Gouty Arthritis

Meyer MF, Rüther W. · Medizinische Klinik I, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Ruhr-Universität Bochum, Bürkle-de-la-Camp-Platz 1, 44789 Bochum, Deutschland. · Z Rheumatol. · Pubmed #17934741 No free full text.

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Liu-Bryan R, Terkeltaub R. · No affiliation provided · Arthritis Rheum. · Pubmed #16447213 links to  free full text

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Fam AG. · No affiliation provided · BMJ. · Pubmed #12411331 links to  free full text

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Lin CX, Ma HF, Ma WZ, Zhou PJ. · College of Acu-moxibustion, Beijing University of Chinese Medicine, Beijing 100029, China. · Zhen Ci Yan Jiu. · Pubmed #19526812 No free full text.

Abstract: In the present paper, the authors make a summary on the clinical application of acu-moxibustion therapy in the treatment of gouty arthritis in recent 10 years. Acupuncture needles often used are filiform needle, red-hot needle, moxibustion-warmed needle and three-edged needle. Clinical studies have showed that acupuncture therapy has a definite efficacy in relieving gouty arthritis and has its clinical characteristics, such as faster efficacy, lower relapse rate, etc. in comparison with medication.

Edwards NL. · Department of Medicine, University of Florida, Gainesville, 32610-0221, USA. · Curr Opin Rheumatol. · Pubmed #19339923 No free full text.

Abstract: PURPOSE OF REVIEW: The role of uric acid as a mediator of vascular damage is not a new idea but has only recently gained widespread acceptance. Uric acid has previously been viewed as a benign solute in serum until it exceeds its saturation level. Others have viewed it as an important antioxidant. These opinions have given way to strong epidemiologic evidence that uric acid elevation may damage endothelial cells and cause significant medical problems. RECENT FINDINGS: The comorbidities associated with gout include hypertension, renal failure, obesity and diabetes. Multiple large epidemiologic studies cited in this review show that uric acid itself may play an important role in initiating the vascular endothelial dysfunction associated with this cluster of medical problems and ultimately lead to stroke, coronary artery disease and chronic kidney disease. These studies are supported by experiments in animals demonstrating how uric acid can gain entrance into cells and function as a 'pro-oxidant'. SUMMARY: Uric acid has been long recognized as the cause of gouty arthritis and kidney stones. There is mounting evidence that it may also have an important role in the development of vascular conditions such as coronary heart disease, stroke and kidney disease. These findings have important implications for the way we view asymptomatic hyperuricemia and for future therapeutic interventions.

Singh JA. · Rheumatology Section, Medicine Service, VA Medical Center, Rheumatology (111R), One Veteran's Drive, Minneapolis, MN 55417, USA. · Curr Rheumatol Rep. · Pubmed #19296889 No free full text.

Abstract: Significant pain, activity limitation, and disability in patients with acute and chronic gouty arthritis lower health-related quality of life. Although many effective therapies are available for gouty arthritis, medication errors are common. One goal of therapy is to reduce the frequency of gout flares by lowering serum uric acid. Further, evidence suggests that the quality of care provided to patients with gout may also impact health-related quality of life. This article reviews evidence concerning quality of care and quality of life for patients with gout.

Magliano M. · Department of Rheumatology, Stoke Mandeville Hospital, Mandeville Road, Aylesbury HP21 8AL, UK. · Menopause Int. · Pubmed #19037063 No free full text.

Abstract: Obesity affects over 20% of the UK's adult population and its prevalence is rising. Obesity can lead to a variety of musculoskeletal problems and is independently associated with locomotor disability and joint pain. Obesity increases the risk of radiographic knee osteoarthritis (OA), but has a lesser effect on disease progression. The association with hip and hand OA is weaker, but implies that excess adipose tissue produces humoral factors, altering articular cartilage metabolism. It has been postulated that the leptin system could be a link between metabolic abnormalities in obesity and increased risk of OA. Although obesity was initially thought to increase the risk of rheumatoid arthritis (RA), further studies showed, that heavier patients with RA have less radiological disease progression and possibly better survival. On the other hand, obesity is strongly associated with hypeuricaemia and gouty arthritis. High body weight correlates independently with metabolic syndrome and may contribute to increased cardiovascular morbidity in patients with gout. Weight reduction should be an important part of treatment for OA and gout. Because obesity at a young age correlates with the development of OA and gout in later life, preventive public health strategies aimed at lowering the incidence of obesity are of most importance.

