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PubMed1992

[Combined ursodeoxycholic acid plus colchicine--treatment of primary biliary cirrhosis: results of a placebo-controlled double-blind study].

In the present pilot study we investigated the effects of urso treatment alone in comparison to a combined treatment with urso plus colchicine in PBC. 22 patients with PBC in the histological stages 1-3 entered the study. All patients were pretreated with urso alone (10-12 mg/kg) for 12 months. Thereafter treatment was continued in a double-blind randomized fashion with urso plus placebo or urso plus colchicine (1 mg/day) for another 12 months. During the initial 12 months urso treatment liver function tests improved significantly in all patients, pruritus improved in 60% of patients. After randomization to the different treatment groups the biochemical parameters stabilized at the lower level and no significant differences could be found between urso plus placebo and urso plus colchicine treatment concerning aminotransferases, alkaline phosphatase, bilirubin, cholinesterase, albumin or cholesterol. The results of this pilot study suggest that the addition of colchicine to an initial urso treatment does not lead to further improvement of aminotransferases, alkaline phosphatase, bilirubin or clinical symptoms like pruritus.

Colchicine↗
PubMedDate not supplied

Colchicine-induced leukopenia in a patient with familial Mediterranean fever: the cause and a possible approach.

A young patient with familial Mediterranean fever (FMF) developed leukopenia each time she took colchicine. However, when she discontinued the drug the white cell and the platelets counts increased but she experienced FMF attacks. Later it was found that the patient also had concomitant cytomegalovirus (CMV) infection. This complex situation posed several diagnostic and therapeutic issues concerning the real cause for the leukopenia and the possible approach to take in such conditions. We propose that when an essential drug (such as colchicine for FMF) causes leukopenia, one should look for concurrent CMV or another viral infection. If there is no such infection, it is suggested that the mechanism leading to leukopenia be clarified. In the case of bone marrow suppression, colchicine should be continued with injections of G-CSF, whereas if the bone marrow is hypercellular it is suggested to use steroids and colchicine concomitantly.

Adult↗
PubMed2005

Colchicine inhibits heterotopic ossification: experimental study in rabbits.

BACKGROUND: Heterotopic ossification is a common complication of hip surgery and musculoskeletal or brain trauma. OBJECTIVES: To confirm by in vivo study that colchicine inhibits osteoblast cell proliferation with marked decrease in tissue mineralization. METHODS: Heterotopic ossification was induced in three groups of New Zealand white rabbits (females, 6 months old, weight 3-3.5 kg) by injecting 2 ml bone marrow drawn from the iliac crest into their right thigh muscle. To prevent heterotopic ossification, colchicine (0.25 mg/ day) was administered orally for 4 weeks to two groups of adult rabbits: group A (preload group)--1 week preceding bone marrow injection; group B--on day of injection; and group C--control group. RESULTS: After 4 weeks the rabbits were evaluated by radiographs and ultrasound for evidence of heterotopic ossification. At the end of the study histologic samples were taken from all the thighs. Imaging and histologic studies showed, with statistical significance, almost complete prevention of heterotopic ossification formation in group A (preload) and a marked decrease in group B, when compared with the controls where large new bone had formed at the injection site. These results indicated the inhibitory effects of colchicine on a bone-forming process in soft tissue such as heterotopic ossification. CONCLUSIONS: The role of colchicine in preventing heterotopic ossification in other bone-forming conditions, such as hip arthroplasty or pelvic trauma, and after brain trauma, remains to be evaluated in a clinical setting.

Animals↗
PubMedDate not supplied

Enhanced superoxide generation and the decreased superoxide scavenging activity of peripheral blood leukocytes in Behçet's disease--effects of colchicine.

Enhanced superoxide radical (O2-) generation by polymorphonuclear cells (PMN) has been suggested to mediate tissue damage associated with Behçet's disease (BD). Because superoxide dismutase (SOD) provides protection from O2- we investigated whether the superoxide scavenging activity (SSA) of PMN, mononuclear cells (MNC) or plasma has a correlation to the amount of O2- generated by PMN in BD. We also studied the effects of colchicine, a potent inhibitor of phagocytosis, on the SSA of PMN. In BD, O2- release by both non-stimulated PMN and those stimulated with opsonized zymosan (OZ), or 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA), was enhanced. The SSA of PMN, but not MNC and plasma, was significantly lower in BD patients as compared with healthy controls. The SSA of PMN showed a strong negative correlation with their O2- release. The SSA of PMN was lower in the BD patients with elevated erythrocyte sedimentation rates and C-reactive protein levels than in those with normal test results. In addition, we found that colchicine treatment increased the SSA of PMN toward normal levels in BD patients. In vitro studies demonstrated that the SSA in PMN obtained from healthy adults was decreased after stimulation with either OZ or PMA. Colchicine could prevent the decrease in the SSA when PMN were stimulated with OZ, but not when stimulated with PMA. Our results suggest that the enhanced O2- release by PMN in vivo may be responsible for the decreased SSA of PMN in BD and the PMN might be able to release more O2- in tissues. Colchicine may increase the SSA of PMN toward normal levels by blocking phagocytosis.

