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PubMed2004

Evaluation of the colchicine-like activity of Gloriosa superba-extracted fractions for mosquito (Diptera: Culicidae) cytogenetic study.

Four fractions of Gloriosa superba L., i.e., hexane fraction, dichloromethane fraction 1, dichloromethane fraction 2, and methanol fraction, were investigated for colchicine-like activity using a mosquito cytogenetic assay. The results revealed that the latter three fractions yielded promisingly high colchicine-like activity, whereas the hexane fraction yielded very low activity compared with 1% colchicine in a 0.85% sodium chloride solution. The metaphase rates and average number of metaphase chromosomes per positive brain ganglion (range) of Aedes aegypti L. larvae after incubation with 0.25-2% solutions of dichloromethane fraction 1, dichloromethane fraction 2, 0.5-2% solutions of methanol fraction, and 1% colchicine solution were 90-100% and 7 (2-19) to 22 (7-47); 90-100% and 4 (1-11) to 30 (4-73); 95-100% and 11 (1-28) to 17 (2-62); and 100% and 6 (2-11), respectively. The temperature stability tests of the three promising fractions were performed by heating 0.5% working solution at 121 degrees C for 15 min and preparing 0.5% working solution from stock frozen at -20 degrees C for 10 mo. These fractions also yielded satisfactory outcomes of metaphase rates and an average number of metaphase chromosomes per positive brain ganglia compared with 1% colchicine solution.

Animals↗
PubMed2000

Rapid colchicine competition-binding scintillation proximity assay using biotin-labeled tubulin.

We have developed a rapid [3H]colchicine competition-binding scintillation proximity assay (SPA) to evaluate antimitotic compounds that bind to the colchicine-binding site on tubulin. The premise of our assay is that compounds will compete with radiolabeled colchicine for the tubulin-binding domain. Biotin-labeled tubulin is incubated first with unlabeled compound and radiolabeled ligand. Streptavidin-labeled SPA beads are added, and the radiolabel associated with tubulin is directly counted with no separation steps. Under our experimental conditions, the dissociation constant of binding (Kd) for colchicine to tubulin was determined to be 1.4 microM, which was consistent with previously reported values. Assay validation was performed by competitively inhibiting [3H]colchicine binding to tubulin with known microtubule inhibitors and comparing their inhibition constants (Ki). Our SPA bead method is a powerful tool since it overcomes the disadvantage of traditional filtration techniques, as there are no separation steps. It is extremely easy to set up, multiple samples can be assayed and supply and labor costs are reduced because of the minimal volume and test reagents used.

Aminophenols↗
PubMed1996

Colchicine myopathy.

Colchicine myopathy typically presents as painless muscle weakness. This report describes a post renal-transplant patient who presented with pain in both extremities bilaterally that was refractory to narcotic analgesics. He had been on low dose daily colchicine for 7 years. Laboratory, EMG, and biopsy findings all supported the diagnosis of colchicine myopathy. Symptoms subsided after discontinuation of colchicine. Myalgia as chief complaint is an unusual presentation of colchicine myopathy.

Aged↗
PubMed1980

Systemic effects of colchicine on phosphate metabolism in innervated and denervated, slow and fast muscles of the rat.

A single systemic injection of 75 micrograms colchicine/100 g body weight increases the permeability to inorganic phosphate of both fast gastrocnemius and extensor digitorum longus muscles and of the slow soleus muscle. In the two fast muscles, there is a significant interaction between colchicine treatment and 5-d- or 30-d- surgical denervation. In the slow soleus muscle there is no interaction between 5-d-colchicine treatment and the initial decrease in phosphate flow due to 5-d-surgical denervation but a significant interaction between colchicine treatment and the secondary increase in phosphate permeability observed after a 30-d-surgical denervation. Thirty days after a single systemic injection of colchicine the muscle phosphate metabolism is still perturbed especially in the slow soleus muscle in which the initial decrease in radioactive uptake associated with a 5-d-surgical denervation is inapparent. It is proposed that colchicine induces denervation-like alterations in the Pi- and POAS metabolism of skeletal muscles through mechanisms which are also activated -- partly or entirely -- by surgical denervation. These alterations do not result from the interruption of the axonal flow. A direct effect on the muscle membrane seems less likely than a disinhibition or activation of the muscle protein synthesis system.

Animals↗
PubMed1999

Regulation of type I collagen and interstitial collagenase mRNA expression in human dermal fibroblasts by colchicine and D-penicillamine.

