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26 G. RAGHUPATI SARMA ETAL extrapulmonary tuberculosis) was much less than that in our series, and this is most probably due to difference in the definition employed to classify the patients as positive or negative responders to tetracosactrin 1 Further, they observed a significant decrease in plasma cortisol, 3-4 weeks after the start of treatment with a regimen containing daily Rifampicin in addition to Isoniazid, Pyrazinamide and Streptomycin, findings contrary to those reported in our study and by Scott et al 16 The daily regimen employed by us (R-7) was similar to that used by Barnes et al 17 , except that Streptomycin was replaced by Ethambutol, and it seems unlikely that this single change could be responsible for the different findings. Findings in this paper suggest that Rifampicin, whether administered daily or twiceweekly exerts a deleterious effect on the adrenocortical function, in patients with pulmonary tuberculosis. The mechanism of action is not clear; the sustained high plasma cortisol concentrations, even up to 4 weeks in patients receiving Rifampicin, appear to go against a mechanism involving a more rapid systemic clearance of this hormone induced by the drug. Earlier investigations had shown that dexamethasone causes an appreciable suppression of cortisol levels in patients with pulmonary tuberculosis 1 And this suggests that the HPA axis is intact in these patients. As such, a decrease in plasma cortisol caused by an increase in its clearance would trigger the release of ACTH by the pituitary resulting in an increase in the secretion of cortisol by the adrenal cortex. Whether formation of antibodies to Rifampicin or other immunological reactions such as the formation of immune complexes involving mycobacterial antigens precipitated by the rapid killing of the bacteria or the induction of autoimmune antibodies against adrenocortical cells are responsible, is a matter of conjecture. Several drugs such as procainamide, hydrallazine, methyldopa and pencillamine have been shown to induce auto-immune disorders such as systemic lupus erythematosis, myasthenia gravis, haemolysis and hepatitis 18 ' and Rifampicin has been implicated in evoking pemphigus, an autoimmune disease of the skin 19 The diurnal rhythm of cortisol secretion was disturbed in the patients with an evening rise in cortisol levels before the start of treatment. The immune system is known to modulate adrenal production of glucocorticoids and cortisol, in turn, has been shown to regulate certain immune responses. Monokines, particularly interleukin-1, released by activated monocytes, are known to stimulate the hypothalamus, the pituitary and the adrenal cortex 20 ' 21 ' 22 Stimulation of hypothalamus would not only cause an increase in the release of CRF, which would ultimately lead to an increase in the cortisol production, but also of certain other factors such as PGE 2 which cause an elevation in body-temperature 23 ' An evening rise in body-temperature is well-established in patients with tuberculosis, but the association between the two phenomena pre-supposes a circadian rhythm in the release of monokines also. The existence of such a rhythm of several immune responses is now well-recognised. Thus, cytolytic activity of natural killer cells 24 , mitogenic and antigenic responses 25 ' 26 ' 27 ' 28 , the counts of eosinophils and neutrophils 28 and of T and B cell populations of human lymphocytes 2930 have been shown to exhibit a circadian rhythm. The maximal levels of T and B cells were attained at midnight followed by a depression during the day, and Abo et a I 29 have shown that variations in the cell counts were inversely related with plasma cortisol levels in healthy subjects. The diurnal rhythm of cortisol secretion had reverted to a near-normal pattern after 2 months of treatment in all the 3 groups of patients. Response to tetracosactrin was not examined at this time and whether this also returns to normal in a majority of the patients with continued treatment with regimens containing Rifampicin remains to be investigated. Acknowledgements We are grateful to Hindustan Ciba Geigy Limited, Bombay, for their kind gift of synacthen. We wish to thank Mr. K. Jayasankar for technical assistance and the Clinic and Nursing Staff for organising the blood and saliva collections. References 1. Raghupati Sarma G.,. Chandra Immanuel, Geetha Ramachandran., Krishnamurthy P.V., Kumaraswami V., Prabhakar R. Adrenocortical function in patients with pulmonary tuberculosis. Tubercle; 1990, 71, 277.
