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Biomedical subjects

J R Ward

Publications and source records attributed to J R Ward.

At least 91 records · Page 5Linked to original sources
PubMed1984

A case of rheumatoid nodule formation within the central nervous system and review of the literature.

We describe nodule formation within the central nervous system (CNS) in a patient with seropositive rheumatoid arthritis (RA). Review of 13 previous reports of CNS rheumatoid nodule formation suggests that the clinical course is usually one of longstanding seropositive disease. Correlation of neurologic signs and symptoms with anatomic lesions has frequently been tenuous. We conclude that CNS nodules are a rare extraarticular feature of RA which, although often of uncertain clinical significance, should be considered as a possible etiology when neurologic dysfunction occurs in the RA patient.

Arthritis, Rheumatoid↗
PubMed1983

Comparison of auranofin, gold sodium thiomalate, and placebo in the treatment of rheumatoid arthritis. Subsets of responses.

A comparison of placebo, auranofin, and parenteral gold sodium thiomalate therapy in 209 patients with active rheumatoid arthritis was performed in a 21-week prospective, controlled, double-blind multicenter trial. When the 161 patients who completed at least 20 weeks of treatment were analyzed for different degrees of response, no remissions were identified. When 50 percent or greater improvement of pain/tenderness scores were compared for end of trial versus entry values, 9 percent of placebo-treated patients, 34 percent of auranofin-treated patients, and 48 percent of gold sodium thiomalate-treated patients showed important improvement that was statistically significant for both gold treatments. When 50 percent improvement for joint swelling was analyzed, 12 percent of the placebo-treated group, 28 percent in the auranofin-treated group, and 37 percent in the gold sodium thiomalate-treated group showed this degree of improvement. Auranofin almost achieved statistical significance for improvement in joint swelling when compared with placebo (p = 0.07), but gold sodium thiomalate was much better than placebo (p = 0.009). There was no statistically significant difference between the two gold treatments. Thus it appears that a subset of patients had an important response to gold therapy that would not be evident by the usual analyses of mean or median changes. Analysis for predictors of response did not discriminate between responders and nonresponders. Because the trial was limited to 21 weeks of therapy, no prediction of the longer-term-effects, especially for auranofin, should be inferred.

Adolescent↗
PubMed1983

Low-dose D-penicillamine therapy in rheumatoid arthritis. A controlled, double-blind clinical trial.

Two hundred twenty-five patients with active severe rheumatoid arthritis were admitted to a multiclinic, controlled, double-blind trial comparing the use of 500 mg D-penicillamine per day, 125 mg D-penicillamine per day, and placebo. One hundred seventy-one patients completed at least 30 weeks of therapy. The 500 mg D-penicillamine group demonstrated statistically significant improvement over the placebo group in grip strength, average circumference of swollen proximal interphalangeal joints, and patient assessment. While the trend was for greater improvement with the larger dose of D-penicillamine, there was no statistically significant difference among the 3 groups in duration of morning stiffness, walking time, physician's assessment, number of swollen joints, or scores for tender and swollen joints. The slight increase in efficacy of higher dose D-penicillamine was associated with increased toxicity.

Adolescent↗
PubMed1983

Comparison of auranofin, gold sodium thiomalate, and placebo in the treatment of rheumatoid arthritis. A controlled clinical trial.

A prospective controlled, double-blind multicenter trial compared placebo, auranofin (an orally administered gold complex), and parenteral gold sodium thiomalate (GST) in patients with active rheumatoid arthritis (RA). Of 193 patients who received any treatment, the only important improvement identified for either auranofin or GST was for pain/tenderness scores. When 161 patients who completed 20 weeks of treatment were examined, both auranofin and GST treatments were superior to placebo as measured by improvement in number of painful and/or tender joints, joint pain/tenderness scores, physician's assessment of disease activity, and decrease in erythrocyte sedimentation rate when elevated at entry. GST was superior to placebo in improvement of joint swelling scores, anemia, thrombocytosis, and rheumatoid factor. No drug-related remissions were observed. The only statistically significant advantages of GST over auranofin for efficacy were an increase in hemoglobin concentration and decrease of thrombocytosis with GST. Withdrawals for adverse effects were 5 times more frequent with GST treatment. Thrombocytopenia, proteinuria, elevated liver enzymes, "nitritoid" reactions, and "gold pneumonitis" were observed only in the GST treatment group. These results confirm that both parenteral and oral gold may be effective for the treatment of RA, that GST tends to show greater efficacy than auranofin, and that auranofin has fewer significant adverse effects than GST. However, long-term benefits, tolerability, and safety cannot be inferred from this study.

