Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the role of interleukin-6 (IL-6) in inflammatory disease we monitored plasma levels of IL-6 and acute phase proteins such as C-reactive protein (CRP) and renin substrate (RS) in patients with reactive arthritis (ReA), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). Venous plasma samples were collected: (1) during the acute phase or exacerbation of the disease, and (2) several months latter during convalescence. Increased mean [95% confidence intervals (CI)] levels of plasma IL-6 were observed in patients with ReA both in the acute phase and later, 229 (177 to 280) ng/l and 197 (134 to 260) ng/l respectively (P less than 0.001 as compared to controls). The corresponding plasma IL-6 levels in RA patients were 283 (223 to 340) ng/l and 183 (151 to 226) ng/l, respectively (P less than 0.001 as compared to controls). Plasma IL-6 levels in SLE patients were not increased. Plasma RS levels were increased in all patient groups, but no significant correlation to IL-6 or CRP levels was observed, whereas plasma IL-6 and CRP levels showed a positive correlation in ReA and RA patients.
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PMID:Plasma interleukin-6 and renin substrate in reactive arthritis, rheumatoid arthritis, and systemic lupus erythematosus. 138 3

This study was undertaken 1) to determine whether or not renin is present in synovial fluid in patients with rheumatoid arthritis and osteoarthritis, and, if present, 2) to investigate whether it is synthesized in synovial fluid, or it is only transported from the circulation into the synovial cavity. The active renin concentration (indirect) was measured with angiotensin I radioimmunoassay kits. Inactive renin was converted into active renin with Sepharose-bound trypsin. Both active and inactive forms of renin were found in synovial fluid. They were significantly higher in patients with rheumatoid arthritis (n = 9) than in those with osteoarthritis (n = 16). In plasma, the concentration of inactive renin was significantly higher (P less than 0.001) in the former. Albumin, transferrin, alpha 2-macroglobulin, ceruloplasmin and immunoglobulins G and M were also found in synovial fluid. In each disease, a plot of the log ratio of synovial fluid to the serum concentration against the log molecular weight of each protein gave an approximately straight line curve, suggesting that these proteins are derived from the circulation and are transported into the synovial cavity. In contrast, the ratio of synovial fluid to plasma concentrations of active renin was significantly higher than that predicted on the basis of the above-mentioned interrelationships in both diseases, whereas the ratio of inactive renin was significantly lower. These findings suggest that 1) inactive and active renin are filtered into the synovial fluid from the circulation, and that 2) inactive renin is converted into the active form in the fluid.
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PMID:Prorenin-renin axis in synovial fluid in patients with rheumatoid arthritis and osteoarthritis. 138 4

A 69-year-old woman with advanced rheumatoid arthritis (RA) suffered two episodes of hyperkalemic hyperchloremic metabolic acidosis (HCMA). Plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were markedly suppressed in the first episode occurring in paralell with the administration of metoprolol during piroxicam and lobenzarit (CCA) therapy. Rechallenge with diclofenac sodium and CCA lead to the second hyperkalemia, but no significant suppression of the renin-aldosterone axis was seen at that time. This suggests that the different mechanisms contribute to the development of these episodes, including the tubulo-interstitial injury which is not uncommon in RA. The combined use of nonsteroidal anti-inflammatory drugs (NSAIDs) and beta-adrenergic blockers may increase the risk of life-threatening hyperkalemia through their suppressive effect on the renin-aldosterone system, whereas the concomitant administration of CCA with NSAIDs through the impairment in the renal tubular function. These drugs should be most carefully given to patients with a latent defect in renal potassium excretion.
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PMID:[Recurrent hyperkalemia in the course of rheumatoid arthritis--a case report]. 168 99

