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PubMed2004

The outcome of pregnancy in the wives of men with familial mediterranean fever treated with colchicine.

OBJECTIVE: To evaluate the outcome of pregnancies of normal women married to men with familial Mediterranean fever (FMF), some of whom took colchicine during the conception with their wives. PATIENTS AND METHODS: We followed the outcome of pregnancies and deliveries of 60 wives of FMF patients; 53 of the husbands were taking colchicine during that time. As a control group we screened the outcome of pregnancy and delivery from 230 healthy women married to healthy men. RESULTS: The 60 FMF patients- wives had 222 pregnancies, of which 206 ended in term delivery with 209 live births. Sixteen pregnancies ended in spontaneous abortions (7%). Three of the newborns in the study group were born with congenital malformations. In the control group, of 788 pregnancies, 127 ended in abortions (16%). Six of the newborns were born with congenital malformations. The rate of the late abortions (second trimester) in both groups was comparable. CONCLUSIONS: The results of our study indicates that neither FMF nor colchicine increases the rate of abortions or congenital malformations. Therefore we believe that there is no need to discontinue colchicine treatment in men with FMF before the conception with their wives.

Abortion, Spontaneous↗
PubMed2004

Effect of colchicine on cyclosporine nephrotoxicity, reduction of TGF-beta overexpression, apoptosis, and oxidative damage: an experimental animal study.

BACKGROUND: Proinflamatory and profibrotic cytokines may be responsible for the cyclosporine A nephrotoxicity. Increased levels of apoptosis, free oxygen redicals, and transforming growth factor beta (TGF-beta), may play an important roles in the pathogenesis of nephrotoxicity. In this experimental animal study, we sought to investigate the effects of colchicine on the cyclosporine nephrotoxicity. METHOD: Twenty-four Wistar albino rats were divided into three groups: cyclosporine 15 mg/kg subcutaneously (SC); cyclosporine 15 mg/kg SC plus colchicine 30 mcg/kg orally; and a control group; equal doses of olive oil orally were administered to groups 1, 2, and 3. Renal function, cyclosporine levels, and serum malonyldialdehyde (MDA) levels were measured at the end of 4 weeks. Apoptosis, TGF-beta, and other findings were detected in renal tissue with the TUNEL method, with a immunohistochemical method, and with routine staining procedures, respectively. RESULTS: There were significant differences in the values of mean creatinine clearance between group 1 and group 3 and between group 2 and group 3 (P < .05 for each comparison), but not between group 1 and group 2 (P > .05). MDA levels in group 1 were high compared with the control group (P < .05) with a trend toward elevation relative to group 2 but the results were not statistically significant (P > .05). Renal tubular vacuolization in group 1 and group 2 animal were greater than in the control group, but no significant difference were observed between any of the groups (P > .05). Mononuclear cell infiltration in group 1 and group 2 hosts were higher than the control group, but there was no significant differences between the groups (P > .05). Afferent arteriolar hyalinization was observed group 1 and 2 but not group 3. There was a statistically significant difference between group 1 and group 3 and between group 2 and group 3 (P < .05 for each comparison). The expression level of TGF-beta was higher in group 1 than group 2 or group 3 (P <.05 for each comparison) but group 2 and group 3 were similar (P > .05). Apoptotic cell death count of group 1 was higher than that in group 2 or group 3 (P < .05, for each comparison); moreover, group 2 also showed greater numbers of apoptotic cells than group 3 (P < .001). At the end of the 4 weeks, there was no intersititial fibrosis in any of the hosts. CONCLUSION: While cyclosporine caused increased TGF-beta expression and apoptotic cell death in the renal tissue of rats colchicine prevented the increase in MDA serum levels, TGF-beta expression, and apoptosis in renal tissue. Our study suggests that colchicine may diminish the cyclosporine nephrotoxicity by its suppressing the expression of TGF-beta, apoptotic cell death, and MDA production.

Animals↗
PubMed1999

Cardiovascular effects of catecholamines injected into the DBB of rats, influence of urethane anaesthesia and local colchicine.

