The incidence of ADIs was higher in individuals with a current CD4 count of 500-749 cells/µL compared to those with a CD4 count of 750-999 cells/µL, but did not decrease further at higher CD4 counts. Results were similar in patients virologically suppressed on combination antiretroviral therapy, suggesting that immune reconstitution is not complete until the CD4 increases to >750 cells/µL.

Purpose While current osteoporosis management guidelines recommend use of pharmacologic treatment following hip fracture, the care of such patients has been suboptimal. The objective of this cross-national study is to quantify the use of and adherence to osteoporosis medication following hip fracture in three countries with different health care systems- the United States, Korea and Spain. Methods In three cohorts of patients aged ≥65 years hospitalized for hip fracture, we calculated the proportion receiving ≥1 osteoporosis drug after discharge. Adherence to osteoporosis treatment was measured as the proportion of days covered (PDC) during the first year following the hip fracture. Results We identified 86,202 patients with a hip fracture - 4,704 (U.S. Medicare), 6,700 (U.S. commercial), 57,631(Korea), and 17,167 (Spain). The mean age was 77–83 years and 74–78% were women. In the year prior to the index hip fracture, 16–18% were taking an osteoporosis medication. Within 3 months following the index hip fracture, 11% (U.S. Medicare), 13% (U.S. commercial), 39% (Korea), and 25% (Spain) of patients filled ≥1 prescription for osteoporosis medication. For those who filled one or more prescriptions for an osteoporosis medication, the mean PDC in the year following the fracture was 0.70 (U.S. Medicare), 0.67 (U.S. commercial), 0.43 (Korea) and 0.66 (Spain). Conclusions Regardless of differences in health care delivery systems and medication reimbursement plans, the use of osteoporosis medications for the secondary prevention of osteoporotic fracture was low. Adherence to osteoporosis treatment was also suboptimal with the PDC<0.70 in all three countries.

Reperfusion injury is considered primarily an inflammatory response to oxidative stress. In vitro, oxygen free radicals induce the formation of oxidized phospholipids with platelet-activating factor (PAF) activity (PAF-like lipids). We examined the following: 1) whether PAF and PAF-like lipids are released during reperfusion; 2) the relationship between these phospholipids and oxidative damage on the one hand, and leukocyte recruitment in renal tissue on the other; and 3) whether antioxidant treatment influences the behavior of these phospholipids, the renal inflammatory response, and the outcome of postischemic acute renal failure. After 60 min of warm renal ischemia in rabbits, a release of PAF and, particularly, PAF-like lipids was seen in the first 15 min of reperfusion. In addition, the release of those phospholipids was associated with intense tissue DNA oxidation and with an increase in myeloperoxidase activity. Vitamin C was able to attenuate these postischemic oxidative changes, decrease PAF and PAF-like lipid levels, and, consequently, reduce myeloperoxidase activity. After 40 min of warm renal ischemia in rats, vitamin C treatment ameliorated renal function and structure. This is the first in vivo demonstration of the release of phospholipid oxidation products as part of an oxidative-inflammatory response after renal ischemia-reperfusion, with the release of phospholipid oxidation products significantly reduced by antioxidant treatment.

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