{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:16:40Z","timestamp":1784557000884,"version":"3.55.0"},"reference-count":36,"publisher":"Bioscientifica","content-domain":{"domain":["edm.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,9,1]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    A 67-year-old man was referred to our department for thyrotoxicosis with intermittent palpitation and 4-kg weight loss during the previous month. At the first visit, the patient was treated with cyclosporine A (CyA) for membranous nephropathy during the last 3 years and 8 months. Laboratory studies revealed that the serum TSH level was &lt;0.005\u200a\u03bcU\/ml, and free thyroxine (fT\n                    <jats:sub>4<\/jats:sub>\n                    ) and triiodothyronine (fT\n                    <jats:sub>3<\/jats:sub>\n                    ) levels were elevated at 2.76\u200ang\/dl and 5.96\u200apg\/ml respectively. Anti-TSH receptor antibody (TRAb) level was increased at 26.4%. A clinical diagnosis of Graves' hyperthyroidism was given, and then thyrostatic treatment with thiamazole (MMI) at a dose of 10\u200amg daily was initiated after CyA withdrawal. After the initiation of MMI therapy, serum fT\n                    <jats:sub>4<\/jats:sub>\n                    and fT\n                    <jats:sub>3<\/jats:sub>\n                    attained the normal level within 1.5 months, with relief of symptoms followed by a remarkable decrease in urinary protein excretion from 2.0\u20135.2\u200ag\/day to \u22640.03\u200ag\/day. The patient maintained euthyroid with a low titre of TRAb for the succeeding 2 years and then MMI was finally stopped. Neither a relapse of hyperthyroidism nor a flare-up of nephrotic syndrome was observed for 3 years after MMI discontinuation. CyA has conflicting effects on immunologic self-tolerance by modulation of self-reactive T cells and natural CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>+<\/jats:sup>\n                    Foxp3\n                    <jats:sup>+<\/jats:sup>\n                    regulatory T cell (Treg) functions, and possibly becomes a triggering factor in the development of autoimmune disorders. This case may be interesting when considering the effect of each T cell subset on the development of Graves' disease.\n                  <\/jats:p>\n                  <jats:sec>\n                    <jats:title>Learning points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            The balance between intrathyroidal self-reactive T cell and natural CD4\n                            <jats:sup>+<\/jats:sup>\n                            CD25\n                            <jats:sup>+<\/jats:sup>\n                            Foxp3\n                            <jats:sup>+<\/jats:sup>\n                            Treg functions determine self-tolerance in the thyroid.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>CyA not only halts the expansion of self-reactive T cells but also impairs the function of Treg, which can provoke an unwanted immune response.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>A change in thyroid autoimmunity during treatment with CyA may result in the development of autoimmune thyroid diseases (AITD).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Renal involvement in AITD frequently manifests as nephrotic syndrome, and thyrostatic treatment with thiamazole may be effective for excessive proteinuria.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  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