Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 6608837 | [Corticosteroids, non-steroidal antirheumatic agents and the gastroduodenum]. | 1984 Jan | A survey is given on the damaging effect of acetylsalicylic acid, other nonsteroidal anti-inflammatory drugs (NSAID) and corticosteroids on the gastroduodenal mucosa. Especially the results of blood loss studies and endoscopic investigations are reviewed in detail. Epidemiologic data strongly support an association between frequent and heavy intake of acetylsalicylic acid and gastric ulcer as well as gastrointestinal bleeding, whereas the association with duodenal ulcers is far less clearly established. Conclusive evidence proving the superiority of other NSAID in this regard is currently unavailable. Intensive ulcer therapy making use of H2 receptor antagonists often allows healing of small ulcers with a diameter less than 1 cm despite continued treatment with low dose corticosteroids or NSAID, whereas continuation of these drugs is associated with very poor healing in ulcers larger than this size. The danger of perforation has to be taken into consideration. | |
| 303187 | Drug and non-drug factors influencing adverse reaction to pyrazoles. | 1977 | Some of the factors influencing the likelihood of the appearance of adverse drug reactions in patients are identified and discussed. Ways of quantifying some of the risks of adverse reactions in different patients are demonstrated. It is pointed out that adverse reaction data can give valuable guidance for both day-to-day patient management and for the initiation or guidance of research projects. In this latter connection, this study highlights the difference in time of onset between aplastic anaemia and agranulocytosis, suggesting different mechanisms of reaction. The majority of adverse reactions occur during the first three weeks of treatment and it is during this time that patients must be most carefully supervised. The old patients should be watched with particular care. It is concluded that age, sex, disease being treated, length of treatment and even the geographical location where the patient lives, can affect the time, type, frequency and outcome of an adverse drug reaction. | |
| 180797 | Hypergastrinemia induced by glucocorticoid and corticotropin treatment in man. | 1976 May | To elucidate further the pathogenesis of steroid-induced ulceration, plasma gastrin levels, both basal and after a test meal, were studied in normal volunteers and patients treated with glucocorticoids or corticotropin. In normal subjects the acute intravenous administration of 100 mg prednisolone had no effect on plasma gastrin levels. After oral administration of prednisolone (40 mg daily, for four days) a significant increase of the basal, the reactive, and the over 90-min integrated gastrin release was observed. In this group, the glucocorticoid treatment had a slight, but significant influence on gastric acid and pepsin secretion, while acidity and pepsin output stimulated by pentagastrin was not affected. In patients treated with prednisolone for more than 24 weeks, the oral administration of this hormone failed to alter basal gastrin values but affected significantly secretion after the test meal. In patients with multiple sclerosis, after intramuscular administration of corticotropin (60 IU daily, for 12 days), an increase of the basal, the reactive, and the integrated gastrin release also was found. Glucocorticoid-induced hypergastrinemia provides information on the pathogenesis of steroid-induced ulceration. | |
| 6813503 | Protein SAP (serum amyloid P-component) in Waldenström's macroglobulinaemia, multiple mye | 1982 Sep | Serum amyloid P-component (protein SAP) levels in patients with Waldenström's macroglobulinaemia have been determined to be markedly elevated (83 +/- 34 micrograms/ml) compared with healthy adult controls (35 +/- 11 micrograms/ml) and patients with multiple myeloma (39 +/- 17 micrograms/ml). Seropositive rheumatoid arthritis and ankylosing spondylitis patients demonstrated slightly elevated protein SAP levels compared with normals and systemic lupus erythematosus patients, but these values were indistinguishable from those for patients with amyloidosis associated with a rheumatic disease. | |
