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  In this article
   Introduction
   Mechanism of Action
   Pharmacology and...
   Dosages and Admi...
   Uses in Dermatology
   Adverse Effects
   Colchicine Overdose
   Drug Interactions
   Monitoring Guide...
   Conclusion
   References
   Article Figures
   Article Tables

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Year : 2010  |  Volume : 76  |  Issue : 2  |  Page : 201-205

Colchicine in dermatology


1 St. Theresa's Hospital, Sanathnagar, Hyderabad - 500018, India
2 Department of Dermatology, Gandhi Medical College and Hospital, Musheerabad, Hyderabad - 500048, India

Date of Web Publication10-Mar-2010

Correspondence Address:
Angoori Gnaneshwar Rao
Department of Dermatology, Gandhi Medical College and Hospital, Musheerabad, Hyderabad - 500048
India
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DOI: 10.4103/0378-6323.60552

PMID: 20228563

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How to cite this article:
Konda C, Rao AG. Colchicine in dermatology. Indian J Dermatol Venereol Leprol 2010;76:201-5

How to cite this URL:
Konda C, Rao AG. Colchicine in dermatology. Indian J Dermatol Venereol Leprol [serial online] 2010 [cited 2014 Apr 18];76:201-5. Available from: http://www.ijdvl.com/text.asp?2010/76/2/201/60552



  Introduction Top


Colchicine, a toxic natural product, which is the active principle of the plant, Colchicum autumnale (autumn crocus or meadow saffron), and other plants of Colchiaceae family. It is a nitrogen-containing substance often described erroneously as an alkaloid, although its biosynthetic precursor, demecolcine, is an alkaloid. [1] It has been known since antiquity for its medicinal uses. It is still in use today for the treatment of gout and familial  Mediterranean fever More Details. [2] Under suitable qualified medical supervision, isolates from the seeds and tubers of these plants have been used in the treatment of certain skin disorders. Colchicine, was first isolated in 1820 by the two French chemists P.S. Pelletier and J. Caventon. [3] We briefly review here the pharmacological and the therapeutic profiles of colchicine in dermatology.


  Mechanism of Action Top


Anti-mitotic

Its capacity to interrupt mitosis is due to its linkage to dimers of tubulin, a dimeric protein in microtubules. [4] The microtubular toxicity will cause cessation of mitosis in metaphase and interference in cellular mobility.

Anti-inflammatory

Colchicine reduces mobility, adhesiveness, and chemotaxis of polymorphonuclear cells. It interferes with intercellular adhesion molecules, selectins, thus inhibiting T-lymphocyte activation and its adhesion to endothelial cells. [5],[6]

It impairs cellular secretion of procollagen and increases collagenase production that promotes a larger collagenolytic action. [7]

Immunosuppressive action

It inhibits cell-mediated immune responses, [8] by inhibiting immunoglobulin secretion, IL-1 production, histamine release and HLA-DR expression.

Other pharmacological effects

Decrease of the corporal temperature, depression of the respiratory center, increased response to sympathomimetic agents, contraction of blood vessels, hypertension by central vasomotor stimulation, and alteration of the neuromuscular function. [Figure 1]


  Pharmacology and Pharmacokinetics Top


It occurs as pale to greenish yellow crystals or powder. When exposed to ultra-violet radiation, it oxidizes into a dark color [9] and is transformed into different photoisomers. [10] Hence, it must be shielded from exposure to sunlight. It is rapidly absorbed when taken orally; peak plasma levels are reached between 30 and 120 min after ingestion. Fifty percent of the drug circulates and links to plasma proteins. The drug is metabolized in the liver, and the majority is eliminated through bile in the feces. It is also distributed in spleen and kidney. Overall, 10-20% of the dose is eliminated unchanged in the urine.


  Dosages and Administration Top


Oral

Acute gout

Initial dose is 1 mg, reduced to 0.5 mg every 2-3 h, until pain relief is achieved or gastrointestinal toxicity occurs. Course may be repeated after at least 3 drug-free days. Maximum dose: 6 mg/course. Should be stored in an airtight container and protected from light. Initiation of allopurinol treatment must be preceded by daily oral colchicine for at least 2 weeks. This is done as sudden discontinuation of allopurinol results in rapid re-elevation of serum uric acid to pre-treatment levels. Continuation of colchicine for several weeks or months after initiation of allopurinol is recommended by most experts. In patients with tophi, it is advised to continue colchicine prophylaxis until all tophi have dissolved, which often takes years.

