Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 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

A 45-year-old woman with Bartter's syndrome complicated with gouty arthritis is reported. Bartter's syndrome was diagnosed from hypokalemia, metabolic alkalosis, high plasma renin activity, normal blood pressure and attenuated pressor response to exogenous angiotensin II infusion. Serum uric acid was 11.8 mg/dl, the renal clearance of uric acid was low (3.0 ml/min) and fractional excretion of uric acid (FEUA) was 7.0%, being the lower limit of the normal range. Fractional excretion of phosphate was low (5.3%) and fractional free water clearance per fractional distal sodium delivery was 0.51. The mechanism of hyperuricemia in this case is discussed.
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PMID:Bartter's syndrome with gouty arthritis. 142 21

Approximately 60 million people in the United States have hypertension (BP greater than or equal to 140/90 mm Hg), 40 million have arthritis clinically suitable for nonsteroidal anti-inflammatory drug (NSAID) therapy, and millions take NSAIDs for nonarthritic conditions, creating considerable potential for concomitant administration of NSAIDs and antihypertensive agents. It is estimated that more than 20 million people are on concurrent therapy. Most NSAIDs produce mild elevations of normal blood pressure levels and can partially or completely antagonize the effects of many antihypertensive drugs. The effect on blood pressure can vary from no effect to hypertensive crisis. In pooled studies, the average increase in mean arterial pressure was 10 mm Hg, and duration was short-lived or chronic. Significant interactions occur in about 1% of patients per year. The risk is greatest in the elderly, blacks, and patients with low-renin hypertension. NSAIDs may block the antihypertensive effects of thiazide and loop diuretics, beta-adrenergic blockers, alpha-adrenergic blockers, and angiotensin-converting enzyme inhibitors. No interactions have been reported with centrally acting alpha agonists or the calcium channel blockers. The mechanism of the hypertensive effects of NSAIDs seem primarily related to their ability to block the cyclo-oxygenase pathway of arachidonic acid metabolism, with a resultant decrease in prostaglandin formation. The prostaglandins are important in normal modulation of renal and systemic vascular dilatation, glomerular filtration, tubular secretion of salt and water, adrenergic neurotransmission, and the renin-angiotensin-aldosterone system. Blockade of salutary effects of prostaglandins by NSAIDs results in a complex series of events culminating in attenuation of the effects of many antihypertensive agents. High-risk patients treated with NSAIDs should be identified and have blood pressure, renal function, and serum potassium frequently monitored.
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PMID:Nonsteroidal anti-inflammatory drugs and antihypertensives. 190 2

In a randomized, double-blind, controlled study, 28 patients with early scleroderma received dipyridamole (225 mg/day) and aspirin (975 mg/day) or placebo for 1-2 years. No significant clinical or objective laboratory improvement was noted in either group. Platelet survival time, plasma renin activity, and coagulation tests were not predictive of disease course. Biomechanical and vascular tests of the hands correlated with clinical extent of skin induration and presence of finger ulcers, respectively.
Arthritis Rheum 1984 Oct
PMID:Trial of platelet-inhibiting drug in scleroderma. Double-blind study with dipyridamole and aspirin. 638 2

An intravenous infusion of 2,000 ml isotonic saline was performed in 8 normotensive, normoreninemic patients with progressive systemic sclerosis. None of them had clinical evidence of renal disease. Total and proximal fractional excretion of sodium was reduced when compared with that of 8 normal subjects. No correlation was found with para-aminohippurate (PAH) clearance values. Two years after this study was done, 4 patients developed arterial hypertension; interestingly, plasma renin activity remained within the normal range. Reduced sodium excretion is suggested as having a pathogenetic role in the hypertension of progressive systemic sclerosis.
Arthritis Rheum 1981 Jan
PMID:Functional renal involvement in normotensive patients with progressive systemic sclerosis: impaired sodium excretion during isotonic saline infusion. 700 2

We present a patient in whom indomethacin treatment for acute gouty arthritis induced reversible azotaemia and hyperkalaemia. Re-introduction of the drug under controlled conditions of metabolic balance resulted in recurrence of hyperkalaemia and azotaemia, and was associated with a fall in plasma renin activity, but no change was observed in plasma aldosterone. Since potassium retention and hyperkalaemia occurred in the absence of hypoaldosteronism, other factors must be invoked to explain the observed upset in potassium homeostasis. This, and other recent case reports suggest that prostaglandin synthetase inhibitors such as indomethacin should be used with caution, especially in patients with pre-existing azotaemia, congestive heart failure, or gout.
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PMID:Indomethacin-induced azotaemia and hyperkalaemia: a case study. 703 49