| 6679571 | Synovial factors and chondrocyte-mediated breakdown of cartilage: inhibition by hydrocorti | 1983 | Cartilage-synovium interactions were explored in a model culture system. Bovine nasal-cartilage discs were cocultured with minced rheumatoid synovium or synovium-conditioned media (SCM) in the presence or absence of hydrocortisone. Cartilage breakdown was assessed by the release of proteoglycan (PG) and hydroxyproline, and matrix biosynthesis by [35S]sulfate incorporation during pulse labeling. Chondrocyte-dependent breakdown in response to synovial factors (i.e., "catabolin" activity) was assessed by the difference in PG release between living and dead cartilages. Short-term contact with minced synovial membrane or exposure to its products released at a distance was sufficient to induce cartilage degradation in coculture; continued exposure was not required for breakdown to persist. Conditioned media from short-term synovial culture were similarly potent, and the induced breakdown was chondrocyte dependent. Matrix biosynthesis was inhibited in exposed cartilage but could be rapidly restored to normal on synovium removal despite the persistence of cartilage breakdown. Early hydrocortisone treatment suppressed the initiation of cartilage breakdown in cocultures and largely abolished the appearance of inductive factors in SCM. Later applications had little effect either in cocultures or in catabolin assays. We conclude that synovium-induced breakdown is an early event and that chondrocyte catabolic mechanisms once they have been activated are sufficient to maintain breakdown at a high level. Hydrocortisone, as well as limiting proteolysis, inhibits early tissue interactions at the level of synovial catabolin production or release. | |
| 1070995 | Pathology, aetiology and pathogenesis of analgesic nephropathy. | 1976 | 1. The initial site of damage in analgesic abuse is the renal medulla and the characteristic lesion is renal papillary necrosis. The papillary necrosis appears to be an ischaemic infarct. The cortical lesion of chronic interstial nephritis is a non-specific change and secondary to obstruction to tubules in the necrotic medulla. 2. Medullary perfusion and the concentration mechanism appear to be important factors in the genesis of renal papillary necrosis. 3. Experimental and clinical studies suggest that abuse of compound analgesics containing aspirin, phenacetin and caffeine result in renal papillary necrosis and the clinical syndrome of analgesic nephropathy. In the APC mixture aspirin appears to be the major nephrotoxic agent while phenacetin plays a synergistic but secondary role in the renal nephrotoxicity. | |
| 272824 | Ternary copper (II) complexes containing salicylate and nitrogenous chelates such as hista | 1977 | In the introduction the chemistry of some bivalent copper complexes of aspirin and salicylate is briefly reviewed and the biological importance of mixed-ligand complexes of bivalent copper is illustrated. The nature of hydroxy-bridged copper (II) complexes and their possible role in the physiological activity of histamine is also discussed. Several neutral, insoluble copper (II) complexes of the type (Chelate-Cu-salicylate) 0-lambda H2O where chelate = 1, 10-phenanthroline (phen), chi = 1; 2,2'-bipyridyl (bipy), chi = 2; histamine (Ha), chi = 1; and where salicylate (sal) = dianion of salicylic acid have been prepared for the first time. They have been characterised by physico-chemical methods and the role of binuclearhydroxy-bridged copper (II) complex ions in their formation is demonstrated. Such complexes may be relevant to the pharmacological action of histamine and of the salicylates, the copper complexes of which are potential anti-inflammatory drugs. Results of some in vivo experiments that have been carried out with mice are also presented. | |
| 6748050 | The specific detection of IgG, IgA and the complement components C3 and C4 in circulating | 1984 Jun | Four immune complex assays (PEG assays) are described; they are based on the binding of radio-labelled immunospecific antibodies to immune complexes containing IgG, IgA, C3 or C4, and subsequent precipitation with polyethylene glycol. Comparison of the results of the IgA-PEG assay with those of an existing immune complex assay (alpha-IgA-InhBA) showed that the former detects only large-sized (greater than 25 S) material. This was also demonstrated by sucrose density gradient ultracentrifugation of immune complexes in patients' sera as well as in preparations of aggregates containing IgA, C3 or C4. By using aggregates of mixed composition (IgG, IgA, C3 and C4) it was shown that each constituent could be detected by one of the 4 assays. Immune complexes containing the various constituents could also be detected in sera of patients with a variety of disorders. Further studies are needed to establish whether these constituents occur within the same complex or within different complexes. | |
