Undescended parathyroid adenoma.

Undescended parathyroid adenomas are rare, representing 0.08% of all parathyroid adenomas; however, they make up 7% of the underlying cause of failed cervical exploration in patients with persistent primary hyperparathyroidism. A 43-year-old woman with no significant medical or family history presented with fatigue and was diagnosed with primary hyperparathyroidism; however, preoperative imaging including sestamibi scan and ultrasound was unable to identify the hyperfunctioning gland. She underwent a neck exploration and hemithyroidectomy and partial parathyroidectomy with failure of resolution of her disease. Subsequent work up including a CT of the neck demonstrated a 1.9 cm mass adjacent to the left submandibular gland. This was removed with postoperative normalisation of the patient's serum calcium and parathyroid hormone levels.

Analysis of age and disease status as predictors of thyroid cancer-specific mortality using the Surveillance, Epidemiology, and End Results database.

BACKGROUND: Age at diagnosis is incorporated into all relevant staging systems for differentiated thyroid carcinoma (DTC). There is growing evidence that a specific age cutoff may not be ideal for accurate risk stratification. We sought to evaluate the interplay between age and oncologic variables in patients with DTC using the largest cohort to date. METHODS: The Surveillance, Epidemiology, and End RESULTS (SEER) database was queried to identify patients with DTC as their only malignancy for the period 1973 to 2009. Multivariate analyses using a range of age cutoffs and age subgroupings were utilized in order to search for an optimal age that would provide the most significant risk stratification between young and old patients. The primary outcome was disease-specific survival (DSS) and covariates included: age, race, sex, tumor/nodal/metastasis (TNM) stage, decade of diagnosis, and radioactive iodine therapy. RESULTS: A total of 85,740 patients were identified. Seventy-six percent of patients were American Joint Committee on Cancer (AJCC) stage I, 8% were stage II, 7% were stage III, and 8% were stage IV. Age over 45 years (hazard ratio [HR] 19.2, p<0.001) and metastatic disease (HR 13.1, p<0.001) were the strongest predictors of DSS. Other factors that significantly predicted DSS included: not receiving radioactive iodine (RAI; HR 1.3, p=0.002), T3 (HR 2.6, p<0.001), and T4 disease (HR 3.3, p<0.001), and nodal spread (HR 2.6 to 3.3, p<0.001). Female sex showed a significant protective effect (HR 0.7, p=0.001). Adjusting the age-group cutoff from 25 to 55 years showed consistently high HRs for advanced age, without a distinct change at any point. Comparing HRs for T, N, and M stage between young and old patient subgroups showed that advanced disease increased the risk for DSS regardless of age, and was oftentimes a worse prognosticator in young patient groups. CONCLUSIONS: The contribution of age at diagnosis to a patient's DSS is considerable, but there is no age cutoff that affords any unique risk-stratification in patients with DTC.

Using a triggered endocrinology service consultation to improve the evaluation, management, and follow-up of osteoporosis in hip-fracture patients.

BACKGROUND: Nearly 2 million osteoporosis-related fractures occur yearly in the United States, with more than 400,000 requiring hospital admissions. Fewer than 30% receive proper evaluation and care for osteoporosis, representing a large opportunity to enhance secondary prevention of fractures. Methods to improve identification and triage of hospitalized fragility-fracture patients are desirable. METHODS: A multidisciplinary team was created, and definitions were established for an evidence-based best-practice protocol to assess, treat, and document an osteoporosis diagnosis and triage patients with hip-fragility fractures on the basis of the best-practice recommendations from The Joint Commission and the National Osteoporosis Foundation. The team initiated a preauthorized osteoporosis consultation from the endocrinology service for hip-fracture patients, "triggered" via a brief query in admission orders or by the orthopedic service nurse practitioner. Osteoporosis consultations used a consultation template reflecting the protocol. RESULTS: Data were analyzed for 71 baseline patients and 61 intervention patients. The groups possessed similar age, gender, race, and body mass index characteristics. The baseline (on-demand consultation) group suffered from poor performance, with only 3%-21% of patients receiving the desired evaluation, documentation, treatment, or outpatient follow-up. Intervention (triggered-consultation) patients improved markedly postintervention, With performance increasing by 52%-76% on all parameters except outpatient follow-up, which changed insignificantly (6%-15%). CONCLUSION: Although triggered consultation was effective, multimodal layered interventions may achieve even better results and address several identified barriers.

Response of adiponectin and its receptors to changes in metabolic state after gastric bypass surgery: dissociation between adipose tissue expression and circulating levels.