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Polyarteritis Nodosa (PAN) is a rare disease in childhood. No single pattern of clinical presentation characterizes this disease, but abdominal pain, central or peripheral nervous system disease, arthritis, myalgia and skin lesions occur at some time during the course of the illness. In this case a 16-year-old boy who presented with abdominal pain, elevated sedimentation rate associated with hypertension, and a high level of renin, all of which were detected during his hospitalization, suggested the diagnosis of PAN, and renal angiography was performed. Characteristic renal aneurysms were visualized and the diagnosis was confirmed.
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PMID:Diagnostic value of renal arteriography in polyarteritis nodosa. 881 29

Arthritis and hypertension are frequent comorbidities in the elderly hypertensive population. Nonsteroidal anti-inflammatory drugs are often used to relieve pain in arthritic patients but a side effect is sodium retention and consequent elevation of blood pressure (BP). The effect of dihydropyridine calcium blocking drugs is relatively independent of sodium intake, whereas the angiotensin-converting enzyme (ACE) inhibitors' effects can be blunted by a high-sodium diet. This study compared the effects of indomethacin with placebo in elderly patients with essential hypertension who had been controlled with amlodipine or enalapril. Indomethacin 50 mg twice daily or placebo was administered for 3 weeks in a double-blind crossover study to patients controlled with amlodipine or enalapril. The response was assessed by ambulatory BP measurement. Indomethacin raised BP and lowered pulse rates in patients taking enalapril but had little effect in patients receiving amlodipine. The difference caused by indomethacin between the two groups was 10.1/4.9 mm Hg increase in BP and a 5.6 beats/min fall in pulse in people taking enalapril. Addition of indomethacin to patients taking either drug caused a rise in weight and a fall in plasma renin. It is postulated that the effect is due to inhibition of prostaglandin synthesis, which causes sodium retention. In patients taking amlodipine, the fall in plasma renin ameliorates the effect of sodium retention on BP. In patients taking enalapril, plasma renin falls but this is not translated into an effect because of the blockage of converting enzyme. Thus, the full effect of sodium retention on BP is expressed. In patients treated with indomethacin, fewer patients may respond to ACE inhibitors. However, the major problem is the patient who intermittently takes indomethacin or other nonsteroidal anti-inflammatory drugs, which, if a person is treated by an ACE inhibitor causes BP to go out of control. In such patients amlodipine would appear to be a preferred choice to enalapril.
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PMID:Effect of indomethacin on blood pressure in elderly people with essential hypertension well controlled on amlodipine or enalapril. 1149 4

The renin-angiotensin system (RAS) is involved in a complex mechanism that serves to preserve the blood supply to organs so that they can maintain cellular function. Angiotensin II exerts this effect, independently of the blood pressure generated, through two time-related events: a fast opening of the reserve collateral circulation and a much slower response of new vessel formation or angiogenesis. This effect is observed in rats with ligation of the abdominal aorta and in gerbils with abrupt or progressive unilateral carotid artery ligation. Inhibition of the angiotensin-converting enzyme (ACE) or the angiotensin II receptor represses this effect, and it appears that it is mediated through a non-AT1 receptor site of angiotensin II. Many tumors, both benign and malignant, express renin and angiotensin. It seems that the stimulating action of angiotensin II on angiogenesis could also be involved in preserving the blood supply to tumor cells. Administration of converting enzyme inhibitors increases survival and decreases tumor size in tumor-bearing rats. These observations support the hypothesis that the RAS, directly or indirectly, is involved in situations in which the restoration of blood supply is critical for the viability of cells and that it is present not only in normal but also in pathological conditions such as tumors. In view of the ubiquitous presence of renins and angiotensins, it is also likely to be involved in other conditions, such as inflammation, arthritis, diabetic retinopathy, and retrolental fibroplasia, among others in which angiogenesis is prominent. In addition, angiotensin II could be involved, through the counterbalance of the AT1 and AT2 receptors, in the rarefaction of blood vessels as an etiologic component of essential hypertension.
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PMID:Protection against ischemia: a physiological function of the renin-angiotensin system. 1143 99


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