| 6410903 | Reactive lymphoid hyperplasia with single class (monoclonal) surface immunoglobulin. | 1983 Sep | Lymphoid tissues from 12 patients were diagnosed as reactive lymphoid hyperplasia, but surface immunoglobulin studies revealed monoclonal (single class) immunoglobulin staining patterns. Infectious, autoimmune, and immunodeficient conditions were diagnosed on the basis of histology and clinical features. Such surface immunoglobulin restriction has been used as an indicator of a neoplastic lymphoid proliferation, but the cases of these patients, in whom the histologic diagnosis was benign, emphasize the importance of a multiparameter approach to diagnosis. Although at the time of this report none of the patients still available to follow-up study have developed known lymphoid neoplasms, the possibility that monoclonal SIg patterns are a harbinger of neoplastic disease makes continuing follow-up of such patients important. | |
| 6446444 | Soluble immune complexes in human disease. | 1980 | The great variety in biochemical properties of immune complexes occurring in human and animal disease states has made the detection of such complexes a difficult task. Variability in immune complex size, specificity, and interaction with humoral or cellular receptor systems, such as complement and phagocytes, suggests different pathogenic properties. The introduction of radioimmunoassays and the recently improved knowledge of the immune complex-receptor interactions have lead to the description of a large number of detection procedures, which in turn has widened the catalogue of diseases associated with immune complexes. This widespread occurrence of soluble immune complexes has lead many investigators to think that such complexes may occur either as a transient physiological phenomenon, important for fast clearance of the antigen, or as primary pathogenic factors triggering inflammatory reactions. Among the 50 procedures for immune complex detection known today, the article will select some pertinent tests, which will be discussed with respect to their specificity, sensitivity, and reproducibility. Furthermore, it is well known that when applied to the study of a patient group with one particular immune complex disease, various tests will result in different percentages of patients having complexes. This observation is due to differences in the underlying principle on which the various tests are based. Thus immune complexes must be further characterized with respect to their size, to the antibody class or specificity involved and, most difficult, to the antigenic specificity which participates in the complex. Recent advances in such experimental characterization of immune complexes in vitro and in the clinical evaluation of patients with complement activation associated to the presence of immune complexes will be discussed. | |
| 6197221 | Evidence in patients with systemic lupus erythematosus of the presence of antibodies again | 1983 Dec | Immunoglobulin G (IgG) in six out of 30 patients with systemic lupus erythematosus (SLE) strongly inhibited the activity of RNA-dependent DNA polymerase (RDPase) of baboon endogenous virus, M7, while IgG obtained from scleroderma patients, rheumatoid arthritis patients and normal subjects was less reactive. Experiments with anti-human IgG and with IgG F (ab')2-bound immunoaffinity columns indicated that the inhibition of RDPase was antibody-mediated. The RDPase inhibiting activity of SLE IgG was considered not to be due to cross-reactions of anti-nuclear antibodies including anti-DNA, anti-ribonucleoprotein, anti-Sm and anti-SS.B antibodies. SLE IgG preferably inhibited the RDPase activity of baboon endogenous virus and a feline endogenous virus, RD114. These findings support the hypothesis that retrovirus(es) might be involved in SLE. | |
| 6750446 | [The hand as an indicator for the diagnostic orientation in various systemic diseases invo | 1982 Oct 6 | Radiological aspects of the hand are presented and discussed in connection with some of the more common systemic diseases involving the bones, in which the hand is an ideal diagnostic indicator. Suitable X-ray techniques and xeroradiography are used to identify alterations to the periostium, the bone cortex and marrow and the soft tissues. The different diseases were classified according to the part of the hand involved: a) distal extremities; b) proximal phalanges and metacarpals; c) entire hand; d) wrist area. | |