Adolescent↗
PubMed1983

Spontaneous nasal septal perforation in patients with rheumatoid arthritis.

Nasal septal perforation is known to be associated with various traumatic and disease states, yet spontaneous nasal septal perforation (SNSP) is relatively rare. SNSP has been reported in three patients with seropositive rheumatoid arthritis (RA) and we report an additional seven patients with SNSP and RA, four of whom were seronegative and none of whom had Raynaud's, in contrast to those reported previously. Manifestations of overt infectious, neoplastic or granulomatous disease have not been found in our seven patients over several years of close follow-up. We have identified no obvious pathogenesis or specific etiology for SNSP. We suggest that SNSP may represent an unusual manifestation of RA previously not well recognized.

Adolescent↗
PubMed1983

Evaluating slow-acting antirheumatic drug therapies for rheumatoid arthritis.

Clinical trials with slow-acting or disease-modifying drugs in rheumatoid arthritis are difficult to design and execute. Such trials are expensive and require long periods of observation. However, there is no acceptable alternative to the properly designed and completed controlled clinical trial. Broad principles for the design of such trials and the basic elements of the study design are outlined and discussed.

Anti-Inflammatory Agents↗
PubMed1983

Toxicity but not arthritogenicity of Mycoplasma arthritidis for mice associates with the haplotype expressed at the major histocompatibility complex.

The use of inbred and congenic mouse strains established that toxicity and death induced by Mycoplasma arthritidis associates with the haplotype expressed at the murine major histocompatibility complex. Mice bearing H-2k and H-2d are susceptible, whereas those bearing H-2b are much more resistant. Mice susceptible to toxicity exhibited massive peritoneal adhesions and a decreased ability to clear organisms from the peripheral circulation. However, the severity of acute arthritis developing over a 3-month period was not statistically related to the haplotype expressed at the major histocompatibility complex. Lymphocyte activation in vitro by a soluble T-cell mitogen is also dependent on a similar haplotype expression.

Animals↗
PubMed1983

Comparison of oral and parenteral gold therapy and placebo in the treatment of rheumatoid arthritis.

Two hundred and eight patients entered a prospective, controlled, double-blind multicenter trial comparing auranofin, gold sodium thiomalate (GST), and placebo. One hundred and sixty-one patients completed at least 20 weeks of therapy. No remissions were seen in the trial. Response to a variety of measures of efficacy was generally modest for both gold treatment groups. There was statistically significant improvement with both gold preparations compared to placebo for the number of tender joints, the joint tenderness score, and physician assessment of disease severity. GST was also significantly better than placebo for the joint swelling score. GST demonstrated statistical improvement in patients with anaemia and thrombocytosis compared to the other treatment groups and both gold preparations were statistically superior to placebo in improvement of an elevated erythrocyte sedimentation rate. Approximately 25% of patients on GST were withdrawn from the study for adverse drug reaction with rash and stomatitis being the predominant reaction. Only 6% of patients on auranofin were withdrawn for untoward drug effect. The two gold preparations were similar in efficacy although auranofin was better tolerated.

Administration, Oral↗
PubMed1983

Design and analysis of controlled clinical trials in rheumatic diseases.

Controlled clinical trials can be difficult, expensive, and time-consuming, but are necessary to advance the knowledge concerning rheumatic disease. Proper care in the design of the study and appropriate statistical analysis of the data can result in studies that answer specific questions and are well worth the effort and expense. If the design is well planned before the entry of the first patient, many problems will be avoided and the results will be credible.

