Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colchicine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources
PubMedDate not supplied

[Colchicine poisoning apropos of a pediatric case].

Colchicine has been widely used in the treatment of gout and familial mediterranean fever. Overdose is rare mostly in childhood. Colchicine overdose always causes gastrointestinal side effects, bone marrow depression and sometimes neuropathy. The mechanism of colchicine upon the microtubules, provides a better understanding of the pharmacology and also of the multiorgan involvement. We report the case of a ten year old child who ingested 0.6 mg/kg colchicine with a good outcome.

Child↗
PubMed1994

Colchicine antagonizes the activity of human smooth muscle cells cultivated from arteriosclerotic lesions after atherectomy.

AIM: Proliferative, migratory, and secretory activities of vascular smooth muscle cells are functional determinants of human atherosclerotic plaque and restenosis formation. The present study was designed to examine the effects of interfering with these processes using drugs. MATERIALS AND METHODS: For in-vitro studies of smooth muscle cell activity, arterial smooth muscle cells were cultivated from human plaque tissue excised from 22 coronary and peripheral lesions and treated with the antitubulin colchicine. Smooth muscle cell migratory activity was analyzed by a standardized semi-automatic video system. Transmission electron microscopy was used to examine cytoplasmic structures. RESULTS: Colchicine caused a concentration-dependent decrease in smooth muscle cell proliferative activity at a half-maximal inhibitory concentration (IC50) of 5 nmol/l. Smooth muscle cell migratory activity was reduced by colchicine in a concentration-dependent manner (IC50, 3 nmol/l). Concordantly, transmission electron microscopy revealed severe disorganization of cytoplasmic structures, especially of organelles, indicating metabolic activation. CONCLUSIONS: In-vitro studies with human smooth muscle cells from arteriosclerotic lesions suggest that the antitubulin principle may be useful in producing anti-arteriosclerotic effects, since a pronounced antagonization of smooth muscle cell proliferative, migratory, and secretory processes, indirectly inferred from ultrastructural analysis, was demonstrated with low concentrations of colchicine.

Actin Cytoskeleton↗
PubMed1993

[Influence of colchicine upon morphology of intervertebral disc of rabbit].

The morphological changes of intervertebral disc of rabbit in the culture liquids of containing colchicine was observed by microscopy and transmission microscopy and hydroxyproline density of culture liquids was measured by stages. Meanwhile, set up control groups. Undiscovery that colchicine can produce discolysis and shrinking. We regard as major mechanism of colchicine treating herniated of intervertebral disc is anti-inflammation and anti-microtubule. We advance opposite viewpoint for Michael R. Rask's hypothesis which colchicine can produce herniated of intervertebral disc shrinking.

Animals↗
PubMedDate not supplied

Evaluation of therapy for cast nephropathy: failure of colchicine to alter urinary Tamm Horsfall glycoprotein excretion in normal subjects.

Tamm Horsfall glycoprotein (THG) is a major constituent of renal tubular casts including the light chain casts of myeloma. Animal studies suggest that the anti-inflammatory agent colchicine reduces urinary THG excretion and prevents light chain cast formation. Six normal male subjects were given therapeutic doses of colchicine (0.5 mg twice daily for 6 days) and excretion of THG, albumin, creatinine and N-acetyl glucosaminidase (NAG) was determined. Colchicine therapy had no effect on the urinary excretion of THG, albumin or NAG or on renal function as assessed by creatinine clearance. This suggests that colchicine will not be a useful therapeutic adjunct to the treatment of light-chain nephropathy.

Acetylglucosaminidase↗
PubMed1994

Histopathological evidences for the antifibrogenic effect of colchicine in schistosomiasis mansoni in mice.