Edwards NL. · Department of Medicine, University of Florida, Gainesville, 32610-0221, USA. · Cleve Clin J Med. · Pubmed #18822470 links to  free full text

Abstract: Elevated serum urate levels are recognized as leading to gouty arthritis, tophi formation, and uric acid kidney stones. While serum urate elevations have long been associated with renal disease, they are not usually considered to have a causal role in kidney dysfunction. However, recent epidemiologic studies have identified serum urate elevations as an independent risk factor for chronic kidney disease. Hyperuricemia has also been found to be an independent risk factor for cardiovascular disease and hypertension. An animal model of mild hyperuricemia has shed new light on a potential mechanism of microvascular changes leading to endothelial dysfunction, a precursor to both coronary artery disease and hypertension. Additional animal studies and recent epidemiologic findings have provided further evidence that soluble urate is a risk factor for nonarticular disease.

Mandell BF. · Department of Rheumatic and Immunologic Diseases, Center for Vasculitis Care and Research, Cleveland Clinic, Cleveland, OH 44195, USA. · Cleve Clin J Med. · Pubmed #18822469 links to  free full text

Abstract: Biologically significant hyperuricemia occurs when serum urate levels exceed urate solubility, ie, at approximately 6.8 mg/dL. At serum urate levels above this threshold, manifestations of chronic crystal deposition, including gouty arthritis, may occur, although asymptomatic hyperuricemia often persists for many years without progression. Intercritical asymptomatic periods follow the resolution of acute gout flares, but crystals remain in the joint during these intervals and further deposition may continue silently. Ultimately this may lead to persistent attacks, chronic pain, and, in some patients, joint damage.

Schumacher HR. · University of Pennsylvania, Philadelphia, PA, USA. · Cleve Clin J Med. · Pubmed #18822468 links to  free full text

Abstract: An elevated serum urate level, together with local factors, can result in the deposition of urate crystals into the joints. Once crystals are deposited into a joint, they can be released into the joint space and initiate an inflammatory cascade causing acute gouty arthritis. These acute flares resolve, but the crystals remain in the joint. The way to ultimately correct the underlying metabolic problem of hyperuricemia and the crystal deposition is to lower the serum urate level and dissolve the crystal deposits. This will stop both the acute attacks and the progressive joint damage.

Stapleton JJ, Rodriguez RH, Jeffries LC, Zgonis T. · Foot and Ankle Surgery, VSAS Orthopaedics, Lehigh Valley Hospital, Cedar Crest Campus, Allentown, PA, USA. · Clin Podiatr Med Surg. · Pubmed #18722911 No free full text.

Abstract: Gouty arthropathy about the first metatarsal-phalangeal joint with a superimposed deep infection poses a great challenge to the foot and ankle surgeon. The inflammatory nature of gout compromises the soft-tissue envelope and vasculature to the area. Acute gouty arthropathy is usually a contraindication to surgical intervention secondary to wound-healing complications and possible vasospasm leading to tissue necrosis. However, if deep infection is present this must be managed with adequate surgical débridement followed by delayed soft-tissue and osseous reconstruction to prevent amputation. The authors present an exceptional clinical manifestation of gouty arthropathy of the first metatarsal-phalangeal joint concomitant with deep abscess and osteomyelitis and the surgical approach taken to afford functional limb salvage.

Jacobson JA, Girish G, Jiang Y, Sabb BJ. · Department of Radiology, University of Michigan Medical Center, 1500 E Medical Center Dr, TC-2910L, Ann Arbor, MI 48109-0326, USA. · Radiology. · Pubmed #18710973 No free full text.

