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Disease activity in rheumatoid arthritis (RA) is difficult to measure objectively. Both clinical and laboratory measures were evaluated by the statistical method of consensus analysis. In the literature, laboratory tests as a group have proved more effective; however, studies did not include self-assessment questionnaires. We evaluated the effectiveness of a Modified Health Assessment Questionnaire (MHAQ) relative to other clinical and laboratory tests measuring disease activity in 100 patients with RA. Hemoglobin, hematocrit, mean corpuscular volume, fibrinogen level, Wes-tergren erythrocyte sedimentation rate and C-reactive protein tests, along with tests of morning stiffness, visual analog pain scale, Ritchie index, total joint count, and MHAQ, were evaluated simultaneously. The erythrocyte sedimentation rate was confirmed as a highly effective test to follow disease activity. The MHAQ was the best clinical test; in the methotrexate-treated subgroup it ranked as highly as the most effective laboratory assays. MHAQ is a more effective tool than many laboratory tests currently ordered for monitoring RA disease activity and should be a part of the record of each visit of an arthritis patient.

Little or nothing is known about how the inhibitory effect of aspirin on platelets distributes in the general population. We describe a simple whole-blood assay for the extent of aspirin-induced inhibition of platelet aggregation and its application to 31 aspirin-treated subjects. Platelet inhibition to two or more 325-mg aspirin tablets was measured using a newly developed method in 31 healthy, young adults. These subjects showed a wide range of variation in their response to aspirin, which in subsequent studies was found to be stable over time. The effect persisted even when the steps of gut absorption and liver metabolism were bypassed. We conclude that the response of platelets to aspirin varies to the extent that a significant proportion of the population may be nonresponsive and that this variability may be intrinsic to platelets and/or their blood environment.

The Westergren erythrocyte sedimentation rate (ESR) has been used for many years without any formal procedure for method validation or for quality assurance. In 1988, the International Committee on Standardization in Hematology (ICSH) (Leuven, Belgium) described an ESR validation procedure as well as a method for producing ESR reference material (ICSH reference method) in the laboratory where it is to be used. The ICSH proposal was tested in our laboratory during a consecutive period of 36 months. In this article, a new mathematical relationship between the ICSH recommendation and the Westergren method is developed, which can be easily used for method validation and/or quality assurance. A table has been made that establishes 95% action limits for Westergren ESRs based on ICSH reference ESRs from 5 through 105 mm/h. The table, derived from 36 months of data, has been tested against two new data sets and used to validate two commercial ESR methods. Analysis of outliers was performed with special attention to the mixing of whole blood samples with sodium citrate necessary for the Westergren ESR. This mixing process is best performed in a large-bore test tube as opposed to the use of the Westergren ESR tube as an aliquoting and mixing device.

The activated coagulation time (ACT), commonly used during cardiopulmonary bypass (CPB), is assumed to measure only differences in heparin levels. Studies were undertaken to determine whether platelet activation/inhibition might also influence the test. When either the platelet inhibitor prostacyclin or the platelet activator adenosine diphosphate (ADP) was added to healthy donor blood containing 2 IU of heparin per ml, there was significant prolongation of the ACT (prostacyclin: mean prolongation, 60.6%; ADP: mean prolongation, 52.3%). In blood taken from the extracorporeal circuit of ten CPB cases, the prolongation with the platelet inhibitor carbacyclin, a prostacyclin analogue, was infinite. It is concluded that the ACT as used during CPB must be interpreted as a measure of both platelet procoagulant activity and heparin activity. Furthermore, this dual sensitivity, while fortuitous, is probably advantageous; patients with hyporeactive platelets will automatically receive less heparin.