Prophylaxis of recurrent gouty arthritis

Adult: 0.5-0.6 mg once daily. Dosage range: 0.6 mg every other day to 0.6 mg tid.

Intravenous preparation (iv)

It is given in 0.9% saline (but not in 5% dextrose as it may precipitate) in a dose of 0.5 mg/mL (2 mL). Single intravenous dosages should not exceed 2-3 mg, and cumulative total dosages for an attack should not be more than 4-5 mg. The administration of iv colchicine is contraindicated in patients with renal failure, extrahepatic biliary obstruction, or patients with combined renal and hepatic insufficiency. Although not approved by the Food and Drug Administration (FDA), intravenous (iv) colchicine has been an accepted treatment for acute gout symptoms. Several additional iv uses include treatment of familial Mediterranean fever, pericarditis, primary biliary cirrhosis, amyloidosis, and Behçet's syndrome. [11],[12],[13]

It should not be given intramuscularly or subcutaneously, as it causes severe local irritation.


  Uses in Dermatology Top


Until now, there was no formal indication approved by the FDA for colchicine use in dermatology; however, several uncontrolled studies have showed exciting results [Table 1], mainly in neutrophilic dermatoses.

Gout

Colchicine controls acute attacks by suppressing monosodium urate crystal-induced NACHT-LRR-PYD-containing protein-3 (NALP3) inflammasome-driven caspase-1 activation, IL-1b processing and release, and L-selectin expression on neutrophils. [14] It will not prevent the formation of cutaneous tophi and may, actually increase the development of tophi, by preventing the inflammatory response. Hence, hyperuricemia must be controlled at the same time.

Papulosquamous Dermatoses

Psoriasis was one of the first cutaneous diseases to be treated with colchicine. Wahba and Cohen used oral colchicine in 22 psoriasis patients and found greater than 50% improvement in 11 patients. The results were better in those whose lesions were small papules and plaques. [15] Kaidbey et al. observed usefulness of topical colchicine in patients with recalcitrant plaque psoriasis. [16] This drug is effectively used in psoriatic arthritis. [17] However, it was not found beneficial in a larger study. Colchicine was found to be effective in generalized pustular psoriasis and palmoplantar pustulosis. [18],[19],[20] It is likely that colchicine has a limited therapeutic value in psoriasis.

Recurrent aphthous stomatitis

Colchicine in the dose of 0.6 mg twice or thrice daily was found to decrease morbidity. [21]

Behcet's syndrome

Colchicine was found to be effective in Behcet's syndrome in the treatment of ocular, articular, oral, and genital lesions. [22],[23],[24] It was postulated that by blocking phagocytosis, colchicine may increase superoxide scavenging activity of neutrophils which is impaired in this syndrome.

Sweet's syndrome

Improvement with a daily dose of 1.5 mg colchicine was found in Sweet's syndrome. [25]

Bullous diseases

Several bullous diseases can be treated with colchicine.

Dermatitis herpetiformis

Silvers et al. used colchicine at the dose of 1.2-1.8 mg/day to treat patients with dermatitis herpetiformis. [26] They found it useful as alternate therapy in those who could not take sulfonamides.

Linear IgA disease

Aram found colchicine to be very useful in patients who failed to respond to dapsone. [27] The good response to colchicine in this disease may be based on the fact that there are many neutrophils.

Epidermolysis bullosa acquisita (EBA)

Megahed and Scharrffetter-Kochanek described successful treatment of EBA with colchicine. [28]

Chronic bullous dermatosis of childhood

Colchicine was found to be very useful in chronic bullous dermatosis of childhood (CBDC) with G6PD deficiency. [29]

In all the immunobullous dermatoses listed where colchicine is used, dapsone is the better choice and colchicine is an alternative where the patient cannot take dapsone due to G6PD deficiency or some other reason or dapsone is not effective in a particular patient.

