The Budget Impact of Including Rucaparib on a US Payer Formulary for the Treatment of Patients with Metastatic Ovarian Cancer.

OBJECTIVE: A budget impact model was constructed to assess the incremental budget impact that rucaparib availability would have on a US health plan. METHODS: An incremental budget impact was estimated over a 3-year horizon as the difference in total annual cost of treatment, with and without rucaparib available, for second-line maintenance, third-line treatment, and the combined maintenance and treatment settings. The hypothetical health plan includes one million covered lives, and commercial and Medicare lines of business. Alternative products included in the model were based on the National Comprehensive Cancer Network guidelines. The eligible patient population was estimated using an incidence-based approach. Modeled costs include drug acquisition, intravenous drug administration, required laboratory testing, and medical management of adverse events. RESULTS: In the maintenance setting, average total expenditures over 3 years were estimated to be US$1,465,043 with rucaparib versus US$1,461,350 without it as a treatment option; the average incremental budget impact was US$3693 (US$0.0003 per member per month [PMPM]). In the treatment setting, average total expenditures were estimated to be US$1,320,718 with rucaparib versus US$1,313,736 without it; the average incremental budget impact was US$6982 (US$0.0006 PMPM). Budget impact is smaller in commercial plans than Medicare because of the higher incidence of ovarian cancer in the over-65 population. CONCLUSION: The budget impact of adding rucaparib to the formulary for a health plan adds negligible PMPM costs of < US$0.001 in all tested settings and scenarios due to the small population eligible for therapy.

Phosphate feeding induces arterial medial calcification in uremic mice: role of serum phosphorus, fibroblast growth factor-23, and osteopontin.

Arterial medial calcification is a major complication in patients with chronic kidney disease and is a strong predictor of cardiovascular and all-cause mortality. We sought to determine the role of dietary phosphorus and the severity of uremia on vascular calcification in calcification-prone DBA/2 mice. Severe and moderate uremia was induced by renal ablation of varying magnitudes. Extensive arterial-medial calcification developed only when the uremic mice were placed on a high-phosphate diet. Arterial calcification in the severely uremic mice fed a high-phosphate diet was significantly associated with hyperphosphatemia. Moderately uremic mice on this diet were not hyperphosphatemic but had a significant rise in their serum levels of fibroblast growth factor 23 (FGF-23) and osteopontin that significantly correlated with arterial medial calcification. Although there was widespread arterial medial calcification, there was no histological evidence of atherosclerosis. At early stages of calcification, the osteochondrogenic markers Runx2 and osteopontin were upregulated, but the smooth muscle cell marker SM22alpha decreased in medial cells, as did the number of smooth muscle cells in extensively calcified regions. These findings suggest that phosphate loading and the severity of uremia play critical roles in controlling arterial medial calcification in mice. Further, FGF-23 and osteopontin may be markers and/or inducers of this process.