Health care expenditures for Medicaid‐covered males with haemophilia in the United States, 2008

Summary. Although haemophilia is an expensive disorder, no studies have estimated health care costs for Americans with haemophilia enrolled in Medicaid as distinct from those with employer‐sponsored insurance (ESI). The objective of this study is to provide information on health care utilization and expenditures for publicly insured people with haemophilia in the United States in comparison with people with haemophilia who have ESI. Data from the MarketScan^® Medicaid Multi‐State, Commercial and Medicare Supplemental databases were used for the period 2004?2008 to identify cases of haemophilia and to estimate medical expenditures during 2008. A total of 511 Medicaid‐enrolled males with haemophilia were identified, 435 of whom were enrolled in Medicaid for at least 11 months during 2008. Most people with haemophilia qualified for Medicaid based on ‘disability’. Average Medicaid expenditures in 2008 were $142,987 [median, $46,737], similar to findings for people with ESI. Average costs for males with haemophilia A and an inhibitor were 3.6 times higher than those for individuals without an inhibitor. Average costs for 56 adult Medicaid enrollees with HCV or HIV infection were not statistically different from those for adults without the infection, but median costs were 1.6 times higher for those treated for blood‐borne infections. Haemophilia treatment can lead to high costs for payers. Further research is needed to understand the effects of public health insurance on haemophilia care and expenditures, to evaluate treatment strategies and to implement strategies that may improve outcomes and reduce costs of care.     

Slowing renal function decline in chronic kidney disease patients after nephrology referral

Aim: Late referral of chronic kidney disease (CKD) patients to nephrologists is associated with increased morbidity and mortality and is still quite common and seldom studied in Taiwan because of unique sociocultural factors. We aimed to study the decline in renal function and factors related to the change in renal function before and after referral. Methods: We retrospectively reviewed the changes of estimated glomerular filtration rate (eGFR) in 213 new referrals of patients with CKD stages 3–5 to the nephrology divisions of one medical centre and one regional hospital from 2001–2006. Data on demographics and laboratory investigations were collected for study. Results: The rates of annual eGFR decline slowed significantly from −7.38 ± 0.84 before referral to −1.02 ± 0.45 mL/min per 1.73 m²/year after referral (mean ± standard error of the mean, P < 0.001). The nephrology referral was the most significant factor associated with the slowing of renal function progression, as was younger age and female sex. After nephrology referral, patients with diabetes had an increase in eGFR compared to those without diabetes (P = 0.034). Patients had better control of diastolic blood pressure, sugar and lipid, more frequent use of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and statins, less frequent use of non-steroidal anti-inflammatory drugs, and more serum creatinine measurements after nephrology referral. Conclusion: Slowing renal functional decline in CKD patients after referral addresses the importance of nephrology referral for CKD care, which should be strongly promoted in CKD prevention projects in Taiwan.     

Antiplatelet Effect of Gingerol Isolated from Zingiber officinale

The purpose of this investigation was to determine the antiplatelet mechanism of gingerol. Gingerol concentration-dependently (0·5–20 μm ) inhibited the aggregation and release reaction of rabbit washed platelets induced by arachidonic acid and collagen, but not those induced by platelet-activating factor (PAF), U46619 (9,11-dideoxy-9α,11 α-methano-epoxy-PGF_2α) and thrombin. Gingerol also concentration-dependently (0·5–10μ m ) inhibited thromboxane B₂ and prostaglandin D₂ formation caused by arachidonic acid, and completely abolished phosphoinositide breakdown induced by arachidonic acid but had no effect on that of collagen, PAF or thrombin even at concentrations as high as 300 μ m . In human platelet-rich plasma, gingerol and indomethacin prevented the secondary aggregation and blocked ATP release from platelets induced by adenosine 5′-diphosphate (ADP, 5 μ m ) and adrenaline (5 ä m ) but had no influence on the primary aggregation. The maximal antiplatelet effect was obtained when platelets were incubated with gingerol for 30 min and this inhibition was reversible. It is concluded that the antiplatelet action of gingerol is mainly due to the inhibition of thromboxane formation.