Vasculitis

Leucocytoclastic vasculitis (LCV) and Urticarial vasculitis

Several case reports have described the beneficial effects of colchicine in this condition with involvement of the skin, with or without joint manifestations, and also in urticarial vasculitis. [30] Colchicine was effective in urticarial vasculitis associated with hypocomplementemia. It reduces neutrophilic chemotaxis and motility in both these conditions.

Scleroderma

Some authors have described beneficial effects in localized and systemic scleroderma, [31] whereas others have not. Colchicine's action on production, regulation of collagen, adhesion molecules, and matrix digester enzymes justifies its use in this disease.

Amyloidosis

Cutaneous lesions develop in upto 40% of patients with systemic amyloidosis, both primary and secondary. This drug prevents amyloid deposition and slows disease progression in amyloidosis associated with familial Mediterranean fever. [32] Amyloid originates from degenerated epidermal cells in susceptible subjects. Colchicine probably blocks the release of lysosomal enzymes within these cells thereby preventing conversion of the cells tonofilaments into amyloid. [33] Oral colchicine is useful in the management of primary cutaneous amyloidosis. [34]

Miscellaneous

Colchicine was found to be effective in erythema nodosum leprosum, [35],[36] pyoderma gangrenosum, [37] severe cystic acne, [38] calcinosis cutis, [39] keloids, sarcoid, condyloma acuminata, [40] fibromatosis, [41] relapsing polychondritis, [42] primary anetoderma, [43] subcorneal pustular dermatosis, [44] erythema nodosum, [45] scleredema, [46] and actinic keratosis. [47]


  Adverse Effects Top


Colchicine is usually well tolerated. Gastrointestinal (GI) adverse effects are the most frequent and include diarrhea, nausea, vomiting, and abdominal pain. The GI side effects are due to increase in gut motility by neural mechanisms as well as by inhibition of mitosis in its rapid turnover mucosa. Symptoms decrease on reducing the dose. The iv administration of the drug avoids the occurrence of these gastrointestinal side effects. Long-term therapy may induce steatorrhea, malabsorption with reduced absorption of vitamin B 12 , fat, sodium, potassium, nitrogen, xylose, and other actively transported sugars. It can cause decreased serum cholesterol and carotene concentrations.

Bone marrow suppression -agranulocytosis, thrombocytopenia, and aplastic anemia occurs after prolonged treatment. Colchicine-induced leukopenia occurs with accidental or intentional overdose and prompt administration of G-CSF must be considered in such cases.

Myopathy and neuropathy occur particularly in patients with renal impairment. Colchicine induces autophagic vacuolar changes in muscle. Myopathy presents as proximal muscle weakness, with rise in creatinine phosphokinase, abnormal proximal muscle fibrillations, and axonal neuropathy. Myopathy recovers on withdrawal of colchicine. Neuropathy resolution is more prolonged. Azoospermia is a reported side effect. [48]

Dermatological adverse effects include urticaria, [49] toxic epidermal necrolysis, [50] and precipitation of porphyria cutanea tarda. Alopecia occurs 2-3 weeks after the onset of therapy and involves face, axilla, and pubic area. [51]


  Colchicine Overdose Top


Colchicine has been known for centuries as a poison. Advice on the dangers of colchicine varies from one source to the next. Until recently, there was no maximum dose of colchicine stated in the approved dosage guidelines. There have been published cases of death occurring after colchicine doses as little as 6 or 7 mg. [52] Overdosage can lead to cholera-like syndrome with dehydration, hypokalemia, hyponatremia, metabolic acidosis, renal failure, and ultimately shock. Respiratory distress syndrome, disseminated intravascular coagulation, and bone marrow suppression occur. Patients may develop convulsions, delirium, muscle weakness, neuropathy, and muscle paralysis. After prolonged therapy, leukopenia, aplastic anemia, myopathy and alopecia can occur. Colchicine intoxication is characterized by multi-organ involvement and by the poor prognosis associated with administration of large amounts of the drug. Therapy is basically supportive and symptomatic because of the rapid distribution and binding of colchicine to the affected tissues. Use of anticolchicine antibodies is a novel approach still in an experimental stage. [53]


