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Query: UMLS:C0003873 (rheumatoid arthritis)
53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anaemia in rheumatoid arthritis (RA) is a common and debilitating complication. The most common causes of this anaemia are iron deficiency and anaemia of chronic disease. Investigations have suggested that interleukin 1 (IL-1) or tumour necrosis factor (TNF), or both, from monocytes associated with chronic inflammation are responsible for the anaemia of chronic disease. On bone marrow examination anaemia of chronic disease is characterised by the diversion of iron from the erythropoietic compartment into marrow macrophages. This phenomenon is termed failure of iron utilisation. In this study, CFU-E (colony forming unit erythroid; late red cell precursors) and BFU-E (burst forming unit erythroid; early red cell precursors) stem cells were cultured from 10 normal marrow samples and 12 marrow samples from patients with RA with iron deficiency anaemia and 10 samples from patients with RA with failure of iron utilisation. All patients with RA were anaemic (haemoglobin less than 100 g/l), Potential accessory or inhibitory cells of erythropoiesis (CD4, CD8, or CD14 positive cells) were removed before culture. Control marrow samples were studied in a similar manner. Normal marrow samples yielded 377 (17) CFU-E and 133 (6) BFU-E (mean (SD)) colonies for each 2 x 10(5) light density cells plated. CD4 ablation caused reductions of 62 and 100% in CFU-E and BFU-E colonies respectively. CD14 removal resulted in considerable but lesser reductions of 46% for CFU-E and 25% for BFU-E. In both groups of patients with RA, CFU-E colony numbers were significantly lower than those seen in normal control subjects, 293 (17) for patients with iron deficiency anaemia and 242 (35) for patients with failure of iron utilisation. BFU-E colony numbers were 102 (13) and 108 (20) respectively. In patients with RA, CD4 removal caused a significantly greater loss of CFU-E colonies compared with normal control subjects. Cytolysis of CD14 positive cells caused a reduction in CFU-E colonies in the two RA groups which was similar to that seen in normal subjects. In conclusion, patients with RA seem to have fewer CFU-E progenitors but essentially normal numbers of BFU-E stem cells. Our data suggest a stimulatory role for marrow CD4 and CD14 cells in erythropoiesis in patients with RA. Monocytes-macrophages (CD14 positive) are known to be producers of IL-1 or TNF, or both, however, the predicted increase in the CFU-E colonies on removal of CD14 cells is not seen. Therefore, if IL-1 or TNF, or both, are responsible for the impairment of erythropoiesis in patients with RA, marrow macrophages are unlikely to be the source. Moreover, these results indicate the probability of erythropoietin resistance on the basis of diminished CFU-E colony formation in patients with RA.
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PMID:Anaemia of chronic disease in rheumatoid arthritis: effect of the blunted response to erythropoietin and of interleukin 1 production by marrow macrophages. 161 58

Adult coeliac disease has a broad clinical spectrum and remains undetected for years. Among subclinical deficiency states, attributable to coeliac enteropathy, combined iron and folic acid malabsorption is predominant. An unexplained recurrent iron anaemia is an indication for small intestinal biopsy. Gastro-intestinal disorders are present in only 50% of the cases. Coeliac disease is frequently associated with other major histocompatibility complex (MMC)-linked diseases which are mediated by immunological mechanisms: dermatitis herpetiformis, oral ulcerations, IgA nephropathy, rheumatoid arthritis, sarcoidosis. Dermatitis herpetiformis is a useful model for examination of the spectrum of mucosal changes that typify gluten sensitivity and subliminal lesions without villous atrophy. An increased interest is devoted to the intra-epithelial T-lymphocyte population, not only in the small intestine, but at the level of the stomach and the colon. A "rectal challenge" test has been proposed for detecting gluten sensitivity in coeliac patients. Such a test could be an original method of screening, reducing so the need of small intestinal biopsy. The preliminary results are to be confirmed. Until now, jejunoscopy remains mandatory for the diagnosis and the survey of intestinal lesions related to coeliac disease.
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PMID:[Celiac disease in adults: clinical aspects--role of endoscopy]. 163 35