| 225265 | Regulation of bradykinin-induced cyclic amp response by quinacrine and prostaglandin E2 an | 1979 Jul | Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids. Both these bradykinin-induced reactions are inhibited by quinacrine, an inhibitor of phospholipase A activity. The cyclic AMP response of human synovial fibroblasts to bradykinin is potentiated by prostaglandin E2 and inhibited by prostaglandin F2 alpha. These data emphasize the critical role of the prostaglandin system in reactions induced by bradykinin and suggest mechansims by which inflammatory reactions due to bradykinin may be modulated. | |
| 301941 | Cold-reactive lymphocytotoxic antibodies in mixed connective tissue disease. | 1977 Spring | Eighty-one sera from 18 patients with mixed connective tissue disease (MCTD) and high titers of antibody to ribonucleoprotein (RNP) were investigated for the presence of lymphocytotoxic antibodies. These were found in 59% sera from 14 patients but in only one of 40 normal subjects. Although lymphocytotoxic activity tended to be higher when the disease was active or there was lymphopenia, the correlation was not statistically significant. The lymphocytotoxic antibodies were found to be cold-reactive, and located in the IgM and/or IgG-containing elution fractions from DEAE cellulose columns. IgM-containing fractions tended to be more cytotoxic. Lymphocytotoxic antibodies were partially absorbed out with cerebral cortex but not with ENA-coated sheep red blood cells. Although attention has been focused on the anti-RNP antibodies found in MCTD, other autoantibodies are also present in a high proportion of patients. | |
| 1224931 | [Induction of chromosome aberrations by antirheumatic therapy]. | 1975 | 1. The comparison between mean structural chromosomal aberration rates after immunosuppressive therapy and the rate of induction of malignant tumours after application of the same cytostatic substances to animals revealed a far-reaching parallelism: Highest mean aberration rates after therapy with procarbazine (Natulan) and cyclophosphamide (Endoxan) - fewer aberrations after mannitol mustard (Degranol) and no definite induction of chromosomal aberrations after azathioprine (Imurel) (8). 2. The possibility of the induction of chromosomal aberrations in lymphocytes of the peripheral blood after injection of gold 198 into the knee-joint, could be confirmed (9). 3. The mean chromosomal aberration rates before and after infusiontherapy with phenylbutazone (Butazolidin; 300 mg + 600 mg/die during 9 days) showed no significant difference (10). | |
| 1138712 | [Chronic interstitial nephritis caused by analgesics]. | 1975 May | Interstitial nephritis secondary to analgesic ingestion is apparently an uncommon subject in pediatric literature. Two cases are reported in this article: case 1 is a girl followed for the last fifteen years when she had lipoid nephrosis which was treated initially with corticosteroids; she responded satisfactorily, but presented frequent relapses. After 8 years, she was given cyclophosphamide plus prednisone and lately, she responded and has remained well. Further on, her urinalysis showed specific gravity of 1,033 and no proteinuria. Five years ago, because of protracted headache due to psychological disturbance, she started to ingest a variety of analgesics in progressively increasing doses. For the last 2 years, abdominal pains, paleness, polydipsia and polyuria have been observed; at present, her blood pressure, serum chemistry, and urine sediment are normal, but there is a marked failure in the renal concentration capacity, as well as marked sodium urinary losses. A percutaneous renal biopsy showed tubulo-interstitial fibrosis and edema with normal glomeruli. Case 2 is a girl with rheumatoid arthritis which appeared 3 years ago; for over one year, the patient was given 15 mg/day prednisone plus 1.5 g. acetylsalycilic acid. She was admitted to the hospital because her osteoarticular problem did not improve. Her blood pressure, blood chemistries and urinary sediment were also normal. LE tests were negative. Renal concentrating capacity was reduced and the renal biopsy showed tubular atrophy; there was intestinal edema and mononuclear infiltration. Chronic interstitial nephritis, secondary to analgesics is supported in both cases; polyuria and a marked defect of renal concentrating capacity are the earliest and most characteristic features. Normal urinary sediment is a common finding leading to erroneous assessment of a lack of renal involvement. Pathological lesions are located in the interstice of the renal medulla and sometimes in the papilla. Early arrest of analgesic ingestion may stop and even reverse the renal lesion and the renal insufficiency. | |