Colchicine treated mice showed significant decrease in prevalence of fibrocellular and fibrocellular and fibrous granulomas in liver specimens compared to corresponding control groups. Percentage of spindle cell component and red fibrillar (RF) material showed significant reduction compared to control groups. These evidences of the antifibrogenic effect of colchicine were more prominent when treatment was given early after infection. Combined therapy with colchicine and praziquantel gave the same results. Mice treated with praziquantel alone showed no significant change compared to control groups. Colchicine showed also an immunomodulant effect evidenced by a significant decrease in the intensity of small and medium-sized to large cell components compared to control groups.

Animals↗
PubMed1994

[Relief of recurrent pericarditis by colchicine].

The incidence of recurrence of pericarditis is about 15-32%. The most common causes include trauma, myocardial infarction, and pericardiectomy. The optimal treatment to prevent recurrence has not been fully established. Possible modalities include nonsteroid anti-inflammatory drugs, corticosteroids, azathioprine, and pericardiectomy. We describe a 19-year-old man with osteogenic sarcoma who developed recurrent pericarditis despite treatment with prednisone and pericardiocentesis. Colchicine was administered in an effort to prevent further bouts of pericarditis. During the acute phase he was treated with a combination of prednisone, 60 mg/day, and colchicine, 1 mg/day. The dose of prednisone was then lowered to 5 mg/day. There was a recurrence when he stopped taking colchicine due to abdominal discomfort. On renewal of treatment there were no further attacks during a follow-up of 16 months. We confirm the results of a previous trial which showed that colchicine may be beneficial in preventing the recurrence of pericarditis. However, these results need corroboration by a large double-blind study.

Adult↗
PubMedDate not supplied

Colchicine inhibits spermatozoal motility in vitro.

OBJECTIVE: To study the in vitro effect of colchicine on the motility of normal human spermatozoa. METHODS: Seminal fluid was obtained from 15 normal healthy volunteers. Following the swim-up technique for sperm selection, samples of sperm were incubated with different concentrations of colchicine and their forward motility was assessed after 2, 17, and 24 hours. RESULTS: Colchicine concentrations of 10 micrograms/mL and 20 micrograms/mL reduced spermatozoal motility, while a concentration of 2 micrograms/mL did not have a significant inhibitory effect. Reduction in motility was observed after a minimum incubation of 18 hours. After 24 hours 90-95% of the spermatozoa was shown to be viable by eosin staining. CONCLUSION: Relatively high concentration of colchicine may affect in vitro motility of sperm, probably by its direct effect on the microtubules rather than by causing spermatozoal death.

Cell Survival↗
PubMed1993

The role of the septohippocampal pathway in the mediation of colchicine-induced compensatory changes in the rat hippocampus.

To study the involvement of the septohippocampal pathway in colchicine-induced changes in the hippocampus, colchicine was used to lesion the septum and/or hippocampus of male, Fischer-344 rats. Rats were killed 12 weeks post-lesion and histochemical and biochemical measurements were performed. [3H]-QNB binding, choline acetyltransferase (ChAT) activity and agonist-stimulated release of inositol phosphates (IPs) were measured in hippocampal slices. AChE histochemistry was also performed to visualize AChE positive fibers in the hippocampus. Increases in ChAT activity, AChE staining and carbachol-stimulated IP release observed in hippocampal-lesioned animals were attenuated in animals receiving both septal and hippocampal lesions. However, the decrease observed in [3H]-QNB binding sites after intradentate colchicine was not affected by septal lesions. Subsequent studies also found enhanced sensitivity to excitatory amino acid (EAA)-stimulated IP release in hippocampal-lesioned animals. Similar to the changes observed in carbachol-stimulated PI hydrolysis, this increase was also long-lasting. However, the hyperstimulation of EAA-induced IP release was not attenuated by the septal lesion. Thus, it appears that the neurochemical and morphological changes observed in the hippocampus following intradentate colchicine are dependent upon more than one afferent projection to the hippocampus.

Animals↗
PubMed1996

Enhancement of N-nitrosodiethylamine-initiated hepatocarcinogenesis caused by a colchicine-induced cell cycle disturbance in partially hepatectomized rats.