Clinical Trials as Topic↗
PubMed1982

Chronic arthritis of rabbits induced by mycoplasmas. III. Induction with nonviable Mycoplasma arthritidis antigens.

Preexposure of rabbits to Mycoplasma arthritidis predisposed them to subsequent development of chronic inflammation in knee joints challenged with nonviable M arthritidis antigens. Rabbits sensitized by hyperimmunization developed a more severe arthritis than those sensitized by infection. Unsensitized rabbits responded minimally to intraarticular injection of nonviable organisms. These results suggested that an immune response to a persisting mycoplasmal antigen might be capable of sustaining chronic inflammation in rabbits with arthritis induced by viable M arthritidis.

Animals↗
PubMed1982

Specificity of a mycoplasma mitogen for lymphocytes from human and various animal hosts.

Spleen lymphocytes from Lewis and Buffalo rats and peripheral blood lymphocytes from 10 human donors exhibited high levels of transformation when exposed to Mycoplasma arthritidis supernatants. In contrast, spleen lymphocytes from rabbits and guinea pigs and peripheral blood lymphocytes from sheep and calves failed to transform when exposed to M. arthritidis supernatants. The lymphocytes from all hosts were transformed in the presence of phytohemagglutinin or concanavalin A or both Serological studies failed to provide evidence that the responding hosts were presensitized against M. arthritidis antigens.

Animals↗
PubMed1982

Stimulation of mouse lymphocytes by a mitogen derived from Mycoplasma arthritidis. III. Ir gene control of lymphocyte transformation correlates with binding of the mitogen to specific Ia-bearing cells.

The supernatant from Mycoplasma arthritidis broth cultures (MAS) contains a T cell mitogen that is under Ir gene control. Responsiveness to this mitogen is dictated by the I-E/I-C subregion of the major histocompatibility complex and is dependent upon adherent radioresistant Ia+ accessory cells from responding haplotype animals. In this study, we established that MAS could be removed from culture supernatants by absorption with spleen cells from mice that themselves are responsive to the mitogen (k and d haplotypes), but activity is not removed by spleen cells from mouse strains that are nonresponsive to the mitogen (b, q, and s haplotypes). Absorption studies with lymphoid cells from congenic and recombinant strain mice established that absorption of the mitogen was itself linked to the I-E/I-C subregion of the major histocompatibility complex. Thymocytes from responding haplotype strains were incapable of removing MAS activity, and spleen cells devoid of Thy-1-positive cells retained their full absorbing capacity. The ability to effectively absorb MAS activity was abrogated by the pretreatment of spleen cells with anti-Ia antiserum and complement. Furthermore, the ability of spleen cells from responding haplotype strains to respond to MAS was blocked by the addition of anti-Ia serum to the cell cultures. Whereas the latter treatment resulted in an almost complete elimination of MAS responsiveness, the ability of similarly treated spleen cells to respond to the mitogens PHA and Con A was only minimally depressed. These results are consistent with our hypothesis that the mitogenic moiety of MAS actually binds to I-E/I-C-coded Ia antigens.

Animals↗
PubMed1982

Stimulation of mouse lymphocytes by a mitogen derived from Mycoplasma arthritidis. II. Cellular requirements for T cell transformation mediated by a soluble Mycoplasma mitogen.

The mitogenic property of supernatants from M. arthritidis cultures (MAS) is shown to be nonsedimentable, nondialyzable, labile to 56 degrees C for 1 hr, and active against spleen cells from both normal and germfree mice. Both viable M. arthritidis and MAS were active for T lymphocytes because anti-Thy-1 antiserum and C eliminated responsiveness. Spleen cells enriched for T lymphocytes by passage over nylon columns lost responsiveness unless supplemented with a radioresistant adherent cell population that was shown to bear Ia antigens. Evidence is also presented that the genetic control of T lymphocyte responses to the mycoplasma mitogen was exercised at the level of the Ia-bearing adherent cells. Thus adherent cells from positive responder mouse strains, but not those from nonresponder mouse strains, restored the responses of T cells from F1 hybrids between responder and nonresponder strains.

Animals↗