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PubMed1995

A quantitative study of the phagocytosis of urate crystals in the synovial fluid of asymptomatic joints of patients with gout.

The objective of this study was to determine whether monosodium urate (MSU) crystals are phagocytosed in the synovial fluid (SF) of the asymptomatic joints of patients with gout. SF samples were obtained from 20 asymptomatic knees of 19 different patients. Cell and differential counts were done. Intracellular MSU crystals were identified by ordinary and polarizing light microscopy. We found that in 19 out of the 20 SF samples intracellular MSU crystals have been found. A mean of 22.55% [confidence interval (CI) 13.92, 31.18; range 0-62] of all the cells contained intracellular MSU crystals. The majority of the cells which contained intracellular crystals were mononuclear cells (MC), and polymorphonuclear (PMN) leucocytes containing intracellular crystals accounted only for 0.5% (CI 0, 1.05; range 0-5) of the total. The total cell count was 527 cells/mm3 (CI 226, 828, range;: 30-2670). Poor correlation was found between the percentage of cells with intracellular crystals and both the total cell count (r = -0.22) and the percentage of PMN leucocytes (r = -0.26). We conclude that cells containing phagocytosed MSU crystals--generally mononuclear cells--are a regular finding in the SF of asymptomatic joints of patients with gout. This finding indicates that other factors besides intra-articular interaction between crystals and cells are necessary to produce arthritis in gouty patients.

Crystallization↗
PubMed1995

The effects of alcoholic beverages on urate metabolism in gout sufferers.

The purine contents of commercial, low-alcohol and alcohol-free beers were determined. Four gout sufferers were studied under controlled conditions before and after ingestion of four different beverages containing alcohol, alcohol and purine, purine and neither alcohol nor purine. The results show a significant increase in purine excretion with a fluid load alone and impairment or reversal of this response with the other three beverages. These results are difficult to interpret on the basis of the alcohol and purine contents of the beverages alone. Isohumulones are present in all beers. Their effect on urate metabolism and excretion is unknown but needs further study as a possible explanation of these results. These results suggest that the three beverages other than a fluid load alone are unsuitable for gout sufferers.

Alcohol Drinking↗
PubMed1996

Characterization of E-selectin expression, leucocyte traffic and clinical sequelae in urate crystal-induced inflammation: an insight into gout.

The self-limiting response to urate crystals allows the exploration of events involved in both the onset and resolution of gout. Using i.v. injected radiolabelled anti-E-selectin monoclonal antibody 1.2b6 together with differentially radiolabelled neutrophils, mononuclear cells and albumin, we have characterized the expression of E-selectin in relation to leucocyte traffic, microvascular permeability and clinical sequelae following intracutaneous injection of monosodium urate crystals. We found that the inflammatory response in this model involved several distinct phases. First, E-selectin expression increased over 2-6 h in the context of increases in neutrophil and mononuclear cell accumulation, and albumin leakage. Secondly, leucocyte accumulation rapidly declined despite persisting E-selectin expression. Thirdly, E-selectin expression peaked at approximately 8 h and then fell despite an increase in clinically detectable erythema and induration. Lastly, these clinical manifestations of inflammation resolved despite the continued presence of urate crystals in the tissues. The further dissection of mechanisms regulating these phases will lead to a better understanding of events in both the pathogenesis and resolution of gout. Of broader significance, this inflammatory model may yield information about the protective events that underly resolution of inflammation, and provide insights into factors which determine chronicity.

Albumins↗
PubMed1993

Lead nephropathy, gout, and hypertension.

The EDTA (calcium disodium edetate) lead mobilization test revealed lead as the probable cause of renal disease in industrial lead workers and in patients with gout or essential hypertension. The data reviewed here demonstrate persistence of lead nephropathy in the contemporary scene despite the introduction of modern industrial and environmental exposure standards. Renal function and biopsy studies showed that lead nephropathy is a chronic tubulointerstitial renal disease with modest proteinuria which frequently presents with hyperuricemia, gout and hypertension. Only evaluation of body lead stores by either the EDTA lead mobilization test or by x-ray fluorescence is helpful in diagnosing lead nephropathy. While chelation therapy is safe and helpful in reversing early lead nephropathy, the best treatment is prevention. These studies further raise the possibility that chronic environmental lead poisoning and associated renal disease and hypertension may be a more widespread problem than suspected. Assessment of the true extent of chronic lead poisoning requires large scale epidemiological studies.

