Nephropathy in ankylosing spondylitis.
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Humans↗
Biomedical subjects
E J Pisko
Publications and source records attributed to E J Pisko.
Human rheumatoid factor-producing cell induction by 2-mercaptoethanol: immunomodulation by a simple thiol compound.
Two-mercaptoethanol (2-ME), a simple 2 carbon thiol compound with a wide variety of in vitro and in vivo immunomodulating effects, was evaluated for its usefulness as a molecular probe of human antibody producing cell activation by adding 2-ME to cultures of peripheral blood mononuclear leukocytes from normal human volunteers. Culturing normal human leukocytes with 2-ME induced a significant number of cells producing rheumatoid factor as measured by a hemolytic plaque forming cell (PFC) assay. Dose response studies revealed 5 X 10(-5)M to be the optimum concentration of 2-ME for the induction of rheumatoid factor plaque forming cells (RF-PFC). This concentration of 2-ME also maximally induced PFC making antibodies to sheep red cells coupled to the trinitrophenyl (TNP) hapten demonstrating that 2-ME is a polyclonal inducer of human PFC. The addition of 5 X 10(-5) M 2-ME to cultures containing maximal concentrations of the polyclonal stimulators, pokeweed mitogen and human heat-aggregrated IgG, increased the number of RF-PFC detected in these cultures by approximately 50%, although both lower and higher concentrations of 2-ME suppressed the RF-PFC response. We conclude that 2-ME induces normal human leukocytes to produce rheumatoid factor as part of a polyclonal activation of antibody producing cells. 2-ME also has immunomodulating effects when added to other polyclonal stimulators of antibody producing cells.
Adjuvants, Immunologic↗
Uric acid effects on in vitro models of rheumatoid inflammatory and autoimmune processes.
A neutrophil monolayer system was used to study the effects of uric acid on neutrophil-aggregate interactions important in rheumatoid inflammation. No effect on immunoglobulin G aggregate phagocytosis was seen, but hyperuricaemic levels of uric acid were associated with an enhancement of phagocytosis-induced release of the azurophilic granular enzyme beta-glucuronidase. A trinitrophenyl-coupled mononuclear leucocyte rheumatoid factor plaque-forming assay was utilised to study uric acid effects on polyclonal activation of immunocompetent cells. Low levels of uric acid enhanced and high levels suppressed this system. Hyperuricaemia may enhance some aspects of rheumatoid inflammation, while uric acid may modulate an important component of rheumatoid autoimmunity.
Arthritis, Rheumatoid↗
Chronic liver disease and Still's disease.
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Adult↗
Induction of human rheumatoid factor producing cells by aggregated IgG.
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Adolescent↗
Induction of autoantibody-producing cells after the coculture of haptenated and normal human mononuclear leukocytes.
The coculture of normal human peripheral blood mononuclear leukocytes (PBL) and autologous mononuclear leukocytes coupled to the trinitrophenyl (TNP) hapten (TNP-PBL) was found to induce a polyclonal activation of antibody-producing cells. The polyclonal activation of antibody-producing cells was demonstrated by detecting the induction of cells producing antibody to sheep red blood cells using a complement-dependent, direct, hemolytic plaque-forming cell (PFC) assay. A ratio of four normal to one haptenated mononuclear leukocyte was found to be optimal for inducing the polyclonal activation of antibody-producing cell in these cultures. The plaque-forming cells assay in these experiments utilized monolayers of indicator red cells. Further evidence for the polyclonal induction of antibody-producing cells by TNP-PBL was provided by demonstrating PFC on monolayers of not only sheep red blood cells, but also autologous human red cells, bromelain-treated autologous red cells, TNP-coupled human and sheep red cells, and human autologous red cells coupled to human heat-aggregated IgG with chromic chloride. Thus cells secreting antibody to TNP, human red cells, and human IgG were induced. Anti-IgG and anti-human red cell-producing cells were first detected on Day 2 of culture and were still present on Day 9. Mononuclear leukocytes altered by chemical haptenation polyclonally stimulate normal mononuclear leukocytes to become antibody-producing cells. This polyclonal stimulation of antibody-producing cells includes cells producing antibodies to human IgG and human autologous red blood cells suggesting that autoantibody-producing cells are induced.