Sclerosis is a disease process in which idiopathic hardening occurs in the skin and/or internal organs as a result of the accumulation of type I collagen, induced mainly by transforming growth factor-beta. Colchicine and D-penicillamine are widely used for its treatment. Their effects are known to be due to post-translational down-regulation of type I collagen synthesis, with colchicine also up-regulating interstitial collagenase. To determine whether or not they have any pre-translational effect on type I collagen and MMP-1, and also to observe their effects on the action of TGF-beta, cultured neonatal foreskin fibroblasts were treated with colchicine and D-penicillamine, singly and together. The amount of type I collagen and MMP-1 mRNA were quantitated by Northern blot hybridization. Colchicine suppresses the basal level of type I collagen mRNA but minimally stimulates the mRNA expression of MMP-1, whereas D-penicillamine does not have any significant effects on either. Colchicine was also able to significantly suppress the TGF-beta-induced up-regulation of type I collagen mRNA expression.

Cells, Cultured↗
PubMed1977

Efficacy of intermittent colchicine therapy in familial Mediterranean fever.

Nine patients with familial Mediterranean fever (FMF) were admitted to a controlled, double-blind trial to determine if there are patients with this disease who are able to abort their acute episodes of pain and fever with short courses of colchicine taken at the onset of attacks. Five patients completed their treatment assignments, and colchicine was significantly effective in aborting the attacks of three but was ineffective in two. The remaining four patients could not be assessed because of insufficient numbers of courses. During the 10 months of the trial, 28 courses of colchicine and 31 of placebo were taken during the early stages of FMF attacks. Twenty-one (75%) colchicine courses were followed by attacks considered to have been aborted, compared to only three (10%) placebo courses. This trial shows that patients can recognize the prodrome of their FMF attacks and that some patients can consistently abort their attacks with short courses of colchicine taken at the very onset of symptoms.

Adolescent↗
PubMed1976

Colchicine inhibition of the first phase of amyloid synthesis in experimental animals.

Colchicine was found to inhibit the first phase of casein-induced synthesis of murine amyloid. When mice were treated with colchicine during the first 7 days of an amyloid induction regimen or when colchicine was given to the donor mice in a transfer model, the amyloidogenic stimulus of casein was blocked completely. Amyloid synthesis was however, not interrupted by the administration of colchicine during the last 7 days of the casein regimen nor by colchicine treatment of recipient mice in a transfer model.

Amyloid↗
PubMed1997

Colchicine-induced myopathy in renal failure.

A 60 year-old woman with chronic renal failure developed acute proximal muscle weakness after receiving a regular dosage of colchicine. Elevation of muscle enzymes and electromyography were compatible with myopathy. Muscle biopsy revealed variation in muscle fiber size and few vacuolated fibers which were features of colchicine-induced myopathy. The clinical improvement and decreasing in muscle enzyme level occurred after colchicine withdrawal. Other potential causes of myopathy such as chronic renal failure and other drugs were ruled out. We suggested that colchicine should be used with caution in the presence of renal failure especially when other drugs which affect the metabolism of colchicine are also prescribed.

Acute Disease↗
PubMed2000

[Use of colchicine in chronic pericardial effusion. Presentation of 2 clinical cases and review of the literature].

Colchicine was introduced in 1987 for the treatment of recurrent pericarditis. Up to the present, papers have been published on a total of 117 patients treated with colchicine after the failure of treatment with FANS, corticosteroids and repeated pericardiocentesis. Here two cases of chronic pericardial effusion, one secondary to pericardiotomy, the second idiopathic, are reported. Both were recalcitrant to conventional therapy. Both patients were treated with 2 mg/die colchicine for 1 month followed by 1 mg/die for a further 5 months, without recurrence of the effusion after follow-up of 12 and 24 months respectively. No side-effects were observed. Colchicine is an anti-inflammatory drug which, by inhibiting various leukocyte functions, depresses the action of the leukocytes and of the fibroblasts at the site of the inflammation. We conclude that colchicine is effective in post-pericardiotomic and idiopathic chronic pericardial effusion as already reported in cases of recurrent pericarditis. Given the lack of side-effects, it could be considered as a drug of choice alternatively to FANS and corticosteroids.

Adult↗
PubMed2000

[Efficacy of colchicine in recurrent acute idiopathic pericarditis].

