Abstract

Introduction: Thyrotoxicosis (T) develops as a result of persistent excess of thyroid hormones (TH). There are two groups of diseases that are fundamentally different in pathogenesis. The first group includes those in which the production of TH increases. Diseases of the second group are accompanied by T caused by destruction of the thyroid gland tissue. Therapeutic approaches for different pathogenetic types of T are different, therefore, a careful differential diagnosis of T is necessary, even if at first glance the diagnosis seems obvious. Clinical Case: A 35-year-old patient consulted a physician complaining of weakness, weight loss by 11 kg in 1.5 months, tremors, palpitations, which first appeared about a month ago. The examination revealed TSH <0.0083 mU/l (0.4-4.0), and an endocrinologist’s consultation was recommended. On examination, the thyroid gland is no larger than the distal phalanx of the subject’s thumb, BMI=24 kg/m2, HR=100 bpm, BP=115/80 mm Hg. Laboratory examination: TSH <0.0083 mU/l, free T4 =28.29 pmol/l (9.0-19.05). Ultrasound of the thyroid gland: signs of diffuse changes in tissue, the total volume=16.8 ml3. For differential diagnosis of T, antibodies to TSH receptors were determined, the titer of which turned out to be slightly increased 1.43 IU / L (<1). A diagnosis of Graves’ disease (GD) was made and treatment was prescribed (Tyrozol 30 mg, Bisoprolol 2.5 mg per day). After 3 weeks, the patient noted an improvement in well-being, but weakness, tremor, an increase in free T4 (23.33 pmol/l) and total T3 (3.26nmol / l at a rate of 0.98-2.33) remained. The lack of achievement of the target values of TH levels was regarded as inadequacy of the received dose of Tyrozol, in connection with which it was decided to increase the dose to 40 mg per day. After 2 weeks, an increase in free T4 (27.26 pmol/L) and total T3 (3.84 nmol/L) remained. The lack of positive dynamics called into question the diagnosis of GD. With a more thorough collection of anamnesis, it was found that 1.5 years ago, the patient took amiodarone for 6 months as prescribed by a cardiologist (he does not remember the dose). In this connection, to establish the cause of T, scintigraphy was performed: revealed a weak accumulation of a radiopharmaceutical with diffuse uneven distribution. Based on the data obtained, amiodarone-induced T type 2 was verified. Treatment was corrected: Tyrosol withdrawal and Prednisolone administration, 40 mg/day with positive dynamics from treatment. Conclusion: Clinical case demonstrates how important it is to carefully collect the patient’s history and follow the algorithms for differential diagnosis. Errors in diagnosis lead to incorrectly prescribed treatment, lengthening the duration of symptoms, which affects not only the patient’s quality of life, but also reduces the level of his trust in medical professionals.

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