[Indocyanine green fluorescence angiography in transoral endoscopic thyroidectomy for papillary thyroid cancer]. / Primenenie fluorestsentnoi angiografii s indotsianinom zelenym v transoral'noi endoskopicheskoi tireoidektomii pri papillyarnom rake shchitovidnoi zhelezy.

OBJECTIVE: To evaluate the effectiveness of ICG angiography in patients with papillary thyroid cancer (PTC) undergoing transoral endoscopic thyroidectomy (TOETVA) and selective neck dissection (level VI). MATERIAL AND METHODS: A retrospective analysis included 20 patients with PTC who underwent TOETVA with selective neck dissection (level VI) between September and December 2022. ICG was administered intravenously (5 mg ´ 3 times). We analyzed parathyroid glands by visual examination and ICG angiography. Fluorescence of all glands was assessed. RESULTS: Twenty patients underwent ICG angiography during TOETVA. A total of 68 parathyroid glands were identified. Only 76.5% (52/68) of parathyroid glands were identified at initial visual examination. ICG angiography additionally localized 12 glands that improved detection to 94.1% (64/68). At least one well-vascularized parathyroid gland was demonstrated by ICG angiography in 16 patients. In all these patients, serum parathyroid hormone was normal in 1 and 10 days after surgery. Two out of four patients who failed to identify a well-vascularized parathyroid gland developed transient hypoparathyroidism. There were no intraoperative and postoperative complications associated with ICG angiography. CONCLUSION: ICG angiography was simple, safe and effective for better identification and preservation of parathyroid glands in patients with PTC undergoing TOETVA. This method was valuable for assessing the viability and function of parathyroid glands and predicting postoperative hypocalcemia.

[Diagnosis and treatment policy in familial thyroid cancer].

Thirty-two cases of hereditary medullary thyroid carcinoma (HMTC) and 95 sporadic HMTC (SHMTC), 44 familial papillary TC (FPTC), and 172 sporadic cases were comparatively analyzed to improve the diagnosis and treatment of familial thyroid cancer. A hundred and one DNA samples from patients with MTC and their relatives were examined. BRAF and RET/PTC gene mutations were investigated in 6 patients with FPTC. The frequencies of familial TC, HNTC, and FPTC were 6 6, 26.5, and 4.3%, respectively. The mean age of patients with HMTC and SHMTC was 30.J±13.6 and 46.3±J3.1 years, respectively (p < 0.0001); tumor multicentricity was 87.5 and 36.8% (p < 0 0001) and bilaterality was 87.5 and 0%, respectively (p < 0.001). Inheritable RET mutations were detected in 16 families. Eight asymptomatic carriers of RET mutations were revealed; 3 of them underwent preventive thyroidectomy. There was the commonest (63.6%) codon 634 mutation in which the earliest manifestation and aggressive course of the disease were observed. The efficiency of screening for type 2 multiple endocrine neoplasia syndrome Increased by 1.8 times (from 31.2 to 51.2%). In the mother and daughter with FPTC, silent mutation was found in codon 891 of RET gene exon 15. Genetic examination of the relatives of patients with HMTC made it possible to diagnose the disease at its early stage and to perform preventive surgical treatment. The aggressiveness of HMTC makes it necessary to make total thyroidectomy. The absence of differences in the clinical course of familial and sporadic PTC predetermines uniform treatment policy.

[The diagnosis and treatment of hereditary forms of medullary carcinoma of the thyroid: Clinical and genetic aspects].

Medullary thyroid cancer (MTC) is a fairly rare disease, accounting for 5-7% of all cases of thyroid cancer. The sporadic form of thyroid cancer is observed in 70-80% of cases, family (inherited - autosomal dominant type of inheritance) - in 20-30%. Familial forms of MTCG are caused by point mutations in the RET proto-oncogen (Rearranged during Transfection). To date, about 25 germinal (inherited) mutations are described in the world literature in 19 codons of the RET gene, which are found in 97% of patients with MEN 2A, in 95% with MEN 2B and in 86% of patients with SMR.