BACKGROUND: Adiponectin is an adipokine with anti-atherogenic and insulin-sensitizing properties. Specific adiponectin receptors, adiponectin receptors 1 (AdipoR1) and 2 (AdipoR2), are present in adipose tissue, indicating adiponectin might have autocrine/paracrine effects on its production or action. In addition, endoplasmic reticulum oxidoreductase 1-Lalpha might mediate regulation of its secretion. The study aim was to determine the subcutaneous adipose tissue (SAT) adiponectin gene and protein expression and their correlation to metabolic parameters during metabolically distinct times after gastric bypass surgery. METHODS: A total of 12 morbidly obese male patients underwent SAT biopsy during gastric bypass surgery, active weight loss (negative energy state), and at weight stabilization (steady state energy). The SAT mRNA and protein content of adiponectin, AdipoR1 and AdipoR2, and endoplasmic reticulum oxidoreductase 1-Lalpha protein levels and the serum levels of adiponectin were assessed. RESULTS: SAT adiponectin, AdipoR1, and AdipoR2 gene expression increased significantly at the negative energy state, with no further change at steady state energy (P<.05, P<.05, and P=.04, respectively), without significant increases in protein at any stage. Changes in SAT adiponectin protein correlated with changes in AdipoR1 and AdipoR2 during steady state energy (P=.003 and P=.002, respectively). Changes in SAT adiponectin expression did not correlate with those in circulating levels. Changes in endoplasmic reticulum oxidoreductase 1-Lalpha did not correlate with either SAT or circulating levels of adiponectin. CONCLUSION: Our data indicate distinct functions of adiponectin receptors, AdipoR1 and AdipoR2, mediate the autocrine/paracrine actions of adiponectin. The lack of correlation between changes in SAT adiponectin gene and protein expression and its circulating levels suggests that adipose tissue synthesis and release of adiponectin are highly regulated pathways.

Adiponectin secretion and response to pioglitazone is depot dependent in cultured human adipose tissue.

The subcutaneous (S) and visceral (V) adipose tissue (AT) depots are increasingly recognized as distinct. To test the hypothesis that depot differences exist for adiponectin, fresh and cultured human VAT and SAT from obese type 2 diabetic (T2D) and obese nondiabetic (ND) subjects was examined to determine whether differences in adiponectin content and secretion occurred as a function of depot studied, diabetic status, and response to thiazolidinedione treatment. VAT and SAT were obtained by biopsy and AT explants cultured in defined media for 7 days. Protein expression was assessed by Western blot. Adiponectin content of conditioned medium was determined by radioimmunoassay. Diabetic status had no effect on adiponectin secretion over days 0-2 of culture. In ND SAT, secretion fell over days 2-4 but was sustained at greater levels vs. T2D SAT. In both ND and T2D VAT, adiponectin secretion was low, similar to T2D SAT. Over the 7-day culture period, cellular adiponectin increased in ND SAT and VAT; it remained unchanged in T2D SAT and VAT. Pioglitazone increased adiponectin secretion and content in all SAT. Pioglitazone failed to increase adiponectin secretion from either ND or T2D VAT and increased cellular content only in ND VAT. AT depot differences exist in the secretion of adiponectin and responsiveness to thiazolidinedione treatment. These data suggest that SAT, not VAT, appears to be the major contributor to increased circulating adiponectin levels in response to pioglitazone treatment.

Adiponectin in health and disease.

Adipose tissue is an active metabolic tissue that secretes multiple metabolically important proteins, known as adipokines. Adiponectin is an important adipokine because of its beneficial effects on glucose and lipid metabolism. Low levels of adiponectin are associated with disease states such as diabetes and cardiovascular disease. Direct administration of adiponectin has been shown to be beneficial in animal models of diabetes, obesity and atherosclerosis. Adiponectin levels in humans can be increased through indirect methods such as weight loss or treatment with thiazolidinediones. This article will review the epidemiology and therapeutic options with adiponectin.

Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue.

Glycogen synthase kinase-3 (GSK-3) is a ubiquitous kinase implicated in both insulin action and adipogenesis. To determine how these multiple roles may relate to insulin resistance, we studied the regulation of GSK-3 protein expression and phosphorylation in skeletal muscle and isolated adipocytes from nonobese healthy control (HC), obese control (OC), and obese type 2 diabetic (OT2D) subjects. At baseline there were no differences in the GSK-3 protein expression in adipocytes. OC subjects underwent a 6-mo caloric restriction resulting in a 7% decrease in body mass index (BMI) and a 21% improvement in insulin-stimulated whole body glucose disposal rate (GDR). GSK-3alpha and GSK-3beta expression decreased in adipocytes (P < 0.05), whereas GSK-3alpha protein expression increased in skeletal muscle (P < 0.05). OT2D subjects were treated with troglitazone or metformin for 3-4 mo. After troglitazone treatment GDR improved (P < 0.05) despite an increase in BMI (P < 0.05), whereas metformin had no significant effect on GDR. There was no significant change in GSK-3 expression in adipocytes following troglitazone, whereas both GSK-3alpha and -beta were decreased in skeletal muscle (P < 0.05). Metformin treatment had no significant impact on GSK-3 protein expression in either adipocytes or skeletal muscle. Neither treatment influenced GSK-3 serine phosphorylation in skeletal muscle or adipocytes. These results suggest that there is tissue specificity for the regulation of GSK-3 in humans. In skeletal muscle GSK-3 plays a role in control of metabolism and insulin action, whereas the function in adipose tissue is less clear.