Adult↗
PubMed2006

[Study on induction of polyploidy in Salvia bowleyana by colchicine treatment].

OBJECTIVE: To explore the technique of induction of polyploidy in Salvia bowleyana by colchicine treatment. METHOD: The three kinds of explant of bud, leaf and calli were induced by colchicine treatment. RESULT: The induction effects were better when the calli was treated by colchicines (15 mg x L(-1)) and the leaf was pre-cultured for one week. The doubling rate was 33.33%, while the majority were wholy doubled plants, and the leaves were thicker and broader, the color was darker, the root was thicker and the stoma size was obviously bigger than the diploid plants. The number of chromosome were 8 to 64. Isoenzyme analysis showed that the enzyme activities between the polyploid and the diploid plants were quite different. CONCLUSION: Induction of polyploidy by colchicine treatment is efficacious. The part of the doubled plants were identified as homologmous tetraploids.

Chromosomes, Plant↗
PubMedDate not supplied

Acute colchicine intoxication during clarithromycin administration in patients with chronic renal failure.

Colchicine is an effective antiinflammatory medication. It should be used with great caution, however, in patients requiring dialysis. Coadministration of colchicine and macrolides may impair colchicine elimination, resulting in excess drug exposure and toxicity. We report 2 renal failure cases of colchicine intoxication occurring with the administration of clarithromycin.

Acute Disease↗
PubMedDate not supplied

Treatment options in colchicine resistant familial Mediterranean fever patients: thalidomide and etanercept as adjunctive agents.

OBJECTIVE: Regular colchicine treatment cannot control the typical febrile attacks of FMF in about 5-10% of the compliant patients. Here we report the effect of thalidomide and etanercept in 5 colchicine-resistant cases. METHODS: Five (4M/ 1F) FMF patients between April 2005 and March 2006, who were experiencing at least 2 attacks per month, despite regular colchicine were included to the study. Four male patients were given thalidomide 100 mg/d initially. Two of these patients unresponsive to thalidomide were prescribed subcutaneous injections of etanercept 25 mg, twice a week. The female patient received etanercept as the first choice due to potential side effects. She then had to be converted to thalidomide due to a severe injection site reaction. RESULTS: The median follow up period with thalidomide and etanercept was 8 months. Both thalidomide and etanercept lowered the number of the abdominal attacks. CONCLUSION: Thalidomide and etanercept might be effective as additional treatment in colchicine-resistant cases of FMF.

Adult↗
PubMed1991

Possible modification of metastasis from adenocarcinoma of the prostate by colchicine: a case report.

Laboratory data indicate that colchicine has an antimetastatic effect in tissue culture and in tumor-transplantation experiments in animals. The present case report reveals a lack of perineural and capsular invasion as well as distant metastases from a large adenocarcinoma of the prostate in a 63-year-old patient who had taken colchicine daily for 25 years prior to lesion discovery. Failure to demonstrate metastasis was unexpected both because of lesion size (estimated volume 4.4 ml) as well as its histopathology (Gleason pattern 3S, grade 6). Colchicine may have inhibited metastasis of activated Ki-ras oncogenes during oncogenesis along neural microtubules in the area because of the known inhibitory effect of this drug on particle transport along the microtubule component of the cytoskeleton. Colchicine at therapeutic doses for gout may simultaneously inhibit metastasis of other types of malignancies in man.

Adenocarcinoma↗
PubMed1991

[Effect of colchicine on vasopressin and melanin-concentrating hormone neurons of rat hypothalamus: hybridocytochemistry and immunocytochemistry studies].

48 hrs. after an intra-cerebroventricular injection of colchicine (100 micrograms), antisera to three putative peptides included in the rat melanin-concentrating hormone (MCH) precursor, strongly stained the secretory granules accumulated in perikarya. In control rats, these antisera stained endoplasmic reticulum, Golgi apparatus, or neurosecretory granules respectively. Colchicine also induced a dramatic decrease in hybridization signal obtained with a probe complementary to the prepro-MCH-mRNA. Similarly, colchicine induced a strong increase in vasopressin immunoreactivity in neurons of the paraventricular and supraoptic nuclei, and a strong decrease of the vasopressin precursor mRNA. These results demonstrated that, in two peptidergic neuron populations of the rat hypothalamus, colchicine lowers mRNAs and impairs neuropeptide protein synthesis, consecutively to the accumulation of neurosecretory granules in perikarya.