Animals↗
Choline magnesium trisalicylate does not impair platelet aggregation.
Blood platelet aggregation in response to adenosine diphosphate (ADP), epinephrine or collagen stimulation was measured in 9 mainly arthritic patients continually treated with choline magnesium trisalicylate for an average of 11 months. Aggregation was entirely normal in 5 of the subjects and only minimally reduced in 3 who showed suppression, in 2 cases borderline or minimal, of ADP-induced aggregation only; the reasons were unclear and the possibility of pre-treatment subnormal responses to ADP, in this group, could not be ruled out. The ninth subject showed no secondary wave of aggregation with ADP or epinephrine and only 21% aggregation with collagen, findings typical of aspirin use. She was thought to have ingested this drug unknowingly and to warrant exclusion from the evaluation. It is concluded that protracted use of choline magnesium trisalicylate does not interfere with platelet aggregation under the conditions of this study. The results obtained were consistent with the reported failure of this drug to cause significant faecal blood loss in clinical trials.
Adenosine Diphosphate↗
Pirprofen and aspirin in the treatment of rheumatoid arthritis.
Pirprofen (800 mg/day) or aspirin (3,600 mg/day) was administered in double-blind fashion for up to one year to 40 adult outpatients with rheumatoid arthritis, after a short, single-blind placebo period. There were no statistically significant differences in efficacy between pirprofen and aspirin, as evidenced by patient opinion, observer opinion, grip strength, walking time, number of tender joints, number of swollen joints, or erythrocyte sedimentation rate. Clinically significant pain of gastrointestinal origin occurred in an equal number of patients from each group. Audiologic evaluation revealed 3 pirprofen-treated patients and 5 aspirin-treated patients in whom sensorineural hearing loss progressed during therapy and required either discontinuation or reduction of drug dosage. Ophthalmologic evaluation disclosed a high prevalence of lesions, the most common being decreased visual acuity and cataracts not explained by previous antiarthritic therapy. The high prevalence of audiologic and ophthalmologic pathology reported in the literature in patients with rheumatoid arthritis makes it difficult to establish in our study whether pirprofen or aspirin affected these organ systems.
Adult↗
Detection of anti-neutrophil cytoplasmic autoantibodies using the promyelocytic HL-60 cell-line.
IgG autoantibodies against antigen in the cytoplasm of cells of the neutrophil-monocyte cell lineage have been found in the sera of patients with Wegener's granulomatosis (WG). The indirect immunofluorescence test (IFT) is proving to be a valuable screening test for these antibodies, but obtaining neutrophils for substrate is time-consuming, and interpretation of the fluorescence patterns in ethanol-fixed cells requires considerable experience. We report an improved IFT using HL-60 cells as substrate. The myeloid reactivity of HL-60 cells was characterized and compared to that of neutrophils, with and without prior ethanol fixation. In contrast to neutrophils, myeloperoxidase (MPO) was more completely extracted from HL-60 cells by prior ethanol fixation, eliminating the confusion inherent in trying to distinguish anti-MPO antibodies from Wegener's granulomatosis associated anti-neutrophil cytoplasmic autoantibodies (WG-ANCA) in the IFT. The WG-ANCA reactivity remained intact with ethanol fixation, producing a distinct crescent and half-moon pattern of specific immunofluorescence. This WG-ANCA positive pattern was found in 25 sera from 11 WG patients and was absent in over 1200 control sera from patients referred for autoantibody testing.
Antibodies, Antineutrophil Cytoplasmic↗
Decreased production of suppressive-B-cell factor by synovial membrane B-lymphocytes in rheumatoid arthritis.
