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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antihypertensive properties of the new diuretic tienilic acid were investigated. Thirteen previously untreated hypertensive patients took part in a double-blind crossover study in which 30 days' treatment with tienilic acid 250 mg, bendrofluazide 5 mg, and spironolactone 100 mg were compared. Bendrofluazide caused the greatest natriuresis on the first treatment day and the most rapid fall in blood pressure. The ultimate antihypertensive effect of all three drugs was similar. Tienilic acid caused a noticeable reduction in serum urate concentrations and a rise in urate clearance, in contrast to the other two agents, which caused slight urate retention. Tienilic acid and bendrofluazide caused falls and spironolactone a rise in plasma potassium concentrations. No untoward effects were seen from any of the drugs. It is concluded that tienilic acid is a moderately potent diuretic that lowers plasma urate concentrations. It may be the drug of first choice for hypertensive patients who already have gout or are likely to develop it when taking thiazide diuretics.
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PMID:Comparison of natriuretic, uricosuric, and antihypertensive properties of tienilic acid, bendrofluazide, and spironolactone. 36 52

Naproxen is a propionic acid derivative with analgesic and anti-inflammatory activity which has been widely used in the treatment of rheumatic diseases. Naproxen has been well studied in rheumatoid arthritis and is as effective as aspirin but better tolerated, thus enabling more patients to continue with treatment. For this reason some clinicians now prefer to try propionic acid derivatives, such as naproxen, before aspirin in arthritic patients. In comparative studies with other non-steroidal anti-inflammatory drugs, such as indomethacin, ibuprofen, fenoprofen and others, all drugs were usually of similar overall efficacy although naproxen was sometimes preferred: but as with other non-steroidal anti-inflammatory agents, not all patients will respond to naproxen and in such cases other agents should also be tried until the most satisfactory drug is found for each patient. Naproxen is also effective in degenerative joint diseases of the hip and knee, although further well designed studies are needed to more clearly define its relative place compared with newer drugs such as diclofenac or diflunisal. Results of other comparative studies have shown that naproxen is a suitable alternative to phenylbutazone or indomethacin in ankylosing spondylitis and to aspirin in juvenile rheumatoid arthritis. Naproxen appears to be effective in reducing pain and swelling in acute gout and is an effective analgesic in patients with pain following surgery or trauma and in pain of dysmenorrhoea. Naproxen has generally been better tolerated than aspirin or indomethacin at the dosages used. Because of its relatively long plasma half-life, naproxen can with convenieice be given twice daily, and there is some evidence that once daily dosage is as effective in rheumatoid arthritis.
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PMID:Naproxen up to date: a review of its pharmacological properties and therapeutic efficacy and use in rheumatic diseases and pain states. 38 72

The safety and efficacy of tienilic acid have been evaluated in studies of patients with mild to moderate essential hypertension, salt and water retention states and hyperuricaemia associated with gout. During the course of these studies 675 patients were treated with tienilic acid, 310 were treated with hydrochlorothiazide, 43 were treated with probenecid and 34 were treated with placebo. Overall, adverse reactions characterized as probably drug-related or questinably drug-related were reported in 28% of patients treated with tienilic acid, 24% treated with hydrochlorothiazide, 25% of patients treated with probenecid and 33% treated with placebo. The side effects encountered were mild in severity, reversible and represented extensions of the pharmacological activity of tienilic acid, hydrochlorothiazide and probenecid. These initial studies demonstrate that tienilic acid is safe and effective in the treatment of mild to moderate essential hypertension, salt and water retention states, including oedema associated with congestive cardiac failure or mild to moderate renal dysfunction, and in the management of elevated serum uric acid levels associated with gout.
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PMID:Safety of tienilic acid. 38 98

Ibuprofen was introduced in England in 1967 and in the United States in 1974 as an anti-inflammatory drug in humans. It has weak but definite anti-inflammatory properties similar to those of aspirin, milligram for milligram, but with considerably less adverse effect on the stomach. Ibuprofen is chemically related to fenoprofen and naproxen, but lack of effect for any one in this chemical class of propionic-acid derivatives does not necessarily mean lack of effect for any other in an individual patient. The drug has analgesic properties, probably related to its anti-inflammatory effect. It inhibits prostaglandin synthesis and has no effect on the adrenopituitary axis, making it a nonsteroidal agent. Ibuprofen has been shown to be effective in rheumatoid arthritis and osteoarthritis and is probably effective in ankylosing spondylitis, gout, and Bartter's syndrome.
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PMID:Ibuprofen. 39 Nov 17