Animals↗
PubMed1977

[Immunosuppressive properties of vinblastine and colchicine].

The action of vinblastine and colchicine on the populations of antibody-forming cells, their precursors and stem cells using a model of primary immune response and in the transplantation system was studied using techniques by Jerne and Nordin (1963), Kennedy et al. (1965), and Till and McCulloch (1961). It was discovered that vinblastine and colchicine, at single administration 48 hours after immunization, inhibited immune response completely. The administration of colchicine and vinblastine to a donor gave an exponential decrease of in foci-forming cell number in a recipient in the system of syngenic transfer. But at the same time, vinblastine at small doses stimulated population of antibody-forming and stem cells, whereas at large doses it was not effective. Colchicine, in contrast, strongly inhibited both antibody-forming and haemopoietic cells in the recipient.

Animals↗
PubMed1991

Colchicine is a potent adjuvant for eliciting T cell responses.

The cytotoxic drug colchicine when administered to mice in conjunction with Ag was shown to have a strong adjuvant effect in generating a specific plaque-forming cell response to the protein Ag OVA, human gamma-globulin and BSA. Dissection of this phenomenon revealed that several T cell activities, including Th function, Ag-induced T cell proliferation and T cell-mediated delayed-type hypersensitivity, were also specifically induced by treating mice with colchicine + Ag. The adjuvant effect of colchicine was observed when the drug and Ag were injected in soluble form, i.e., no vehicle (e.g., oil, liposome) was necessary. The potency of colchicine as an adjuvant was equal to or more than that of conventional adjuvants such as CFA or alum.

Adjuvants, Immunologic↗
PubMed1990

[Chronic human colchicine myopathy].

We report a case of myopathy induced by daily administration of colchicine. A 65-year-old man with gout and renal dysfunction had taken 1 mg of colchicine daily for 3 years. The dose was raised to 2 mg per day and two months later, he developed progressive weakness of the proximal limbs and had difficulty in rising from squatting and climbing stairs. Five months after the development of weakness, neurological examination showed proximal muscle weakness without wasting, generalized hyporeflexia and mild sensory loss and dysesthesia of the toes. Serum creatine kinase level was elevated to 788 IU/L and creatinine level was 2.1 mg/dl. Electromyography demonstrated myogenic changes with spontaneous activity. HE preparations of biceps muscle biopsy showed mild increase of variation in fiber size, small vacuoles with and without basophilic rims in some fibers and a few fibers with unevenly stained sarcoplasm. NADH-TR preparations showed numerous moth-eaten and targetoid fibers. The small rimmed vacuoles stained positively for acid phosphatase. Electron microscopy showed accumulation of lysosomes and autophagic vacuoles, and architectural changes and disruptions of myofibrils. After the discontinuation of colchicine, his strength and serum CK level normalized within two masquerading as polymyositis, may occur when customary doses of colchicine are given daily to patients with renal dysfunction.

Aged↗
PubMed1990

Neurotoxic effects of colchicine.

Neurotoxicants have found increasing use as tools to study the structure and function of the central nervous system. One class of compounds which block mitosis and disrupt axoplasmic transport includes colchicine, a chemical which is highly toxic to certain neuronal populations. Colchicine administered directly into the hippocampus of rats results in the preferential destruction of dentate gyrus granule cells without affecting the surrounding pyramidal cells. Injection of colchicine into other brain areas also destroys neurons but with less selectivity than is observed in the hippocampus. The neurotoxicity of colchicine appears to be related to the ability to bind to tubulin, although its exact mechanism remains to be elucidated.

Animals↗
PubMed1979

Effect of colchicine on PGE1 stimulation of cAMP1 formation in human lymphoblastoid and normal lymphocytes.

PGE1 increased cAMP level in human lymphoblastoid cells (RPMI 1788) after 5-60 min of incubation at 37 degrees C. A gradual decrease of cAMP concentration was found at the later time intervals. Colchicine significantly potentiated the stimulatory effect of PGE1, although it did not have any effect on cAMP level in control lymphoblastoid cells. The maximal effect of colchicine on PGE1 stimulation of cAMP formation was at the 0.1-1.0 microM level. Human lymphocytes also responded with increased cAMP formation to colchicine addition. In contrast, no stimulatory effect of colchicine was found in human granulocytes.

Cell Line↗
PubMed1988

[Effect of colchicine on histamine secretion and calcium uptake in mast cells].

