Citations

There is little consensus on what constitutes adequate health insurance coverage. The concept of a lack of adequate coverage, or underinsurance, is a matter of ongoing debate. A measure of adequate coverage is of critical importance as the nature of health insurance products evolves. Changes to health coverage include more direct out-of-pocket spending by consumers and a reduction of covered benefits. This article updates and extends an earlier review of underinsurance measurement published in 1993. We present a conceptual approach to measuring underinsurance and provide a review of the empirical findings obtained from the application of these approaches. A discussion of the limitations in the selection of a measurement approach includes a review of the extant data sources used. We recommend a national effort to develop a consistent approach to monitor changes in the economic and structural dimensions of health insurance coverage with a concerted effort to define and measure underinsurance.

Background— Vasoreactivity tests are fundamental in evaluating pulmonary arterial hypertension (PAH). Mutations of the transforming growth factor-β type II receptor gene, BMPR2 , predispose to the development of pulmonary hypertension and may alter the response to vasodilators. Previous investigations have not examined the relationship of BMPR2 mutations to vasoreactivity. Methods and Results— We identified 133 consecutive unrelated patients with either idiopathic or familial PAH. Sixty-six patients were excluded because we lacked either DNA samples (n=18) or complete data from a vasoreactivity test (n=48). The remaining 67 patients were screened for BMPR2 DNA sequence variations, and specific variations were confirmed by gene sequencing. The vasoreactivity of patients with nonsynonymous BMPR2 variations was compared with that of patients without nonsynonymous BMPR2 variations. We found nonsynonymous BMPR2 variations in 27 of 67 patients with idiopathic (n=16 of 52) or familial (n=11 of 15) PAH. Vasoreactivity was identified in 3.7% of 27 patients with nonsynonymous BMPR2 variations and in 35% of 40 patients without nonsynonymous BMPR2 variations ( P =0.003). Five of the 27 nonsynonymous variations occur commonly in healthy individuals. None of the remaining 22 patients with BMPR2 variations demonstrated vasoreactivity, and the analysis remained unchanged when we assumed that nonsynonymous BMPR2 variations were present in all 15 patients with familial PAH. Conclusions— Patients with familial or idiopathic PAH and nonsynonymous BMPR2 variations are unlikely to demonstrate vasoreactivity. Further trials are required to determine whether long-term therapy can be directed by tests for BMPR2 variations.