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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

What then are the lessons to be learned about prevention and treatment of hemochromatosis? Early diagnosis is essential. The best indicator would be testing of serum iron and total saturation followed by a serum ferritin if elevated. Once these indices are abnormally high, MRI and or a liver biopsy should confirm the stage of the iron over-loaded state. If indeed the patient is not iron-overloaded (normal liver biopsy in the face of high saturation and ferritin level) phlebotomies should be performed until these indices are normal and then maintained at a normal level. This should entail four to six phlebotomies a year. Family members should also be screened and managed in a like manner. HLA typing may be a partially helpful screening device. The abnormal gene is closely linked on chromosome 6 with HLA histocompatibility loci. Now, by means of HLA typing, we can identify heterozygote carriers and homozygous (abnormal) among first degree relatives of patients with hemochromatosis. Unfortunately, HLA typing can only be used within a given family and cannot be used to screen the general population. It is estimated that 70% of hemochromatoics have the antigen HLA-A3; however, so does 28% of the (well) general population. Patients with unexplained cirrhosis, arthritis, liver disease, diabetes, impotency, cardiomyopathy and neurological symptoms should be screened in a like manner. Routine health practice profile chemistries must include a serum iron and iron saturation, and if high followed by a serum ferritin. Once diagnosed, therapy must be maintained with phlebotomy for the life time of the patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemochromatosis: diagnosis and treatment. 179 61

Pathophysiological and therapeutic properties of anemia in rats with adjuvant-induced arthritis (AA) were investigated. Both anemia and chronic inflammation were induced in rats by a single injection of Freund's complete adjuvant. This study confirmed other earlier data that these anemic rats with AA had reduced serum iron levels and that the anemia was characterized as mild, non-progressive, hypochromic, microcytic. In addition, our studies showed that these anemic rats had slightly but significantly enhanced erythropoietin titers, but not renal failure; there was no significant difference in blood urea nitrogen and creatinine levels in anemic and normal groups. The anemia in rats with AA was improved by recombinant human erythropoietin (r-HuEPO) at 30 and 100 U/kg/day, given i.v. for 5 days. In contrast, iron-chondroitin-sulfate colloid (10 mg/kg/day, i.v. for 5 days) failed to improve the anemia and to enhance the effects of r-HuEPO. These data suggest that anemia in rats with adjuvant-induced arthritis is distinguished, pathophysiologically and therapeutically, from iron deficiency anemia, hemolytic anemia, and renal anemia.
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PMID:Recombinant human erythropoietin, but not iron supplementation, improves anemia in rats with adjuvant-induced arthritis. 181 58

The efficacy of a drug containing three heavy metals together has been tested in adjuvant-induced arthritic rats. Treated rats were injected with 22.8 micrograms copper gluconate, 0.2 microgram gold thioglucose and 6.8 micrograms silver proteinate each day during a period of 29 days. The drug treatment was found to diminish the increases in plasma levels of haptoglobin, ceruloplasmin, PGE2, 6-keto-PGF1 alpha and copper, the decrease in the iron plasma level induced by Freund's adjuvant and the paw swelling. No effect was seen on the plasma levels of TXB2, Zn, Se, Mn and Ni. Therefore the simultaneous administration of low doses of gold, copper and silver had a real anti-rheumatic property in this model. These results should be of interest for the long-term treatment of arthritis.
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PMID:Anti-inflammatory properties of a preparation containing low doses of copper, gold and silver. 198 Sep 12

Genetic hemochromatosis, a disorder of iron metabolism, results in the deposition of massive amounts of iron in the tissues. Arthropathy is one of a number of clinical features associated with the disease. Characteristic radiographic features in the wrist and hand have been reported, and an increased incidence of severe hip disease has been observed. In this study, hip radiographs of 112 patients with genetic hemochromatosis and arthritis were reviewed, and histologic examination of 2 femoral heads was performed. Twenty-eight of the 112 patients (25%) had evidence of arthritis of the hip joint. In 23 (82%) of the 28 patients, this feature was thought to be associated with osteoarthritis; 2 of these patients had an atypical arthropathy associated with radiolucency of the femoral head and histologic features of atypical stripping of the cartilage from the subchondral bone. These atypical features were not thought to be due to avascular necrosis, pyrophosphate-associated arthropathy, apatite-associated deposition arthritis, or osteoarthritis, but may be typical of genetic hemochromatosis and possibly the result of increased susceptibility to shearing forces at the bone-cartilage interface. In 5 of the 28 patients (18%), chondrocalcinosis was the sole abnormal finding on radiography. Ten of the 28 patients eventually required hip surgery, which confirms the severity of the hip disease associated with genetic hemochromatosis.
Arthritis Rheum 1991 Mar
PMID:Hip arthropathy in genetic hemochromatosis. Radiographic and histologic features. 200 57