In a previous publication it was shown that 1 microgram colchicine injected into the diagonal band of Broca (DBB) produced a significant decrease in femoral artery blood pressure (and/or volume) measured in urethane-anaesthetised rats. In order to test if the central catecholamines were involved in this effect, guide cannulae were implanted in the DBB and a catheter in the femoral artery. On-line pressure recordings were taken before during and after alpha1, alpha2 and beta adrenoreceptor agonists and antagonists were injected into the region of the DBB of non-anaesthetised and urethane anaesthetised male Wistar rats with and without injection of colchicine. Arterial pressure was significantly increased in the non-anaesthetised rats (114.6+/-2.6 n=11 vs. 149.3+/-3.3 mmHg n=12, p<0.01) yet significantly reduced (82.0+/-3.9 n=11 vs. 63.8+/-4.5 mmHg n=12, p<0.01) in the urethane treated rats by the alpha2 agonist clonidine. The alpha2 antagonist yohimbine blocked these effects in both preparations. In contrast, the beta adrenoreceptor agonist isoprenaline produced a significant decrease in arterial pressure in both preparations (107.7+/-3.9 n=11 vs. 85.9+/-4.0 mmHg n=12, p<0.01) (102.6+/-6.7 n=11 vs. 81.7+/-3.4 mmHg n=12, p<0.01) and this effect was blocked by the beta antagonist propranolol. Colchicine injected into the DBB abolished the effects of the alpha2 agonist and antagonist in the non-anaesthetised but not the anaesthetised rats. The responses to the beta agonist and antagonist were not greatly affected by the colchicine in the non-anaesthetised rats whereas in the anaesthetised rat beta agonist injection tended to totally depress arterial pressure. These results suggest that the sympathetic nervous system in the DBB plays a significant role in the central control of arterial pressure and that the alpha2 component is significantly affected by the state of anaesthesia.

Adrenergic beta-Agonists↗
PubMed1978

Long-term colchicine therapy of familial Mediterranean fever.

Familial Mediterranean fever is a disorder characterized by recurrent fever and polyserositis. Continuous prophylactic colchicine therapy has been effective in suppressing attacks in affected adults. From 30 children with FMF, 14 were selected for colchicine therapy. Eight children continued prophylactic colchicine therapy for 29 months (mean) and experienced a marked decrease in the frequency of attacks. Six other children did not comply with the treatment regimen. Although no deleterious side effects were noted, the safety of long-term colchicine administration in childhood is unknown.

Adolescent↗
PubMed1983

Effect of colchicine on rat small intestinal absorptive cells. I Formation of basolateral microvillus borders.

Treatment of rats with colchicine (0.5 mg/100 g of body weight) for more than 3 hr causes formation of microvillus borders along lateral and basal surfaces of absorptive cells in the small intestine. Morphologically, these strongly resemble the apical brush border inclusive of the terminal-web region. Formation of basolateral microvilli is restricted to mature absorptive cells. At 6 hr after administration of colchicine, 3.47% (+/- 1.94%) of the basolateral cell surfaces exhibit "implantation" of microvillus borders. The results show that colchicine induces formation of surface differentiations at lateral and basal surface regions that are restricted to the apical cell surface in controls. Redistribution of constituents of the plasma membrane from apical to basolateral membrane portions, as well as rearrangement in the organization of microfilaments can be considered to underlie formation of basolateral microvillus borders. From the antimicrotubular effect of colchicine it may be deduced that microtubules exert a regulative function in the formation of surface differentiations on absorptive cells of the small intestine and in the maintenance of the polarity of the cells.

Animals↗
PubMed2003

Neuroprotective action of flavopiridol, a cyclin-dependent kinase inhibitor, in colchicine-induced apoptosis.

Flavopiridol was developed as a drug for cancer therapy due to its ability to inhibit cell cycle progression by targeting cyclin-dependent kinases (CDKs). In this study, we show that flavopiridol may also have a neuroprotective action. We show that at therapeutic dosage (or at micromolar range), flavopiridol almost completely prevents colchicine-induced apoptosis in cerebellar granule neurones. In agreement with this, flavopiridol inhibits both the release of cyt c and the activation of caspase-3 induced in response to colchicine treatment. We demonstrate that in this cellular model for neurotoxicity, neither re-entry in the cell cycle nor activation of stress-activated protein kinases, such as c-Jun N-terminal kinase (JNK) or p38 MAP kinase, is involved. In contrast, we show that colchicine-induced apoptosis correlates with a substantial increase in the expression of cdk5 and Par-4, which is efficiently prevented by flavopiridol. Accordingly, a cdk5 inhibitor such as roscovitine, but not a cdk4 inhibitor such as 3-ATA, was also able to protect neurons from apoptosis as well as prevent accumulation of cdk5 and Par-4 in response to colchicine. Our data suggest a potential therapeutic use of flavopiridol in disorders of the central nervous system in which cytoskeleton alteration mediated by cdk5 activation and Par-4 expression has been demonstrated, such as Alzheimer's disease.