Fifteen serum samples and 29 synovial fluids of patients with rheumatoid arthritis (RA) were examined for the presence of tumour necrosis factor (TNF). The assay for TNF was based on the cytotoxic activity of this cytokine for human melanoma cells in tissue culture. High concentrations of TNF were found in serum samples of patients with severe RA, who had increased erythrocyte sedimentation rate and serum alpha 2 macroglobulin, but decreased haemoglobin and serum iron concentrations. Tumour necrosis factor was also found in the synovial fluid of 16 out of 29 patients. High TNF concentrations were found in fluids with greater than 10(10) leucocytes/l. Tumour necrosis factor was not detected in the serum of normal subjects or in synovial fluid of patients with osteoarthritis. A mediator of inflammation, such as TNF, may contribute to the severity of RA.
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PMID:Tumour necrosis factor in serum and synovial fluid of patients with active and severe rheumatoid arthritis. 170 Jun 72

Haemoglobin concentration was determined in all patients (530) over 70 years of age in a general practice in Oslo during an eight month period. 72 had anaemia and were investigated further. Iron deficiency was found in 13 patients and was most often caused by gastrointestinal blood loss. Chronic diseases, particularly chronic infections and rheumatoid arthritis, were responsible for anaemia in 34 patients. Renal failure caused anaemia in 14 patients. In 10 patients we found no explanation for the anaemia. Nine patients with a previously undiscovered disease were found, six of whom could be offered some kind of treatment. We conclude that anaemia in elderly patients in general practice is often caused by chronic diseases. The main cause of iron deficiency is blood loss, and routine prescription of iron is not justified in this age group. The therapeutic benefit from routine measurement of haemoglobin concentration is small and the test should be used selectively.
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PMID:Anaemia in elderly patients. Incidence and causes of low haemoglobin concentration in a city general practice. 175 48

Haemochromatosis (HC) is a group of phenotypically heterogeneous clinical syndromes, which may have a common molecular basis. Classical genetic haemochromatosis (GHC) is one of these syndromes and is a disorder of iron storage due to an increase in intestinal iron absorption, which results in progressive and massive iron deposition leading to fibrosis and organ malfunction. The liver, pancreas, heart and pituitary are commonly involved. There is a specific arthropathy and an association with osteoporosis. Clinically, the arthropathy may resemble rheumatoid arthritis, with acute attacks of inflammation associated with bilateral destruction of the metacarpophalangeal joints. However, bony joint swelling may occur, suggestive of osteoarthritis. Hip arthritis may be unduly severe and disabling. Haemochromatosis arthritis is composed of three radiographic categories: isolated chondrocalcinosis, hypertrophic osteoarthritis which is indistinguishable from pyrophosphate associated arthropathy, and disease specific changes such as subchondral radiolucency of the femoral head, hook-like osteophytes on the metacarpal heads and a degenerative predilection for the metacarpophalangeal joint rather than the scapholunate. The characteristic histological changes are: abnormal amounts of iron deposits, little or no signs of synovial inflammation and CPPD deposition. Subchondral radiolucency of the femoral head and atypical stripping of the cartilage from the subchondral bone are thought to be specific radiographic and histological changes of HC. The pathogenesis of HC arthritis has been associated with the presence of iron in joint tissue, a defect in cartilage metabolism and immunological dysfunction. Treatment has little effect on clinical, radiological or histological progression.
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PMID:Rheumatic manifestations of haemochromatosis. 175 88

Thirty patients of rheumatoid arthritis comprising 16 classical and 14 definite cases based on the ARA criteria were evaluated in a prospective and controlled study for iron status with special reference to serum ferritin levels. Serum ferritin levels were estimated by RIA technique and marrow iron status was ascertained by semi-quantitative estimation after Pearl's staining of marrow aspirate (G 0-6). Marrow iron stores were found absent to decreased in 17 patients (56.7%), normal in 2 (6.7%) and increased in 11 patients (36.6%). The serum ferritin levels in the iron depleted rheumatoid arthritis patients were significantly lower in comparison to patients with normal to increased marrow iron stores (23.91 +/- 11.45 ug/L vs 69.94 +/- 24.7 ug/L, p less than 0.001). There was a strong positive correlation between serum ferritin levels and marrow iron stores (r = +0.08, p less than 0.001). A serum ferritin value of less than or equal to 32 ug/L was a good predictor of decreased iron stores in the bone marrow, with a sensitivity of 88.2% and specificity of 84.5%. The test had a predictive value of 83.33%. There was no correlation between marrow iron stores and conventional indicators or iron status i.e. serum iron, TIBC, transferrin saturation and MCHC. It is concluded that serum ferritin correlates well with marrow iron stores and can be used as a simple non-invasive test for predicting iron-deficiency in patients of rheumatoid arthritis.
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PMID:Iron status in patients of rheumatoid arthritis with special reference to serum ferritin levels. 181 99

