OBJECTIVE Continuous glucose monitoring (CGM) use is associated with improved outcomes in type 1 diabetes, but racial-ethnic disparities exist in use. We were interested in examining whether addressing structural healthcare barriers would change provider prescribing behaviors to make CGM access more equitable. Continued focus is needed on upstream interventions that affect downstream determinants of CGM use. RESEARCH DESIGN AND METHODS From January 2019 to December 2021, we initiated several non-grant-funded practice transformations targeted toward equity, including developing a type 1 diabetes clinic, conducting social needs assessment and management, training support staff to place trial CGMs at the point of care, optimizing prescription workflows, and educating providers on CGM. We included multilevel stakeholders in development of transformations to improve feasibility, acceptability, and sustainability. To examine effect, we collected monthly aggregate data from the electronic medical record and performed multiple linear regression to examine change in CGM prescriptions over the 3 years of transformation. RESULTS In total, we included our four diabetes practice sites of approximately 25 endocrinologists and 1,357 adults with type 1 diabetes (mean ± SD age 38 ± 18 years; 30% Black [n = 406], 45% Hispanic [n = 612], 12% White [n = 164]; and 74% publicly insured [n = 1,004]). CGM prescription rates increased overall from 15% to 69% (P < 0.001). Improvements were seen equally among Black (12% to 72%), Hispanic (15% to 74%), and White adults (20% to 48%) (between-group P = 0.053). CONCLUSIONS Diabetes practice transformations can have powerful effects on provider prescribing behaviors to reduce root causes of inequity in CGM among underserved adults with type 1 diabetes. Our efforts at including multilevel stakeholder input provide an example of how to improve the likelihood of success and sustainability of health care delivery changes.
Clinically silent double pituitary adenomas consisting of corticotroph and somatotroph cells are an exceedingly rare clinical finding. In this report, we present the case of a 28-year-old man with a 1-year history of recurrent headaches. Imaging revealed a 2.1 (anterior-posterior) × 2.2 (transverse) × 1.3 (craniocaudal) cm pituitary adenoma invading into the left cavernous sinus and encasing the left internal carotid artery. Endoscopic transnasal resection was performed without complications. Immunohistochemical staining revealed a double adenoma consisting of distinct sparsely granulated somatotroph and densely granulated corticotroph cells that were positive for growth hormone and adrenocorticotropic hormone, respectively. Ki-67 index labeling revealed a level of 6% within the corticotroph adenoma. No increase in serum growth hormone or adrenocorticotropic hormone was found, indicating a clinically silent double adenoma. While transsphenoidal surgery remains a first-line approach for silent adenomas presenting with mass effects, increased rates of proliferative markers, such as the Ki-67 index, provide useful insight into the clinical course of such tumors. Determining the Ki-67 index of silent pituitary adenomas could be valuable in predicting recurrence after initial surgical resection and identifying tumors that are at an increased risk of needing additional therapeutic interventions or more frequent surveillance imaging.
Background: The most common cause of primary hyperparathyroidism (PHPT) is overproduction of PTH by a parathyroid gland adenoma. While definitive therapy is parathyroidectomy, 4% of patients develop persistent PHPT - a sustained hypercalcemic state that is detected within six months of parathyroidectomy. A missed parathyroid adenoma is the most common cause of persistent PHPT, and accurately locating these glands presents a diagnostic challenge. We describe a rare case of persistent PHPT due to a missed mediastinal parathyroid adenoma. Case: A 54-year-old woman with a history of PHPT presented with abdominal pain, nausea, and decreased oral intake. She underwent parathyroidectomy six months ago with reimplantation of one parathyroid gland into the right sternocleidomastoid muscle (SCM). She was now hypercalcemic to 13.9 mg/dL (8.5–10.5) with intact PTH 1273 pg/mL (15.0–65.0), vitamin D 25-OH 31.4 ng/mL (>30.0), and normal PTHrP. She was not taking calcium, and other causes of hyperparathyroidism were excluded. Sestamibi scintigraphy localized only to the right SCM, and the initial impression was recurrent HPT due to the previously implanted gland. Follow-up CT neck with and without contrast failed to localize any regrowth in the SCM, but did reveal a 1.4 cm mediastinal soft tissue mass, suspicious for an ectopic parathyroid adenoma. She subsequently underwent video-assisted thoracoscopic excision, and pathology was consistent with ectopic hypercellular parathyroid tissue. Post-operatively, her PTH down-trended and calcium normalized. Conclusion: This case describes a small yet biochemically aggressive mediastinal adenoma causing persistent PHPT. While sestamibi scans have ~90% sensitivity for localization of ectopic adenomas, they can fail to identify a small culprit lesion in 12% of patients, whereas CT imaging with and without contrast has increased sensitivity for adenomas <2 cm. Thus, diagnosing persistent PHPT requires sestamibi scan in combination with other imaging modalities for accurate diagnosis of missed adenomas.
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