Cost-effectiveness of telehealth with remote patient monitoring for postpartum hypertension.

OBJECTIVE: Evaluate cost-effectiveness of telehealth with remote monitoring for postpartum hypertensive disorders from the hospital's perspective. METHODS: A decision tree was developed using results from a non-randomized controlled trial comparing telehealth to standard outpatient blood pressure monitoring. At discharge, postpartum women with a hypertensive disorder received a Bluetooth tablet, blood pressure monitor, and scale to submit vitals daily for 6 weeks. Women were managed and treated with a standard protocol. We performed a cost-effectiveness analysis using data from the hospital, device manufacturer supplied charges, and utilities. A cost-effectiveness threshold was set at $100,000/quality-adjusted life years. One-way and two-way sensitivity analyses were performed to evaluate the robustness of our results compared to baseline assumptions. RESULTS: Telehealth monitoring significantly reduced postpartum readmissions, 3.7% (8/214) versus 0.5% (1/214), and resulted in higher quality-adjusted life years. Telehealth monitoring was cost-effective and cost-saving. Average cost of telehealth per patient was $309, and was cost-effective to a cost of $420 per patient. Telehealth monitoring remained cost-effective down to an admission cost of $10,999 compared to our baseline-estimate for the average admission cost of $14,401. Telehealth monitoring also remained cost-effective when the postpartum readmission rate was 3.0% or higher with standard monitoring. With a cost saving of $93 per patient and an estimated 333,253 pregnant women with hypertension in the US a year, telehealth could reduce health care costs in the US by approximately $31 million a year. CONCLUSIONS: This study demonstrates telehealth with remote blood pressure monitoring may be a cost-effective and cost-saving solution for management of postpartum hypertension.

Adding Azithromycin to Cephalosporin for Cesarean Delivery Infection Prophylaxis: A Cost-Effectiveness Analysis.

OBJECTIVE: To investigate the cost-effectiveness of adding azithromycin to standard cephalosporin regimens of cesarean delivery prophylaxis by considering the maternal outcomes in the current and potential subsequent pregnancies. METHODS: A cost-effectiveness model was created using TreeAge to compare the outcomes of using azithromycin-cephalosporin with cephalosporin alone in a theoretical cohort of 700,000 women, the approximate number of nonelective cesarean deliveries annually in the United States that occur during labor or after membrane rupture. Outcomes examined included endometritis, wound infection, sepsis, venous thromboembolism, and maternal death in the current pregnancy and uterine rupture, cesarean hysterectomy, and maternal death in subsequent pregnancies, including cost and quality-adjusted life-years for both pregnancies. Probabilities, utilities, and costs were derived from the literature, and a cost-effectiveness threshold was set at $100,000 per quality-adjusted life-year. Sensitivity analyses were used to determine the robustness of our results. RESULTS: Compared with cephalosporin alone for prophylaxis, our model showed 16,100 fewer cases of endometritis, 17 fewer cases of sepsis, eight fewer cases of venous thromboembolism, and one fewer maternal death with azithromycin-cephalosporin. Additionally, this strategy prevented 36 uterine ruptures and four cesarean hysterectomies in the subsequent pregnancy. Overall, the addition of azithromycin led to both lower costs and higher quality-adjusted life-years when compared with standard cephalosporin prophylaxis. In sensitivity analysis, we found that as long as the cost of azithromycin remained below $930 (baseline cost $27), it was cost-effective. CONCLUSION: For women who undergo cesarean delivery in labor or after membrane rupture, compared with cephalosporin alone, the addition of azithromycin to cesarean delivery infection prophylaxis is less costly and leads to better maternal outcomes in the index delivery and subsequent deliveries. These findings support the use of prophylactic azithromycin at the time of cesarean delivery.

What is the optimal gestational age for women with gestational diabetes type A1 to deliver?

