ECTOPIC THYROID TISSUE MASQUERADING AS A FUNCTIONAL CAROTID BODY PARAGANGLIOMA.

OBJECTIVE: Ectopic thyroid tissue (ETT) is a rare entity resulting from thyroid gland dysembryogenesis. We present a case of ETT confirmed by histopathology that was misdiagnosed clinically as a carotid body tumor. METHODS: A 34-year-old female with a history of thyroidectomy for a goiter presented with 1 year of worsening tachycardia (heart rate ranging from 82 to 111 beats per minute), anxiety, hot flashes, and intolerance to heat. For further evaluation, we obtained imaging of her neck, including a thyroid ultrasound, a computed tomography (CT) scan, and an octreotide scan. We also performed laboratory studies including fractionated 24-hour urine meta-nephrines and thyroid function tests. RESULTS: Her thyroid ultrasound showed a mass at the right carotid bifurcation, which was confirmed on CT as well as on an octreotide scan. Her free thyroxine was 0.6 ng/dL (normal, 0.7 to 1.5 ng/dL) and her thyroid-stimulating hormone was 4.51 mIU/L (normal, 0.45 to 4.5 mIU/L). Her fractionated 24-hour total urine metanephrines were 1,502 mcg/24-hour (normal, 149 to 535 mcg/24-hour). She underwent resection of a vascular mass from the carotid bifurcation. Histologic examination revealed ETT with dilated follicles filled with colloid with no evidence of paraganglioma/carotid body tumor. CONCLUSION: The somatostatin receptor is typically present in paragangliomas; however, there are reports of octreotide uptake within thyroid goiters. It has been demonstrated that psychoactive medications can increase urine metanephrines. Given the patient's psychiatric history and that no other tumors were identified on imaging, it was felt that the elevated urine normetanephrine in this case was most likely due to psychoactive medication use. This case demonstrates the preoperative imaging findings and postoperative pathologic confirmation of an unusual presentation of ETT.

The Use of a Smart Bolus Calculator Informed by Real-time Insulin Sensitivity Assessments Reduces Postprandial Hypoglycemia Following an Aerobic Exercise Session in Individuals With Type 1 Diabetes.

OBJECTIVE: Insulin dosing in type 1 diabetes (T1D) is oftentimes complicated by fluctuating insulin requirements driven by metabolic and psychobehavioral factors impacting individuals' insulin sensitivity (IS). In this context, smart bolus calculators that automatically tailor prandial insulin dosing to the metabolic state of a person can improve glucose management in T1D. RESEARCH DESIGN AND METHODS: Fifteen adults with T1D using continuous glucose monitors (CGMs) and insulin pumps completed two 24-h admissions in a hotel setting. During the admissions, participants engaged in an early afternoon 45-min aerobic exercise session, after which they received a standardized dinner meal. The dinner bolus was computed using a standard bolus calculator or smart bolus calculator informed by real-time IS estimates. Glucose control was assessed in the 4 h following dinner using CGMs and was compared between the two admissions. RESULTS: The IS-informed bolus calculator allowed for a reduction in postprandial hypoglycemia as quantified by the low blood glucose index (2.02 vs. 3.31, P = 0.006) and percent time <70 mg/dL (8.48% vs. 15.18%, P = 0.049), without increasing hyperglycemia (high blood glucose index: 3.13 vs. 2.09, P = 0.075; percent time >180 mg/dL: 13.24% vs. 10.42%, P = 0.5; percent time >250 mg/dL: 2.08% vs. 1.19%, P = 0.317). In addition, the number of hypoglycemia rescue treatments was reduced from 12 to 7 with the use of the system. CONCLUSIONS: The study shows that the proposed IS-informed bolus calculator is safe and feasible in adults with T1D, appropriately reducing postprandial hypoglycemia following an exercise-induced IS increase.

Recent Exposure to Hypoglycemia Increases Glucose Variability Following a Hyper/Hypoglycemic Metabolic Challenge in T1D.