  Drug Interactions Top


The coadministration of colchicine with known inhibitors or substrates of CYP3A4 may inhibit its metabolism resulting in toxicity such as by macrolide antibiotics. It may increase the serum concentration of cyclosporine, and verapamil, and vice versa. It may cause malabsorption of vitamin B 12 leading to megaloblastic anemia. Coadministration of simvastatin with colchicine may induce acute myopathy. [54]


  Monitoring Guidelines Top


It is suggested that complete blood counts, platelet count, serum multiphasic analysis (i.e. tests of renal and hepatic function), and urinalysis be performed at least every 3 months. Monthly laboratory monitoring for the first few months of therapy is a reasonable protocol. Colchicine should not be used during pregnancy (risk of teratogenicity) [55]


  Conclusion Top


Colchicine has many useful actions in dermatological disorders and is well tolerated. Although colchicine is not a first-line medication for any of the conditions mentioned, we are more likely to use it early in patients with leukocytoclastic vasculitis, Sweet's syndrome, and aphthous ulcers. This medication is inexpensive and safe in moderate doses than most immunosuppressive agents.

 
  References Top

1.BoDD (Botanical Dermatology Database) monographs (COLCHICACEAE) latest update:03 Jan 2009.  Back to cited text no. 1      
2.Surajana G, Bhattacharyya B. The colchicine -tubulin interaction: A review. Curr Sci 1997;73:1.   Back to cited text no. 2      
3.Pelletier PS, Caventon J. [Title unknown]. Ann Chim Phys 1820;14:69.  Back to cited text no. 3      
4.Davis S. Newer uses of older drugs -an update. In: Wolverton S, editor.Comprehensive dermatologic drug therapy. Indianapolis: WB Saunder; 2001. p. 426-44.   Back to cited text no. 4      
5.Cronstein BN, Molad Y, Reibman J, Balakhane E, Levin RI, Weissmann G. Colchicine alters the quatitative and qualitative display of selectins on endothelial cells and neutrophils. J Clin Invest 1995;96:994-1002.   Back to cited text no. 5      
6.Perico N, Ostermann D, Bontempeill M, Morigi M, Amuchastegui CS, Zoja C, et al. Colchicine interferes with L-selectin and leukocyte function-associated antigen-1 expression on human T lymphocytes and inhibits T cell activation. J Am Soc Nephrol 1996;7:594-601.  Back to cited text no. 6      
7.Sabroe R. Colchicine. In: Wakelin SH, Maibach HI, editors. Handbook of systemic drug treatment in dermatology. London: Manson; 2003. p.105.  Back to cited text no. 7      
8.Mekori YA, Baram D, Goldberg A, Klajman A. Inhibition of delayed hypersensitivity reactions in mice by colchicine. I. Mechanism of inhibition of contact sensitivity in vivo. Cell Immunol 1989;120:330-40.  Back to cited text no. 8      
9.Sullivan TP, King LE Jr, Boyd AS. Colchicine in dermatology. J Am Acad Dermatol 1998;39:993-9.   Back to cited text no. 9      
10.Sagorin C, Ertel NH, Wallace SL. Photoisomeration of colchicine. Loss of significant antimitotic activity in human lymphocytes. Arthritis Rheum 1972;15:213-7.   Back to cited text no. 10      
11.Simons RJ, Kingma DW. Fatal colchicine toxicity. Am J Med 1989;86:356-7.  Back to cited text no. 11      
12.Bonnel RA, Villalba ML, Karwoski CB, Beitz J. Deaths associated with inappropriate intravenous colchicine administration. J Emerg Med 2002;22:385-7.  Back to cited text no. 12      
13.Simmons JW, Harris WP, Koulisis CW, Kimmich SJ. Intravenous colchicine for low back pain: a double-blind study. Spine (Phila Pa 1976) 1990;15:716-7.  Back to cited text no. 13      
