Key Points Question Can the diagnosis of benign disease or cancer in thyroid nodules with indeterminate cytology be established by molecular testing instead of diagnostic surgery? Findings This prospective, blinded, multicenter cohort study of a multigene genomic classifier (ThyroSeq v3) test included 257 indeterminate cytology thyroid nodules with informative test results. It demonstrated a high sensitivity (94%) and reasonably high specificity (82%), with 61% of the nodules yielding a negative test result and only 3% residual cancer risk in these nodules. Meanings Up to 61% of patients with indeterminate cytology thyroid nodules may avoid diagnostic surgery by undergoing multigene genomic classifier testing.

Atrial fibrillation is the most common postoperative arrhythmia with significant consequences on patient health. Postoperative atrial fibrillation (POAF) complicates up to 8% of all noncardiac surgeries, between 3% and 30% of noncardiac thoracic surgeries, and between 16% and 46% of cardiac surgeries. POAF has been associated with increased morbidity, mortality, and longer, more costly hospital stays. The risk of POAF after cardiac and noncardiac surgery may be affected by several epidemiologic and intraoperative factors, as well as by the presence of preexisting cardiovascular and pulmonary disorders. POAF is typically a transient, reversible phenomenon that may develop in patients who possess an electrophysiologic substrate for the arrhythmia that is present before or as a result of surgery. Numerous studies support the efficacy of beta-blockers in POAF prevention; they are currently the most common medication used in POAF prophylaxis. Perioperative amiodarone, sotalol, nondihydropyridine calcium channel blockers, and magnesium sulfate have been associated with a reduction in the occurrence of POAF. Biatrial pacing is a nonpharmacologic method that has been associated with a reduced risk of POAF. Additionally, recent studies have demonstrated that hydroxymethylglutaryl-CoA reductase inhibitors may decrease the risk of POAF. Finally, based on recent evidence that angiotensin converting enzyme inhibitors and angiotensin receptor blockers reduce the risk of permanent atrial fibrillation, these medications may also hold promise in POAF prophylaxis. However, there is a need for further large-scale investigations that incorporate standard methodologies and diagnostic criteria, which have been lacking in past trials.

Objective To characterize the metabolic phenotype of 2 cases of normal weight young women who developed type 2 diabetes (T2D), severe insulin resistance (insulin requirement >200 units/day), marked hypertriglyceridemia (>2000 mg/dL), and hepatic steatosis beginning 9 years after undergoing total body irradiation (TBI) and bone marrow transplantation for childhood cancer. Methods Fasting plasma glucose, insulin, free fatty acids (FFAs), leptin, adiponectin, resistin, TNFα, and IL-6 were measured in each case and in 8 healthy women; Case 1 was also assessed after initiating pioglitazone. Coding regions and splice junctions of PPARG, LMNA, and AKT2 were sequenced in Case 1 and of PPARG in Case 2 to evaluate for familial partial lipodystrophies. Genotyping of APOE was performed in Case 1 to rule out type III hyperlipoproteinemia. Results Both cases had elevated plasma levels of insulin, leptin, resistin, and IL-6, high-normal to elevated TNFα, and low to low-normal adiponectin in keeping with post-receptor insulin resistance and adipose tissue inflammation. Case 1 experienced a biochemical response to pioglitazone. No causative mutations for partial lipodystrophies or type III hyperlipoproteinemia were identified. Conclusion Though metabolic derangements have previously been reported in association with TBI, few cases have described insulin resistance and hypertriglyceridemia as severe as that seen in our patients. We speculate that early childhood TBI may impede adipose tissue development leading to metabolic complications from an attenuated ability of adipose tissue to accommodate caloric excess, and propose that this extreme metabolic syndrome be evaluated for as a late complication of TBI.

Silent, or clinically nonfunctioning, pituitary adenomas can arise from any anterior pituitary cell type. Some are "clinically silent" in that they result in a supranormal serum concentration of the hormonal product of the cell type from which the adenoma arose but do not cause the clinical manifestations typical of excessive levels of that hormone. Others are "totally silent" in that they result in neither hormonal excess nor clinical manifestations. Gonadotroph and null cell adenomas are the most prevalent types and are typically silent. Somatotroph and corticotroph adenomas typically cause clinical syndromes but occasionally are clinically or totally silent. Those that are silent are usually larger and grow more aggressively than those that cause clinical syndromes. Silent adenomas are usually not discovered until they become very large and cause neurologic defects, such as visual impairment, but are also often discovered incidentally when neuroimaging is performed for another reason. Silent adenomas may become, rarely, clinically apparent over time. The diagnosis of a silent pituitary adenoma begins with the detection of a sellar mass by MRI. Biochemical testing can identify the adenoma cell type in those that are clinically silent. Silent adenomas that cause neurologic deficits require transsphenoidal surgery, but those that do not can be followed by MRI. Residual or recurrent disease is treated by radiation therapy, which is usually effective in preventing further growth but results in hormonal deficiencies in about half of patients. Dopamine agonists and somatostatin analogs are usually ineffective, but occasionally have been associated with reduced adenoma size.