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NOTE Effect of Corticosteroids in 10 Cases of Methimazole

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NOTE Effect of Corticosteroids in 10 Cases of Methimazole Endocrinol. Japon. 1981, 28 (6), 823-827 NOTE Effect of Corticosteroids in 10 Cases of Methimazole- Induced Agranulocytosis NOBORU HAMADA*, KUNIHIKO ITOH, NAOKO MOTOTANI, YOSHIHIKO NISHIKAWA, TAKASHI MIMURA, AND HIROTOSHI MORII*, Itoh Hospital, Jingumae, Shibuya-ku, Tokyo and *Second Department of Internal Medicine, Osaka City University Medical School, Abeno-ku, Osaka Abstract The effect of corticosteroids on the inception of remission was investigated in 10 patients with methimazole induced agranulocytosis. While remission started 6.00±0.92 days (mean±SE) after discontinuation of methimazole in 6 patients to whom corti- costeroids were administered immediately after the cessation of methimazole treat- ment, it started at a significantly later date (9.25±0.48days after discontinuation of methimazole) in 4 patients in whom the corticosteroid treatment was started 5.5±0.5 days after methimazole ceased to be used. The results suggested that corticosteroids may quicken the recovery from methimazole-induced agranulocytosis. The use of adrencorticosteroidsin cases were treated for Graves' disease at Itoh Hospital, of acute agranulocytosishas been controver- Tokyo where patients with Graves' disease numbered 6430 during that period. They all had a clinical sial. Palva et al. (1972) reported that corti- picture of acute onset, sore throat, fever, a low level costeroidsmay quicken the recovery from of neutrophils below 100/μl, and no evidence of other agranulocytosisin cases of an immunological blood disorders. The clinical data of the patients type of agranulocytosis. While antithyroid are shown in Table I. There was no apparent age predilection. The doses of methimazole were 30mg drugs are known to cause agranulocytosis per day in 9 patients and 20mg per day in one (Moore, 1946), the pathogenetic mechanism patient. Patients developed agranulocytosis 18 to 67 has not been clarified(Roseve, 1977) and days after the commencement of methimazole treat- there has been no report analyzing the effect ment. The period from the start of methimazole therapy to the onset of agranulocytosis was 24.0±3.2 of corticosteroids. days (mean±SE) in 3 patients with previous methi- In this communication, the effectof corti- mazole therapy and 43.3±5.6 days in 7 patients costeroidson the inception of remission was without it. One patient (Case No.7) died of hemorrhage evaluated in 10 patientswith methimazole- following necrosis of the tonsils, although hema- induced agranulocytosis. tologic improvement had set in. The use of methimazole was strictly avoided during antibiotic therapy to control infections. Cor- Subjects and Methods ticoseroids were given at various intervals after the cessation of methimazole, as shown in Table II. Most of the patients received prednisolone orally in Ten patients with acute agranulocytosis induced a daily dose of 40 to 80mg or the equipotent amount by methimazole administration during the period of other corticosteroids. White blood cell counts and 1978-1980 were included in this study. The patients their differential counts were taken daily or every other day (Table II). The inception of remission Received October 5, 1981. was defined as the indication of an apparent increase Endocrinol. Japon. 824 HAMADA et al. December 1981 Table 1 Clinical data of 10 patients with methimazole ( MM1 )-induced agranulocyt o s i s *represents t h e lowest counts o bserve d. Vol.28, No6 METHIMAZOVLE-INDUCED AGRANULOCYTOSIS 825 Table 2. The change in white blood *represe the day when corticosteroid treatmen ce l l and neutrophil c ounts after cessation of methimazo l e t was started .§ represents the incepion of remission determined by an apparent increase of neutrophils in the peripheral blood that continued during th e following days . ¶ This patient died on the 9th day after the c essation of methimazol .Values on numerator and denominator represent the counts of neutrophil and white blood cell/ μl, respectively . Endocrinol. Japon. 826 HAMADA et al. December 1981 in neutrophils in the peripheral blood that continued Two pathogenetic mechanisms have been during the following days. The Student's t-test was described in drug-induced agranulocytosis; used for statistical analysis. i.e., from immunologic and toxic as- pects. However, information that might Results shed some light on the pathogenesis of a- granulocytosis caused by the antithyroid Remission began 3 to 10days after the drug is meager, and fundamental questions cessation of methimazole treatment (Table regarding its mechanism still remain unans- II). The period from the cessation of me- wered. Rosove (1977) said in his review thimazole to the beginning of remission was of agranulocytosis and antithyroid drugs that there may be a biochemical susceptibility 6.00•}0.93days (mean•}SE) in 6 patients in whom the corticosteroid therapy was involving some essential metabolic pathway started simultaneously with the cessation