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Year : 2004  |  Volume : 70  |  Issue : 1  |  Page : 42-43

Diabetes mellitus and immunosuppressives

Consultant Dermatologist, Rohtak, Haryana

Correspondence Address:
Skin V. D. and Allergy Clinic, Jhajjar Road, Rohtak - 124001
[email protected]

How to cite this article:
Bansal R. Diabetes mellitus and immunosuppressives. Indian J Dermatol Venereol Leprol 2004;70:42-3

How to cite this URL:
Bansal R. Diabetes mellitus and immunosuppressives. Indian J Dermatol Venereol Leprol [serial online] 2004 [cited 2021 Jan 23];70:42-3. Available from:

Immunosuppressive agents like azathioprine, cyclophosphamide, methotrexate (MTX) or cyclosporine A (CYA) are often used as adjuvants with corticosteroid therapy for patients with chronic dermatological disorders like pemphigus. Such patients may also have diabetes mellitus (DM), which is a relative contraindication for corticosteroid therapy, and may need immunosuppressive therapy. Many dermatologists hesitate to use these agents in patients with diabetes mellitus (DM). I would like to discuss this issue.

Azathioprine (AZA), a synthetic purine analogue is one of the main immunosuppressive drugs used in dermatology. Its immunosuppressive effects are caused by the substitution of naturally occurring purine bases in DNA by its active intracellular metabolite 6-thioguanine in actively dividing cells.[1] AZA is effective in the treatment of autoimmune diseases at doses which don't cause lymphopenia, leukopenia or bone marrow depression.[2] Although AZA can inhibit T-cell function,[3] patients treated with the standard immunosuppressive doses of AZA generally fail to exhibit significant suppression of cell mediated immunity despite a clinical response to therapy.[4] There is little evidence for any consistent effect of AZA on the normal humoral immune response and often AZA fails to inhibit it.[5] The fact that treatment with AZA is associated with an increased incidence of viral infections but not with an increase in bacterial infections has been taken as evidence against any major inhibition of humoral immunity.[6] Swanson et al[2] found that patients with immunologic diseases don't become agammaglobulinemic as a result of antimetabolite therapy and that adequate levels of immunoglobulins having the usual spectrum of antiviral and antibacterial activities are maintained. He concluded that when used cautiously AZA does not result in a harmful degree of immunosuppression in patient with immunologic diseases. Sharma et al used AZA in four patients who had both parthenium dermatitis and DM and observed its corticosteroid sparing effect.[7]

Cyclophosphamide (CPA) is the most potent immunosuppressant among the synthetic alkylating agents.[8] Several investigators have reported that there is no change in the relative percentage of circulating B and T cells during CPA induced lymphopenia.[5]

Cyclosporine A (CYA) is a fungal metabolite with potent immunosuppressant effect without significant myelotoxicity. In three large controlled studies,[9],[10],[11] use of CYA was found to be successful in blocking or reducing the cytotoxic process in order to favor beta cell regeneration in patients newly diagnosed with insulin dependent diabetes mellitus (IDDM).[12]

IDDM results from autoimmune beta cell destruction which is thought to be triggered by an infection or environmental stimulus.[13] Bansal et al suggested that lack of adequate insulin levels in DM impairs T lymphocyte activity and the elevated levels of immunoglobulins in DM could be due to subclinical infection.[14] Infections are thought to be due to incompletely defined abnormalities in phagocyte function associated with hyperglycemia, as well as diminished vascularization secondary to long-standing DM.[15],[16] Hyperglycemia probably aids the colonization and growth of a variety of organisms.[13]

In view of the inconsistent effects of immunosuppressive agents on T and B cells, their use in a diabetic patient with optimal glycemic control is justified. The impaired immunity of diabetic patients does not debar them from using these agents. In spite of impaired immunity, diabetic patients have been successfully immunosuppressed by using triple therapy with CYA, AZA and prednisone for renal transplantation for many years.[17] Dermatologists can not afford to ignore these drugs in diabetic patients if they are required, particularly in situations where corticosteroids have to be given for a long duration or are contraindicated. 

