ASA Use Research Articles

Aspirin resistance after coronary artery bypass grafting.

The antiplatelet effect of aspirin may be compromised by an enhanced platelet turnover, generating an increased fraction of platelets that is able to form thromboxane within the dosing intervals (usually 1 day). This may be of particular relevance for patients undergoing CABG after cardiopulmonary bypass, when postoperative platelet turnover is increased. The present work examines whether the antiplatelet effect of aspirin, which is based on the inhibition of platelet thromboxane production, may be impaired by an increased platelet turnover. Determination of thromboxane in collagen-stimulated platelet-rich plasma after CABG showed a remarkable enhancement of the capacity for thromboxane formation, despite the fact that aspirin was administered at an antiplatelet dose (100 mg once daily) that largely suppressed thromboxane synthesis in healthy control subjects. Aspirin is widely used to reduce graft thrombosis after coronary artery bypass grafting (CABG).1 However, aspirin appears to not always be an effective inhibitor of platelet function because considerable individual variations in the antiplatelet effect of aspirin have been reported in patients assigned to CABG.2 ASPIRIN RESISTANCE AFTER CORONARY ARTERY BYPASS GRAFTING

Sedation and general anaesthesia in children undergoing MRI and CT: adverse events and outcomes

Quality assurance data were collected prospectively for children who were sedated (n = 922) or given general anaesthesia (n = 140) for magnetic resonance imaging (MRI) or computerized tomography (CT). The data included patient characteristics, concurrent medication, adequacy of sedation, adverse events and requirement for escalated care. The quality of scans was evaluated. Reasons for preselection of general anaesthesia included previously failed sedation (28%), potential for failed sedation (32%) and perceived medical risk (14%). Hypoxaemia occurred in 2.9% of sedated children, and was more common in children classified as ASA III or IV. Sedation was inadequate for 16% of children and failed in 7%. Failed sedation was associated with greater age (P = 0.009), higher ASA status (P = 0.04) and use of benzodiazepines as sole sedatives (P < 0.03). More of the children who underwent general anaesthesia were ASA III or IV than sedated children, yet the procedure was successful in all the children who underwent general anaesthesia, with one incident of laryngospasm. Excessive motion was noted in 12% of scans of sedated children and 0.7% of those completed with general anaesthesia. We conclude that sedation of children for MRI and CT is associated with risks of hypoxaemia and of inadequate or failed sedation. These adverse events were more likely to occur in older children, those with a higher ASA status and those in whom benzodiazepines had been used as sole sedatives. For a preselected high-risk group of children, general anaesthesia may make MRI and CT scans more successful with minimal adverse events.

Clinical effects of early angiotensin-converting enzyme inhibitor treatment for acute myocardial infarction are similar in the presence and absence of aspirin: Systematic overview of individual data from 96,712 randomized patients

OBJECTIVESWe sought to determine whether the clinical effects of early angiotensin-converting enzyme (ACE) inhibitor (ACEi) treatment for acute myocardial infarction (MI) are influenced by the concomitant use of aspirin (ASA).BACKGROUNDAspirin and ACEi both reduce mortality when given early after MI. Aspirin inhibits the synthesis of vasodilating prostaglandins, and, in principle, this inhibition might antagonize some of the effects of ACEi. But it is uncertain whether, in practice, this influences the effects of ACEi on mortality and major morbidity after MI.METHODSThis overview sought individual patient data from all trials involving more than 1,000 patients randomly allocated to receive ACEi or control starting in the acute phase of MI (0–36 h from onset) and continuing for four to six weeks. Data on concomitant ASA use were available for 96,712 of 98,496 patients in four eligible trials (and for none of 1,556 patients in the one other eligible trial).RESULTSOverall 30-day mortality was 7.1% among patients allocated to ACEi and 7.6% among those allocated to control, corresponding to a 7% (standard deviation [SD], 2%) proportional reduction (95% confidence interval 2% to 11%, p = 0.004). Angiotensin-converting enzyme inhibitor was associated with similar proportional reductions in 30-day mortality among the 86,484 patients who were taking ASA (6% [SD, 3%] reduction) and among the 10,228 patients who were not (10% [SD, 5%] reduction: chi-squared test of heterogeneity between these reductions = 0.4; p = 0.5). Angiotensin-converting enzyme inhibitor produced definite increases in the incidence of persistent hypotension (17.9% ACEi vs. 9.4% control) and of renal dysfunction (1.3% ACEi vs. 0.6% control), but there was no good evidence that these effects were different in the presence or absence of ASA (chi-squared for heterogeneity = 0.4 and 0.0, respectively; both not significant). Nor was there good evidence that the effects of ACEi on other clinical outcomes were changed by concomitant ASA use.CONCLUSIONSBoth ASA and ACEi are beneficial in acute MI. The present results support the early use of ACEi in acute MI, irrespective of whether or not ASA is being given.