Renin-angiotensin-aldosterone++ system was investigated in 60 patients suffering from rheumatoid arthritis. Forty-four of them (group 1) had arterial hypertension (144 +/- 4/94 +/- 2 mm Hg), sixteen were free of hypertension (120 +/- 3/80 +/- 1 mm Hg). Twenty-nine control subjects comparable by AH standing and demographic parameters had essential hypertension stage IB-IIA by A. L. Myasnikov classification (141 +/- 3/89 +/- 1 mm Hg). A tendency to renin suppression was dominating in 72% of group 1 patients (plasma renin activity less than 1.0 ng/ml/h). In this group there appeared high concentrations of A II (14.2 +/- 3.1 pg/ml) and plasma aldosterone++ (238 +/- 94 ng/ml). Rheumatoid vasculitis manifested in 86% of patients. Control subjects exhibited plasma renin activity greater than 3.0 ng/ml/hin 48%, average A II concentration was similar to that of group 1 (12.4 +/- 2.7 ng/ml/h, p greater than 0.05), plasma aldosterone++ level was significantly lower (176 +/- 29 ng/ml, p less than 0.05). Correlations were established between A II concentration and ESR (r = 0.39, p less than 0.05), A II and rheumatoid factor titers (r = 0.40, p less than 0.05). These indicate that immunopathological reactions are responsible for shifts in renin-angiotensin-aldosteron system in hypertensive rheumatoid arthritis subjects.
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PMID:[The renin-angiotensin-aldosterone system and arterial hypertension in patients with rheumatoid arthritis]. 187 68

This case was a 51-year-old woman, who had been diagnosed as having rheumatoid arthritis at some clinic and had been treated with both non-steroidal anti-inflammatory drugs and steroid 3 years before visiting our clinic. When she noticed a decrease in visual acuity and general fatigue in June 1985, she was referred to an ophthalmologist of our hospital, and found to have blood pressure of 240/150 mmHg and KW grade IV retinal findings. She was admitted in our department to examine and treat malignant hypertension. On admission, remarkable hypergammaglobulinemia (29.3%), arthralgia, arthral deformity and pericardial effusion were present thus, she was suspected to be suffering from malignant rheumatoid arthritis. Anti-nuclear antibody (64X), anti-nuclear ribonucleoprotein antibody (64X) and anti-RNase sensitive antibody of anti-extractable nuclear antigens (ENA) antibody (81920X) were positive, while anti-RNase resistant antibody of anti-ENA antibody was negative. Immunologically, her condition was consistent with mixed connective tissue disease (MCTD). Since urinary protein was positive and creatinine clearance was 46.0 ml/min, renal function was thought to be diminished. Her chest roentgenogram revealed cardiomegaly (CTR 67.5%) and an increase in pulmonary vascular shadow. An echocardiogram demonstrated the presence of pericardial effusion. Plasma renin activity was 3.3 ng/ml/h and it was suspected that an intrarenal ischemic change resulted in increased renin release from the juxta-glomerular apparatus, leading to the marked hypertension. Treatment was started with prednisolone 60 mg/day during 4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of mixed connective tissue disease complicated with malignant hypertension]. 219 30

The value of plasma renin and its inactive precursor, prorenin, were examined as a marker for vasculitis in rheumatoid arthritis (RA). Plasma renin and prorenin rise when the renin-angiotensin system is activated; an isolated increase of prorenin may be a marker for microvascular complications in diabetes mellitus. Renin concentrations in plasma obtained from 34 patients with RA (seven with vasculitis, 27 controls) were measured under standard conditions, before and five days after stopping non-steroidal anti-inflammatory drugs; creatinine clearance was also measured. At first the median renin concentration in the patients with vasculitis was 19 (range 12-63) mU/l (normal less than 61 mU/l) and in the controls 9 (3-43) mU/l. The median prorenin concentration in patients with vasculitis was 233 (144-428) mU/l (normal less than 358 mU/l) and in the controls 144 (25-364) mU/l. Renin and prorenin concentrations increased significantly in both groups after withdrawal of nonsteroidal anti-inflammatory drugs. The creatinine clearance was similar in both groups and did not correlate with renin concentrations. In conclusion, it was found that, unlike patients with diabetes mellitus, patients with RA with vasculitis had slightly raised concentrations of both renin and prorenin. These findings signal activation of the renin-angiotensin system and might indicate early cardiac or renal involvement by vasculitis.
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PMID:Raised plasma renin and prorenin in rheumatoid vasculitis. 220 Mar 59