Acute idiopathic pericarditis is complicated by recurrence in 15 to 30% of cases. The preventive treatment of recurrences is not well codified. Aspirin, non-steroidal anti-inflammatory drugs and corticoids are the commonest prescribed treatments. The objective of this study was to assess the value of colchicine in the prevention of recurrences of acute idiopathic pericarditis. Twenty-eight cases of recurrent acute pericarditis (2 episodes, 1 month between each episode) admitted to a department of internal medicine between 1989 and 1999 were reviewed. Analysis was concentrated on the 13 idiopathic forms. The subjects were 7 women and 6 men with an average age of 41 years (10-62) at the time of the first episode of acute pericarditis. These 13 patients were treated with colchicine (1 to 2 mg/day) after failure of conventional treatment (aspirin 13/13, NSAID 13/13, steroids 9/13 and pericardiocentesis 3/13). Ten patients were followed up regularly (6 months after starting colchicine) and were improved with respect to number, duration and intensity of their recurrences. The average duration of colchicine therapy was 17 +/- 14 months (6-48). Progressive withdrawal of NSAID and steroids was obtained in 8/10 cases. The authors conclude that colchicine is useful in the prevention of recurrence of acute pericarditis. It may be proposed as treatment of choice, especially in the idiopathic forms.

Acute Disease↗
PubMed2002

[Induction of morphologically and genetically unstable calluses of Fagopyrum tataricum by colchicine].

A study was made of colchicine effect on genetic and morphological stability of morphogenic calli of the tatar buckwheat Fagopyrum tataricum (L.) Gaertn. A prolonged exposure of the morphogenic callus in colchicins-containing medium led to its morphological changes: the callus became more friable, and proembryogenic cell complexes disappeared. Genetic non-stability started from the first days of culturing in colchicine-containing indicated by amitotic divisions and K-mitoses, leading to the formation of micronuclei and increased variability in chromosome number. As a result of colchicine action, a few lines of heterogeneous calli were obtained differing in morphology, chromosome numbers, and ability to morphogenesis from the primary morphogenic callus. Genetic instability appeared in the following passages, when the treated calli were subcultured in the medium without colchicine: a wide range of abnormal nuclear division and chromosome aberrations was observed. This prolonged genetic instability was accompanied by a prominent increase in the formation of friable clones, which was 20-30 times higher than in the control. The formation of friable clones seems to result from one or two point mutations.

Colchicine↗
PubMed1976

[Effects of colchicine, vinblastine and mercury p-hydroxybenzoate on the multiplication of adenovirus 5 in HeLa cells].

After 30 min incubation at 37 with 10(-4) M PHMB (p-hydroxymercuribenzoate), monolayers of HeLa cells are not affected; after 3 h exposure to 10(-5) M colchicin or 2.5 X 10(-5) M vinblastine, HeLa cells are not altered morphologically but the number of cells is decreasing between 1 and 2 days post treatment. When cells are kept in suspension after trypsinization, their ability to adhere to the Petri dishes is not altered with 10(-4) M PHMB but only 50% of the cells are able to attach after treatment with colchicine or vinblastine. Adenovirus type 5 is unsensitive to the effect of colchicine and vinblastine at various concentrations, after 3 h incubation at 37. With 10(-3) M PHMB, the virus is inactivated, infectivity and hemagglutinating activity are almost abolished but the particles are unsensitive to pancreatic DNase, so that the structure of the viral particle is intact. This effect is reduced with 10(-4) M PHMB. The adenovirus 5 multiplication is not affected when HeLa cells are treated with 10(-5) M colchicine or 2.5 X 10(-5) M vinblastine, before and during adsorption of the virus. The viral production decreases after 24 h treatment with colchicine or vinblastine. Treatment with 10(-4) M PHMB does not influence intra- or extracellular viral yield.

Adenoviridae↗
PubMed2004

Uptake of [111In-DTPA0]octreotide in the rat kidney is inhibited by colchicine and not by fructose.

UNLABELLED: The high renal uptake of radiolabeled somatostatin analogs is dose limiting. Lowering this uptake permits higher radioactivity doses and, thus, tumor doses to be administered. We tested the effects of the microtubule drug colchicine on renal uptake of [(111)In-DTPA(0)]octreotide. Also, the effects of fructose were tested. METHODS: Organ radioactivity 24 h after injection of [(111)In-DTPA(0)]octreotide was determined in rats. RESULTS: Coinjection of 1 mg of colchicine per kilogram did not influence renal uptake of [(111)In-DTPA(0)]octreotide, whereas this dose administered 5 h before [(111)In-DTPA(0)]octreotide resulted in significant renal uptake reduction (63%). D-Lysine plus colchicine reduced the uptake by 76% (P < 0.01 vs. D-lysine alone). Liver and blood radioactivity levels were significantly elevated by colchicine. Fructose did not affect the biodistribution of [(111)In-DTPA(0)]octreotide. CONCLUSION: Renal uptake of [(111)In-DTPA(0)]octreotide is dependent on microtubule function in rats. The addition of colchicine to amino acid protocols may permit administration of higher doses, improving the therapeutic window of peptide receptor radionuclide therapy.