Stroke outcome in patients already taking aspirin

Background Although aspirin (ASA) has been shown to be effective for secondary (but not primary) stroke prevention and to have some beneficial influence on outcome when taken early after stroke onset, studies regarding the impact of prior use of ASA on stroke severity are conflicting. To determine whether ASA therapy begun before stroke onset lessens the severity of stroke. Prospective clinical information was collected for all patients admitted with their first acute ischemic stroke between July 1996 and July 1998. National Institutes of Health Stroke Scale (NIHSS) scores were noted on admission and at discharge. Barthel Index (BI), Modified Rankin Scale (MRS), and Glasgow Outcome Scale (GOS) scores were also noted at discharge. Stroke severity was classified as severe if the NIHSS score was 9 or greater, BI score was 55 or less, the MRS score was 4 or greater, or the GOS score was 3 or greater. Group comparisons were performed by using the X(2) tests. 178 patients were evaluated. Forty-two were taking ASA and 136 were not taking ASA or any other anti-thrombotic drug. There were no differences between the 2 groups in terms of age, gender, baseline hematocrit or blood glucose, history of hypertension, diabetes, atrial fibrillation, smoking, or stroke subtype. There were no significant differences between the 2 groups on any of the scales, either on admission or at discharge. Our data do not suggest that ASA use before stroke onset lessens the severity of first stroke. Until this question is definitively settled, however, it would be prudent to ensure balanced distribution of recent ASA use in acute stroke treatment trials.

NSAIDs, aspirin, and esophageal strictures: are over-the-counter medications harmful to the esophagus?

There are several studies that suggest that aspirin (acetylsalicylic acid [ASA]) and nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with esophagitis or esophageal stricture formation. There are limited data on the potential of low-dose ASA and over-the-counter (OTC) NSAIDs to cause esophageal injury. The goal of this study was to determine whether there is an association between esophageal strictures and ASA/NSAID use, including low-dose ASA and OTC NSAIDs. A total of 79 consecutive patients (mean age, 52.8 years; 38 men, 41 women) referred for endoscopy from 4/1/96 to 11/15/96 for chronic gastroesophageal reflux disease symptoms were evaluated. Data collected include gender, race, and age, NSAID or ASA use, as well as an assessment of dysphagia, heartburn duration, and heartburn frequency. Patients taking NSAIDs or ASA at least twice a week were considered ASA/NSAID users. There were 46 patients without strictures and 33 patients with peptic strictures. Patients with strictures were older than patients without strictures (mean age, 58.7 versus 48.6 years; p < 0.01), had longer duration of heartburn symptoms (8.6 versus 6.4 years, p < 0.05), and were more likely to have mucosal injury (50% versus 26.1%). Stricture patients were more likely to use ASA/NSAIDs (63.6% versus 26.1%; p < 0.01). In particular, stricture patients were more likely to use low-dose ASA than patients without strictures (30.3% versus 2.2%; p < 0.01). Otherwise, there were no significant differences with regard to gender, race, or heartburn duration or frequency. Linear regression analysis showed that ASA/NSAID use had a greater influence on the incidence of peptic strictures than age. There is an association between esophageal stricture and ASA/NSAID use, which includes OTC NSAIDs and low-dose ASA.