A qualitative and semi-quantitative evaluation of synovial iron deposits in 20 patients with rheumatoid arthritis (RA) and in 12 patients presenting with degenerative and traumatic joint disease was carried out. Ferric iron deposits, abundant and preferentially distributed in the superficial and deeper connective tissue layers in the RA patients, were more limited and prevalently sited in the synovial lining layer in the controls. These results further underline the increase in synovial iron stores found in active RA and the role played by iron deposits in sustaining inflammation, as has been reported in the literature.
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PMID:Histopathological study of iron deposit distribution in the rheumatoid synovium. 195 97

A prospective phase II trial was conducted to assess the feasibility, tolerance, and efficacy of a device designed for selective removal of rheumatoid factor from the plasma of rheumatoid arthritis patients. The device contained terpolymer hydrogel-coated plates with chemically attached, aggregated human immunoglobulin G, and it operated as an immunoaffinity column. Sixty-one patients aged 25 to 73 underwent weekly plasmapheresis treatments (the primary therapy phase). During the trial, patients continued current rheumatoid arthritis medications without dose adjustments. All patients received two to six treatments (primary therapy). Responding patients were eligible to continue apheresis treatment every 2 to 6 weeks (maintenance therapy). No serious, untoward side effects were noted in the course of this study; of 640 treatments, only 2 (in different patients) were aborted, one because of complaints of dizziness and angioedema and the other because of chest tightness and shortness of breath. Except for a significant (p less than 0.05) decrease in serum iron, no significant changes in complete blood count, serum electrolytes, renal and hepatic function tests, or serum C3 and C4 were noted. Although the trial was not designed to determine clinical efficacy, patients noted less morning stiffness, longer time to onset of fatigue, and improved global pain assessment (p less than 0.004); significant objective improvements were noted in joint pain, tenderness, swelling, and the number of affected joints (p less than 0.001). One-half of the treated patients had at least a 50 percent improvement in objective measures of antirheumatic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective in vivo removal of rheumatoid factor by an extracorporeal treatment device in rheumatoid arthritis patients. 199 91

In 50 patients with confirmed or classical rheumatoid arthritis the serum iron level (FeS) was examined (in some repeatedly), the total number of examinations being 82. In 51.1% reduced values were recorded. In 27 subjects of the group the total iron binding capacity was assessed. In none of the patients reduced values were found, in 24 the values were at the upper borderline of normal values and in one instance the value was elevated. In 13 patients with a low FeS with a normal or elevated total iron binding capacity Ferronat Retard was administered. The FeS level reached relatively rapidly normal values which in the author's opinion is rather a manifestation of receding activity of rheumatoid arthritis. They consider administration of iron preparations even in patients with a relatively high total iron binding capacity problematical, except when there is justified suspicion of iron ion losses via the gastrointestinal tract or in malnutrition. Iron administration did not cause deterioration of the rheumatic process.
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PMID:[Plasma iron levels in patients with rheumatoid arthritis]. 205 7

We investigated the serum erythropoietin (Epo) response in 11 rheumatoid arthritis (RA) patients without anaemia, 7 with RA and iron deficiency (ID) and 12 with RA and anaemia of chronic disease (ACD). In all patients the serum Epo was higher than in healthy subjects. Apparently this increase was insufficient to prevent anaemia in ID and ACD. Serum Epo correlated negatively with serum ferritin. Ten RA patients with ACD were treated with the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1). No obvious toxicity signs occurred after one week of treatment. It effectively released iron from iron stores. The Hb rise (in 70% of the patients) was correlated positively with an Epo increase and negatively with a serum ferritin decrease. We conclude that a serum Epo increase does not overcome ACD. Epo response might correlate inversely with iron stores. L1 treatment effectively chelates iron from iron stores. The effects of L1 on erythropoiesis and serum Epo and its safety need further substantiation after prolonged treatment in more RA patients.
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PMID:Impaired erythropoietin responsiveness to the anaemia in rheumatoid arthritis. A possible inverse relationship with iron stores and effects of the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one. 205 65


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