THYROID TUMORS
Thyroid carcinomas TC are rare (3.6% of all human tumors), but are the most common malignant endocrine tumors. Their incidence has increased in recent decades, with the detection of carcinomas <1cm, through the use of neck ultrasound. The male to female ratio is 4 / 1. The average age at diagnosis is 45-50 years, children are rarely affected.
The risk factor recognized so far is exposure to ionizing radiation. Differentiated thyroid carcinoma DTC is the most common and are categorized in papillary thyroid carcinoma PTC 80% and follicular thyroid carcinoma FTC 10%, PDTC poorly differentiated thyroid carcinoma, ATC anaplastic thyroid carcinoma, MTC medullary thyroid carcinoma are respectively 5% 2% 7%.
The most common oncogenic changes in PTC are RET / PTC rearrangements 20% and BRAFV600E mutation 45%. Other rarer changes have been found recently. The most common oncogenic changes in PTDC and ATC are p53 and TERT promoter point mutations. The diagnosis of DTC (including poorly differentiated forms) involves pathological and molecular evaluations before and after surgery.
Pre-operative FNA for cytology is not required for nodules with a size of 1 cm. Decisions on aspirating larger nodules should be guided by the size of the lesion and the sonographic appearance. Cytology findings are classified into diagnostic categories associated with different risks of malignancy. Most malignant thyroid tumors can be identified cytologically.
INITIAL TREATMENT
According to the latest international guidelines for surgery treatment in cases with TC, it can be either hemithyroidectomy or lobectomy LB, or a total thyroidectomy TT. Prophylactic node dissection is not recommended in DTC. Surgery of the central or lateral lymph nodes is done if US shows metastases in lymph nodes.
If MTC is diagnosed before surgery, TT and prophylactic central node dissection are always indicated. After TT, DTX with an intermediate or high risk of recurrence should be treated with radioiodine after TSH stimulation. PTDC and ATC should be treated locally with palliative intent external radiotherapy. 131 I therapy plays no role in MTC since they originate from C parafollicular cells which have a neuroendocrine origin and are not capable of absorbing iodine.
Surgical complications of LB or TT to be considered are vocal cord paralysis and hypoparathyroidism both of which may be transient or permanent. PTDC and ATC are usually locally very advanced with infiltration of other neck structures making surgical intervention rare.
TREATMENT OF ADVANCED CASES
In DTC chemotherapy mainly doxorubicin was ineffective. Certainly, no chemotherapy has been shown to be effective in advanced and symptomatic MTCs which moreover cannot be treated with 131 I due to their nature. RAS and BRAF mutations are the main reason for treating advanced DTC and MTC with tyrosine kinase inhibitors TKI.
ATC are still outside a treatment scheme. Other therapeutic strategies are under evaluation such as the use of selumetinib, a MEK inhibitor to restore the lost ability to absorb 131 I. Immunotherapies used alone or in combination with levatinib are being considered based on the frequent association of TC with lymphatic infiltration.