Quality of human immunodeficiency virus viral load testing in Australia.

This study determined the proficiencies of laboratories measuring human immunodeficiency virus type 1 (HIV-1) viral loads and the accuracies of two assays used for HIV-1 viral load measurement in Australia and investigated the variability of the new versions of these assays. Quality assessment program panels containing (i) dilutions of HIV-1 subtype B, (ii) replicates of identical samples of HIV-1 subtype B, and (iii) samples of subtype E and B were tested by laboratories. Total variability (within and between laboratories) was tested with quality control samples. The coefficients of variation (CVs) for the Roche AMPLICOR HIV-1 MONITOR version (v) 1.0 and Chiron Quantiplex bDNA 2.0 assays ranged from 53 to 87% and 22 to 31%, respectively. The widespread occurrence of invalid runs with the AMPLICOR HIV-1 MONITOR 1.0 assay was identified. The CVs of the new versions of the assays were 82 to 86% for the AMPLICOR HIV-1 MONITOR v 1.5 assay and 16 to 23% for the Quantiplex bDNA 3.0 assay. For virus dilution samples, all but 5 of 19 laboratories obtained results within 2 standard deviations of the mean. The Quantiplex bDNA 2.0 assay reported values lower than those reported by the AMPLICOR HIV-1 MONITOR version 1.0 assay for samples containing HIV-1 subtype B, whereas the reverse was true for subtype E. Identification and resolution of the problem of invalid runs markedly improved the quality of HIV-1 viral load testing. The variability observed between laboratories and between assays, even the most recent versions, dictates that monitoring of viral load in an individual should always be by the same laboratory and by the same assay. Results for an individual which differ by less than 0.5 log(10) HIV-1 RNA copy number/ml should not be considered clinically significant.

Indomethacin inhibits the effects of dietary supplementation with marine oils on vasoconstriction of human forearm resistance vessels in vivo.

OBJECTIVE: Dietary supplementation with marine oils attenuates the responses to noradrenaline and angiotensin II in human forearm resistance arteries. The mechanisms underlying these effects were the subject of the present study. METHODS: Twenty-two normal male adults were allocated to one of three groups. The first group (n = 11) received 10 g/day marine oil capsules (maxEPA) for 28 days. The second group (n = 7) received maxEPA plus 25 mg indomethacin three times a day on days 28 and 29. The third group (n = 4) received 10 g/day mixed-oil placebo capsules for 28 days, plus indomethacin on days 28 and 29 as in group 2. Forearm venous occlusion plethysmography was performed before and immediately after each treatment period. RESULTS: Responses to acetylcholine, sodium nitroprusside or reactive hyperaemia (area under the time-response curve: pre-maxEPA 14,850 +/- 3502, post-maxEPA 17,118 +/- 4576 units) were unaffected by maxEPA. The suppressive effect of maxEPA on responses to noradrenaline and angiotensin II (from group 1) was no longer apparent in the group receiving indomethacin in addition to maxEPA. Indomethacin, in subjects on placebo capsules, had no effect on the responses to either agonist. CONCLUSION: We conclude that the suppressive effects of maxEPA result from alterations to in vivo prostanoid profiles.

Marine oils dose-dependently inhibit vasoconstriction of forearm resistance vessels in humans.

The effects of dietary supplementation with marine oils on vascular reactivity in human forearm resistance arteries were studied. Healthy male adults (six to nine subjects per group) were given either maxEPA capsules (content: eicosapentaenoic acid, 0.178 g/g; docosahexaenoic acid, 0.116 g/g) at doses of 20, 10, or 5 g/day or placebo capsules at 20 g/day for 28 days. Capsule compliance was confirmed by measurement of platelet membrane incorporation of n-3 fatty acids. Blood pressure was not affected by either maxEPA or placebo. The influence of treatment interventions on forearm vasoconstrictive responses to local infusions of angiotensin II and norepinephrine was examined using venous occlusion plethysmography before and after treatment. Responses to both agonists were significantly suppressed by 20 g/day maxEPA (slopes before and after maxEPA, respectively: angiotensin II, 3.34 and 0.89; norepinephrine, 0.91 and 0.41). When analyzed as difference in area under the dose-response curves, the suppressive effects of maxEPA were clearly dose dependent (angiotensin II: 20 g area reduced by 72%, 10 g by 67%, 5 g by 33%). Similarly, responses to norepinephrine were dose-dependently suppressed by maxEPA (20 g area reduced by 61%, 10 g by 63%, and 5 g by 33%). Placebo had no effect on the responses to either constrictor. The responses to both agonists returned to preoil levels after 2 months' discontinuation of 20 g/day maxEPA. We conclude that the suppressive effects of marine oils on vascular reactivity may, in part, contribute to their cardioprotective influence in humans.