Standardizing Quality of Virtual Urgent Care: Using Standardized Patients in a Unique Experiential Onboarding Program.

Introduction: Virtual urgent care (VUC) provides real-time evaluation, triage, and treatment of low-acuity medical problems; however, VUC physicians have varying levels of telemedicine training. We created a workplace-based experiential onboarding program that deployed standardized patients (SPs) into a VUC clinic to evaluate and deliver feedback to independently practicing physicians, providing quality assurance and identifying areas for improvement. Methods: We simulated evaluation of an adult with upper respiratory symptoms. To replicate a real-life encounter, we developed a mock electronic medical entry with demographic and medical information and scheduled SPs into the clinic's actual patient queue. SPs provided seamless, realistic training within the real-world virtual clinic environment. Using an adapted assessment tool anchored to not done, partly done, or well done, SPs evaluated communication, disease-specific, and telemedicine skills by observing behaviors. We surveyed participants to evaluate the program. Results: Twenty-one physicians participated. All performed well in core communication and disease management domains. Ninety-three percent of behaviors (SD = 11%) were rated well done within the information gathering domain, 90% (SD = 8%) within relationship development, and 95% (SD = 5%) within disease management. Physicians struggled with telemedicine-specific skills-55% (SD = 38%) well done-and education and counseling-32% (SD = 34%) well done-highlighting specific behaviors most ripe for improvement. All queried participants indicated that this simulation improved communication and telemedicine skills. Discussion: This workplace-based experiential onboarding program uncovered knowledge gaps within telemedicine skills and patient education domains. Identification of these gaps can help drive new virtual care curricula.

Insulin-like growth factor-I inhibition with pasireotide decreases cell proliferation and increases apoptosis in pre-malignant lesions of the breast: a phase 1 proof of principle trial.

INTRODUCTION: Estrogen inhibition is effective in preventing breast cancer in only up to 50% of women with precancerous lesions and many experience side effects that are poorly tolerated. As insulin-like growth factor I (IGF-I) underlies both estrogen and progesterone actions and has other direct effects on mammary development and carcinogenesis, we hypothesized that IGF-I inhibition might provide a novel approach for breast cancer chemoprevention. METHODS: In total, 13 women with core breast biopsies diagnostic of atypical hyperplasia (AH) were treated for 10 days with pasireotide, a somatostatin analog which uniquely inhibits IGF-I action in the mammary gland. They then had excision biopsies. 12 patients also had proliferative lesions and one a ductal carcinoma in situ (DCIS). Primary outcomes were changes in cell proliferation and apoptosis after treatment. Expression of estrogen receptor (ER), progesterone receptor (PR), and phosphorylated Insulin-like growth factor I receptor (IGF-1R), protein kinase B (AKT) and extracellular signal-regulated kinases 1/2 (ERK1/2) were also assessed. Core and excision biopsies from 14 untreated patients served as non-blinded controls. Hyperglycemia and other side effects were carefully monitored. RESULTS: Pasireotide decreased proliferation and increased apoptosis in all AH (from 3.6 ± 2.6% to 1.3 ± 1.2% and from 0.3 ± 0.2% to 1.5 ± 1.6%, respectively) and proliferative lesions (from 3.8 ± 2.5% to 1.8 ± 1.8% and from 0.3 ± 0.2% to 1.3 ± 0.6%, respectively). The DCIS responded similarly. ER and PR were not affected by pasireotide, while IGF-1R, ERK1/2 and AKT phosphorylation decreased significantly. In contrast, tissue from untreated controls showed no change in cell proliferation or phosphorylation of IGF-1R, AKT or ERK 1/2. Mild to moderate hyperglycemia associated with reduced insulin levels was found. Glucose fell into the normal range after discontinuing treatment. Pasireotide was well tolerated and did not cause symptoms of estrogen deprivation. CONCLUSIONS: IGF-I inhibition by pasireotide, acting through the IGF-1R, was associated with decreased proliferation and increased apoptosis in pre-malignant breast lesions and one DCIS. Assuming hyperglycemia can be controlled, these data suggest that inhibiting the IGF-I pathway may prove an effective alternative for breast cancer chemoprevention. TRIAL REGISTRATION: NCT01372644 Trial date: July 1, 2007.