Suppressive-B-cell factor (SBF) is an autoregulatory B-cell lymphokine produced by heat-aggregated-IgG stimulated B-lymphocytes which suppresses polyclonal immunoglobulin production. SBF production by rheumatoid arthritis (RA) patients' peripheral blood B-lymphocytes inversely correlates with disease activity and in vitro rheumatoid factor production. To further define the role of SBF in the pathogenesis of RA, the present study measured SBF production by surgically-obtained synovial membrane mononuclear leukocytes. SBF production by RA synovial leukocytes was similar to the levels previously described for RA peripheral blood leukocytes. Both RA and osteoarthritis (OA) synovial leukocytes produced significantly less SBF than leukocytes obtained from otherwise healthy patients with plica. OA patients produced less SBF than RA patients, but the difference was not statistically significant. SBF values for combined RA patients and controls with OA or plica correlated with the degree of histological plasma cell infiltration providing further evidence for SBF production by cells of the B-lymphocyte lineage. Depletion studies also demonstrated that synovial SBF was produced by B-lymphocytes. The molecular weight (34,000) of synovial SBF was similar to the molecular weight of peripheral blood SBF. Decreased SBF production by RA synovial B-lymphocytes is a functional abnormality in RA which may contribute to the perpetuation of synovial rheumatoid factor production and chronic synovial inflammation.
Adult↗
Successful symptomatic treatment of melorheostosis with nifedipine.
Melorheostosis is an unusual sclerotic dysplasia of bone. We describe a patient with melorheostosis who showed improvement in pain and vasomotor function after treatment with nifedipine. Peripheral vascular disturbances may be responsible for the pain associated with this disorder and vascular abnormalities could possibly be related to the pathogenesis of this disease.
Adult↗
Rheumatoid pleural effusion. A transmission and scanning electron microscopic evaluation.
The pathognomonic triad of a rheumatoid pleural effusion (round multinucleated inflammatory giant cells, large elongated cells and a background of granular material) has only rarely been reported, with only one case examined by electron microscopy. This paper present an additional case with emphasis on its ultrastructural features and immunochemical characteristics. Our data support an origin of the components of the effusions in the pleural rheumatoid nodules.
Adult↗
Temporal arteritis in Sjögren's syndrome.
We report the first case of co-existing temporal arteritis and Sjögren's syndrome in the English language literature. Characteristic clinical and laboratory findings of both disorders were present. The combination of these two illnesses could be on the basis of chance alone or there may be a common etiology. Temporal arteritis could therefore be an addition to the spectrum of vasculitis diseases seen in Sjögren's syndrome.
Aged↗
Inhibition of neutrophil phagocytosis and enzyme release by hyaluronic acid.
Hyaluronic acid at a concentration found in normal joints (4 mg/ml) inhibited the uptake of aggregated IgG by human peripheral blood polymorphonuclear leukocytes, but concentrations of hyaluronic acid found in inflammatory joints (1 mg/ml) did not. Similarly, hyaluronic acid at 4 mg/ml, but not 1 mg/ml, inhibited the release of lysozyme from aggregated IgG stimulated polymorphonuclear leukocytes. beta-Glucuronidase release was inhibited by both concentrations of hyaluronic acid. Physiological concentrations of hyaluronic acid inhibit this model system for the fluid phase of rheumatoid arthritis and hyaluronic acid may be an important immunomodulating substance in the rheumatoid joint.
Cell Adhesion↗
Ocular pathology, tear production, and tear lysozyme in rheumatoid arthritis.
Ninety-seven rheumatoid arthritis (RA) patients receiving investigational nonsteroidal antiinflammatory drugs were found to have a 31.9% prevalence and 24.5%/year incidence of ocular pathology. None of these ocular lesions were definitely related to their RA or drug therapy. Twenty-one of these patients were studied further for evidence of keratoconjunctivitis sicca. None of these patients had abnormal rose bengal staining, but over half had decreased tear production on both stimulated and unstimulated Schirmer's testing and many patients had high tear lysozyme levels. Increased tear lysozyme levels and decreased Schirmer's tests correlated with a modified rheumatoid activity index.
Adult↗