To report ten-year experience with a parathyroid hormone (PTH)-guided Calcium (Ca) and calcitriol supplementation protocol in reducing the incidence of hypocalcemia after total thyroidectomy (TT). Single-institution, retrospective chart review of patients who underwent TT. One hundred forty-eight patients had an operation prior to the protocol introduction and 735 had surgery after the protocol was started. Total serum Ca < 8 mg/dL was defined as hypocalcemia. The 4h-PTH stratified patients into low (>30 pg/mL), intermediate (15-30 pg/mL), and high (<15 pg/mL) hypocalcemia risk groups, to guide Ca and calcitriol management. Demographic information, pre- and post-operative characteristics, and outcomes were recorded. Fisher's exact test and Wilcoxon rank sum test were used to compare the characteristics between the 2 groups. Multivariable logistic regression was used to account for confounding variables. Area under the ROC curve was used to determine optimal 4h-PTH value as predictor of hypocalcemia. The post-protocol group had significantly lower hypocalcemia incidence (9.9% vs. 20.9%, p<0.001) and related readmissions (0.9% vs. 4.7%, p=0.004) than the pre-protocol group. Lymph node dissection and parathyroids embedded in thyroid tissue were significant risk factors for hypocalcemia. Hypocalcemia occurred in 24.3% of patients with PTH 30pg/mL. Lymph node dissection and parathyroids embedded in thyroid tissue were significant risk factors. . A PTH-guided Ca and calcitriol supplementation protocol significantly reduces post-TT hypocalcemia and related readmissions and may represent a useful approach in managing suitable candidates for outpatient TT.

Introduction: BRAFV600E mutation (BRAF^mut) is common in papillary thyroid cancer (PTC), and most patients have an excellent outcome. However, a TERT-promoter mutation (pTERT^mut) in the presence of BRAF^mut (BRAF^mutpTERT^mut) has been demonstrated to confer a more aggressive behavior to PTC. Lymphocytic infiltration is often present in PTC. In this study, we sought to decipher the relationship between the BRAF and pTERT mutations and immune gene dysregulation in tumor samples from a cohort of 147 samples of PTC.Methods: The abundance of 770 immune gene transcripts was determined by multiprex capture/detection and digital counting of mRNA transcripts using the NanoString nCounter^® PanCancer Immune Profiling Panel.Results: We identified 40 immune transcripts differentially expressed in BRAF^mutpTERT^mutvs BRAF^mutpTERT wildtype (pTERT^wt) (P<0.05). Transcripts induced by BRAF^mut alone were significantly repressed in BRAF^mutpTERT^mut samples, such as genes expressed by lymphoid cells, antigen-presenting cells, and cytotoxic cells, including chemokines, cytokines, checkpoint control proteins, interferon downstream markers, TNF superfamily proteins and BMP markers. A validation analysis using 444 samples from The Cancer Genome Atlas (TCGA) PTC dataset yielded similar results. Deconvolution analysis confirmed differences in the immune cell populations such as increased presence of M2 macrophages in the BRAF^mutpTERT^mut Mayo cohort and a lower abundance of M1 macrophages in the BRAF^mutpTERT^mut TCGA cohort compared to BRAF^mutpTERT^wt. Most of the immune gene pathways were enriched in the BRAF^mutpTERT^wt tumors in both Mayo and TCGA cohorts but not in BRAF^mutpTERT^mut. BRAF^mutpTERT^wt had higher stromal lymphocytes infiltration as compared to BRAF^wtpTERT^wt tumors, corroborating the transcriptomic findings.Discussion: To our knowledge this is the first report of a potential link between TERT and the immune microenvironment, offering an explanation for the aggressive nature of BRAF^mutpTERT^mut PTC.

Background/Objectives: Autoimmune inner ear disease (AIED) causes sensorineural hearing loss that classically presents as fluctuating, asymmetric loss of hearing. Associated vestibular and other ear symptoms can be present in many patients. First-line treatment of AIED is high-dose corticosteroids. AIED can present either as a primary condition limited to ear involvement or secondary, as part of an underlying systemic autoimmune rheumatic disease, the most common of which include vasculitis and relapsing polychondritis. We described our cohort of primary AIED, including demographics, treatment, and outcomes. We excluded from this review sensorineural hearing loss in the context of vasculitis and relapsing polychondritis. Methods: We performed a chart review of patients with the diagnosis of AIED at Mayo Clinic and compared the cohort by sex. Results: Thirty-one patients met the inclusion criteria. The mean age was 48.5 years, and 17 were men. Patients were initially evaluated at the Department of Otorhinolaryngology or Internal Medicine, and 29 patients were subsequently referred to the Department of Rheumatology, with a mean of 12.2 weeks after the first evaluation. Treatment with corticosteroids showed improvement in hearing and vestibular symptoms during the first month but no further improvement by the end of the third month. Other immunosuppressive medications were used with various degrees of response. Methotrexate was the second most used therapy, with 11 of 17 patients reporting an improvement in symptoms. Conclusions: Corticosteroid therapy is an effective initial treatment for AIED and should be followed with corticosteroid-sparing agents to prevent further damage to the cochlea.

Amiodarone is known to cause thyroid dysfunction, due to both direct cytotoxicity and high iodine content. Due to its lipophilic properties, amiodarone gets stored in the adipose tissue and may induce delayed amiodarone-induced thyrotoxicosis (AIT), months after discontinuation. We present the case of a 60-year-old man admitted with new-onset atrial fibrillation. He had a history of ventricular tachycardia, treated with amiodarone that was discontinued 14 months earlier. On admission, thyrotropin was undetectable, with markedly elevated free thyroxine and total triiodothyronine. He had no previous history of thyroid dysfunction or recent exposure to iodinated contrast. Additional history revealed that the patient had been taking tirzepatide 10 mg weekly resulting in a 54-kg weight loss over the previous 12 months. With this information, a spot urine iodine/creatinine (Cr) was measured and found to be significantly increased at 2323 µg/g Cr (SI: 2075 µmol/mol Cr) (normal reference range <584 µg/g Cr, [SI: <521 µmol/mol Cr]). He was treated with prednisone and methimazole with eventual resolution of hyperthyroidism. Delayed AIT should be considered in the differential diagnosis of new-onset thyrotoxicosis in patients previously treated with amiodarone who experience significant weight loss.