Normocalcemic hyperparathyroidism: Intervention to differentiate primary from secondary hyperparathyroidism.

BACKGROUND: Normocalcemic hyperparathyroidism can occur, but surgery should not be considered until common etiologies for secondary hyperparathyroidism are comprehensively excluded. Calcium deficiency is an underrecognized cause of normocalcemic parathyroid hormone elevation, and we aim to determine if the implementation of a preoperative calcium challenge can be used to reduce unnecessary parathyroidectomy. METHODS: Consecutive patients referred for parathyroidectomy (1/21-6/22) with normocalcemia (serum calcium <10 mg/dL) and concurrently elevated parathyroid hormone levels were routinely treated with supplemental calcium and vitamin D3, and follow-up laboratory studies were assessed. RESULTS: A total of 29/314 (9%) patients had normocalcemic parathyroid hormone elevation with mean calcium, parathyroid hormone, and vitamin D 25OH levels of 9.5 ± 0.3 mg/dL, 109.9 ± 34.9 pg/mL, and 42.7 ± 23.8 ng/mL respectively. Confounding factors included estimated glomerular filtration rate <60 in 2, loop diuretic use in 4, and prior gastric bypass or gastric sleeve surgery in 4. Follow-up biochemical evaluation was available in 27 (92%); results were unchanged in 7 patients (26%); normalization of parathyroid hormone levels with persistently normal calcium levels occurred in 15 (55%), thus confirming secondary hyperparathyroidism and hypercalcemia with elevated parathyroid hormone levels (classic primary hyperparathyroidism) was diagnosed in 5 (19%). Parathyroid exploration has been completed for 3 of 5 patients with classic primary hyperparathyroidism to date. CONCLUSION: A preoperative calcium challenge was prospectively initiated in normocalcemic patients with parathyroid hormone elevation, and there was high compliance (92%). Short-interval calcium supplementation revealed ∼50% to have resolved secondary hyperparathyroidism due to insufficient calcium intake, which avoided unnecessary surgery. In contrast, classic patients were unveiled in 20%, allowing for prompt and correct surgical intervention.

An Unusual Case of Hashimoto's Thyroiditis Presenting as Impending Cardiac Tamponade in a Patient with Acquired Immune Deficiency Syndrome (AIDS).

BACKGROUND Cardiac tamponade is a life-threatening pericardial compressive disorder that is a common downstream manifestation of infections, malignancy, and metabolic disorders. Hypothyroidism is a rare cause of tamponade that is attributed to the slow accumulation of effusive fluid into the intrapericardial space. In individuals living with HIV/AIDS, tamponade is commonly associated with infection or malignancy. To our knowledge, this is the first reported case of a patient with HIV/AIDS to have been identified with tamponade secondary to hypothyroidism. CASE REPORT Herein, we describe the case of a 52-year-old male patient with a history of AIDS, who presented with nausea, vomiting, diarrhea, and episodic gastrointestinal discomfort for the past several weeks, in conjunction with progressive fatigue. At initial presentation, he had no hemodynamic or clinical signs of tamponade, but pericardial effusion was incidentally found on imaging. Further investigations revealed an undiagnosed Hashimoto's thyroiditis as a function of restored immunocompetency, which ultimately led to the impending tamponade in this patient. We describe his clinical course through diagnosis of autoimmune hypothyroidism, review cardiac tamponade and hypothyroidism in the context of people living with HIV/AIDS, and discuss this rare manifestation of restored immunocompetency. CONCLUSIONS Hypothyroidism should be ruled out in all patients presenting with pericardial effusions or cardiac tamponade, even in people living with HIV/AIDS or those with a history of immune deficiencies.

ACTH Infusion Impairs Baroreflex Sensitivity-Implications for Cardiovascular Hypoglycemia-Associated Autonomic Failure.

CONTEXT: Hypoglycemia attenuates cardiovascular homeostatic autonomic control. This attenuation, known as the cardiovascular component of hypoglycemia-associated autonomic failure (HAAF), is characterized most notably by decreased baroreflex sensitivity (BRS) that begins during hypoglycemia and persists until at least the next day, despite return to euglycemia. Understanding the mechanisms underlying this reduction in BRS is important because BRS attenuation is associated with increased morbidity and mortality. OBJECTIVE: The objective of this work is to investigate the role of the adrenocorticotropin (ACTH)-adrenal axis in decreasing BRS. We tested the hypothesis that infusion of ACTH 1-24 (cosyntropin), as compared to placebo, would acutely suppress BRS, and that this decrease in BRS would be present the next day. DESIGN: A double-blind, placebo-controlled, random-order, cross-over study was conducted. SETTING: This study took place in a clinical research center. PARTICIPANTS: Participants included healthy men and women. INTERVENTIONS: Interventions included an intravenous infusion of cosyntropin (70 µg/hour for 2.5 hours in the morning and again in the early afternoon) vs normal saline placebo. MAIN OUTCOME MEASURES: Outcome measures included BRS during and 16 hours after cosyntropin vs placebo infusions. RESULTS: Cosyntropin infusion attenuated BRS (mm Hg/ms) as compared to placebo (baseline 17.8 ±â€…1.38 vs 17.0 ±â€…2.07; during 14.4 ±â€…1.43 vs 17.3 ±â€…1.65; and next day 14.8 ±â€…1.42 vs 18.9 ±â€…2.04; P < .05, time by treatment, analysis of variance). BRS was decreased during the final 30 minutes of the morning cosyntropin infusion as compared to baseline (P < .01) and remained suppressed the next day (16 hours after afternoon infusion) (P < .025). Placebo infusion did not significantly change BRS. Corrected QT interval was not affected. CONCLUSIONS: ACTH attenuates BRS, raising the possibility that hypoglycemia-induced increases in ACTH may contribute to the cardiovascular component of HAAF.

Mechanical characterization of collagen-glycosaminoglycan scaffolds.

Tissue engineering scaffolds are used extensively as three-dimensional analogs of the extracellular matrix (ECM). However, less attention has been paid to characterizing the scaffold microstructure and mechanical properties than to the processing and bioactivity of scaffolds. Collagen-glycosaminoglycan (CG) scaffolds have long been utilized as ECM analogs for the regeneration of skin and are currently being considered for the regeneration of nerve and conjunctiva. Recently a series of CG scaffolds with a uniform pore microstructure has been developed with a range of sizes of equiaxed pores. Experimental characterization and theoretical modeling techniques have previously been used to describe the pore microstructure, specific surface area, cell attachment and permeability of these variants. The results of tensile and compressive tests on these CG scaffolds and of bending tests on the individual struts that define the scaffold network are reported here. The CG scaffold variants exhibited stress-strain behavior characteristic of low-density, open-cell foams with distinct linear elastic, collapse plateau and densification regimes. Scaffolds with equiaxed pores were found to be mechanically isotropic. The independent effects of hydration level, pore size, crosslink density and relative density on the mechanical properties was determined. Independent control over scaffold stiffness and pore size was obtained. Good agreement was observed between experimental results of scaffold mechanical characterization and low-density, open-cell foam model predictions for uniform scaffolds. The characterized scaffold variants provide a standardized framework with defined extracellular environments (microstructure, mechanics) for in vitro studies of the mechanical interactions between cells and scaffolds as well as in vivo tissue engineering studies.