The present study has shown that in some patients parathyroid cell allotransplantation may be considered a method of treatment for permanent hypoparathyroidism after thyroid surgery. Graft function and/or survival did not depend on the baseline viability or secretory activity of cultured cells used for transplantation.
Thyroid-associated orbitopathy is a set of ophthalmic symptoms resulting from an autoimmune process in which the swelling of extraocular tissues leads to exophthalmos either caused by hypersecretion and accumulation of glycosaminoglycans in the orbit fibroblasts or being the result of inflammatory processes in the oculomotor. These changes cause eyeball motility disturbances, keratopathy, and the pressure on the optical nerve. Thyroid-associated orbitopathy accompanies Graves' disease in most cases, whereas the Hashimoto's disease in only 5%. In the present case, other reasons for the exophthalmos such as tumors of the orbit and sinuses, intracranial tumors, aneurysms and vascular fistulas and orbit tissue inflammation of different etiology were excluded. Additional examinations showed that thyrotropin level was 26 µIU/ml (normal range 0.27-4.0), antithyroglobulin antibody level was 1763 IU/ml (normal range 0-115), antithyrotropin antibody level was 4.93 IU/l (normal range 0-1), and anti-thyroid peroxidase antibody level was 1609 IU/ml (normal range 0-35). An ultrasound examination showed a thyroid gland of 9.8 ml volume. A cytological presentation obtained by thin-needle aspiration biopsy demonstrated inflammatory infiltration of lymphocytes, indicating an autoimmune process. The iodine uptake after 24 hours was 9%. The active form of orbitopathy was diagnosed in the patient with hypothyreosis in the course of Hashimoto's disease. Moreover, the coexistence of another autoimmune disease, pernicious anemia was diagnosed. The administration of the methylprednisolone pulse therapy and levothyroxine caused remission of ophthalmic symptoms, and euthyreosis was obtained. Our report presents a rare coexistence of thyroid orbitopathy and Hashimoto's disease.
BackgroundThyroid disorders are very common in adults. Despite advances in conservative management, surgery remains a treatment modality of choice in many cases. The mortality and morbidity of thyroidectomy are low, but long-term postoperative hypoparathyroidism (HPT) remains a prominent complication of the procedure.The aim of this study was to assess the incidence of permanent HPT and identify the risk factors for this complication in a cohort of post-thyroidectomy patients followed at a District Endocrine Clinic.Material/MethodsThis was a retrospective analysis of 401 patients followed up at a Regional/District Endocrine Clinic, who had undergone thyroid surgery in the years 1993–2011. The percentage of patients with permanent (>12 months) HPT was the primary endpoint of the study. The statistically analyzed data of patients with permanent HPT versus the remaining patients free from postoperative complications included their demographic data, indications for surgical treatment of their thyroid disorder, and extent of the thyroid resection. The risk factors for postoperative hypoparathyroidism were assessed using logistic regression analysis.ResultsPermanent HPT following surgery on the thyroid gland occurred in 8.5% of the patients. It was more frequent following total thyroidectomy (20.2%) than near-total thyroidectomy (6.7%) or subtotal thyroidectomy (4.2%); p<0.0001. A multivariate statistical regression analysis demonstrated that primary total thyroidectomy was a significant risk factor for permanent HPT (OR 6.5; 95% CI: 2.9–14.4; p<0.0001).ConclusionsTotal thyroidectomy was associated with increased prevalence of permanent hypoparathyroidism when compared to less extensive thyroid resection modes in patients with benign thyroid diseases.
Radioiodine treatment of hyperthyroid patients with autonomous thyroid nodule leads to cellular DNA damage not only in thyrocytes but also in peripheral blood lymphocytes. The purpose of this study was to evaluate DNA breakage and base damage in thyrocytes and lymphocytes in patients treated with 131-I. In all the patients thyroid scintiscan was performed using 131-I. Damage to DNA was estimated by comet assay. Samples were taken before radioiodine treatment, and 12 and 54 days afterwards. Our results indicate high diversity in the level of DNA damage among the individual patients. However, in all cases, after 54 days the level of DNA damage in lymphocytes was similar or even lower than that in the controls. In contrast, in hot nodule the DNA damage persisted until the 54th day after 131-I application. Differences in the type of DNA damage between thyrocytes and lymphocytes were also observed. In lymphocytes there was more base damage, whereas in thyrocytes single strand breaks prevailed. This may indicate different mechanisms of DNA damage induction and/or DNA repair.
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