Interaction Between Enalapril and Aspirin on Mortality After Acute Myocardial Infarction: Subgroup Analysis of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II)

The use of angiotensin-converting enzyme (ACE) inhibitors early after an acute myocardial infarction to reduce mortality has been studied in several trials with inconsistent results. Aspirin (ASA) has become a well-documented therapeutic adjunct in patients with coronary heart disease. Attention has recently been focused on a possible interaction between ASA and ACE inhibitors. We therefore reanalyzed data from the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II) to find any evidence of differential effects of the ACE inhibitor enalapril in subgroups defined by use of ASA at baseline. Logistic regression tested the multiplicative interaction. We used Rothman synergy index S, which would be equal to unity under additivity, and less than unity when suggesting antagonism, to examine the postulated interaction with departure from an additive model. Logistic regression showed that the enalapril-ASA interaction term was a significant predictor of mortality at the end of the study (p = 0.047), and was a borderline significant predictor of mortality 30 days after randomization (p = 0.085). The Rothman synergy index S was 0.66 (95% confidence interval 0.46 to 0.94) for mortality at the end of the study, and 0.68 ( 0.44 to 1.04) for 30-day mortality, indicating antagonism between enalapril and ASA with departure from an additive model. Thus, we found evidence of enalapril-ASA interaction. The effect of enalapril was less favorable among patients taking ASA than among patients not taking ASA at baseline.

Ticlopidine and Aspirin Pretreatment Reduces Coagulation and Platelet Activation During Coronary Dilation Procedures

Objectives. It is unknown whether a therapeutic combination of aspirin (ASA) and ticlopidine might effectively decrease activation of hemostasis.Background. Percutaneous transluminal coronary angioplasty (PTCA), rotational atherectomy and stent implantation are procedures that fracture or ablate endothelium and plaque, a situation that activates hemostasis.Methods. In 85 patients undergoing PTCA for a 77.8 ± 1% stenosis, we measured markers of coagulation and platelet activation (thrombin-antithrombin complexes [TAT], prothrombin fragment 1 + 2 [F1+2] serotonin and the presence of circulating activated platelets reacting with monoclonal antibodies against glycoproteins exposed on platelet membranes). Blood samples were drawn from a peripheral vein and from the coronary ostium before the procedures. Both immediately and 10 min after angioplasty, and 10 min afterward, samples were collected from a probing catheter (0.018 in. [0.46 cm]) positioned beyond the stenosis. All patients were being treated with antianginal drugs and ASA, 250 mg/day. Seventy of them had taken ticlopidine, 250 mg, twice daily for ≤1 day (≤24 h) (n = 28) or for ≥3 days (≥72 h) (n = 42). Heparin (150 U/kg) was administered before angioplasty. Thirty patients underwent PTCA; 15 of them were not treated with ticlopidine and 15 were given ticlopidine (≥72 h). Thirty-five patients had stent implantation, 20 rotational atherectomy.Results. Before and during the procedures, there was greater thrombin generation (expressed by higher TAT and F1+2plasma levels) in patients not taking ticlopidine or taking it for ≤24 h (p < 0.05). Platelet activation and plasma serotonin levels were also significantly higher in the no ticlopidine or ≤24-h ticlopidine groups.Conclusions. The combined use of ticlopidine, ASA and heparin effectively controls activation of coagulation in patients with stable or unstable angina undergoing coronary dilation.(J Am Coll Cardiol 1997;29:13–20)>

Fetal Wastage Syndrome due to Blood Protein/Platelet Defects: Results of Prevalence Studies and Treatment Outcome with Low-Dose Heparin and Low-Dose Aspirin

Fetal wastage syndrome is characterized by recurrent spontaneous abortion. Many syndromes are associated with recurrent fetal loss, including anatomical anomalies, endocrine/hormonal abnormalities, and coagulation defects, with coagulation defects accounting for ∼30% of cases. Most procoagulant factor defects are due to inadequate fibrin-mediated implantation of the fertilized ovum into the decidua. However, blood protein/ platelet defects leading to hypercoagulability and thrombosis are associated with thrombosis of placental vessels, precluding viability of the implanted ovum or later fetus. During the past 2 years, we have seen 46 patients with fetal wastage syndrome due to thrombosis-associated hemostasis defects. In this group, there have been three patients with sticky platelet syndrome, one patient with dysfibrinogenemia, four patients with congenital protein S deficiency, 35 patients with anticardiolipin antibodies, and one patient with a lupus anticoagulant. Patients were started on one low-dose aspirin (ASA), 81 mg per day preconception, at time of diagnosis, and low-dose s.c. porcine heparin at 5,000 units every 12 h was added immediately postconception. The combination of low-dose ASA plus low-dose s.c. porcine heparin was used throughout pregnancy. All patients achieving pregnancy have had uneventful, normal deliveries. It appears that blood protein/platelet defects leading to thrombosis and associated with recurrent fetal loss can be successfully managed with the use of preconception low-dose ASA, followed by immediate postconception addition of fixed low-dose porcine heparin, both used throughout pregnancy. Using this regimen, our success rate has been 100%. Ideal heparin doses, which might be much lower than our empirically chosen and currently used doses, remain to be defined in this particular indication. Key Words: Fetal wastage syndrome—Heparin—Aspirin.