RIFAMPICIN AND ADRENOCORTICAL FUNCTION 27 2. Ohnhaus E.E., Park B.K. Measurement of urinary 6—ft—hydroxycortisol excretion as an in vivo parameter in the clinical assessment of the microsomal enzyme-inducting capacity of antipyrine, phenobarbitone and Rifampicin. Eur. J. Clin. Pharmacol; 1979,15,139. 3. Edwards O.M., Courtney-Evans R.J., Galley J.M., Hunter J., Tait A.D. Changes in cortisol metabolism following Rifampicin therapy. Lancet; 1974, ii, 549. 4. Buffington G A., Dominguez J.H., Piering W.F., Herbert L.A., Kauffman M., Lemann J. Interaction of Rifampicin and glucocorticoids. Adverse effect on renal allograft function. JAMA.; 1976, 236,1958. 5. McAlister W.A.C., Thompson P;J., Al-Habet S.M., Rogers H.J. Adverse effects of Rifampicin on prednisolone disposition. Thorax; 1982, 37, 792. 6. McAlister WA.C., Thompson P.J., Al-Habet S.M., Rogers H.J. Rifampicin reduces effective ness and bio-availability of prednisolone. Br. Med. J.; 1983, 286, 923. 7. Elansary E.H., Earis J.E. Rifampicin and adrenal crisis. Br. Med. J.; 1983, 286, 1861. 8. Wilkins E.G.L., Hnizdo E., Cope A. Addisonian crisis induced by treatrnent with Rifampicin. Tubercle; 1989, 70, 69. 9. Acocella G., Pagani V., Marchetti M., Baroni G.C., Nicolis F.B. Kinetic studies on Rifampicin. I. Serum concentration analysis in subjects treated with different oral doses over a period of two weeks. Chemotherapy; 171,16, 356. 10. Chandra Immanuel., Jayasankar K., Narayana A.S.L., Raghupati Sarma G. Self-induction of Rifampicin metabolism in man. Ind J. Med Res.; 1985, 82, 381. 11. Campbell I.A., Dyson A.J. Lymph node tuberculosis : A comparison of various methods of treatment. Tubercle; 1977, 58, 171. 12. Chambers ST., Hendricks W.A., Record C., Rudge P., Smith H. Paradoxical expansions of intra-cranial tuberculomas during chemo therapy. Lancet; 1984, ii, 181. 13. Smith H. Paradoxical -responses during the chemotherapy of tuberculosis. J. Infect.; 1987, 15,1. 14. Jawahar M.S., Sivasubramanian S., Vijayan V.K., Ramakrishnan C.V., Paramasivan C.N., Selvakumar N., Paul S., Tripathy S.P., Prabhakar R. Short-course chemotherapy for tuberculous lymphadenitis in children. Br. Med. J.; 1990, 301,359. 15. Ellis M.E., Tayoub F. Adrenal function in tuberculosis. Br. J. Dis. Chest; 1986, 80, 7. 16. Scott G.M., Murphy P.G., Gemidjioglu M.E. Predicting deterioration of treated tuberculosis by corticosteroid reserve and C-reactive protein. J. Infect; 1990, 21, 61. 17. Barnes D.J., Naraqi S., Temu P., Turtle J.R. Adrenal function in patients with active tuberculosis. Thorax; 1989, 44, 422. 18. Russel A.S. Drug-induced autoimmune disease. Clin. Immunol. Allergy; 1981, 1, 57. 19. Gange R.W., Rhodes E.L., Edwards C.O. Pemphigus induced by Rifampicin. Br. J. Dermatol; 1976, 95, 445. 20. Besedovsk H.O., del Ray A.E., Sorkin E. What do immune system and brain known about each other ? Immunol Today; 1983, 4, 342. 21. Woloski B.M.R.N.J., Smith E.M., Meyer W.J., Fuller G.M., Blalock J.E. Corticotrophinreleasing activity of monokines. Science; 1985, 235,1035. 22. Whitcomb R.W., Linehan G.M., Wahl L.M., Khazek R.A. Monocytes stimulate cortisol production by cultured human adrenocortical cells. J. Clin. Endocrinol. Metab.; 1988, 66,33. 23. Hamblin A.S. Lymphokines in haematopoiesis, cytotoxicity and inflammation. In Male D, Rickwood D, ed Lymphokines. Oxford : IRL Press 1988, 45-52. 24. Williams R.M., Kraus L.J., Dubey D.P., Yunis E.J., Halberg F. Circadian bioperiodicity in natural killer cell activity of human blood. Chronobiologia; 1979, 6, 172 (Abstract). 25. Tavadia H.B., Fleming K.A., Hume P.D., Simpson H.W. Circadian rhythmicity of human plasma cortisol and PHA-induced lymphocyte transformation. Clin. Exp. Immunol; 1975, 22, 190. 26. Kaplan M.S., Byers V.S., Levin A.S., German D.F., Fudenberg H.H., Lecam L.N. Circardian rhythm of stimulated lymphocyte blastogenesis. J. Allergy. Clin. Immunol; 1976, 58, 180. 27. Leskila H., Molnar F.G., Soppi E. Biological rhythm of cell-mediated immunity in man. Clin. Exp. Immunol; 1976, 26, 253.
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