The relationship between transforming growth factor-β with erythema nodosum leprosum recurring events based on immunoglobulin M anti-phenolic glycolipid-1 and cortisol
Keywords:
ENL, TGF-β, IgM anti-PGL-1, cortisol, leprosy, erythema nodosum leprosumAbstract
ABSTRACTObjective To examine the relationship between transforming growth factor (TGF)-β with recurrent erythema nodosum leprosum (ENL) based on the anti-phenolic glycolipid (PGL)-1 IgM antibody and cortisol in leprosy patients. Methods This research included 44 patients of leprosy MB type; 22 leprosy patients with recurrent ENL reactions as subjects and 22 patients with nonrecurring reaction as controls. We examined the serum levels of TGF-β by ELISA using Human TGF-β Bio legend kit (USA), anti-PGL-1 IgM antibody with the Laboratory of Leprosy Institute of Tropical Disease kit, Airlangga University Surabaya, and cortisol using Stress Xpress Cortisol EIA kit (StressMarq Canada). Results There were 22 subjects with recurrent ENL reaction (16 male, 6 female, mean age 34.9 year). Mean TGF-β was 62.6 ± 30.4 pg/ml, the IgM anti PGL-1 was 2029 ±1687 µg/ml, and the cortisol was 6.61 ± 1.99 µg/dl, and 22 subjects nonrecurring reaction as controls (15 male, 7 female, mean age 47 year) the mean of TGF-β level was 47.2 ± 23 pg/ml, anti PGL-1 IgM antibody was 629 ±1043 µg/ml and the cortisol was 5.07 ± 2.01 µg/dl. The t-independent statistic test the influence of leprosy MB type group to the recurrent ENL reaction and the un-recurrent ENL patients to TGF-β, IgM anti-PGL-1 and cortisol had p value = 0.015, 0.001 and 0.035 (p <0.05), respectively implying significant difference between subjects and controls. The result of logistic binary test of TGF-β, IgM anti-PGL-1 and cortisol was 0.25, 0.016 and 0.771. This means that IgM anti-PGL-1 has correlation as variable of TGF-β with recurrent ENL. Conclusion There was significant difference between the levels of TGF-β, anti-PGL-1 IgM antibody and cortisol in leprosy patients with the recurrent ENL reaction and those with nonrecurring ENL reaction. There was a correlation between the levels of TGF-β with recurrent ENL based on the IgM anti-PGL-1. The increasing levels of TGF-β and IgM anti-PGL-1 level on patients with leprosy MB type can be a predictor of the recurrent reaction.References
REFERENCES :
Fitnes J, . Genetics of susceptibility to leprosy (Review), Genes and Immunity 2002, 3 : 441.
Naafs B,. Current views on Reaction in Leprosy.Indian j Leprosy 2000, Vol 72(1) :
– 122.
Fava V, Orlova M, Cobat A, Alcais A, et al ,. Genetic of Leprosy reaction : an overview, Mem Inst Oswaldo Cruz 2012, 107 (1) : 1 -7.
Sampaio E.P.Oliveira R.B., Davies J.W et al. T cell-monocyte contact enhances Tumor Necrosis Factor-alpha production in response to Mycobacterium leprae. Journal of Infectious Disease 2000, 182 : 1463 -72.
Yamamura M,. Defining protective responses to pathogens: cytokine profiles in leprosy lesions. Science 1992, 255:12.
Goulart MB, Mineo JR and Foss MT,. Production of transforming growth factor- β1 (TGF-β) by blood monocytes from patient with different clinical forms of leprosy 2000, Clin Exp Immunol 122 : 330 –4.
Gorelik L, Constant S, and Flavel RA,. Mechanism of Transforming Growth Factor-β inducedinhibiton of T Helper type 1 Disorientation, J Exp Med 2001, 195 ; 11 : 1499 – 505
Rojas R E, Demichelis S O, Sarno E N, Eiras A S,. IgM anti-phenolic glycolipid I and IgG anti 10-kDp a hat shock protein antibody in sera and immune complexes isolated from leprosy patients with or without erythema nodosum leprosum and contacts. FEMS Immunology and medical microbiology 1997,19 : 65 -74
Stevani MMA, Martelli CMT, Morais-Neto OL et al,. Assesment of Anti PGL-l as a prognostiv marker of leprosy reaction, International Journal of Leprosy 2012, 66 ; 3:356-60.
Moura RS, Calado KL, Olivveira MLW and Skula SB,.Leprosy serologi using PGL-I : a systemic review, Rev Soc Bras Med Trop 2008, 41: 11 – 18.
Kar HK, Sharma P ,. Management of Leprosy Reaction, IAL Textbook of Leprosy, first edition, Ajanta Offset and Packagings Ltd, Ne Delhi, India 2010, : 387-99.
Leal AM, Magalhaes PK, Souza CS, Foss NT. Adrenocortical hormones and interleukin patterns in leprosy, Eur J ClinMikcrobiol. Parasite Immunology 2003 ; 25 : 457- 61.
Cooper MS, Stewart PM,. Corticosteroid insufficienmcy in acutely ill patients. New England Journal of Med 2003, 348 : 727 – 734.
WHO. Guide to eliminate leprosy as public health problem, Geneva 2000 :1-5 .
Pocaterra L, Jain S, Reddy R,. Clinical course of erythema nodosum leprosum : an 11 yeear cohort study in Hyderabad India. Am J TropMed Hyg 2006, 74 (5) : 868 -79.
Jopling WH,. Leprosy reaction (reactional states), Handbook of leprosy, Fifth ed. CBs Publisher & distributor 1996, India : 82 -91.
Manandhar R, Master LJW, Roche PW,. Risk factor for Erythema Nodosum Leprosum ,Int Journal of Leprosy 1999, 67,3, Sept : 270 – 8.
Balagon VF, GelberRH, Abalos RM, Cellona RV, . Reactions following completion of 1 and 2 year multydrug therapy (MDT). Am J Trop Med Hygiene 2010, 83 (3): 637-44.
Kahawita IP, Walker SL, Lockwood DNJ,. Towards understanding the pathology of erythema nodosumleprosum. Ryal society of Tropical Medicine and Hygiene 2008, 102 :329 -37.
Silva EA, Iyer A, Ura S.,Is ., et al. Utility of measuring serum levels of anti PGL-1 antibody, neopterin and c-reactive protein in monitoring leprosy patients during multidrug treatment and reactions. Trop Med and Int Med 2007, 12 : 1450 – 1458
Zenha EMR, Ferreira MAN and Foss NT,. Use of anti-PGL-1antibodies to monitor therapy regimens in leprosy patients, Braz J Med Biol Res 2009, 42 ; 10 : 868 – 97.
Rook GAW, Baker W,. Cortisol metabolism, cortisol sensitivity and the pathogenesis of leprosy reaction. Tropical Medicine and International Journal Health 1999, 4 (7) : 493 – 498.
Cooper MS, Stewart PM,. Corticosteroid insufficienmcy in acutely ill patients. New England Journal of Med 2003, 348 : 727 – 734.
Van Veen NHJ, Lockwood DNJ, Van Brakel WH , et al . Intervention for erythema nodosum leprosum. Cochrana Database of Systematic review 2009, Issue 3 : 1 – 53.