Clinical experience with the Thrombostat 4000.

Bleeding times are presently widely used to screen patients with primary hemostasis defects although their accuracy and reliability has been questioned by many investigators. Platelet aggregation studies are not suited for routine use. We investigated the performance characteristics of the Thrombostat 4000, a device that assesses primary hemostasis. Tests can be performed by adding ADP, epinephrine, CaCl2 or NaCl to the collagen onto which platelets adhere. It was found, using normal volunteers and patients, that ADP and epinephrine had acceptable reference ranges with coefficients of variance between 9-12% for within run and between runs. However, major differences were seen when different filter badges were used--a reflection of differences in collagen. Regular citrated blood, routinely drawn for coagulation studies, can be used; test performance can be delayed for up to five hours when the blood is kept at room temperature. The effects of aspirin on volunteers could be detected when epinephrine was used, but not with ADP. ADP addition allowed the detection of more patients with primary hemostasis defects than bleeding times, and epinephrine was as useful as ADP in detecting these abnormalities. The data suggest that the broadest spectrum of platelet defects (ASA use and platelet dysfunction) can be detected with epinephrine. Inconsistencies in collagen used for coating of the filters is a major drawback for the routine use of this device in screening primary hemostasis defects.

Hemostaseological management of urological operations in patients taking aspirin using the Thrombostat 4000.

A clinical study was started in order to examine the suitability of the Thrombostat (in vitro bleeding test) (IVBT) as a diagnostic tool to prevent perioperative bleeding due to aspirin (ASA) and/or platelet function disorders of other origins. This report is based on preliminary data. Eighty three patients who had ingested ASA in the last two weeks and/or with a history of bleeding and/or documented hemorrhagic disorders requiring distinct urological operations, were included in the study. In all patients the IVBT with CaCl2, in addition to common coagulation tests, were performed. Thirteen patients stopped ASA ingestion until IVBT became normal and did not show any increased bleeding tendency. The residual patients were classified by the various operations. The following operation groups were formed: Male genitals (n = 11), inguinal/suprapubic operations (n = 7), transurethral tumor resections of the bladder (TURB) (n = 17), transurethral prostate resection (TURP) (n = 12), tumor nephrectomy (n = 8), radical prostatectomy (n = 9). Thirty six patients with a history of ASA use, but normal IVBT, served as control group (C). Thirty one patients with a history of ASA ingestion had normal in vivo bleeding times (BT) and abnormal IVBT with CaCl2 (A). Seven patients had a bleeding history and/or documented hemorrhagic disorders (B). None of the patients (A) with abnormal IVBT but normal BT displayed clinically relevant bleeding. However, the blood loss was somewhat higher compared to the controls (C), especially in patients with TURB and radical prostatectomy (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

901-76 Antagonism Between Enalapril and Aspirin: Subgroup Analysis of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II)

Several drugs have been investigated regarding their effect on mortality when given early after an acute myocardial infarction. The use of angiotensinconverting enzyme (ACE) inhibitors has been studied in several trials with inconsistent results. Aspirin (ASA) has become a well documented therapeutic adjunct in patients with coronary heart disease. Attention has recently been focused on a possible interaction between aspirin and ACE inhibitors. We therefore reanalyzed data from the CONSENSUS II to find any evidence of differential effects of the ACE inhibitor enalapril in subgroups defined by use of ASA at baseline. Stepwise logistic regression tested the multiplicative interaction. The enalapril-ASA interaction term was a significant predictor of at the end of the study (odds ratio 1.442, p = 0.047), and was a borderline-significant predictor of mortality 30 days after randomization (odds ratio 1.450, p = 0.085). We used Rothman synergy index S to examine the postulated interaction with departure from an additive model. S would be equal to unity under additivity, and less than unity when suggesting antagonism. The synergy index was 0.66 (95% confidence interval 0.46 to 0.94) for mortality at the end of the study, and 0.68 (0.44 to 1.04) for 30-day mortality, indicating antagonism between enalapril and ASA. No significant interaction was found regarding nonfatal major events. We found evidence of enalapril-ASA interaction. Excess mortality occurred when enalapril was randomized to patients using ASA at baseline.