Principal concepts concerning the anemia of RA are summarized in Tables 7 and 8. These concepts have been validated by our analysis of 93 anemic RA patients and by our review of the literature. The fact that anemia in RA may have one or more etiologies, occasionally in the same patient, mandates a reasoned approach to the analysis of anemia in every RA patient in whom it may occur. In particular, iron deficiency is common and determination of bone marrow iron content via an aspirate may be required for a definitive diagnosis. In those RA patients with anemia of chronic disease, the best therapy remains control of the underlying disease, most commonly with second line drugs and/or corticosteroids. The place for recombinant erythropoietin in the therapy of this anemia has not been defined; one specific role for erythropoietin may be in the preparation of RA patients for elective surgery, particularly hip arthroplasty, where correction of the anemia may either obviate the need for transfusion or may allow for donation of blood for purposes of autologous transfusion perioperatively. The pathogenesis of the anemia of chronic disease, as seen in RA anemia, is not completely understood. Inflammatory mediators, particularly the cytokines, appear to be important factors in the impairment of erythropoiesis. The mechanism by which these cytokines impair erythroid progenitor growth and hemoglobin production in developing erythrocytes is an important area for future study.
Semin Arthritis Rheum 1990 Feb
PMID:The pathogenesis of anemia in rheumatoid arthritis: a clinical and laboratory analysis. 218 69

Anterior cruciate ligament transection (ACLT) in the dog produces changes in the articular cartilage of the unstable knee that are consistent with those of osteoarthritis (OA). To determine whether the degrees of severity of OA cartilage changes, of synovitis, and of synovial iron deposition were related to adequacy of hemostasis at the time of ACLT, a modified surgical technique was devised, whereby electrocautery was used to obtain meticulous control of bleeding when the ligament was severed and irrigation was used to remove intraarticular blood before closure of the joint. When no particular attention was given to hemostasis, 69% of the dogs showed synovitis in the OA knee 10 weeks after ACLT; when electrocautery and irrigation were used to maintain hemostasis, synovitis was present in only 24% of the OA knees 10 weeks after ACLT (P less than 0.01). Iron deposits were present in 75% of synovial samples obtained after routine ACLT, but in only 6% (P less than 0.001) when attention was given to hemostasis. Hypertrophy of articular cartilage, chondrocyte cloning, fibrillation, and changes in tangential zone chondrocytes were less prominent in the OA knee when electrocautery and irrigation were used. However, the water content, uronic acid concentration, and rate of net 35S-labeled glycosaminoglycan synthesis were similarly increased regardless of the surgical technique used, and presumably, these changes reflect the reaction of joint cartilage to mechanical instability in this model of OA.
Arthritis Rheum 1990 Sep
PMID:Synovitis and osteoarthritic changes in canine articular cartilage after anterior cruciate ligament transection. Effect of surgical hemostasis. 240 3

Methods are described for the quantification of certain acute phase reactants (albumin, iron, fibrinogen, seromucoid, haptoglobin, and ceruloplasmin) in small amounts of plasma using the COBAS-BIO centrifugal analyzer. These methods have been applied to determine the concentrations of these acute-phase reactants (APRs) in rat plasma during the first 5 days of adjuvant-induced arthritis. The levels of the APRs alter with the degree of inflammation in a dose-related manner. Administration of the antiinflammatory and antirheumatic drugs (indomethacin, dexamethasone, and clobuzarit [CLOZIC]) during the course of the adjuvant-induced arthritis reduced the inflammatory response as judged by the measurement of oedema. These compounds, however, show differential effects on the profile of APRs as systemic measurements of the inflammatory disease. The present study shows that specific classes of drug have defined effects on acute-phase protein concentration. We believe that the multiple analysis of APR levels during the course of inflammation may help to distinguish between and elucidate the mechanisms of action, of antiinflammatory and antirheumatic drugs.
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PMID:Automated quantification of rat plasma acute phase reactants in experimental inflammation. 247 Oct 18