Animals↗
PubMed1992

Treatment of gout and crystal arthropathies and uses and mechanisms of action of nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory agents have anti-inflammatory, analgesic, and antipyretic actions. Nonsteroidal anti-inflammatory drugs are the preferred class of agents for the treatment of gout and other crystal-induced arthropathies. The use of colchicine for other than the prophylaxis of acute attacks is discouraged owing to side effects, which include death. The inhibition of the enzyme prostaglandin H synthase by most nonsteroidal anti-inflammatory drugs explains many of their effects and toxicities. However, it is likely that additional biologic actions are important. These include the inhibition of the transcription of the gene for prostaglandin H synthase, a direct central effect on peripheral inflammation, and the modulation of the functions of a variety of cells (eg, neutrophils, lymphocytes, and chondrocytes). This review focuses on the current controversy in the treatment of gout and discusses the recent literature on the actions of nonsteroidal anti-inflammatory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Gout and mechanisms of crystal-induced inflammation.

Since last year's review of gout and hyperuricemia, investigators have described new potential mechanisms that may contribute to urate crystal deposition and the propagation, self-limitation, and therapeutic control of gouty inflammation. The clinical presentation of gout in women continues to be described in greater detail. Also, new information on oral allopurinol desensitization is now available to help approach the difficult problem of allopurinol hypersensitivity.

Aged↗
PubMed1994

Hyperuricemia and gout.

Due to high uric acid clearance, which occurs prior to puberty, hyperuricosuria rather than hyperuricemia may be the only clue to diagnosis of purine overproduction in children who have enzymatic defects or who develop the condition in the course of treatment of malignancies. The probable inclusion of hyperuricemia as a part of syndrome X associated with insulin resistance may help in understanding its clinical associations, including coronary artery disease. Gout, hypertension, and lead often go together; thus, perhaps we should check for lead toxicity routinely in this setting. Asymptomatic joints of patients with gout contain monosodium urate crystals, and research on the factors that determine the occurrence of clinical inflammation in this setting continues as an area of current interest. Coating of the crystals by different proteins may modify their inflammatory potential and may be an important modulating mechanism.

Arthritis, Gouty↗
PubMed2001

Gout: diagnosis, pathogenesis, and clinical manifestations.

Gout is a common form of arthritis, in which many of the risk factors, pathogenetic mechanisms, and clinical features have been recognized for years. Nevertheless, new information has become available regarding the normal physiologic role of uric acid as an antioxidant, and greater insight has been obtained regarding the inflammatory process in acute gout. New studies have improved our understanding of the role of genetic and environmental factors responsible for hyperuricemia, and we know more about the significance of the association of hyperuricemia with other diseases. Clinically, rare complications and disease manifestations in new populations continue to be discussed, and diagnostic methods continue to be refined.

Arthritis, Gouty↗
PubMedDate not supplied

Monoarticular gout following trauma: MR appearance.

We report a case of gout with monoarticular tophaceous involvement of the proximal interphalangeal joint of the middle finger, emphasizing MR findings. To the best of our knowledge, the MR appearance of gout is not commonly known.

Arthritis, Gouty↗
PubMed1978

Synovial membrane histopathology in the differential diagnosis of rheumatoid arthritis, gout, pseudogout, systemic lupus erythematosus, infectious arthritis and degenerative joint disease.

The synovial membrane histologic sections from patients with six common rheumatic diseases were reviewed without knowledge of the clinical diagnosis. After histopathologic evaluation, the synovial membrane characteristics were grouped according to the patient's clinical diagnosis, and included 29 patients with rheumatoid arthritis, 13 with systemic lupus erythematosus, 17 with degenerative joint disease, 10 with acute bacterial arthritis, 8 with gout, and 13 with pseudogout. The only specific characteristics identified were bacteria (infectious arthritis), crystals (gout, pseudogout), and lymphoid follicles (rheumatoid arthritis). Nevertheless, other characteristic features of differential diagnostic utility were recognized, including the intensity and nature of synovial lining cell hyperplasia and of leukocyte infiltration. Light microscopic histopathologic changes in the common rheumatic diseases are not specific, but are of diagnostic utility. Complete and exhaustive review of each pathologic synovial membrane characteristic provides more justification for the routine use of synovial membrane biopsy as an adjunct to arthrocentesis in the evaluation of common rheumatic diseases.

Arthritis↗
PubMed1988

Polyarticular versus monoarticular gout: a prospective, comparative analysis of clinical features.