Strategies for Reducing Blood Transfusions in Hepatic Resection

A comparison of 60 blood transfused and 71 nonblood transfused hepatic resection patients was done to evaluate strategies for reducing blood transfusions during hepatic surgery. There were no significant differences between the two groups with regard to preoperative laboratory data, except for prothrombin time and hematocrit value. The mean operative blood loss was 1990 ml and 760 ml in the blood transfused and nonblood transfused groups, respectively. A multivariate analysis suggested that the patient’s body weight, preoperative prothrombin time, and operative blood loss independently predicted the need for intraoperative blood transfusion. Major postoperative complications developed more frequently in the blood transfused group than in the nonblood transfused group (31.7 vs. 11.3%, p<0.005). These results suggest that the difference in operative blood loss between the two groups was related to the prolonged prothrombin time and a susceptibility for blood transfusion was found to exist particularly in patients with a lower hematocrit value as well as a lower body weight. Thus, the improvement of these preoperative laboratory data combined with avoiding the use of the hematocrit value as a determining factor for intraoperative transfusion could correspond to a reduction in operative blood loss, while curtailing the demands on blood bank facilities, and lowering the risk of postoperative complications.

THE EFFECTS OF ASPIRIN ON MICROVASCULATURE AFTER PHOTODYNAMIC THERAPY

The effects of aspirin (acetylsalicylic acid: ASA) on vessel behavior and tumor response were measured during and after photodynamic therapy (PDT). Changes to vessel constriction, macromolecular leakage, tumor interstitial pressure, and tumor response were examined. Animals were randomly placed into treatment groups and injected with 0-25 mg/kg Photofrin and given 0 or 135 J/cm2 light treatment. The light treatment was standardized to 75 mW/cm2 at 630 nm over a 30 min treatment interval (135 J/cm2). The treatment groups were further subdivided to receive Photofrin alone or Photofrin plus 100 mg/kg ASA. A cremaster muscle model in Sprague-Dawley rats was used to directly observe microvascular response and changes in vessel permeability to macromolecules. A tumor interstitial pressure model was designed to measure pressure changes in a chondrosarcoma tumor over time. This model indirectly measures macromolecular leakage, among other factors, in the tumor tissue. Groups of 10-20 rats were implanted subcutaneously with chondrosarcoma and were subjected to PDT to assess tumor response to the various treatments. Statistically significant differences in vessel leakage and changes in interstitial pressure were observed between animals given ASA plus PDT as compared to animals given PDT alone. The administration of ASA significantly inhibited venule leakage of albumin and reduced increases in interstitial pressure after treatment. The use of ASA had no effect on vessel constriction or tumor response after PDT. These findings suggest that the increases in vessel permeability observed during and after PDT, using Photofrin, do not significantly contribute to tumor response.

Significant Role of Aspirin Use in Patients With Esophagitis

This study determines objectively the extent of nonsteroidal anti-inflammatory drug (NSAID) use in upper gastrointestinal (GI) mucosal acid-peptic diseases by supplementing the conventional interview with two tests of current aspirin (ASA) use--high-performance liquid chromatography (HPLC) for the presence of salicylates in serum and platelet cyclooxygenase activity, which detects ASA use within 5 days of testing. Of 186 consecutive patients undergoing upper endoscopy, 62% of 55 patients with esophagitis had evidence of current NSAID use, vs. 26% of 42 control patients with normal endoscopy (p less than 0.001), 12% of 17 patients with recently healed peptic ulcer (p less than 0.001), and 36% of 25 patients who had an active peptic ulcer (p less than 0.05), five of whom had concomitant esophagitis. Another 52 patients were ineligible for this analysis. Testing for platelet cyclooxygenase activity uncovered 26% more ASA users than history alone. In considering age, sex, smoking and drinking habits, arthritis, and ASA use by logistic regression, ASA use was the only factor contributing to esophagitis; ASA could not be further associated with severity, stricture or symptoms, however. In these patients, 95% of NSAID use was chronic, and 84% of that was ASA. These data show a previously unreported, strong association of ASA use with esophagitis, which suggests that ASA may be a significant factor in the resistance of esophagitis to current therapies as well as the frequently rapid relapse after therapy is withdrawn.