of to antithyroid drugs in some persons. On methimazole and 9.25•}0.48days in 4 pa- the other hand, some studies have shown tients in whom the cortisteroid therapy was the possibility of drug-dependent immune started 4 to 6days after the cessation of destruction of leucocytes in those patients. methimazole. The difference in the period Patients with methimazole-induced agranu- locytosis showed neutrophil opsonisation needed for the inception of remission be- tween these two groups was significant (p due to a complement-dependent mechanism apparently induced by an IgM antibody <0.05), whereas the beginning of remission occurred 8 to 9days after the corticosteroid (Weitzman et al., 1078). Bilezikian et al. therapy in 2 cases in the former group. (1976) reported that serum samples taken The period required for the neutrophil count from patients during the acute phase of to exceed 1.0•~103/ƒÊl from the cessation of agranulocytosis had an inhibitory effect on methimazole was shorter in the former group phagocytosis-associated hexose monophos- (9.66•}1.05, n=6) than in the latter group phate shunt activity in leucocytes from both normal donors and patients who had re- (13.00•}0.57, n=3), but the difference was not significant. covered from agranulocytosis. In addition, There were 5 patients who were taking the patients with propylthiouracil-induced methimazole even after the onset of symp- agranulocytosis possessed serum factors that toms. The correlation between the incep- inhibited 14CO2 release by particle-stimulated tion of remission, and the period during leucocytes incubated with C-1[14C] glucose which methimazole was taken after the (McIntyre et al., 1971). onset of symptoms was not significant (r= Corticosteroids increase the count of -0 .145, p>0.05). Furthermore, even in granulocytes in the peripheral blood by a Case No.1, who had been taking me- combination of an increased marrow release thimazole for 6days after the onset of rate and decreased efflux of cells from the symptoms, remission started 3days after blood (Bishop et al., 1968). Hewever, it ceasing to use this drug. cannot be expected that the release rate of granulocytes is increased further by corti- costeroids in agranulocytosis, because release Discussion rate of granulocytes from the marrow is increased (Marsh and Lewitt, 1971) and the It was demonstrated in this study that granulocyte reserves of the marrow are corticosteroids induced early remission in exhausted in this condition (Young and patients with methimazole-induced agranu- Vincent, 1980). Hence, Palva et al. (1972) locytosis. stated that the favorable effect of cortico- Vol.28, No.6 METHIMAZOLE-INDUCED AGRANULOCYTOSIS 827 steroids in agranulocytosis is probably limited to cases of an immunological type. The References findings obtained in this study suggest that methimazole-induced agranulocytosis may be Bilezikian, S. B., Y. Laleli, M. F. Tsan, B. A. Hod- kinson, S. Ice and P. A. McIntyre (1976). Im- an immunological type. This concept may, munological reactions involving leukocytes: III. furthermore, be supported by the following Agranulocytosis induced by antithyroid drugs. two pieces of evidence: that agranulocytosis Johns. Hopkins. Med. J. 137, 124-129. occurred earlier in patients with previous Bishop, C. R., J. W. Athens, D. R. Boggs, H. R. Warner, G. E. Cartwright and M. M. Wintrobe methimazole therapy and that the inception (1968). Leukokinetic studies. XIII. A non-steady- of remission was not retarded in patients state kinetic evaluation of the mechanisms of cor- who took methimazole even after the onset tisone-induced granulocytosis. J. Clin. Invest. 47, 249-260. of symptoms. In this study, no significant Marsh, J. C. and M. Lewitt (1971). Neutrophilia- difference in the period required for complete inducing activity in plasma of eeutropenic human recovery from agranulocytosis was observed beings. Blood. 37, 647-656. between the 2 groups. It may be because McIntyre, P. A., Y. R. Laleli, B. A. Hodkinson corticosteriods were administered to both and H. N. Wagner (1971). Evidence for anti- leukocyte antibodies as a mechanism for drug groups even with a time interval. induced agranulocytosis. Trans. Assoc. Am. Phys. It is not clear whether methimazole-in- 84, 217-228. duced agranulocytosis occurred immunologi- Moore, F. D. (1946). Toxic manifestations of thiouracil therapy, J. A. M. A. 130, 315-319. cally in all cases, since there were 2 cases Palva, P., O. O. Mustala and S. J. Salokannel in which the start of remission was observed (1972). Drug-induced agranulocytosis III. Res- 8 to 9days after the corticosteroid treat- ponse to corticosteroids. Acta. Med. Scand. 192, ment. However, the use of corticosteroids 51-53. Rosove, M. H. (1977). Agranulocytosis and antithy- would be recommended for the cases of roid drugs. West. J. Med. 126, 339-343. methimazole-induced agranulocytosis. Weitzman, S. A., T. P. Stossel and M. Desmond (1978). Drug-induced immunological neutropenia. Lancet. I, 1068-1072. Young, G. A. R. and P. C. Vincent (1980). Drug- induced agranulocytosis. Clin. in Haematol. 9, 483-504..
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