Amino Acid Chloromethyl Ketones↗
PubMed1988

Protective effect of colchicine on acute liver damage induced by carbon tetrachloride.

Pretreatment of rats with colchicine (10 micrograms/day) for 7 days protected against CCl4-induced acute liver damage. CCl4 intoxication was demonstrated histologically and by increased serum activities of glutamic-pyruvic transaminase, alkaline phosphatase and gamma-glutamyl transpeptidase. Furthermore, an increase in liver lipid peroxidation and a decrease in plasma membrane gamma-glutamyl transpeptidase activity were found. Colchicine increased the LD50 of CCl4 2.5-fold and prevented the release of intracellular enzymes, as well as the decrease in gamma-glutamyl transpeptidase activity in the plasma membrane. It also completely prevented the lipid peroxidation produced by CCl4 and limited the extent of the histological changes. Our results suggest that the protective effect of colchicine may be mediated through its action on an early toxic event, because treatment of the animals with colchicine produced a significant decrease in CCl4-induced lipid peroxidation.

Animals↗
PubMed1996

Effects of additional administration of colchicine in ursodeoxycholic acid-treated patients with primary biliary cirrhosis: a prospective randomized study.

BACKGROUND/AIMS: Although ursodeoxycholic acid is effective for the treatment of primary biliary cirrhosis, some patients do not respond to this treatment. The objective of the present study was to investigate the effects of additional administration of colchicine in ursodeoxycholic acid-treated patients with primary biliary cirrhosis. METHODS: Twenty-two patients with primary biliary cirrhosis treated with ursodeoxycholic acid (600 mg/day) for 30 months were randomly assigned to two groups: group 1, colchicine (1 mg/day) and ursodeoxycholic acid (n = 10); group 2, ursodeoxycholic acid alone (n = 12). RESULTS: In group 1, there were significant decreases in mean serum levels of alkaline phosphatase, total bilirubin, gamma-glutamyltranspeptidase, alanine aminotransferase, aspartate aminotransferase, and IgM, and these changes were more remarkable in those who responded poorly to ursodeoxycholic acid. In contrast, there were no significant changes in those values in group 2. CONCLUSIONS: Additional administration of colchicine to ursodeoxycholic acid may be beneficial for patients with primary biliary cirrhosis, especially those who respond poorly to ursodeoxycholic acid. It is necessary, however, to further confirm the efficacy of colchicine by examining histological changes and following the patients for longer periods.

Aged↗
PubMed1984

Colchicine for treatment of relapsing polychondritis.

This report describes the effectiveness of oral colchicine, 0.6 mg twice daily, in abating three attacks of chondritis in two patients who fulfilled the diagnostic criteria for relapsing polychondritis (RP). Chondritis of the pinnae of the ears was utilized as a therapeutic guideline toward improvement. Collagen antibodies and urinary mucopolysaccharides were negative during flares and after improvement; antinuclear antibodies (ANA) and anti-deoxyribonucleic acid (DNA) were present in one patient. Both patients experienced a continued chondritis for at least 10 days before colchicine was started. Marked improvement was observed in 4 days, and complete resolution occurred after 7 days' treatment with colchicine. These observations indicate that the effectiveness of colchicine, as a relatively safer medicine, should be evaluated further in the treatment of RP.

Adult↗
PubMed1985

Colchicine is effective in controlling chronic cutaneous leukocytoclastic vasculitis.

Chronic cutaneous leukocytoclastic vasculitis is commonly difficult to control. In an attempt to avoid potentially toxic therapy with corticosteroids and/or immunosuppressives or to allow tapering of corticosteroid therapy, I instituted oral colchicine therapy in thirteen patients. Complete control of disease occurred in nine patients, partial control (as evidenced by my ability to lower the corticosteroid dosage) was obtained in three patients, and one patient had no demonstrable effects during a 1-month period of colchicine therapy. Effect was uniformly noted within 1 week after institution of therapy. Side effects were uncommon but, when they occurred, consisted mainly of abdominal cramping and/or diarrhea. Seven patients had a relapse of their cutaneous vasculitis when colchicine was stopped, but reinstitution again led to a rapid control of the disease manifestations. Therapy has been safely continued for up to 2 1/2 years without evidence of toxicity. Thus colchicine appears to be a safe and effective therapy for chronic cutaneous leukocytoclastic vasculitis.

