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Introduction: The Clinical Affairs Committee of the American Thyroid Association has developed this statement to describe recent changes in the billing and coding of ultrasound-guided fine needle aspiration procedures of thyroid nodules, and to raise awareness of the adverse consequences that have arisen as a result. Review: A reduction in payment of ultrasound-guided fine needle aspiration procedures was enacted by the Centers for Medicare and Medicaid Services in 2019. The Clinical Affairs Committee has sought to examine the effects of the change in reimbursement on the care of patients with thyroid diseases. Summary: The historical background of the changes in payment structure for ultrasound-guided fine needle aspiration of thyroid nodules is discussed. The years 2019 and 2020 saw a significant decline in claims for ultrasound-guided fine needle aspiration procedures, concomitant with a shift in the performance of these procedures away from non-facility outpatient settings and a rise in costs to the health care system. Conclusion: Several negative consequences of the decrease in reimbursement for ultrasound-guided fine needle aspiration of thyroid nodules have arisen. This has led to significant concern among clinicians who care for patients with thyroid diseases regarding delays in patient access to care and diagnosis, and a diminished pool of qualified thyroid specialists to perform these procedures in the future. [ABSTRACT FROM AUTHOR]

We report that two widely-used drugs for erectile dysfunction, tadalafil and vardenafil, trigger bone gain in mice through a combination of anabolic and antiresorptive actions on the skeleton. Both drugs were found to enhance osteoblastic bone formation in vivo using a unique gene footprint and to inhibit osteoclast formation. The target enzyme, phosphodiesterase 5A (PDE5A), was found to be expressed in mouse and human bone as well as in specific brain regions, namely the locus coeruleus, raphe pallidus, and paraventricular nucleus of the hypothalamus. Localization of PDE5A in sympathetic neurons was confirmed by coimmunolabeling with dopamine β-hydroxylase, as well as by retrograde bone-brain tracing using a sympathetic nerve-specific pseudorabies virus, PRV152. Both drugs elicited an antianabolic sympathetic imprint in osteoblasts, but with net bone gain. Unlike in humans, in whom vardenafil is more potent than tadalafil, the relative potencies were reversed with respect to their osteoprotective actions in mice. Structural modeling revealed a higher binding energy of tadalafil to mouse PDE5A compared with vardenafil, due to steric clashes of vardenafil with a single methionine residue at position 806 in mouse PDE5A. Collectively, our findings suggest that a balance between peripheral and central actions of PDE5A inhibitors on bone formation together with their antiresorptive actions specify the osteoprotective action of PDE5A blockade. [ABSTRACT FROM AUTHOR]

The primitive neurohypophyseal nonapeptide oxytocin (OXT) has established functions in parturition, lactation, appetite, and social behavior. We have shown that OXT has direct actions on the mammalian skeleton, stimulating bone formation by osteoblasts and modulating the genesis and function of bone-resorbing osteoclasts. We deleted OXT receptors (OXTRs) selectively in osteoblasts and osteoclasts using Col2.3Cre and Acp5Cremice, respectively. Both male and female Col2.3Cre+:Oxtrfl/fl mice recapitulate the low-bone mass phenotype of Oxtr+/- mice, suggesting that OXT has a prominent osteoblastic action in vivo. Furthermore, abolishment of the anabolic effect of estrogen in Col2.3Cre+:Oxtrfl/fl mice suggests that osteoblastic OXTRs are necessary for estrogen action. In addition, the high bone mass in Acp5Cre+:Oxtrfl/fl mice indicates a prominent action of OXT in stimulating osteoclastogenesis. In contrast, we found that in pregnant and lactating Col2.3Cre+:Oxtrfl/fl mice, elevated OXT inhibits bone resorption and rescues the bone loss otherwise noted during pregnancy and lactation. However, OXT does not contribute to ovariectomy-induced bone loss. Finally, we show that OXT acts directly on OXTRs on adipocytes to suppress the whiteto- beige transition gene program. Despite this direct antibeiging action, injected OXT reduces total body fat, likely through an action on OXT-ergic neurons. Consistent with an antiobesity action of OXT, Oxt-/- and Oxtr-/- mice display increased total body fat. Overall, the actions of OXT on bone mass and body composition provide the framework for future therapies for osteoporosis and obesity. [ABSTRACT FROM AUTHOR]