14.Nuki G. Colchicine: Its mechanism of action and efficacy in crystal-induced inflammation. Curr Rheumatol Rep 2008;10:218-27.  Back to cited text no. 14      
15.Wahba A, Cohen H. Therapeutics trials with oral colchicines in psoriasis. Acta Derm Venereol 1980;60:515-20.  Back to cited text no. 15      
16.Kaidbey KH, Petrozzi JW, Kligman AM. Topical colchicine therapy for recalcitrant psoriasis. Arch Dermatol 1975;111:33-6.  Back to cited text no. 16      
17.Seideman P, Fjellner B, Johannesson A. Psoriatic arthritis treated with oral colchicine. J Rheumatol 1987;14:777-9.   Back to cited text no. 17      
18.Horiguchi M, Takigawa M, Imamura S. Treatment of generalized pustular psoriasis with methotrexate and colchicine. Arch Dermatol 1981;117:760.  Back to cited text no. 18      
19.Zachariae H, Kragballe K, Herlin T. Colchicine in generalized pustular psoriasis: clinical response and antibody-dependent cytotoxicity by monocytes and neutrophils. Arch Dermatol Res 1982;274:327-33.  Back to cited text no. 19      
20.Mori S, Hino K, Izumi H, Hino H. Clinical manifestations and treatment of pustulosis palmaris et plantaris. J Dermatol 1976;86:671.  Back to cited text no. 20      
21.Katz J, Langevitz P, Shemer J, Barak S, Livneh A. Prevention of recurrent aphthous stomatitis with colchicine: an open trial. J Am Acad Dermatol 1994;31:459-61.  Back to cited text no. 21      
22.Mangelsdorf HC, White WL, Jorizzo JL. Behcet's disease. Report of 25 patients from the United States with prominent mucocutaneous involvement. J Am Acad Dermatol 1996;34:745-50.  Back to cited text no. 22      
23.Aktulga E, Altaç M, Müftüoglu A, Ozyazgan Y, Pazarli H, Tüzün Y, et al. A double blind study of colchicine in Behcet's disease. Haematologica 1980;65:399-402.  Back to cited text no. 23      
24.Sander HM, Randle HW. Use of colchicine in Behçet's syndrome. Cutis 1986;37:344-8.  Back to cited text no. 24      
25.Suehisa S, Tagami H. Treatment of acute febrile neutrophilic dermatosis (Sweet's syndrome) with colchicine. Br J Dermatol 1981;105:483.  Back to cited text no. 25      
26.Silvers DN, Juhlin EA, Berczeller PH, McSorley J. Treatment of dermatitis herpetiformis with colchicine. Arch Dermatol 1980;116:1373-4.  Back to cited text no. 26      
27.Aram H. Linear IgA bullous dermatosis: Successful treatment with colchicine. Arch Dermatol 1984;120:960-1.  Back to cited text no. 27      
28.Megahed M, Scharffetter-Kochanek K. Epidermolysis bullosa acquisita: Successful treatment with colchicine. Arch Dermatol Res 1994;286:35-46.  Back to cited text no. 28      
29.Zeharia A, Hodak E, Mukamel M, Danziger Y, Mimouni M. Successful treatment of chronic bullous dermatosis of childhood with colchicine. J Am Acad Dermatol 1994;30:660-1.  Back to cited text no. 29      
30.Wiles JC, Hansen RC, Lynch PJ. Urticarial vasculitis treated with colchicine. Arch Dermatol 1985;121:802-5.  Back to cited text no. 30      
31.Bibas R, Gaspar NK, Ramos-e-Silva M. Colchicine for dermatological diseases. J Drugs Dermatol 2005;4:196-204.  Back to cited text no. 31      
32.Zemer D, Pras M, Sohar E, Modan M, Cabili S, Gafni J. Colchicine in the prevention and treatment of the amyloidosis of familial Mediterranean fever. N Engl J Med 1986;314:1001-5.  Back to cited text no. 32      
33.Nath D. Probable mechanism of action of colchicine in macular and lichen amyloidosis. Indian J Dermatol Venereol Leprol 1999;65:48-9.  Back to cited text no. 33    Medknow Journal  
34.Chakravarty K, Chanda M. Role of colchicine in primary localised cutaneous amyloidosis. Indian J Dermatol Venereol Leprol 1995;61:268-9.  Back to cited text no. 34    Medknow Journal  