   References Top

1.Anstey A. Azathioprine in dermatology: a review in light of advances in understanding methylation pharmacogenetics. J R Soc Med 1995;88:155-60.  Back to cited text no. 1    
2.Swanson MA, Schwartz RS. Immunosuppressive therapy: the relationship between clinical response and immunologic competence. N Engl J Med 1967;277:163-70.  Back to cited text no. 2  [PUBMED]  
3.Bach MA, Bach JF. Activities of immunosuppressive agents in vitro-different timing of azathioprine and methotrexate in inhibition and stimulation of mixed lymphocyte reaction. Clin Exp Immunol 1972;11:89-98.  Back to cited text no. 3  [PUBMED]  
4.Denman EJ, Denman AM, Greenwood BM, Gall D, Heath RB. Failure of cytotoxic drugs to suppress immune responses of patients with rheumatoid arthritis. Ann Rheum Dis 1970;29:220-31.  Back to cited text no. 4  [PUBMED]  
5.Bassen CR. Immunosuppressive agents. In: Thaler MS, Klausner RD, Cohen HJ, editors. Medical immunology. Philadelphia: JB Lippincott; 1977. p. 415.  Back to cited text no. 5    
6.Hamburger J, Crosnier J, Dormont J. Renal transplantation-theory and practice. Boston: Williams & Wilkins; 1972.  Back to cited text no. 6    
7.Sharma VK, Chakrabarti A, Mahajan V. Azathioprine in the treatment of parthenium dermatitis. Int J Dermatol 1998;37:299-302  Back to cited text no. 7    
8.Bach JF. The mode of action of immunosuppressive agents. Front Biol 1975;41:1-374.  Back to cited text no. 8    
9.Mandrup-Poulsen T, Nerup J, Stiller CR, Marner B, Bille G, Heinrichs D, et al. Disappearance and reappearance of islet cell cytoplasmic antibodies in cyclosporine treated insulin dependent diabetics. Lancet 1985;i:599-602.  Back to cited text no. 9    
10.Feutren G, Papoz I, Assan R, Vialettes B, Karsenty G, Vexiau P, et al. Cyclosporine increases rate and length of remission in insulin dependent diabetes of recent onset. Lancet 1988;ii:119-23.  Back to cited text no. 10    
11.Boughneres PF, Carel JC, Castano L, Boitard G, Gardin JP, Landias P, et al. Factors associated with early remission of type 1 diabetes in children treated with cyclosporine. N Engl J Med 1988;318:663-70.  Back to cited text no. 11    
12.Mohan V, Kumaraswami V, Vishwanathan M. Immunology of diabetes. J Asso Phys Ind 1982;40:461-4.  Back to cited text no. 12    
13.Foster DW. Diabetes mellitus. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, editors. Principles of internal medicine. 14th ed. New York: McGraw-Hill; 1998. p. 2060.  Back to cited text no. 13    
14.Bansal AS, Wilson PB, Humphrey RSH, Boulton AJ, Malik RA. Cellular and humoral immunity in patients with insulin-dependent diabetes (Letter). Lancet 1993;342:246.   Back to cited text no. 14    
15.Hadzimejilic M, Redzepagic B, Macanovic M. Cellular and humoral immunity in diabetes mellitus with and without complications. In: Bajaj JS, editor. Diabetes mellitus in developing countries. New Delhi: Interprint; 1984. p 99-103.  Back to cited text no. 15    
16.Narang NK, Gupta RC, Singh N. Immunity in diabetes mellitus (Letter). J Asso Phys Ind 1989;37:614.  Back to cited text no. 16    
17.Kronson JW, Gillingham KJ, Sutherland DE, Matas AJ. Renal transplantation for type II diabetic patients compared with type I patients and patients over 50 years old: a single-centre experience. Clin Transplant 2000;14:226-34.  Back to cited text no. 17    


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