Background: Differentiated thyroid cancer (DTC) is the most prevalent cancer of thyroid and is among the most frequently diagnosed cancers in the United States. The practice guidelines of the American Thyroid Association (ATA) for DTC management in adult patients (previously combined with thyroid nodules) were published initially in 1996, with subsequent revisions based on advances in the field. The goal of this update is to provide clinicians, patients, researchers, and those involved in health policy with rigorous, comprehensive, and contemporary guidelines to assist in the management of adult patients with DTC, emphasizing the patient journey beginning with a thyroid cancer diagnosis. Methods: The questions addressed were based, in part, on prior versions of the guidelines, with input from a larger, more diverse complement of stakeholders. The panel included members from multiple specialties involved in thyroid cancer care, including a patient advocate and an expert in systematic reviews/meta-analyses/guidelines who educated and supported task force members. The panel conducted systematic literature reviews to inform the recommendations and commissioned two additional systematic reviews. Published English-language articles were eligible for inclusion, with a final search date of July 1, 2024. A modified Grading of Recommendations Assessment, Development and Evaluation system was used for critical appraisal of evidence and determining the quality of data. The guidelines panel had editorial independence from the ATA. Competing interests of task force members were pre-vetted, regularly updated, communicated with task force members, and assessed and managed by ATA leadership and the Clinical Practice Guidelines and Statements Committee. Results: These revised guidelines begin with the initial cancer diagnosis and continue with recommendations for staging and risk assessment, initial treatment decisions, assessment of treatment responses, monitoring approaches, diagnostic testing, and subsequent therapies based on the strength of evidence for response and consideration of side effects and outcomes. Patient-reported outcomes and identified areas of need for additional high-quality research are highlighted. Conclusions: These revised evidence-based recommendations inform clinical decision-making in the management of DTC that reflect the changing science and optimize the evidence-based clinical care of patients throughout their journey with DTC. Critical areas of need for additional research are highlighted.

Thyroid eye disease (TED) remains challenging for clinicians to evaluate and manage. Novel therapies have recently emerged, and their specific roles are still being determined. Most patients with TED develop eye manifestations while being treated for hyperthyroidism and under the care of endocrinologists. Endocrinologists, therefore, have a key role in diagnosis, initial management, and selection of patients who require referral to specialist care. Given that the need for guidance to endocrinologists charged with meeting the needs of patients with TED transcends national borders, and to maximize an international exchange of knowledge and practices, the American Thyroid Association and European Thyroid Association joined forces to produce this consensus statement.

Context: Breastfed infants rely on adequate maternal dietary iodine intake. Objective: Our objective was to measure breast milk iodine and perchlorate, an inhibitor of iodide transport into the thyroid and potentially into breast milk, in Boston-area women. Participants: The study included 57 lactating healthy volunteers in the Boston area. Measurements: Breast milk iodine and perchlorate concentrations and urine iodine, perchlorate, and cotinine concentrations were measured. For comparison, iodine and perchlorate levels in infant formulae were also measured. Results: Median breast milk iodine content in 57 samples was 155 μg/liter (range, 2.7–1968 μg/liter). Median urine iodine was 114 μg/liter (range, 25–920 μg/liter). Perchlorate was detectable in all 49 breast milk samples (range, 1.3–411 μg/liter), all 56 urine samples (range, 0.37–127 μg/liter), and all 17 infant formula samples (range, 0.22–4.1 μg/liter) measured. Breast milk iodine content was significantly correlated with urinary iodine per gram creatinine and urinary cotinine but was not significantly correlated with breast milk or urinary perchlorate. Conclusions: Perchlorate exposure was not significantly correlated with breast milk iodine concentrations. Perchlorate was detectable in infant formula but at lower levels than in breast milk. Forty-seven percent of women sampled may have been providing breast milk with insufficient iodine to meet infants’ requirements.

Diabetes mellitus is the leading cause of end‐stage renal disease (ESRD) in the U.S. and many countries globally. The role of improved glycemic control in ameliorating the exceedingly high mortality risk of diabetic dialysis patients is unclear. The treatment of diabetes inESRDpatients is challenging, given changes in glucose homeostasis, the unclear accuracy of glycemic control metrics, and the altered pharmacokinetics of glucose‐lowering drugs by kidney dysfunction, the uremic milieu, and dialysis therapy. Up to one‐third of diabetic dialysis patients may experience spontaneous resolution of hyperglycemia with hemoglobin A1c (HbA1c) levels <6%, a phenomenon known as “Burnt‐Out Diabetes,” which remains with unclear biologic plausibility and undetermined clinical implications. Conventional methods of glycemic control assessment are confounded by the laboratory abnormalities and comorbidities associated withESRD. Similar to more recent approaches in the general population, there is concern that glucose normalization may be harmful inESRDpatients. There is uncertainty surrounding the optimal glycemic target in this population, although recent epidemiologic data suggest that HbA1c ranges of 6% to 8%, as well as 7% to 9%, are associated with increased survival rates among diabetic dialysis patients. Lastly, many glucose‐lowering drugs and their active metabolites are renally metabolized and excreted, and hence, require dose adjustment or avoidance in dialysis patients.

Purpose of review To summarize the mechanisms of iodine-induced hypothyroidism and hyperthyroidism, identify the risk factors for thyroid dysfunction following an iodine load, and summarize the major sources of excess iodine exposure. Recent findings Excess iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Sources of increased iodine exposure include the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients, excess seaweed consumption, and various miscellaneous sources. Summary Iodine-induced thyroid dysfunction may be subclinical or overt. Recognition of the association between iodine excess and iodine-induced hypothyroidism or hyperthyroidism is important in the differential diagnosis of patients who present without a known cause of thyroid dysfunction.