PEDIATRIC ULCER DISEASE: NEW PERSPECTIVES

We retrospectively studied 70 children with endoscopically proven ulcers (age 1day-18yrs) to determine whether gastric ulcers (GUD) were different from duodenal ulcers (DUD) with respect to epidemiology, aspirin (ASA) use and clinical presentation. GUD occurred in 64% and DUD in 36% of patients. GUD occurred in all age groups but DUD was rare in the young child. GUD was present in 51% of children under 6 yrs of age, compared to 8% of DUD. GUD showed a strong seasonal influence with 80% occurring between November and April, the period of increased viral illnesses and presumed increased ASA use. DUD showed no such seasonal predilection. Of the 36 patients with GUD during these months, 67% were acute (symptoms <1 mo), 36% had a prodromal illness and 47% were exposed to ASA. Of the remaining 9 GUD patients who presented in the summer months, 78% were acute in onset but only 18% had a prior illness or were exposed to ASA. In contrast, of the 25 DUD patients, 52% presented with chronic symptoms, 16% had an antecedent illness and only 28% had ASA. Symptomatically, pediatric DUD presents similarly to adult DUD, with epigastric pain (76%) as the primary symptom and GI bleeding in only 16%. GUD more commonly presents with vomiting (53%) and GI bleeding (49%) with pain in only 44%. In conclusion, it appears that pediatric GUD is a unique problem, distinctively different from DUD. GUD usually occurs in the winter months and commonly follows a viral illness. More importantly, GUD is seen after the use of ASA which may in part account for the high frequency of acute gastrointestinal bleeding found in these children.

PROSPECTIVE EVALUATION OF RANITIDINE (R) IN PEDIATRIC ULCER DISEASE (PUD)

(PUD) is no longer a rare problem. Despite various claims for efficacy, there are few objective data available to support any treatment regimens for PUD. We are prospectively evaluating the safety, pharmacokinetics and therapeutic efficacy of R(R), a new H2 antagonist in the treatment of PUD. Nine children (C) (3.5-6.5yrs) who presented with complaints of epigastric pain (8), vomiting (8), nausea (7), hematemesis (3) and melena (1) have been studied. Six C had chronic complaints (>3 wks) and 2 C had a hx of recent ASA use. All C (5M:4F) had endoscopically proven ulcers (5 gastric, 2 pyloric, 2 duodenal). Therapy was designed to achieve gastric acid suppression and ulcer healing. After basal acid output (BAO) was determined a R infusion was given to achieve 90% suppression of BAO. Individual pharmacokinetics were determined and an effective serum concentration 22.6 ng/ml (9-65 ng/ml) was required to achieve 90% suppression. Once C were eating and placed on oral R, dosage was adjusted to account for individual differences in bioavailability. Weekly followup revealed no clinical, biochemical, hepatic or renal abnormalities. Eight C were asymptomatic within the first 3 wks of R therapy. One child has shown steady symptomatic improvement but nausea persists. Complete ulcer healing has been endoscopically documented after 6 wks of therapy. An oral dose of 0.5 mg/kg q 12h is effective in healing ulcers healing in C. R appears to be a safe and effective drug for the treatment of PUD.

Personality, disease parameters and medication in rheumatoid arthritis

This study examined the inter-relationships of three variables: patients' personalities as defined by the Cattell 16 PF instrument, several parameters of rheumatoid disease activity and treatment as defined by medication. The personality profile of the total sample of 56 rheumatoid arthritic patients revealed tendencies to low ego strength, anxiety and dependency, characteristics that are not unique to rheumatoid patients. The only significant relationship was found between patients' personalities and the dependency upon oral corticosteroid drugs. In comparison with those who had never received oral corticosteroids, those who had received such drugs were found to be less persevering, more depressed and taciturn, complaintive and demanding, dependent and easily upset. Except with the use of gold salts and ASA, no significant relationships existed between any of the drugs—antimalarials, phenylbutazone, indomethacin and oral corticosteroids—and indices of disease activity. We hypothesize that the prescription of oral corticosteroids, a potentially hazardous measure, might be contingent upon the psychological and not specific rheumatological needs of the rheumatoid patient.