The role of iron in arthritis was studied by administering ferric citrate (Fe-cit) to age-matched, female Sprague-Dawley rats immunized with chick type II collagen on Day 0. Rats received intravenously (iv) either Fe-cit (7.7 mg/kg body wt) or an identical concentration of sodium citrate on varying days after immunization. Transferrin saturation peaked (88-95%) 1 hr post-Fe-cit and returned to baseline values within 24 hr. Injection of Fe-cit on either Day 3 or Day 5, but not on Day 7 or Day 9, significantly (P less than 0.03) increased the incidence of arthritis. Synovium from the infrapatellar fat pad was harvested on Days 0-10 for analysis by immunocytochemistry. The inceptual morphologic change in the synovium following collagen immunization in rats not injected iv was an increase in the number of CD4+ and transferrin receptor+ mononuclear cells in perivascular regions; compared to Day 0 both cell types had increased two- to threefold by Day 3. On Day 7, an increase in CD8+ mononuclear cells occurred and the first polymorphonuclear leukocytes were noted. These alterations resulted in a peak in the CD4-CD8 ratio on Day 3, with a gradual decline thereafter. Although Fe-cit administration promoted the ingress of these mononuclear cells, it did not change the CD4-CD8 ratio significantly or recruit polymorphonuclear leukocytes into the joint tissue. Serum antibody titers to type II collagen, measured 20 days after immunization by an enzyme-linked immunosorbent assay, and delayed-type hypersensitivity to collagen, measured by a radiometric ear assay on Day 23, did not differ significantly between the groups. As well as showing that the initial intrasynovial event in collagen arthritis is perivascular infiltration by members of the CD4+ T cell subset displaying a phenotypic sign of activation, these findings demonstrate that iron administered at a critical time after immunization enhances the induction of collagen arthritis. The coincidence of this brief period of susceptibility with maximum CD4-CD8 ratios within the synovium and its occurrence prior to the stage of neutrophil infiltration are consistent with the possibility that the augmenting effect of iron is mediated by the inducer T cell subset.
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PMID:Collagen arthritis in the rat is initiated by CD4+ T cells and can be amplified by iron. 252 77

Both purified hyaluronic acid (HA) and bovine synovial fluid react with OCI-, the major oxidant produced by the myeloperoxidase (MPO)/H2O2/CI- system, resulting in a decrease in their specific viscosity. This reaction is inhibited in the presence of excess methionine. H2O2 alone decreases the viscosity of HA, presumably by the Fenton reaction, in the absence (but not in the presence) of the iron chelator, diethyltriaminepentacetic acid (DETAPAC). In the presence of DETAPAC, incubation of HA with the complete MPO/H2O2/CI- system lowered the viscosity of HA. Analysis of 3H-HA exposed to OCI- by gel filtration chromatography indicated that cleavage of HA occurred only at higher OCI- concentrations. We suggest that the reduction in viscosity of HA by the MPO/H2O2/CI- system may be due to a combination of oxidative cleavage and changes in the conformation of the molecule. We speculate that the changes in the molecular size of rheumatoid synovial fluid HA may be due to the action of the neutrophil MPO/H2O2/CI- system.
Arthritis Rheum 1989 Apr
PMID:Changes in the viscosity of hyaluronic acid after exposure to a myeloperoxidase-derived oxidant. 215 12

Long-term hemodialysis is complicated by rheumatological problems. They can vary from pain syndromes without clinical signs to severe destructive arthritis. The latter is often associated with severe disability. Its origin can be related to deposition of amyloid or synovial overloading with aluminium or iron. Different factors influence its occurrence, such as the type of dialysis membrane used or the quantity of aluminium consumed by these hemodialysed patients. The authors evaluated the frequency and the type of rheumatic disorders in the hemodialysis center of the HCU in Geneva. A comparison of these findings with previous reports is presented and the etiopathogenesis is discussed.
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PMID:[Rheumatologic complications in patients treated with intermittent hemodialysis]. 266 29


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