35.Kar HK, Roy RG. Comparison of colchicine and aspirin in the treatment of type 2 lepra reaction. Lepr Rev 1988;59:201-3.  Back to cited text no. 35      
36.Sarojini PA, Mshana RN. Use of colchicine in the management of erythema nodosum leprosum. Lepr Rev 1983;54:151-3.  Back to cited text no. 36      
37.Rampal P, Benzaken S, Schneider S, Hebuterne X. Colchicine in pyoderma gangrenosum. Lancet 1998;351:1134-5.  Back to cited text no. 37      
38.Jeong S, Lee CW. Acne conglobata: Treatment with isotretinoin, colchicine, and cyclosporin as compared with surgical intervention. Clin Exp Dermatol 1996;21:462-3.  Back to cited text no. 38      
39.Fuchs D, Fruchter L, Fishel B, Holtzman M, Yaron M. Colchicine suppression of local inflammation due to calcinosis in dermatomyositis and progressive systemic sclerosis. Clin Rheumatol 1986;5:527-30.  Back to cited text no. 39      
40.Von Krogh G. Topical treatment of penile condyloma acuminata with podophyllin, podophyllotoxin and colchicine. Acta Dermatol Venereol 1978;58:163-8.  Back to cited text no. 40      
41.Dominguez-Malagon HR, Alfeiran-Ruiz A, Chavarria-Xicotencatl P, Duran-Hernandez MS. Clinical and cellular effects of colchicine in fibromatosis. Cancer 1992;69:2478-83.  Back to cited text no. 41      
42.Eng AM, Reddy VB. Relapsing polychondritis responding to colchicine. Int J Dermatol 1994;33:448-9.  Back to cited text no. 42      
43.Braun RP, Borradori L, Chavaz P, Masouyé I, French L, Saurat JH. Treatment of primary anetoderma with colchine. J Am Acad Dermatol 1998;38:1002-3.  Back to cited text no. 43      
44.Pavithran K. Colchicine in the treatment of subcorneal pustular dermatosis. Indian J Dermatol Venereol Leprol 1995;61:56-7.  Back to cited text no. 44    Medknow Journal  
45.Wallace SL. Erythema nodosum treatment with colchicine. JAMA 1967;202:1056.   Back to cited text no. 45      
46.Gruson LM, Franks A Jr. Scleredema and diabetic sclerodactyly. Dermatol Online J 2005;11:3.  Back to cited text no. 46      
47.Grimaître M, Etienne A, Fathi M, Piletta PA, Saurat JH. Topical colchicine therapy for actinic keratoses. Dermatology 2000;200:346-8.  Back to cited text no. 47      
48.Merlin HE. Azoospermia caused by colchicine. A case report. Fertil Steril 1972;23:180-1.  Back to cited text no. 48      
49.Cabili S, Shemer Y, Revach M. Allergic reaction and desensitization of colchicine in familial Mediterranean fever. Rheumatologie 1982;12:207.  Back to cited text no. 49      
50.Arroyo MP, Sanders S, Yee H, Schwartz D, Kamino H, Strober BE. Toxic epidermal necrolysis-like reaction secondary to colchicine overdose. Br J Dermatol 2004;150:581-8.  Back to cited text no. 50      
51.Malkinson FD, Lynfield YL. Colchicine alopecia. J Invest Dermatol 1959;33:371-84.  Back to cited text no. 51      
52.Macleod JG, Phillips L. Hypersensitivity to colchicine. Ann Rheum Dis 1947;6:224-9.   Back to cited text no. 52      
53.Putterman C, Ben-Chetrit E, Caraco Y, Levy M. Colchicine intoxication:clinical pharmacology, risk factors, features and management. Semin Arthritis Rheum 1991;21:143-55.  Back to cited text no. 53      
54.Porter RS, editor. Colchicine drug information-2008. The merck manual's online medical library: Merck Research Laboratories: 2004.  Back to cited text no. 54      
55.Callen JP, af Ekenstam E. Cutaneous leukocytoclastic vasculitis: clinical experience in 44 patients. South Med J 1987;80:848-85.  Back to cited text no. 55      


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