In HIV-infected patients with limited treatment options, raltegravir plus optimized background therapy provided better viral suppression than optimized background therapy alone for at least 48 weeks. (ClinicalTrials.gov numbers, NCT00293267 and NCT00293254.)

No abstract

Inflammatory mechanisms have been implicated in Alzheimer's disease (AD) and might be mediated via the COX-2 enzyme. Previous studies with the selective COX-2 inhibitors, rofecoxib and celecoxib, have shown that they do not alter the progression of AD. We conducted a double-blind study to investigate whether rofecoxib could delay a diagnosis of AD in patients with mild cognitive impairment (MCI), a group with an expected annual AD diagnosis rate of 10-15%. MCI patients X65 years were randomized to rofecoxib 25 mg (N ¼ 725) or placebo (N ¼ 732) daily for up to 4 years. The primary end point was the percentage of patients with a clinical diagnosis of AD. The estimated annual AD diagnosis rate was lower than the anticipated 10-15%: 6.4% in the rofecoxib group vs 4.5% in the placebo group (rofecoxib : placebo hazard ratio ¼ 1.46 (95% CI: 1.09, 1.94), p ¼ 0.011). Analyses of secondary end points, including measures of cognition (eg the cognitive subscale of the AD Assessment Scale (ADAS-Cog)) and global function (eg the Clinical Dementia Rating (CDR)), did not demonstrate differences between treatment groups. There was also no consistent evidence that rofecoxib differed from placebo in post hoc analyses comparing ADAS-Cog and CDR-sum of boxes scores in overlapping subgroups of patients who had Mini Mental State Exam scores of 24-26 in the present MCI study and in a previous AD treatment study with a similar design. The results from this MCI study did not support the hypothesis that rofecoxib would delay a diagnosis of AD. In conjunction with the lack of effects observed in previous AD studies, the findings suggest that inhibition of COX-2 is not a useful therapeutic approach in AD.

The failure of selective cyclo-oxygenase-2 inhibition to slow the progression of AD may indicate either that the disease process is too advanced to modify in patients with established dementia or that cyclo-oxygenase-2 does not play a significant role in the pathogenesis of the disorder.

The patient with a history of current opioid consumption presenting in the acute postoperative setting presents a challenge for pain management. Standard treatment dosages and strategies are often ineffective in providing pain relief. This retrospective case-control study reviews 4 years' experience of the Acute Pain Service (APS) at our institution providing care for 202 chronic pain and opioid-consuming (CPOC) patients, 6.6% of 3058 patients undergoing urologic, gynecologic, orthopedic and general surgical procedures. Controls matched for age, gender, date and type of surgery, and postoperative pain relief modality were found for 180 (89%) of these patients. Patients were provided patient-controlled analgesia (PCA), or epidural opioid analgesia (EOA with boluses of preservative-free morphine or bupivacaine (1:16% + 2 micrograms/ml fentanyl (B/F)). Records were reviewed for patient demographics, diagnoses, surgical procedures, pre-operative opioid use, days-on-service, analgesic requirement, pain scores and incidence of moderate/severe side effects. Patient demographics were similar between CPOC and control groups. When considering PCA alone, mean 24-h usage in controls was 42.8 (32.0) mg morphine (MS) equivalents differing significantly from CPOC patients' use of 135.8 (68.5) mg MS equivalents (P = 0.0001). EOA and B/F case studies showed similar results. Moderate sedation was experienced by 50% of CPOC patients receiving PCA. Differences in opioid usage, side effects, pain scores, sedation and prescribed treatment with anxiolytics were shown between CPOC patients and matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)