulin-ANS) complexes. While pure native tubulin readily incorporated 0.8 atom of Co2+ per tubulin alpha-beta dimer, incorporation was reduced to 0.4 atom of Co2+ per mole of tubulin when it was complexed with colchicine, indicating that the conformational change induced in tubulin by the binding of colchicine leads to a reduced accessibility of the divalent cation binding site linked to the E site without necessarily changing the intrinsic binding constant. The fluorescence emission spectra of tubulin-bound colchicine, allocolchicine, and ANS displayed a strong overlap with the Co2+ absorption spectrum, identifying these as adequate donor-acceptor pairs. Fluorescence energy-transfer measurements were carried out between tubulin-bound colchicine (or allocolchicine) and ANS as donors and tubulin-complexed Co2+ as acceptor. It was found that the distance between the ANS and the high-affinity divalent cation binding sites is greater than 28 A, while that between the colchicine and the divalent cation binding sites is greater than 24 A.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilino Naphthalenesulfonates↗

PubMed1984

Binding to tubulin of the colchicine analog 2-methoxy-5-(2', 3', 4'-trimethoxyphenyl)tropone. Thermodynamic and kinetic aspects.

The thermodynamics and kinetics of the binding to tubulin of the colchicine analog 2-methoxy-5-(2', 3', 4'-trimethoxyphenyl) tropone (termed AC because it lacks the B-ring of colchicine) have been characterized by fluorescence techniques. The fluorescence of AC is weak in aqueous solution and is enhanced 250-fold upon binding to tubulin. The following thermodynamic values were obtained for the interaction at 37 degrees C: K = 3.5 X 10(5) M-1; delta G0 = -7.9 kcal/mol; delta H0 = -6.8 kcal/mol; delta S0 = 3.6 entropy units. The AC-tubulin complex is 1-2 kcal/mol less stable than the colchicine-tubulin complex. The change in fluorescence of AC was employed to measure the kinetics of the association process, and quenching of protein fluorescence was used to measure both association and dissociation. The association process, like that of colchicine, could be resolved into a major fast phase and a minor slow phase. The apparent second order rate constant for the fast phase was found to be 5.2 X 10(4) M-1 S-1 at 37 degrees C, and the activation energy was 13 kcal/mol. This activation energy is 7-11 kcal/mol less than that for the binding of colchicine to tubulin. The difference in activation energies can most easily be rationalized by a mechanism involving a tubulin-induced conformational change in the ligand ( Detrich , H. W., III, Williams, R. C., Jr., Macdonald, T. L., Wilson, L., and Puett , D. (1981) Biochemistry 20, 5999-6005). Such a change would be expected to have a small activation energy in AC because it possesses a freely rotating single bond in place of the B-ring of colchicine.

Animals↗

PubMed1987

Fertility and obstetric history in patients with familial Mediterranean fever on long-term colchicine therapy.

The obstetric histories were examined for 36 women with familial Mediterranean fever (FMF) on long-term colchicine treatment followed for periods ranging between 3 and 12 years. Seven of 28 pregnancies (25%) associated with colchicine therapy ended in miscarriage. Thirteen women (36%) had periods of infertility; these were due to ovulatory dysfunction in six women, to peritoneal adhesions in four and remained unexplained in three women. The rates for miscarriage and infertility are high but are similar to those reported for women with FMF before colchicine therapy was introduced. All 16 infants born to mothers who had taken colchicine during pregnancy were healthy. Currently, we do not advise discontinuation of colchicine before planned pregnancy but recommend amniocentesis for karyotyping and reassurance.

Abortion, Spontaneous↗

PubMed1986

Low-dose colchicine inhibits astrocyte, fibroblast, and retinal pigment epithelial cell migration and proliferation.