AIMS: In type 1 diabetes (T1D), repeated hypoglycemic episodes may reduce hormonal defenses and increase the risk for severe hypoglycemia. In this work, we investigate the effect of a structured hyper/hypoglycemic metabolic challenge on the postintervention glucose variability in T1D subjects studied at home. METHODS: Thirty T1D subjects using insulin pump were monitored with blood glucose meters (SMBG) during a 1-month observation period. After 2 weeks of monitoring, participants were admitted at the University of Virginia Clinical Research Unit to undergo an 8-hour metabolic challenge. The intervention was designed to create hyperglycemia shortly followed by hypoglycemia, mimicking a real-life scenario of underbolused meal followed by overcorrection. After the intervention, subjects were monitored for 2 more weeks. Glycemic variability was assessed before and after the challenge using the low blood glucose index (LBGI). Glucagon counterregulation (GCR) response to induced hypoglycemia was also measured. LBGI variation and GCR were linked to prior exposure to hypoglycemia. RESULTS: Subjects significantly exposed to hypoglycemia in the 2 weeks before the intervention had a significant increase of postchallenge LBGI ( P < .001) and lower GCR response ( P < .05). Recent occurrence of hypoglycemia and number of years not using an insulin pump were identified as significant predictors of postchallenge LBGI ( P < .001). CONCLUSION: Glycemic swings, a common result of suboptimal insulin treatment, have a significant impact on future (days) glycemic control in T1D subjects with a recent history of hypoglycemia, as measured in the field. Choice of past insulin therapy may also mediate this effect.

Decrease of Serum IGF-I following Transsphenoidal Pituitary Surgery for Acromegaly.

BACKGROUND: In the immediate postoperative period following resection of growth hormone (GH)-secreting pituitary tumors, serum concentrations of GH have limited ability to predict remission of acromegaly. Since many actions of GH actions are mediated by insulin-like growth factor-1 (IGF-I), we aimed to determine the rates of fall of IGF-I during 72 h after surgical resection of pituitary tumors. METHODS: We studied patients who were undergoing pituitary surgery for acromegaly. IGF-I was measured by LC-MS and GH by immunoassay. Remission was defined by the combination of serum GH <0.4 ng/mL during oral glucose tolerance testing performed 8 weeks after the surgical procedure and normal IGF-I at ≥8 weeks. RESULTS: During the first 72 h after surgery, the mean (SD) rate of decline of IGF-I was 185 (61) ng/mL per 24 h in those who achieved remission (n = 23), with a mean (SD) apparent half-life of 55 (19) h. IGF-I had decreased to <65% of the preoperative IGF-I on postoperative day 2 in 20 of 23 remission patients (87%) vs none of 5 patients who did not achieve remission. GH was <2.7 ng/mL on day 2 in 21 of 23 remission patients (91%), but in none of the nonremission patients. The combination of IGF-I and GH on day 2 separated the remission and nonremission groups of patients. CONCLUSIONS: Rapid decline of serum IGF-I during the immediate postoperative period warrants further study as an analytically independent adjunct to GH measurement for early prediction of biochemical remission of acromegaly.

Intrarenal ghrelin infusion stimulates distal nephron-dependent sodium reabsorption in normal rats.

Ghrelin is a 28-amino acid peptide hormone that exerts powerful orexigenic effects. Ghrelin receptor expression has been reported in the kidney, but the role of ghrelin in the kidney is unknown. The present studies confirmed ghrelin receptor mRNA expression in the kidneys of normal Sprague Dawley rats (n=6) using reverse transcription polymerase chain reaction (PCR) and sequencing of the 588-bp PCR product. To test intrarenal ghrelin action, uninephrectomized rats received 3 cumulative 1-hour renal interstitial (RI) infusions of 5% dextrose in water (vehicle, n=21), ghrelin (n=10), ghrelin plus specific ghrelin receptor antagonist [D-Lys-3]-GHRP-6 (n=24), or [D-Lys-3]-GHRP-6 alone (n=32). Mean arterial pressure (MAP), urine sodium excretion rate (U(Na)V), glomerular filtration rate (GFR), fractional excretion of sodium (FE(Na)), and fractional excretion of lithium (FE(Li)) were calculated for each period. RI ghrelin infusion significantly decreased U(Na)V to 86 ± 4.9% (P<0.05), 74 ± 6.5% (P<0.01), and 62 ± 10% (P<0.01) of baseline during periods 1 to 3, respectively. Ghrelin also significantly decreased FE(Na) to 68 ± 11% (P<0.05), 57 ± 8.6% (P<0.001), and 59 ± 12% (P<0.01) of baseline, without changing GFR or FE(Li). Identical ghrelin infusions in the presence of [D-Lys-3]-GHRP-6 failed to permit reductions in U(Na)V or FE(Na). Following [D-Lys-3]-GHRP-6 infusion alone, U(Na)V increased from 0.06 ± 0.01 to 0.18 ± 0.03 µmol/min (P<0.0001). Concomitant increases in FE(Na) were also observed (0.23 ± 0.03% to 0.51 ± 0.06% [P<0.001]), without changes in MAP, GFR, or FE(Li). Together, these data introduce a novel intrarenal ghrelin-ghrelin receptor system, which, on activation, significantly increases Na(+) reabsorption at the level of the distal nephron.