Ultrasonography of the thyroid and ultrasonographically guided fine-needle aspiration can help determine whether a nodule is probably benign or malignant. In the absence of growth or suspicious clinical or radiologic findings, nodules with a benign finding on FNA can be monitored.

Thyroid cancer incidence is increasing at an alarming rate, almost tripling every decade. In 2017, it was the fifth most common cancer in women. Although the majority of thyroid tumors are curable, about 2–3% of thyroid cancers are refractory to standard treatments. These undifferentiated, highly aggressive and mostly chemo-resistant tumors are phenotypically-termed anaplastic thyroid cancer (ATC). ATCs are resistant to standard therapies and are extremely difficult to manage. In this review, we provide the information related to current and recently emerged first-line systemic therapy (Dabrafenib and Trametinib) along with promising therapeutics which are in clinical trials and may be incorporated into clinical practice in the future. Different categories of promising therapeutics such as Aurora kinase inhibitors, multi-kinase inhibitors, epigenetic modulators, gene therapy using oncolytic viruses, apoptosis-inducing agents, and immunotherapy are reviewed. Combination treatment options that showed synergistic and antagonistic effects are also discussed. We highlight ongoing clinical trials in ATC and discuss how personalized medicine is crucial to design the second line of treatment. Besides using conventional combination therapy, embracing a personalized approach based on advanced genomics and proteomics assessment will be crucial to developing a tailored treatment plan to improve the chances of clinical success.

Untreated or unrecognized hypothyroidism may progress to severe decompensated hypothyroidism or myxedema coma. Relatively few cases are reported in the literature since the first case was apparently reported from the St. Thomas Hospital in London in 1879. The paucity of cases may be due to either underreporting or improvement in the diagnosis and treatment of uncomplicated hypothyroidism. However, despite the ready availability of sensitive thyrotropin assays, the recognition and treatment of myxedema coma remains a challenge. Although thyroid hormone treatment is highly effective when combined with ventilatory and hemodynamic support in the intensive care unit setting, controversies abound on the optimal and most effective choice of thyroid hormone preparation: thyroxine and triiodothyronine and in what amount. Accumulated evidence now shows that proper use of either thyroxine alone or in combination with triiodothyronine may be effective therapy.

Background: In the United States, many women with hypothyroidism are on thyroid hormone replacement during pregnancy. The optimal management strategy for thyroid hormone dosing in hypothyroid women during pregnancy is controversial. We hypothesized that dosage requirements during pregnancy might differ depending upon the nature of the underlying hypothyroidism. Methods: We conducted a retrospective review of 45 pregnancies from 38 women whose hypothyroidism was managed during pregnancy. Thyroid function tests were obtained when pregnancy was confirmed, then every 4–8 weeks. The thyrotropin (TSH) goal was 0.4–4.1 μU/mL (SI unit conversion: multiply TSH by 1.0 for mIU/L). Results: On average, the entire group required a cumulative increase from baseline in levothyroxine (LT₄) dosage of 13% in the first trimester, 26% in the second trimester, and 26% in the third trimester (p < 0.001, p < 0.001, p < 0.001, respectively). Average baseline LT₄ dose for patients with primary hypothyroidism was 92.5 ± 32.0 μg daily. These patients required small cumulative dose increases of 11%, 16%, and 16% from baseline in each trimester, respectively (p values = 0.125, 0.016, 0.016). Average baseline LT₄ dose for patients with hypothyroidism resulting from treated Graves' disease or goiter was 140.4 ± 62.4 μg daily. These patients required the largest cumulative increases in LT₄ dosage (first trimester, 27%; second trimester, 51%; third trimester, 45%; p = 0.063, 0.063, 0.063, respectively). Average baseline LT₄ dose for patients with thyroid cancer was 153.2 ± 30.3 μg. The cumulative LT₄ dose increases for patients with thyroid cancer were 9%, 21%, and 26% in each trimester, respectively (p = 0.03, p < 0.001, p < 0.001). Conclusions: The etiology of hypothyroidism plays a pivotal role in determining the timing and magnitude of thyroid hormone adjustments during pregnancy. Patients require vigilant monitoring of thyroid function upon confirmation of conception and anticipatory adjustments to LT₄ dosing based on the etiology of their hypothyroidism.

Amiodarone is a class III antiarrhythmic drug containing 37% iodine by weight, with a structure similar to that of thyroid hormones. Deiodination of amiodarone releases large amounts of iodine that can impair thyroid function, causing either hypothyroidism or thyrotoxicosis in susceptible individuals reflecting ~20% of patients administered the drug. Not only the excess iodine, but also the amiodarone (or its metabolite, desethylamiodarone) itself may cause thyroid dysfunction by direct cytotoxicity on thyroid cells. We present an overview of the epidemiology and pathophysiology of amiodarone-induced thyroid disorders, with a focus on the various forms of clinical presentation and recommendations for personalized management of each form.

Serum thyrotropin (TSH) is considered the single most sensitive and specific measure of thyroid function in the general population owing to its negative logarithmic association with free triiodothyronine and free thyroxine concentrations. It is therefore often the test of choice for screening, diagnosis, and monitoring of primary hypothyroidism. Serum TSH concentrations can be analyzed quantitatively using third-generation immunoassays, whereas its bioactivity can be measured by TSH activity assays in cell culture. Theoretically, if serum TSH concentrations are directly related to TSH activity, the two tests should yield comparable results. However, on occasion, the results are discordant, with serum concentrations being higher than TSH biological activity. This review focuses on the dissociation between the clinical state and serum TSH concentrations and addresses clinically important aspects of TSH analysis.