The condition of generalized periarthritis calcarea (hydroxyapatite deposition disease) is characterised by multiple periarticular calcification which can be localised around practically any joint and also in proximity to the spine. This calcification consists of hydroxyapatite crystals which are responsible for the episodes of acute, subacute or chronic periarticular or articular inflammation so typical of the condition. Because of this one can classify periarthritis calcarea along with gout and chondrocalcinosis in the group of crystal deposition diseases. The actual cause of the calcification remains unknown but it is probable that, along with hereditary factors, disturbances in metabolism play an important role. The diagnosis of generalised periarthritis is made from the characteristic X-ray picture in conjunction with the clinical findings and, on occasion, the demonstration of hydroxyapatite crystals in the affected tissues. In the differential diagnosis gout, chondrocalcinosis, various inflammatory rheumatic conditions and septic arthritis must be excluded and various calcification processes, particularly interstitial calcinosis and lipocal cinogranulomatosis, must also be considered. Since the etiology of the calcification remains unknown to specific treatment is available. Symptomatic treatment with colchicine is mostly inadequate which is why one often has recourse to the use of non-steroid anti-inflammatory drugs and corticosteroids.
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PMID:[Generalized periarthritis calcarea (generalized hydroxyapatite disease)]. 39 90

Evidence favoring genetic predisposition to each of the major classes of rheumatic diseases is reviewed, including juvenile-onset rheumatoid arthritis, rheumatic fever, ankylosing spondylitis and other syndromes associated with spondylitis, adult-onset rheumatoid arthritis, gout and pseudogout, and systemic lupus erythematosus. In addition, simply inherited genetic diseases that may present with arthritis are noted for purposes of differential diagnosis. The importance of heterogeneous causes and mechanisms within each major class of disease is emphasized, both for patient care and for clinical investigation.
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PMID:Genetics of rheumatic diseases. 40 Aug 31

Diagnosis of gout by crystal identification in synovial fluid is simple and definitive. To treat gout effectively, the physician must determine whether overproduction or underexcretion of uric acid is the underlying mechanism. The acute attack is treated initially with antiinflammatory agents. After the acute phase is controlled, lifelong definitive therapy for hyperuricemia is begun.
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PMID:Hyperuricemia and gout. A modern approach to diagnosis and treatment. 42 48

A family is reported where four males have developed hyperuricemia, renal damage and, except for the youngest person affected, gout at an early age. The disease appears to be inherited as an X-linked recessive metabolic error. Clinically the patients have developed classical, tophaceous gout before the age of 25 and have suffered repeated attacks of renal colic. Renal tubular damage with decreased ability to concentrate and acidify urine was seen in a family member of only 16 years of age. Progressive renal failure seems to develop slowly. None in the family has shown neurologic symptoms, and two of the four affected men are apparently of at least average intelligence, two slightly below average. One female carrier has repeatedly passed uric acid stones. Studies of the red blood cell lysate have shown a normal activity of enzyme hypoxanthine phosphoribosyltransferase, and an increased level of adenine phosphoribosyltransferase. Skin fibroblasts from affected family members grew normally in the presence of 8-azaguanine. Administration of azathioprine to the patients did not decrease their serum uric acid levels. This is the first family described with this type of disorder of the purine metabolism.
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PMID:Recessive X-linked hyperuricemia with gout and renal damage, normal activity of hypoxanthine phosphoribosyltransferase and resistance to azaguanine. 42 44

The diagnosis of gout depends on showing urate crystals in synovial effusions or, with less certainty, recognizing a characteristic clinical presentation. The management of gout has four phases: control of inflammation, diagnostic evaluation, education of the patient, and treatment for the hyperuricemia. Sound logical principles guide each aspect. Careful attention to these four phases of management should lead to highly satisfactory control of the syndrome of gout.
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PMID:Management of gout. 43 90

Using the Intralipid lipid tolerance test we could not demonstrate any direct effect of serum triglyceride on uric acid or any influence of hyperuricaemia on triglyceride removal. This result supports previous studies suggesting that hyperuricaemia and hypertriglyceridaemia are linked through the association of obesity and alcohol excess rather than a direct cause and effect mechanism. It was possible to demonstrate significant reductions of serum triglyceride in patients with gout by reducing either their alcohol intake or body weight. Reduction of serum uric acid by probenecid had no effect on serum triglyceride or cholesterol. Similarly, allopurinol had no significant effect on serum triglyceride, but a significant fall of serum cholesterol was observed.
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PMID:Mechanism and treatment of hypertriglyceridaemia in gout. 43 44


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