The effects of a colchicine-induced M-phase block of regeneration after partial hepatectomy on early-stage liver carcinogenesis were studied in rats. When administered 1 or 3 days after N-diethylnitrosamine initiation and partial hepatectomy, colchicine increased the mitotic index of regenerating hepatocytes at days 4-6 without evidence of liver cell necrosis. When the protocol was combined with a selection procedure (E. Cayama et al., Nature (Lond.), 275: 60-62, 1978), a significant increase in the size but not number of gamma-glutamyltranspeptidase-positive foci at week 5 was observed in a colchicine dose-dependent manner. This was associated with an elevated incorporation of 5-bromo-2-deoxyuridine into the gamma-glutamyltranspeptidase-positive cells. In a longer-term experiment, the numbers, sizes, and 5-bromo-2-deoxyuridine labeling index of persistent nodules were increased significantly in colchicine-treated rats at week 9. This was associated with significant increases in the incidences and numbers of hepatocellular carcinomas at week 42. The above results raise the interesting possibility that a cell cycle disturbance in the early stage of liver carcinogenesis provides a persisting growth advantage for initiated cells, resulting in enhanced growth of foci and persistent nodules that evolve into hepatocellular carcinomas.

Animals↗
PubMed1997

Colchicine affects cortical and amygdalar neurochemical changes differentially after middle cerebral artery occlusion in rats.

Recently, we have shown increases in the immunoreactivity for neuropeptide Y and tyrosine hydroxylase in the insular cortex surrounding the focal infarction after middle cerebral artery occlusion. In addition, the immunoreactivity for neuropeptide Y, leucine-enkephalin, dynorphin, and neurotensin increased ipsilaterally in the amygdala. Increases in immunoreactivity were observed in nerve terminals and fibers; changes in the neuropeptides were maximal 3 days after stroke. Local excitotoxic injury of the insular cortex also elicited similar neuropeptide changes unilaterally in the same regions. In this study, immunohistochemistry was used following intracerebroventricular injection of colchicine and stroke to determine whether blockade of axonal transport would prevent these neurochemical changes. These experiments would also locate the putative cellular origins of the neurochemicals involved. Control rats received either colchicine injection or middle cerebral artery occlusion alone. Injection of colchicine enhanced the periinfarct increase in neuropeptide Y but did not alter the increase in tyrosine hydroxylase. The neuropeptide Y increase was observed in local cortical neurons. Colchicine prevented the increases in immunoreactivity for the neuropeptides in the amygdala on the side of stroke, although there were small perikarya that showed immunoreactivity for these neuropeptides within the amygdala on both sides. We conclude that local cortical neurons are responsible for the increase in neuropeptide Y in the periinfarct region, that the cortical increase in tyrosine hydroxylase is not dependent on fast axonal transport, and that axonal transport of signals from the insular cortex to the amygdala is critical in mediating the amygdalar neuropeptide changes seen after stroke.

Amygdala↗
PubMed1997

Effects of colchicine on the number of T2 vesicles in the tegument of Fasciola hepatica.

The role of microtubules in the secretory processes in the tegument of adult trematode Fasciola hepatica L. is studied by estimating the effects of colchicine, a substance known to disrupt microtubules, on the number of T2 vesicles. Tissue slices of the worm are incubated in Hedon-Fleig medium with or without 5 x 10(-4) M colchicine. The dynamics of the colchicine-provoked secretory block is examined by morphometry on samples processed for electron microscopy. T2 vesicles are estimated as a total number or separately within three levels (apical, sub-apical and central) of the distal tegument. The secretory block is demonstrated as reduction in the total number of T2 vesicles. The separate counting within three levels of the distal tegument demonstrates in control samples a trend of sub-apical condensation of T2 vesicles. This pattern of T2 distribution remains unchanged in colchicine-treated samples in spite of the reduction of the mean T2 counts within each of the levels examined. The data illustrate the role of microtubules in both the tegumental transport of secretory vesicles and the stratification of the organelles within the tegument.

