35-year-old female with albinism since 10 years of age and type 1 diabetes mellitus since 12 years of age, recently treated with insulin pump, smoking about 10 cigarettes a day, reported due to clinical and laboratory signs of Graves’ disease. Laboratory evaluation at admission revealed reduced concentration of TSH and elevated levels of fT3 and fT4. In addition, abnormal levels of antibodies against thyroid peroxidase (anti-TPO) and against TSH receptor (TRAb) were established – hormone levels before and after treatment are presented in the table 1. Physical examination revealed significantly enlarged thyroid gland, smooth, with audible vascular murmur, and bilateral exophthalmos. In addition, the medical interview indicated that the patient had difficulties in controlling diabetes mellitus over the last 3 months. Thiamazole was administered in the initial dose of 40 mg/day, which was gradually reduced. Despite treatment with thiamazole and gradual improvement in thyroid parameters, exophthalmos gradually increased and double vision additionally occurred. Based on the clinical picture and imaging evaluations (MRI of the head, ultrasound evaluation of the orbital cavities, VEP), an active phase of thyroid orbitopathy with involved external eye muscles and double vision (class IV according to ATA) was diagnosed, and it was decided that it was necessary to use intravenous systemic corticotherapy (SoluMedrol 6 x 500 mg and 6 x 250 mg every week over 12 weeks). This method of therapy is currently recognized as the most effective in treatment of Graves’ orbitopathy (1). Due to poor prognosis in terms of obtaining permanent remission after treatment with thyrostatic drug, large goiter, and maintaining a high level of TRAb antibodies during treatment with corticoids, it was decided that treatment with radioiodine was necessary. Therapeutic dose of ¹³¹I 15 mCi was administered. After treatment with radioiodine, administration of maintenance doses of thiamazole was continued. After one year following administration of radioiodine, hypothyroidism occurred and it was necessary to administer thyroxine in initial dose of 25 μg/day.

As early as during the first intravenous infusion of SoluMedrol in the dose of 500 mg, a significant increase in glycemia occurred, which exceeded 350 mg/dL, and abnormal concentration of glucose maintained over the next 3 days, despite attempts undertaken by the patient in order to regain control. It was necessary to establish a course of action in order to avoid the risk of occurrence of hyperglycemia and potential ketoacidosis in this patient during the next courses of treatment. During the next courses of treatment, a gradual change in insulin dosing was established. Increased demand for insulin took place shortly after starting infusion of SoluMedrol. After approximately 2-3 hours following start of the infusion, a 2-fold increase in basal insulin was necessary (programmed by the patient as the base “steroids”), and 3-fold after completion of administration of SoluMedrol. Another increase of the base was executed by the patient by using rectangular bolus extended over about 12 hours. Simultaneously, on the day of administration of corticoid, a 3-fold increase in doses of pre-meal boluses was necessary. On the second day of treatment, demand for basal insulin decreased to the level of two times higher than normal basal infusion, and demand for pre-meal boluses was similarly higher. On the third day following administration of SoluMedrol, doses of the basal infusion and pre-meal boluses were 1.5 times higher than usual. On the fourth day, it was possible to use regular dosing. During the next courses of treatment with SoluMedrol in the dose of 500 mg, demand for insulin increased to the same level and it did not undergo any further changes. During infusions of SoluMedrol in the dose of 250 mg, demand for insulin was insignificantly lower.