Adult↗
PubMed1996

Colchicine for epidermolysis bullosa acquisita.

BACKGROUND: Epidermolysis bullosa acquisita (EBA) is a chronic subepidermal blistering disease that is difficult to treat. Recently one patient with severe EBA was described who responded dramatically to colchicine. OBJECTIVE: Our purpose was to determine the efficacy of colchicine in the treatment of EBA. METHODS: Four patients with severe EBA refractory to conventional therapy were treated with colchicine 0.6 to 1.5 mg a day for up to 4 years. RESULTS: In all four patients the lessening of skin fragility and the decrease in spontaneous blister formation were dramatic; few side effects were noted. CONCLUSION: Colchicine should be considered in the treatment of EBA.

Adult↗
PubMed1998

Comparative study on effects of pentoxifylline, prednisolone and colchicine in experimental alveolitis.

Neutrophil alveolitis is a hallmark of cryptogenic fibrosing alveolitis (CFA), known for its poor prognosis. Corticosteroids, as the remedy of choice, are ineffective in a majority of patients. More and more evidence indicates that pentoxifylline (POF) could be an effective therapeutic alternative. Furthermore, colchicine has been proposed for therapy of CFA for many years now. We conducted an experimental study comparing the efficacy of these drugs in preventing neutrophil alveolitis in vivo. Alveolitis was induced in male rats by intratracheal instillation of bleomycin. Treatment consisted of daily injections of POF i.p., colchicine i.p., or prednisolone i.m. After 8 days the animals were sacrificed and body weights, cell differentials in BAL, amount of proliferating interstitial cells as determined by KI-67 staining of lung tissue, and collagen concentrations in lungs were determined. Bleomycin instillation was followed by a significant weight loss in the animals, a neutrophil alveolitis in BAL and an increased amount of proliferating cells in lung interstitium. POF significantly inhibited any of the parameters named, whereas prednisolone and colchicine had little effect. Data cannot be applied directly in human disease. There are however many similarities between CFA and bleomycin-induced lung injury and alveolitis. We conclude that POF is an effective inhibitor of neutrophil alveolitis, whereas neither colchicine nor prednisolone exerted significant influence in our model. We suggest POF effects should be further investigated regarding anti-inflammatory and anti-fibrotic properties.

Animals↗
PubMed1997

S100beta promotes the extension of microtubule associated protein2 (MAP2)-immunoreactive neurites retracted after colchicine treatment in rat spinal cord culture.

S100beta, a glial derived calcium-binding protein with neurotrophic activity in the central nervous system, stimulates neurite extension of fetal raphe, cortex, spinal cord, and dorsal root ganglion neurons. The effects of S100beta on neurite length and microtubule associated protein2 (MAP2) immunoreactivity (IR) after microtubule disruption with colchicine were investigated in primary rat spinal cord culture. The incubation with S100beta (20 ng/ml) for 3 h after exposure to colchicine (10(-6) M) for 30 min altered the distribution of MAP2-IR. The length of MAP2-IR neurites increased by 65% compared to that in colchicine treatment alone. MAP2-IR intensity in the cell body was reduced by 26% compared to that in colchicine treatment alone. These results indicate that neurites shrink when the microtubular cytoskeletal system is disrupted and S100beta rapidly promotes re-assembly and/or stabilization.

Animals↗
PubMed2000

Colchicine-induced bone marrow suppression: treatment with granulocyte colony-stimulating factor.

Bone marrow aplasia is a frequent complication of colchicine poisoning. This typically occurs on day 3 to 5 postexposure, and the blood cell counts remain depressed for a week or more. Unfortunately, because patients suffering from colchicine toxicity develop multiple organ complications and sepsis, the morbidity and mortality associated with bone marrow depression is high. In this article, we present three cases of colchicine toxicity in which granulocyte colony-stimulating factor (G-CSF) was used to treat bone marrow depression. In all three cases, there was a dramatic increase in the white cell count and, to a lesser extent, the platelet count. In view of the critical nature of the bone marrow depression and multi-organ toxicity induced by colchicine, we believe that consideration of the use of G-CSF to shorten the duration of neutropenia is warranted.