Animals↗
PubMedDate not supplied

[Protective effect of colchicine on tissue damage caused by free radicals in hepatic cirrhosis: an experimental study in rats].

The present study was undertaken to evaluate the effect of colchicine on oxidative stress in cirrhosis assessed by lipid peroxidation products. Wistar rats were used and induced hepatic cirrhosis by carbon tetrachloride. After the cirrhosis-induced period colchicine was administrated daily during 90 days. Lipid peroxidation was evaluated by the thiobarbituric acid reactive substances method (TBARS) and chemiluminescence initiated by tert-butyl hydroperoxide. The liver was submitted to histological evaluation to check whether cirrhosis was present. The results demonstrated an higher increase in lipid peroxide levels in cirrhotic tissue when compared with normal tissue and it was decreased by colchicine treatment (P < 0.05). Observing this study, we can conclude that hepatic cirrhosis produce an higher oxidative stress than normal liver and it can be decreased by colchicine treatment.

Animals↗
PubMed1985

Selective 1H-NMR relaxation investigations of membrane-bound drugs in vitro. 1. Colchicine.

Binding of colchicine to dipalmitoylphosphatidylcholine bilayer vesicles was detected by measuring the 1H-NMR selective spin-lattice relaxation rates of the low-field protons of colchicine. From the temperature dependence of the selective rates, preferential binding was observed above the temperature of transition. In the same way, binding of colchicine to red blood cells was detected and the equilibrium constant determined. Binding to the lipid matrix of red blood cells accounted only partially for the binding of colchicine to whole cells.

Journal Article↗
PubMed2001

Colchicine induced neuromyopathy in a patient with normal renal function.

A 69-year-old male on colchicine 0.6 mg twice a day for more than a year developed subacute onset of painless proximal muscle weakness with significant elevation of creatine phosphokinase (CPK) levels. He also experienced numbness and tingling in the extremities. Nerve conduction studies revealed a mild axonal neuropathy affecting the arms and legs while needle electromyography was unremarkable. He refused a muscle biopsy. After withdrawal of colchicine, muscle strength and serum CPK levels returned to normal over a period of 4 months. Neuromyopathy is a well documented side effect of colchicine, and impaired renal function has been the major risk factor in previously reported cases. In our patient, neurological toxicity occurred in the presence of normal renal function. The neuromyopathy is generally reversible on withdrawal of the drug. Colchicine is to be used with caution in patients with impaired renal function, and even if kidney function is normal, muscle strength must be monitored and serum CPK levels checked if myopathy is suspected.

Journal Article↗
PubMed1971

Dissociation by colchicine of the hexose monophosphate shunt activation from the bactericidal activity of the leukocyte.

The effect of the in vitro addition of colchicine on various aspects of leukocyte metabolism was investigated. Colchicine in 6 mm concentration reduced the oxygen uptake of phagocytizing leukocytes to below the level of resting cells. A similar concentration of colchicine inhibited the increase in glucose-1-(14)C oxidation by 90% and the quantitative nitroblue tetrazolium reduction by about 50%. Experiments with broken cell preparations indicate that the inhibition of the hexose monophosphate shunt is due to an inhibition of the activity of the shunt enzymes glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. In spite of these pronounced metabolic changes, the addition of 6 mm colchicine had no observable effect on the bactericidal activity of the leukocyte against three test organisms. These results support a mechanism for phagocytosis in which the hexose monophosphate-shunt activation is a secondary phenomenon which is not required for the actual killing process.

Journal Article↗
PubMed2006

Colchitaxel, a coupled compound made from microtubule inhibitors colchicine and paclitaxel.