Ten patients with rheumatoid arthritis (RA) and concomitant heart failure were treated with either naproxen or sulindac in an open randomized study to study the drugs' effects on the urinary excretion of prostaglandins on the plasma renin level and on the renal function of the group. Both drugs were given for 14 days and caused a similar and marked decrease in renal excretion of the prostaglandins PGE2 and PGF2 alpha and in plasma renin in all patients. There was no significant effect on the diastolic blood pressure, the body weight or the 24-h creatinine clearance and the clinical effect on the joint symptoms was identical. We conclude that both sulindac and naproxen inhibit the renal prostaglandin synthesis in patients with RA.
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PMID:The renal excretion of prostaglandins and changes in plasma renin during treatment with either sulindac or naproxen in patients with rheumatoid arthritis and thiazide treated heart failure. 639 59

The influence of carprofen and indomethacin on renal salt and water homeostasis was investigated. Carprofen is a new nonsteroidal antiinflammatory drug that is currently undergoing clinical trials in the United States. Both drugs were administered in usual clinical doses to steady state in six healthy individuals and in six individuals with rheumatoid arthritis. Blood pressure, weight, plasma renin activity, urine volume, creatinine clearance, fractional excretion of sodium and potassium, and free water reabsorption were determined. Both drugs were found to suppress plasma renin activity. Indomethacin suppressed plasma renin activity more than carprofen. Neither drug produced clinically significant changes in any of the other parameters. In healthy individuals and in patients with rheumatoid arthritis renal homeostatic mechanisms may compensate for the salt- and water-retaining effects of nonsteroidal antiinflammatory drugs.
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PMID:Effects of indomethacin and carprofen on renal homeostasis in rheumatoid arthritis patients and in healthy individuals. 703 67

Non-steroidal anti-inflammatory drugs are efficacious treatments for rheumatoid arthritis and osteoarthritis. However, an adverse effect of treatment with non-steroidal anti-inflammatory drugs is acute renal failure, particularly in a subset of patients that are in a state of effective volume depletion. The frequency of this side-effect in the general treated population is not known, but is probably less than 1% per year. Non-steroidal anti-inflammatory drugs act by inhibiting the synthesis of prostaglandins, which are important mediators of renal function. In the volume-depleted state prostaglandins may counter the vasoconstriction associated with the activation of the renin-angiotensin system. Cyclooxygenase is the rate-limiting enzyme involved in the synthesis of prostaglandins. Cyclooxygenase exists in two forms: a constitutive form (cyclooxygenase-1) and an inducible form (cyclooxygenase-2), which is associated with inflammation. Non-steroidal anti-inflammatory drugs are non-specific inhibitors of both forms of cyclooxygenase. New data are emerging regarding the role of cyclooxygenase-2 in the control of renal function. In normal rat and dog kidney, cyclooxygenase-2 is sparsely expressed in the macula densa, but expression is upregulated when animals are volume depleted. This review explores the possible role of cyclooxygenase-2 in the maintenance of normal renal function in volume depleted states.
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PMID:Non-steroidal anti-inflammatory drug-induced renal failure: a brief review of the role of cyclo-oxygenase isoforms. 944 67

Local functional renin-angiotensin systems (RAS) have been demonstrated in many organ and tissue systems. Angiotensins, the effector growth factors of the RAS, are essentially cytokines and growth factors which actively contribute to many inflammatory reactions. Among the components of RAS, angiotensin-converting enzyme (ACE) and renin have been previously investigated separately in RA. In this study, ACE levels and renin concentrations were measured in the sera of 16 patients with RA (median age: 45 (26-69), male/female: 3/13), 13 patients with osteoarthritis (OA) (median age: 55 (28-72), male/female: 5/8), and 11 healthy adults (median age: 44 (35-70), male/female: 6/5). Synovial ACE levels and renin concentrations were also measured concurrently in patients with RA and OA. Serum ACE levels were comparable between the groups. However, synovial fluid ACE levels were significantly higher in the patients with RA than in patients with OA. Likewise, synovial fluid renin concentrations were higher in RA patients than in OA patients, while serum renin concentrations were similar in patients with RA and OA and in healthy controls. Moreover, there was a significant negative correlation between the duration of the disease and synovial renin concentrations in RA patients. In conclusion, locally-generated active renin and ACE could contribute to joint destruction in rheumatoid arthritis.
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PMID:Renin and angiotensin-converting enzyme (ACE) as active components of the local synovial renin-angiotensin system in rheumatoid arthritis. 1576 28


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