This investigation was undertaken to define prospectively the clinical characteristics of patients with crystal-documented gouty arthritis simultaneously involving multiple joints. Of 106 consecutive patients with gouty arthritis (GA), 42 (40%) had articular inflammation at 2 or more sites. Comparison of these 42 patients with GA with the 64 patients with GA who presented with monoarthritis yielded the following conclusions: 1) Polyarticular gout represents one end of a generally predictable spectrum of GA, reflecting chronicity associated with poor patients understanding, poor patient compliance, and suboptimal physician management. 2) Polyarticular patients with GA tend to develop attacks of more smoldering onset and increasing duration, while joint involvement tends to occur in an ascending but asymmetrical fashion, with upper extremity joints later added to repeatedly active lower extremity sites. 3) There may be a significant discrepancy between the site (or sites) of the GA patient's chief complaint and clinically involved joints on careful physical examination. 4) Recognition of polyarticular joint involvement increases the number of sites for potential joint and/or tophus aspiration, permitting greater ease of establishing a definitive diagnosis. 5) No single laboratory or synovial fluid value meaningfully distinguishes patients with polyarticular from those with monoarticular gout.

Adult↗
PubMedDate not supplied

The radiographic appearance of gout.

Gout is a disease that often leads to gouty arthritis, an arthropathy caused by elevated serum uric acid. Bony changes are not usually seen until years after the first clinical symptoms. This article describes gout and gouty arthritis with special reference to radiographic changes associated with the disease.

Gout↗
PubMed1987

NSAID-masked gout.

The use of NSAIDs masked the diagnosis of gout in nine patients with the chronic polyarticular form of the disease. The escape from detection of chronic polyarticular gout resulted in a needless dependence on NSAIDs, failure to correct the metabolic problem, and in some cases progression of joint destruction. Although acute inflammation was modified, basic pathogenic mechanisms remained unchecked and joint disease continued. The indiscriminate use of NSAIDs may, by promoting misdiagnosis, become a major obstacle to effective control of this, perhaps the most remediable of arthritic disorders.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1979

Recessive X-linked hyperuricemia with gout and renal damage, normal activity of hypoxanthine phosphoribosyltransferase and resistance to azaguanine.

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.

Adenine Phosphoribosyltransferase↗
PubMed1987

Does colchicine work? The results of the first controlled study in acute gout.

We have performed the first controlled study of colchicine in acute gout, to determine its efficacy and toxicity, and to define the natural history of acute gout. Two-thirds of colchicine-treated patients improved after 48 hours, but only one-third of the patients receiving placebo demonstrated similar improvement. The colchicine-treated patients responded earlier; significant differences from placebo were shown after 18-30 hours. All patients given colchicine developed diarrhea after a median time of 24 hours (mean dose of colchicine 6.7 mg). This side effect occurred before relief of pain in most patients.

Acute Disease↗
PubMed1966

The kidney in hepatic disease and in gout: clinical and pathologic aspects.

The role of the kidney in hepatic disease and in gout has been surveyed. Kidney involvement is more common but less severe in hepatic disease, whereas it is less common but more severe in gout. The underlying pathology of the kidney lesions in both diseases (including studies by electron microscopy and immunofluorescence) is presented, with emphasis on the role this pathologic substratum plays in the renal insufficiency. The clinical aspects, including the diagnostic approach and therapeutic management of the "hepatorenal syndrome" and "gouty kidney" are discussed, as are the prognostic implications of the natural history of these "complications" and measures aimed at their prevention.

Glomerular Filtration Rate↗
PubMed1977

Multicentre trial of naproxen and phenylbutazone in acute gout.

Naproxen 750 mg as a single dose followed by 250 mg three times daily has been compared with phenylbutazone 200 mg four times daily for 48 hours followed by 200 mg three times daily for treatment of acute gout in an open study on 41 patients. The drugs were equally effective with few and relatively mild side effects. Naproxen is a useful alternative agent for the treatment of acute gout.

Acute Disease↗
PubMed1980

Controlled inpatient study of tienilic acid in treatment of gout and hypertension.

Under inpatient controlled conditions 4 patients with gout and hypertension were treated with varying doses of tienilic acid, a new uricosuric diuretic. Plasma urate levels were reduced by an average of 50% in association with significantly increased urinary urate excretion. A twice-daily regimen was considerably more effective than a single morning dosage in reduction of plasma urate, though both regimens were equally effective in antihypertensive potency. The single daily regimen produced greater diurnal fluctuations in plasma urate and was more frequently associated with the development of acute gout attacks.

Blood Pressure↗