BACKGROUND: Tumor promoters enhance tumor yield in experimental animals without directly affecting the DNA of the cell. Promoters may play a role in the development of cancer, as humans are exposed to them in the environment. In work based on computer-assisted microscopy and sophisticated classification methods, we showed that cells could be classified by reference to a database of known normal and cancerous cell phenotypes. Promoters caused loss of properties specific to normal cells and gain of properties of cancer cells. Other compounds, including colchicine, had a similar effect. Colchicine given together with paclitaxel, however, caused cells to adopt properties of normal cells. This provided a rationale for tests of microtubule inhibitor combinations in cancer patients. The combination of a depolymerizing and a stabilizing agent is a superior anti-tumor treatment. The biological basis of the effect is not understood. RESULTS: A single compound containing both colchicine and paclitaxel structures was synthesized. Colchicine is an alkaloid with a trimethoxyphenyl ring (ring A), a ring with an acetamide linkage (ring B), and a tropolone ring (ring C). Although rings A and C are important for tubulin-binding activity, the acetamide linkage on ring B could be replaced by an amide containing a glutamate linker. Alteration of the C-7 site on paclitaxel similarly had little or no inhibitory effect on its biological activity. The linker was attached to this position. The coupled compound, colchitaxel (1), had some of the same effects on microtubules as the combination of starting compounds. It also caused shortening and fragmentation of the + end protein cap. CONCLUSION: Since microtubule inhibitor combinations give results unlike those obtained with either inhibitor alone, it is important to determine how such combinations affect cell shape and growth. Colchitaxel shows a subset of the effects of the inhibitor combination. Thus, it may be able to bind the relevant cellular target of the combination. It will be useful to determine the basis of the shape reversal effect and possibly, the reasons for therapeutic efficacy of microtubule inhibitor combinations.

Journal Article↗
PubMed1996

Myotonia in colchicine myoneuropathy.

Colchicine may induce a myoneuropathy in patients with renal insufficiency. To date, myotonia has not been described in this disorder. We recently studied 4 patients treated with routine doses of colchicine who, in the setting of renal insufficiency, developed a severe myoneuropathy characterized by prominent myotonic discharges on electromyography. In addition, 1 of the 4 patients had profound clinical myotonia. In the 3 patients in whom biopsies were performed, marked myopathic change with intracytoplasmic vacuolization was identified. All 4 patients improved rapidly with discontinuation of the medication. The patient in whom electrophysiologic studies were repeated had a complete resolution of the myotonic discharges. Colchicine myoneuropathy can present with prominent clinical and electrophysiologic myotonia that resolves completely with discontinuation of the medication.

Adult↗
PubMed2004

A severe autosomal-dominant periodic inflammatory disorder with renal AA amyloidosis and colchicine resistance associated to the MEFV H478Y variant in a Spanish kindred: an unusual familial Mediterranean fever phenotype or another MEFV-associated periodic inflammatory disorder?

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurring short attacks of fever and serositis. Secondary AA amyloidosis is the worst complication of the disease and often determines the prognosis. The MEFV gene, on chromosome 16p13.3, is responsible for the disease and around 30 mutations have been reported to date. Colchicine is the standard FMF treatment today, and prevents both attacks and amyloid deposition in 95% of patients. Here we describe a three-generation Spanish kindred with five family members affected by a severe periodic inflammatory disorder associated with renal AA amyloidosis and colchicine unresponsiveness. Clinical diagnosis of definite FMF disease was made based on the Tel-Hashomer criteria set. Genetic analyses revealed that all subjects were heterozygous for the new H478Y MEFV variant, segregating with the disease. In addition, mutations in the TNFRSF1A and CIAS1/PYPAF1/NALP3 genes, related to the dominantly inherited autoinflammatory periodic syndromes, were ruled out. However, the dominant inheritance of the disease, the long fever episodes with a predominant joint involvement, and the resistance to colchicine in these patients raise the question of whether the periodic syndrome seen in this kindred is a true FMF disease with unusual manifestations or rather another MEFV-associated periodic syndrome. We conclude that the new H478Y MEFV mutation is the dominant pathological variant causing the inflammatory periodic syndrome in this kindred and that full-length analyses of the MEFV gene are needed to obtain an adequate diagnosis of patients with clinical suspicion of a hereditary periodic fever syndrome, especially those from non-ancestral populations.

Adult↗