The function of contractile system of microtubules on the mechanism of mast cell exocytosis by using colchicine, a depolymerizing alkaloid of the microtubular system, has been studied. The response of histamine release and 45Ca-uptake in isolated rat mast cells treated with colchicine has been determined. The incubation of mast cells in the presence of 10(-8)-10(-3) M colchicine slightly inhibits histamine secretion induced by the stimulant concentration 50 micrograms/ml of compound 48/80 (35 +/- 5%). Similarly colchicine does not significantly affect histamine values spontaneously elicited in unstimulated mast cells; the percentages of secretion are never greater than 10%. However, high doses of this alkaloid are found to markedly inhibit entry of calcium ions into the cell. These results suggest that microtubules do not participate in the secretory process of mast cells, although they significantly decrease calcium uptake. The microtubules might be connected to the membrane, so that the depolymerization of this contractile system could damage the membrane structures through which Ca2+ is transported.

Animals↗
PubMed1989

[Changes in amino acid metabolism at the onset of colchicine resistance in Dzungarian hamster fibroblast cell culture].

We have studied amino acid up-take from incubation media by colchicine-resistant and colchicine-sensitive Djungarian hamster fibroblast cells. It has been shown that arginine and asparagine amino acid contents in the medium are different for colchicine-sensitive and colchicine-resistant cells. Amino acids concentration is not reduced in the medium after incubation of resistant cells, while it is decreased after incubation of sensitive cells. We can suggest that penetration of low-weight sources of nitrogen into sensitive cells is hampered. It can also be suggested that protein macromolecules are the main source of nitrogen for these cells. The protein up-take levels from the incubation medium, as assessed by the ammonia and amino acid contents of cell counts don't exceed 5% of their initial concentrations in the medium.

Amino Acids↗
PubMed1989

Effectiveness of vitamin E and colchicine in amelioration of paraquat lung injuries using an experimental model.

The major cause of death in paraquat poisoning is a rapidly progressive respiratory failure due to an oxidative insult to the alveolar epithelium with subsequent fulminant obliterating fibrosis. The present study evaluates the effectiveness of vitamin E in combination with colchicine in ameliorating paraquat lung injuries in rats. Vitamin E is a biologic antioxidant interfering with lipid peroxidation, and colchicine reduces collagen synthesis which is significantly augmented in pulmonary fibrosis. Eight normal rats were given a single i.p. dose of paraquat at 15 mg/kg. The treated group included eight animals that received, in addition to i.p. paraquat (15 mg/kg), daily doses of vitamin E (100 mg/kg i.p.) and colchicine (0.1 mg/kg i.p.). All the rats in the paraquat group died within 42 to 96 h, six of them within 60 h, following severe respiratory failure. The treated rats developed a somewhat milder form of respiratory insufficiency, six of them dying within 48 to 72 h. Less severe intra-alveolar hemorrhages were observed in this group. Two rats survived, and these had only mild emphysema on autopsy at 21 days. Our preliminary results suggest that the combination of vitamin E with colchicine may be effective in ameliorating lung injuries caused by paraquat, and warrant further studies.

Animals↗
PubMed1989

A morphometric analysis of functionally defined subpopulations of neurons in the paraventricular nucleus of the rat with observations on the effects of colchicine.

Two populations of neurons in the paraventricular nucleus of the hypothalamus that have different efferent projections and physiological roles in the regulation of visceral responses were characterized morphologically with a combined intracellular filling, retrograde tracer, and immunohistochemical method. Neuroendocrine cells were retrogradely labeled by an intravenous injection of Fast blue, and distinguished from descending neurons that were retrogradely labeled by an injection of fluorogold into the spinal cord. Retrogradely labeled neurons were selectively penetrated and filled intracellularly with Lucifer yellow to visualize detailed features of their morphology. Corticotropin-releasing hormone (CRH)-containing neurons were distinguished from other neuroendocrine cells by immunostaining the tissue with an antiserum to rat CRH. Morphometric features of defined populations of neurons were then quantified and reconstructed graphically to generate multicellular montage drawings that demonstrate their spatial organization. Descending neurons were further separated into dorsal and ventral medial parvicellular components, while the neuroendocrine population was differentiated into parvicellular and magnocellular groups. The mean somal areas, total dendritic lengths, and spine densities were compared between groups of neurons, and these showed significant differences across cell types. These measures were also dramatically affected by colchicine, which appears to induce the formation of new dendritic appendages, swelling of the soma, and reduction of dendritic length. Whether colchicine is acting directly upon cytoskeletal structures or indirectly by altering the physiology of the cell is unclear. However, the precise effects of colchicine on mean somal area, total dendritic length, and spine density appear to be dependent upon individual cell type. Colchicine may therefore act in a nonspecific, but nonetheless highly selective, manner in disrupting an endogenous mechanism regulating the number, morphology, and location of spines.

Animals↗