We studied the effect of low-dose colchicine on cell proliferation and migration. Colchicine at doses well below the level of ocular toxicity was found to be a potent inhibitor of astrocyte, fibroblast, and retinal pigment epithelial (RPE) cell proliferation and migration. A colchicine concentration of 1.3 X 10(-8) mol/L, 10(-8) mol/L, and 1.7 X 10(-8) mol/L showed a 50% inhibition of proliferation for RPE, astrocytes, and fibroblasts, respectively. At 10(-7) mol/L, colchicine inhibited 44%, 46%, and 93% of RPE, astrocyte, and fibroblast migration, respectively. Low-dose colchicine appears to be an effective inhibitor of RPE, astrocyte, and fibroblast migration and proliferation in vitro.

Astrocytes↗

PubMed1984

Influence of colchicine and vinblastine on the intracellular migration of secretory and membrane glycoproteins: III. Inhibition of intracellular migration of membrane glycoproteins in rat intestinal columnar cells and hepatocytes as visualized by light and electron-microscope radioautography after 3H-fucose injection.

In the first paper of this series (Bennett et al., 1984), light-microscope radioautographic studies showed that colchicine or vinblastine inhibited intracellular migration of glycoproteins out of the Golgi region in a variety of cell types. In the present work, the effects of these drugs on migration of membrane glycoproteins have been examined at the ultrastructural level in duodenal villous columnar cells and hepatocytes. Young (40 gm) rats were given a single intravenous injection of colchicine (4.0 mg) or vinblastine (2.0 mg). At 10 min after colchicine and 30 min after vinblastine administration, the rats were injected with 3H-fucose. Control rats received 3H-fucose only. All rats were sacrificed 90 min after 3H-fucose injection and their tissues processed for radioautography. In duodenal villous columnar cells, 3H-fucose labeling of the apical plasma membrane was reduced by 51% after colchicine and by 67% after vinblastine treatment; but there was little change in labeling of the lateral plasma membrane. Labeling of the Golgi apparatus increased. This suggests that labeled glycoproteins destined for the apical plasma membrane were inhibited from leaving the Golgi region, while migration to the lateral plasma membrane was not impaired. In hepatocytes, labeling of the sinusoidal plasma membrane was reduced by 83% after colchicine and by 85% after vinblastine treatment. Labeling of the lateral plasma membrane also decreased, although not so dramatically. Labeling of the Golgi apparatus and neighboring secretory vesicles increased. This indicates that the drugs inhibited migration of membrane glycoproteins from the Golgi region to the various portions of the plasma membrane. Accumulation of secretory vesicles at the sinusoidal front suggests that exocytosis may also have been partially inhibited. In both cell types, microtubules almost completely disappeared after drug treatment. Microtubules may, therefore, be necessary for intracellular transport of membrane glycoproteins, although the possibility of a direct action of these drugs on Golgi or plasma membranes must also be considered.

Animals↗

PubMed2002

A randomized controlled trial to evaluate the slow-acting symptom-modifying effects of colchicine in osteoarthritis of the knee: a preliminary report.

OBJECTIVE: To determine if colchicine added to nimesulide may have a beneficial effect on osteoarthritis (OA) of the knee. METHODS: Colchicine 0.5 mg twice daily or placebo was added to nimesulide (a nonsteroidal antiinflammatory drug) in 36 patients with OA of the knee in a randomized, double-blind, placebo-controlled trial over a 5-month period. RESULTS: The 30% improvement rate at 20 weeks was higher in the colchicine group than in the control group receiving placebo, as measured by total Western Ontario and McMaster University Osteoarthritis scores (57.9% versus 23.5%) and visual analog scale for index knee pain (52.6% versus 17.6%) (primary measures of response). The significance persisted on combined analysis by Mantel-Haenszel test (P = 0.062). Comparison of means also showed significant improvement in the colchicine group versus the control group in a multivariate analysis performed using T(2) test (P = 0.0115). CONCLUSION: Among patients with OA of the knee, the group receiving colchicine plus nimesulide exhibited significantly greater symptomatic benefit at 20 weeks than did the control group receiving nimesulide plus placebo.

Anti-Inflammatory Agents, Non-Steroidal↗