OBJECTIVE: Type A1 gestational diabetes mellitus (A1GDM), also known as diet-controlled gestational diabetes, is associated with an increase in adverse perinatal outcomes such as macrosomia and Erb palsy. However, it remains unclear when to deliver these women because optimal timing of delivery requires balancing neonatal morbidities from early term delivery against the risk of intrauterine fetal demise (IUFD). We sought to determine the optimal gestational age (GA) for women with A1GDM to deliver. STUDY DESIGN: A decision-analytic model was built to compare the outcomes of delivery at 37-41 weeks in a theoretical cohort of 100,000 women with A1GDM. Strategies involving expectant management until a later GA accounted for probabilities of spontaneous delivery, indicated delivery, and IUFD during each week. GA-associated risks of neonatal complications included cerebral palsy, infant death, and Erb palsy. Probabilities were derived from the literature, and total quality-adjusted life years were calculated. Sensitivity analyses were used to investigate the robustness of the baseline assumptions. RESULTS: Our model showed that induction at 38 weeks maximized quality-adjusted life years. Within our cohort, delivery at 38 weeks would prevent 48 stillbirths but lead to 12 more infant deaths compared to 39 weeks. Sensitivity analysis revealed that 38 weeks remains the optimal timing of delivery until IUFD rates fall <0.3-fold of our baseline assumption, at which point expectant management until 39 weeks is optimal. CONCLUSION: By weighing the risks of IUFD against infant deaths and neonatal morbidities from early term delivery, we determined that the ideal GA for women with A1GDM to deliver is 38 weeks.

Synergistic induction of human cathelicidin antimicrobial peptide gene expression by vitamin D and stilbenoids.

SCOPE: The cathelicidin antimicrobial peptide (CAMP) gene is induced by 1α,25-dihydroxyvitamin D3 (1α,25(OH)2 D3), lithocholic acid, curcumin, nicotinamide, and butyrate. Discovering additional small molecules that regulate its expression will identify new molecular mechanisms involved in CAMP regulation and increase understanding of how diet and nutrition can improve immune function. METHODS AND RESULTS: We discovered that two stilbenoids, resveratrol and pterostilbene, induced CAMP promoter-luciferase expression. Synergistic activation was observed when either stilbenoid was combined with 1α,25(OH)2 D3. Both stilbenoids increased CAMP mRNA and protein levels in the monocyte cell line U937 and synergy was observed in both U937 and the keratinocyte cell line, HaCaT. Inhibition of resveratrol targets sirtuin-1, cyclic AMP production and the c-Jun N-terminal, phosphoinositide 3 and AMP-activated kinases did not block induction of CAMP by resveratrol or synergy with 1α,25(OH)2 D3. Nevertheless, inhibition of the extracellular signal regulated 1/2 and p38 mitogen-activated protein kinases, increased CAMP gene expression in combination with 1α,25(OH)2 D3 suggesting that inhibition of these kinases by resveratrol may explain, in part, its synergy with vitamin D. CONCLUSION: Our findings demonstrate for the first time that stilbenoid compounds may have the potential to boost the innate immune response by increasing CAMP gene expression, particularly in combination with 1α,25(OH)2 D3.

Do RCAN1 proteins link chronic stress with neurodegeneration?

It has long been suspected that chronic stress can exacerbate, or even cause, disease. We now propose that the RCAN1 gene, which can generate several RCAN1 protein isoforms, may be at least partially responsible for this phenomenon. We review data showing that RCAN1 proteins can be induced by multiple stresses, and present new data also implicating psychosocial/emotional stress in RCAN1 induction. We further show that transgenic mice overexpressing the RCAN1-1L protein exhibit accumulation of hyperphosphorylated tau protein (AT8 antibody), an early precursor to the formation of neurofibrillary tangles and neurodegeneration of the kind seen in Alzheimer disease. We propose that, although transient induction of the RCAN1 gene might protect cells against acute stress, persistent stress may cause chronic RCAN1 overexpression, resulting in serious side effects. Chronically elevated levels of RCAN1 proteins may promote or exacerbate various diseases, including tauopathies such as Alzheimer disease. We propose that the mechanism by which stress can lead to these diseases involves the inhibition of calcineurin and the induction of GSK-3ß by RCAN1 proteins. Both inhibition of calcineurin and induction of GSK-3ß contribute to accumulation of phosphorylated tau, formation of neurofibrillary tangles, and eventual neurodegeneration.