P-082 CHALLENGES IN PATIENT CARE WITH CUSHING DISEASE AND COMORBIDITIES (PRIMARY HYPERPARATHYROIDISM, GRAVES’ DISEASE)

P-082 库欣病合并症(原发性甲状旁腺功能亢进症、格雷夫斯病)患者护理中的挑战

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Abstract

INTRODUCTION: Successful treatment of Cushing disease and decrease of cortisol level may be associated with reactivation of the immune system and enhanced risk of onset of various autoimmune diseases. MATERIAL-METHODS: Clinical case of Cushing's disease in combination with primary hyperparathyroidism and further development of Graves’ disease. CLINICAL CASE: Female patient K., at aged 52 reported facial plethora (matronism), weight gain of 10 kg, striae, hypertension up to 200/130 mm Hg, a height decrease of -4 cm. Cushing's disease was confirmed based on appropriate laboratory tests and pituitary adenoma on MRI. A densitometry revealed a BMD decrease in lumbar spine (T-score -3.2 SD) and the proximal femur (T-score -1.7 SD). Primary hyperparathyroidism was also identified: mild hypercalcemia, parathyroid hormone 78 pg/mL (11-62), an adenoma of the left inferior parathyroid gland was found. Patient had 2 components of MEN 1 syndrome (pituitary adenoma and primary hyperparathyroidism), genetic analysis of MENIN was performed—no mutations were identified. The first stage of treatment was pituitary adenomectomy (histology: pituitary adenoma with nuclear polymorphism). In the postoperative period, secondary hypocortisolism and secondary hypothyroidism developed. Therapy with hydrocortisone and levothyroxine as well as bisphosphonates was initiated – with a positive effect. During observation period 12 months after the adenomectomy, the patient's free T4 level gradually increased. Levothyroxine was discontinued, without treatment free T4 was 40 pmol/l (9-19.1), and level TSH receptor antibodies was highly increased. An ultrasound examination showed diffuse enlargement of the thyroid gland with enhanced vascularization and the adenoma of the left inferior parathyroid gland. Thus thyroidectomy and left parathyroid adenomectomy were performed, and hormonal replacement therapy was adjusted (levothyroxine, hydrocortisone). Cholecalciferol, calcium carbonate, zoledronic acid were initiated for osteoporosis. CONCLUSION: The patient with Cushing's disease had coexisted primary hyperparathyroidism that worsened the patient's condition and exacerbated bone loss. After resolution of hypercortisolism, hyperthyroidism due to primary autoimmune thyroid disease developed in addition to the secondary postoperative hypothyroidism. Careful monitoring and a multidisciplinary approach led to the successful compensation of this patient's complex condition.

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