Does greater Medicare HMO enrollment cause adverse selection into Medigap?

This paper examines the interaction between public and private insurance in the context of the US Medicare program, which serves those aged 65 and older as well as the disabled who meet specific eligibility requirements. Specifically, the paper examines the extent to which increasing enrollment in Medicare managed care (which provides more comprehensive coverage than basic Medicare) influences premiums in the privately purchased Medicare supplemental insurance market (called 'Medigap'). We employ a fixed effects instrumental variables approach to analyze the association between premiums charged by two large Medigap insurers and Medicare HMO penetration rates, examining over 60 geographic areas during the period 1994-2000. It is hypothesized that greater Medicare HMO penetration will lead to adverse selection into the Medigap market, resulting in higher premiums. The findings suggest a moderate upward effect on premiums, with elasticities ranging from 0.09 to 0.25. Controlling for other factors, moving from a 12% to a 22% Medicare HMO penetration rate would raise average Medigap premiums from $1,314 to $1,615. We discuss the implications of these results with respect to the design of national health care systems that include both public and private insurers.

Does open enrollment control premiums? A case study from the "Medigap" market.

This article analyzes a change in "Medigap" regulations that occurred in Missouri in 1999. It allows Medicare beneficiaries in the state to switch to a different carrier each year so long as they retain the same standardized policy type, without losing their open enrollment privileges. The analysis is based on a comparison of various outcomes in Missouri and those in two comparison states, Kansas and Florida. We found little evidence that the policy change affected premiums charged by insurance carriers in Missouri, but conclude that other desirable aspects of the change make it potentially attractive for other states to follow.

Medigap reform legislation of 1990: a 10-year review.

The 1990 Medigap reform legislation sought to make it easier for consumers to compare policies, provide market stability, promote competition, and avoid adverse selection. Evidence is that the standardization of benefits has simplified consumer choice and is strongly supported by consumers and State regulators. The 1990 reforms also decreased carrier and agent abuses. However, loss ratios (the proportion of premiums paid in benefits versus being retained for administration and profit) have changed little since 1990, bringing into question whether price competition has been enhanced. The prescription drug benefit, which is included in 3 of the 10 standardized plans, provides only limited financial protection yet is expensive, one reason being adverse selection. Access to coverage for Medicare disabled beneficiaries is problematic in most States.

Prescription drug benefits: cost management issues for Medicare.

Little attention has been devoted in policy circles as to how Medicare would manage an outpatient prescription drug benefit. This article, first, discusses the role of the pharmacy benefits manager (PBM), the entity that processes claims and otherwise helps administer the benefit. It then discusses the major decisions that will be necessary regarding such matters as: which drugs should be covered; how broad should the pharmacy network be; whether there should be incentives to obtain generic rather than brand-name drugs when available; for drugs with no generic equivalent, should there be incentives to obtain less expensive, medically appropriate brand-name drugs; and how should prescription drug utilization be managed.

Influence of alpha thalassaemia on the retinopathy of homozygous sickle cell disease

Homozygous alpha+ thalassaemia (alpha-/alpha-) ameliorates some of the clinical manifestations of homozygous sickle cell (SS) disease but its effect on retinal complications remains unknown. This has been assessed by visual examination and flourescein angiography in 39 subjects with SS disease and homozygous alpha+ thalassaemia and in 39 age/sex matched controls with SS disease but with a normal alpha genotype (alpha alpha/alpha alpha). The results indicate that homozygous alpha+ thalassaemia reduces the extent of peripheral retinal vessel closure but has no apparent effect on the frequency of proliferative sickle retinopathy (AU)

Laser photocoagulation for proliferative retinopathy in sickle haemoglobin C disease

The effect of sectoral, scatter laser photocoagulation on proliferative sickle retinopathy (PSR) was investigated by reviewing florescein angiograms of 88 sickle cell-haemoglobin C patients enrolled in a controlled, randomised trial. Follow-up was for a median period of 2.9 years. Complete infarction of all PSR in an eye occurred in 7 of 74 treated eyes and 2 0f 60 control eyes. Treatment resulted in significantly greater regression (decrease in number and size of PSR lesions) in eyes of patients aged <25 years at enrollment but not in eyes of patients> or = 25 years at enrollment. Infarction of the individual PSR lesions was significantly more common in treated eyes. Treated PSR was significantly more likely to infarct if small (< 15 degrees circumferential involvement) and if flat rather than elevated. New PSR was significantly less likely to develop in treated eyes.

Risk factors for proliferative sickle retinopathy

The prevalence, incidence, and risk factors associated with proliferative sickle retinopathy (PSR) were investigated in 786 patients with homozygous sickle cell (SS) disease and 533 patients with sickle cell hemo globin C (SC) disease. PSR was more common in SC disease, in which there was a significant predominance of males, and it increased with age in both genotypes. In SC disease the risk of developing PSR was highest between 15 and 24 years in males, between 20 and 39 years in females, and in SS disease between 25 and 39 years in both sexes. PSR tended to be bilateral, especially in SC disease. There was no evidence of familial clustering of PSR in SC siblings, and insufficient numbers of SS siblings were available to test for clustering. Haematological risk factors associated with PSR in SS disease were a high haemoglobin in males and a low fetal haemoglobin in both sexes and in SC disease, a high mean cell volume, and a low fetal haemoglobinin females. (AU)