| 6233690 | [Study of plasma androgens in women with autoimmune diseases]. | 1984 Mar | The exact significance of a reported androgen deficiency in women with lupus has not yet been determined. The authors decided to study plasma androgen concentrations not only in lupus, but also in other auto-immune diseases as well as non-auto -immune diseases. 43 patients (rheumatoid arthritis (RA): 10; systemic lupus erythematosus (SLE): 11; multiple sclerosis (MS): 11; patients without auto-immune disease: 11) were compared to 13 normal women. The age and the hormone concentrations of these different groups were compared by analysis of variance and by the Kruskal-Wallis test. A statistically significant reduction in androgen levels was only detected in the women with lupus. It therefore appears that the androgen deficiency is not a non-specific consequence of any disease, that it does not represent a predisposing factor for auto-immune disease in general, but that it is specific for lupus. | |
| 292777 | The etiology, diagnosis, and treatment of TMJ dysfunction-pain syndrome. Part I: Etiology. | 1979 Dec | Craniomandibular pain has five major causes: neurologic, vascular, the temperomandibular joint itself, muscular, and hysterical conversion. When the pain source is purely in the muscles it has been termed MPD (myofascial pain dysfunction) by Laskin. However, when the TMJ itself is also involved it is called TMJ dysfunction-pain syndrome. | |
| 1080421 | Immunologic characterization of the mononuclear cell infiltrates in rheumatoid synovia, in | 1975 Jul | Two subcutaneous rheumatoid nodules and 8 rheumatoid synovia from patients with rheumatoid arthritis (RA); and 2 parotid glands, 1 "pseudolymphoma," and 6 lip biopsies from patients with Sjogren's syndrome (SS) were studied to identify mononuclear cells. The palisading mononuclear cells in subcutaneous nodules had a surface membrane receptor for complement. B lymphocytes surrounded by larger numbers of non-B lymphocytes were found in RA synovium and between salivary ducts of SS lip biopsies. A "pseudolymphoma" obtained from a patient with SS consisted primarily of B lymphocytes. The predominant mononuclear cell in rheumatoid synovia and salivary glands in patients with RA and SS do not have surface membrane receptors from complement and are thus probably T lymphocytes or null cells. | |
| 842146 | [Calcium, phosphorus, hydroxyproline and nitrogen in inflammatory joint diseases]. | 1977 Jan | The elimination of calcium, phosphorus, hydroxyproline and nitrogen was studied in 127 patients with inflammatory joint diseases and )6 healthy controls for 4 days. On the third day, 186 mg of calcium was administered intravenously. Provoked hypercalciuria tests were made in 35 males, 116 females with rheumatiod arthritis (RA), 18 males with ankylosing spondylitis (ASp), 8 postinfectious arthritis (PA) and 18 healthy controls (C). In 120 patients comparison was made between the ratios of eliminated P/hydroxyproline, Ca/hydroxyproline and P/Ca with regards to the results obtained in healthy controls. The kinetics of 47Ca were studied in 7 males with ASp and 4 C. The ratios Ca/P in serum and P/Ca in urine were studied in the same patients and compared with 21 C. The results show that the bone symptomatology of PA manifests itself by elimination of elevated amounts of all of the indicators studied, especially phosphorus. In RA there may be considerable oscillations of flow of urine due to the perspiration of patients. RA differs from decompensated coxarthrosis and gonarthrosis in that the patients eliminate significantly less calcium and phosphorus. Corticosteroids stimulate the elimination of hydroxyproline. Younger patients with RA (25-44) show changes compatible with osteoporosis, older females (45-64) display changes similar to those seen in osteomalacia, the oldest female patient (65-84) appear to have insufficient binding capacity for calcium. The hyposthesis is proposed that at the disease onset RA is characterized by an extremely marked syndrome of osteopathy. ASp is characterized by significantly reduced elimination of hydraxyproline, higher metabolic pool of calcium, lower elimination of calcium in urine and faeces and lower accretion to bone. |