Adenosine Triphosphate↗
PubMed1992

Acute colchicine intoxication--possible role of erythromycin administration.

A 29-year-old patient with familial Mediterranean fever and amyloidosis involving the kidney, liver, and gastrointestinal tract received longterm colchicine, 1 mg daily. In the last year she developed diarrhea and abdominal pain, that coincided with toxic colchicine blood levels. After 2 weeks of oral erythromycin therapy she was hospitalized for acute, life threatening colchicine toxicity, with fever, diarrhea, abdominal pain, myalgia and lower extremity parasthesias and later convulsions and alopecia. Pancytopenia evolved into rebound leukocytosis, disturbed liver function and hypoglycemia. After a long stormy course she improved. Colchicine toxicity with combined liver and renal impairment and the role of erythromycin in her colchicine toxicity are discussed.

Acute Disease↗
PubMed2005

Acute renal failure associated with an accidental overdose of colchicine.

CASE SUMMARY: A 47-year-old man with a history of polyarticular gout was admitted to the nephrology service because of severe renal insufficiency (creatinine 6.25 mg/dl). Three days before admission he had a pain crisis in his knees and ankles and self-administered 20 x 1 mg granules of colchicine p.o. over a period of 4 - 5 hours together with six suppositories each containing 100 mg of indomethacin. The patient began vomiting within 24 hours, experienced diarrhea which persisted for three days and then came to the hospital. The patient reported oliguria during the preceding 24 hours. In hospital, attempts to correct water and electrolyte balance were initiated. The patient became stabilized hemo-dynamically, the diarrhea disappeared within 24 hours, diuresis resumed and the renal function progressively improved. Leukopenia and thrombopenia were diagnosed, the transaminases increased: AST = 79 U/l, ALT = 132 U/l on the eighth day after taking the colchicine. The serology for hepatitis A, B, C and HIV viruses was negative; the serology for CMV and VEB revealed a previous infection. After being discharged from hospital 11 days after admission, the patient presented with the following parameters: hematocrit 39%, leukocytes 5,920/microl (3 470 neutrophils), prothrombin time 13 seconds, urea 44 mg/dl, creatinine 1.29 mg/dl, AST 16 U/l and ALT 35 U/l. DISCUSSION: The patient mistakenly ingested 20 mg ofcolchicine p.o. (0.22 mg/kg). The intoxication was associated with gastroenterocolitis, dehydration and renal failure during the first three days after ingestion. The patient also developed leukopenia, thrombopenia and mild hepatocellular injury. Renal failure due to colchicine intoxication is due to various factors such as depletion of volume/hypotension, rhabdomyolysis and multiorgan failure. In this case, the hypovolemia was probably the fundamental cause of the acute renal insufficiency as demonstrated by the quick recovery after administering fluids. It is possible that indomethacin may have enhanced the toxic effect of colchicine on the kidneys and bone marrow. Some colchicine intoxications, as in this case, are caused by an error in interpreting the dose for treating an acute attack of gout. A way to prevent these errors would be to use a low-dose treatment protocol.

Acute Kidney Injury↗
PubMed2006

Medication errors with the use of allopurinol and colchicine: a retrospective study of a national, anonymous Internet-accessible error reporting system.

OBJECTIVE: To more closely assess medication errors in gout care, we examined data from a national, Internet-accessible error reporting program over a 5-year reporting period. METHODS: We examined data from the MEDMARX database, covering the period from January 1, 1999 through December 31, 2003. For allopurinol and colchicine, we examined error severity, source, type, contributing factors, and healthcare personnel involved in errors, and we detailed errors resulting in patient harm. Causes of error and the frequency of other error characteristics were compared for gout medications versus other musculoskeletal treatments using the chi-square statistic. RESULTS: Gout medication errors occurred in 39% (n = 273) of facilities participating in the MEDMARX program. Reported errors were predominantly from the inpatient hospital setting and related to the use of allopurinol (n = 524), followed by colchicine (n = 315), probenecid (n = 50), and sulfinpyrazone (n = 2). Compared to errors involving other musculoskeletal treatments, allopurinol and colchicine errors were more often ascribed to problems with physician prescribing (7% for other therapies versus 23-39% for allopurinol and colchicine, p < 0.0001) and less often due to problems with drug administration or nursing error (50% vs 23-27%, p < 0.0001). CONCLUSION: Our results suggest that inappropriate prescribing practices are characteristic of errors occurring with the use of allopurinol and colchicine. Physician prescribing practices are a potential target for quality improvement interventions in gout care.

Adverse Drug Reaction Reporting Systems↗
PubMedDate not supplied

Colchicine treatment of liver fibrosis.