Adolescent↗
PubMed1986

[Acute respiratory distress syndrome in adults in colchicine poisoning].

Two cases of adult respiratory distress syndrome were treated in a series of 26 patients suffering from colchicine overdose. The syndrome appeared between the 24th and 72nd hours. It was characterized by the presence of interstitial as well as alveolar oedema seen on chest roentgenograms. Haemodynamic investigation showed a hyperkinetic state with moderate precapillary pulmonary arterial hypertension. In addition, multivisceral phenomena were observed in all cases. Post-mortem examination revealed interstitial and alveolar pulmonary oedema with haemorrhagic or macrophagic alveolitis often accompanied by hyaline membrane. The physiopathology of ARDS occurring in colchicine poisoning appeared to involve such different factors as infection, the presence of a state of shock and disseminated intravascular coagulopathy. The direct toxic action of colchicine on pneumocyte microtubules and the inhibition of surfactant production were a probable cause. The responsibility of colchicine in leukocyte aggregation remains to be determined.

Adult↗
PubMedDate not supplied

Analysis of colchicine-induced chromosomal aberrations in embryos obtained from XO mice.

A high incidence of chromosomal anomalies has been observed in the offspring of our XO mouse colony. However, the reason(s) are unknown. We hypothesized that XO dams might be more susceptible to certain chromosomal mutagens. Therefore, we assessed whether the oocytes of XO mice are more susceptible to colchicine. Pregnant XO and XX mice were intraperitoneally (i.p.) injected with colchicine, 0.2 mg/kg, 6 h after mating (between resumption of meiosis II and extrusion of the second polar body). Contrary to our expectation, the incidence of chromosomal anomalies induced by colchicine exposure did not differ between XX and XO dams. These findings suggest that the chromosomal stability of the oocytes from XO mice may not be affected by colchicine exposure at the stage of extrusion of the second polar body. The effects of chromosomal imbalance inherent in XO mice on chemical susceptibilities should be further investigated.

Animals↗
PubMed1989

The degradation of collagen in pig synovium in vitro and the effect of colchicine.

Colchicine induced a rapid destruction of the collagenous matrix of pig synovial explants in culture in the presence of serum. The most efficacious doses were 0.01-0.1 micrograms/ml (2.5 x 10(-8) M - 2.5 x 10(-7) M). The histological progression of the tissue breakdown induced by colchicine was very similar, although faster, to that described for other agents (Fell et al., 1986), with cells having basophilic nuclei accumulating in areas of fibril degradation. The loss of collagen correlated with an increase in collagenase production and at the peak of resorption (6 to 8 days) active collagenase was present in the culture media. Immunocytochemical methods demonstrated active collagenase bound to collagen fibrils after only 4 days in culture, before significant collagen degradation could be observed histologically. Collagen breakdown was completely inhibited by cortisol, and partially inhibited by indomethacin: only the inhibition by indomethacin could be reversed by exogenous prostaglandin E2. Vinblastine at a higher dose was as effective as colchicine but the lumicolchicines, which do not disrupt microtubules, were ineffective. Although the precise mechanism of action of colchicine is unknown, this culture system provides a useful in vitro model for increasing our understanding of the cellular mechanisms of tissue breakdown and for elucidating the roles of active collagenase and related metalloproteinases.

Animals↗
PubMed1998

Regulation of parathyroid hormone-related protein expression in a canine squamous carcinoma cell line by colchicine.

The regulation of parathyroid hormone-related protein expression by colchicine, vinblastine, nocodazole, taxol, transforming growth factor-beta1 (TGFbeta1), and epidermal growth factor (EGF) was investigated in a canine squamous carcinoma cell line (SCC 2/88 cells). SCC 2/88 cells were stably transfected with a human P2/P3 PTHrP promoter-luciferase reporter gene construct and gene expression was measured after chemical treatments. The greatest increase in reporter gene expression was observed after colchicine treatment and small increases occurred after treatment with vinblastine, taxol, TGFbeta1, or EGF. Nocodazole had no significant effect on reporter gene expression. Colchicine also increased PTHrP steady state mRNA expression and PTHrP secretion by SCC 2/88 cells. These results demonstrated that PTHrP production was increased in SCC 2/88 cells by colchicine and suggested that factors or events during mitosis are capable of stimulating PTHrP production. An increase in PTHrP production during mitosis of malignant epithelial cells may be important in the pathogenesis of humoral hypercalcemia of malignancy.

Animals↗