Aplastic Anemia and Other Bone Marrow Failure Syndromes by Mehdi Tavassoli (auth.), Nasrollah T. Shahidi (eds.)

By Mehdi Tavassoli (auth.), Nasrollah T. Shahidi (eds.)

During the earlier decade, there were quite a few direct and oblique medical contributions to either the etiology and treatment of aplastic anemia and similar bone marrow failure syndromes. scientific observations, akin to autologous bone marrow restoration after conditioning with immunosup­ pressive brokers for bone marrow transplantation; failure to accomplish en­ graftment in a few exact twins with no earlier immunosuppressive ther­ apy; and hematologic reaction to immunosuppressive brokers, have ended in the concept that of immune-mediated etiology of obtained aplastic anemia. this sort of suggestion was once additional bolstered through laboratory findings, implicat­ ing the position of activated cytotoxic T lymphocytes and irregular produc­ tion of inhibitory lymphokines. The immunologic mechanisms can also follow to the idiosyncratic bone marrow aplasias linked to medications, poisonous chemical compounds, and viruses. those brokers may well modify general mobile recog­ nition websites by way of interacting with mobile elements and bring about lack of self tolerance. Immunologic mechanisms have lengthy been endorsed in lots of different organ disasters, and the hemopoietic organ isn't any exception. it's of curiosity that parallel medical and laboratory investigations in juvenile diabetes mellitus variety I and in rodent types of this ailment have yielded effects suitable with an identical pathogenic mechanisms. The infiltration of pancreatic islets through activated T lymphocytes, useful and morphological adjustments of islet cells upon incubation with lymphokines resembling gamma interferon and tumor necrosis issue, and scientific reaction to cyclosporine are a couple of examples.

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Treatment of aplastic anemia by bone marrow transplantation in identical twins. Blood 1980; 55:1033-1039. 86. Ershler WB, Ross J, Finlay JL, et al. Bone marrow microenvironment defect in congenital hypoplastic anemia. N Engl J Med 1980; 302: 1321- 1327. 87. Dexter TM, Testa NG. Differentiation and proliferation of hemopoietic cells in culture. Methods Cell Bioi 1978; 14:387 -405. 88. Dexter TM, Allen TD, Lajtha LG. Conditions controlling the proliferation of hemopoietic cells in vitro. J Cell Physiol 1977; 91:335-344.

In: Najean Y, ed. Medullary Aplasia. New York: Masson, 1980: pp. 43-51. 40. Zeldiis JB, Deinstag JL, Gale RP. Aplastic anemia and non-A non-B hepatitis. Am J Med 1983; 74:64-8. 41. Smith D, Gribble TJ, et al. Spontaneous resolution of severe aplastic anemia associated with viral hepatitis A in a 6-year-old child. Am J Hematol 1978; 5:247. 42. Casciato DA, Klein CA, Kaplowitz N, et al. Aplastic anemia associated with type B viral hepatitis. Arch Intern Med 1978; 138:1557-1558. T. Shahidi 43. McSweeney PA, Carter JM, Green GJ, et al.

4 •S There is also a significant difference in age. For instance, in Sweden 80% of patients with aplastic anemia are 50 years old or older at the time of onset, whereas in Korea only 12% are over 50 years of age. Aplastic anemia comprises a heterogeneous group of pancytopenia linked only by clinical and hematologic findings. The bone marrow destruction may be caused by a variety of drugs/chemicals and viral agents directly or indirectly through immunological mechanisms. 1. Implication of these drugs in the pathogenesis of aplastic anemia is based on circumstantial evidence accumulated over the years.

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