BACKGROUND/AIMS: Because of its antifibrotic and anti-inflammatory effects, colchicine has been proposed as a treatment for liver disease. The results from clinical trials have however been inconsistent. The aim of the present study was to evaluate the effect of colchicine in the treatment of patients with hepatic fibrosis of various etiologies. METHODOLOGY: Thirty-eight patients were randomized to receive either colchicine 1 mg per day (n=21, group A) or no antifibrotic agent (n=17, group B). Treatment lasted for at least 12 months. Liver biopsy was performed prior to entry and after 12 months. Liver function tests, serum aminoterminal peptide of procollagen III (PIIINP) levels and CD4:CD8 ratio of peripheral blood T lymphocytes (PBTLs) were performed at baseline and bimonthly or every 4 months post-treatment. RESULTS: Mean albumin serum levels increased 12 months post-treatment period only in group A (p<0.05). Mean serum PIIINP levels did not change significantly after 12 months of treatment in group A; in 7 patients a reduction in mean serum PIIINP levels was noticed during 24-month post-treatment follow-up period (p<0.05). At baseline, a correlation between focal or bridging necrosis and CD4:CD8 ratio of PBTLs was noticed in group A (p < 0.05). The mean serum CD4:CD8 ratio was increased after 12 months of colchicine treatment (p<0.05) associated with abrogation of this correlation; comparison between the two groups revealed increased CD4:CD8 ratio in group A at 12 months (p<0.05). The histological findings according to Knodell criteria in both groups remained unchanged after 12 months follow-up. The treatment was well tolerated in all patients. CONCLUSIONS: Long-term colchicine treatment in patients with hepatic fibrosis appears to exert an anti-inflammatory, anti-fibrotic and immunomodulatory effect.

Adult↗
PubMed1991

Differences in signal transduction between Fc gamma receptors (Fc gamma RII, Fc gamma RIII) and FMLP receptors in neutrophils. Effects of colchicine on pertussis toxin sensitivity and diacylglycerol formation.

Studies on the role of microtubule integrity in stimulus-response coupling in neutrophils have generated contradictory data. To determine the role of microtubule integrity in stimulus-response coupling elicited by two different mechanisms, i.e., engagement of the Fc receptors (FcR gamma II, FcR gamma III) or engagement of the receptor for FMLP, we utilized colchicine (10 microM), which reduces pericentriolar microtubules to 29% of control, and compared its effect with that of nocodazole (50 microM) and lumicolchicine (10 microM). We now demonstrate that treatment of neutrophils with colchicine but not lumicolchicine, inhibits degranulation elicited by engagement of Fc receptors but augments degranulation in response to FMLP. In contrast to the ligand-specific effect of microtubule-disruption on degranulation, superoxide anion production (assembly of the NADPH oxidase) is unaffected by colchicine regardless of the ligand. To determine whether intact microtubules were required for responses elicited by ligation of Fc gamma RII(CD32) or Fc gamma RIII(CD16), mAb directed against these receptors were employed. Treatment of neutrophils with mAb KuFc79 directed against Fc gamma RII(CD32) or mAb 3G8 directed against Fc gamma RIII(CD16) inhibited degranulation of neutrophils elicited by immune complexes (IC). In contrast, removal of most of Fc gamma RIII by phosphatidylinositol-specific phospholipase C did not significantly alter degranulation in response to IC. We conclude that degranulation elicited by IC results from ligation of both Fc gamma RII and phosphatidylinositol-specific phospholipase C-insensitive Fc gamma RIII. The importance of microtubule integrity on the generation of intracellular signals was also examined. Degranulation of neutrophils proceeds via pertussis toxin-sensitive and insensitive pathways; treatment of cells with colchicine did not augment the action of pertussis toxin. Stimulation of neutrophils by chemoattractants results in a biphasic increase in 1,2-sn-diacylglycerol; a rapid increase ("triggering") secondary to the action of a phosphatidylinositol-specific phospholipase C, and a late increase ("activation") secondary to the action of a phosphatidylcholine-specific phospholipase C. Treatment of cells with colchicine altered the production of both [3H]-arachidonic acid-diacylglycerol and diacyl[14C]glycerol in parallel to its effect on degranulation. These studies indicate that the requirement of intact microtubules for degranulation is ligand-specific. Furthermore, assembly of the respiratory burst oxidase does not require intact microtubules. Microtubules most likely alter the cycling of specific receptors or the generation of specific intracellular signals required for stimulus-response coupling in the course of degranulation. Intact microtubules are not uniformly required for the discharge of granule contents during exocytosis.

Antigens, Differentiation↗