Abstract: In the presence of joint space narrowing, it is important to differentiate inflammatory from degenerative conditions. The presence of osteophytes, bone sclerosis, and subchondral cysts and the absence of inflammatory features such as erosions suggest osteoarthritis. Typical osteoarthritis involves specific joints at a particular patient age. When osteoarthritis involves an atypical joint, occurs at an early age, or has an unusual radiographic appearance, then other causes for cartilage destruction should be considered, such as trauma, crystal deposition, neuropathic joint, and hemophilia. There are several types of arthritis, such as juvenile chronic arthritis and gouty arthritis, that may have a variable appearance compared with that of other common inflammatory arthritides.

Krishnan E. · S709 BST South, 3500 Terrace Street, Pittsburgh, PA 15215, USA. · Curr Rheumatol Rep. · Pubmed #18638434 No free full text.

Abstract: Gout is the leading cause of inflammatory arthritis, typically affecting men and characterized by intermittent, abrupt onset of intense inflammation. The association between gout, atherosclerosis, and vascular disease has been noted in medical literature since the end of the 19th century, yet it has not been well studied. This review critically appraises the few epidemiologic studies that ask if gout is a risk factor for coronary artery disease. An exhaustive literature search using search engines and cross-referencing found four major studies and several smaller studies that have evaluated gout as a risk factor for coronary artery disease. The available studies were too heterogeneous to permit formal meta-analysis. Although there are gaps in evidence pointing to a causative pathway, overall, evidence exists for a relationship between gouty arthritis and coronary artery disease independent of traditional risk factors.

Nuki G. · University of Edinburgh, Osteoarticular Research Group, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom. · Curr Rheumatol Rep. · Pubmed #18638431 No free full text.

Abstract: New light has been shed on the mechanisms of action of colchicine in crystal-associated arthropathies. Colchicine, long used to treat gout, arrests microtubule assembly and inhibits many cellular functions. At micromolar concentrations, it suppresses monosodium urate crystal-induced NACHT-LRR-PYD-containing protein-3 (NALP3) inflammasome-driven caspase-1 activation, IL-1beta processing and release, and L-selectin expression on neutrophils. At nanomolar concentrations, colchicine blocks the release of a crystal-derived chemotactic factor from neutrophil lysosomes, blocks neutrophil adhesion to endothelium by modulating the distribution of adhesion molecules on the endothelial cells, and inhibits monosodium urate crystal-induced production of superoxide anions from neutrophils. Cyto-chrome P450 3A4, the multidrug transporter P-glycoprotein, and the drugs that bind these proteins influence its pharmacokinetics and pharmacodynamics. Trial evidence supports its efficacy in acute gout and in preventing gout flares, but it has narrow therapeutic index, and overdosage is associated with gastrointestinal, hepatic, renal, neuromuscular, and cerebral toxicity; bone marrow damage; and high mortality.

Fodor D, Albu A, Gherman C. · 2nd Internal Medicine and Rheumatology Department, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania. · Ortop Traumatol Rehabil. · Pubmed #18449120 No free full text.

Abstract: The aim of this paper is to describe the ultrasonographic findings in rheumatologic pathology due to crystal deposition. There are four main types of crystals involved: monosodium urate, calcium pyrophosphate dihydrate, basic calcium phosphate (hydroxyapatite), and calcium oxalate. In gout the joint fluid is anechoic only at the first gouty attack; afterwards the synovium begins to proliferate. Double contuour sign, a focal or diffuse enhancement of the superficial margin of the articular cartilage is a specific finding. Bursitis has chronic features from the beginning. The ultrasonographic aspect of tophi depends on their age and size (at first small, hypoechoic and homogenous nodules, then echoic with hyperechoic edges and finally pseudotumoral, inhomogeneous). The depositions in the superficial layer are hyperechoic, well delimited only in the absence of inflammatory reaction. The depositions at the entheseal level are leading to the gouty enthesopathy. In knee involvement irregularities of the anterior surface of patella are found. In chondrocalcinosis the most important ultrasonographic signs are the thin hyperechoic band, parallel to the surface of the hyaline cartilage and the punctuated pattern of the fibrocartilage. In hydroxyapatite associated disease, calcifications are frequent in the shoulder or in the great trochanter of the hip, with aspects depending of the calcification phase. Milwakee shoulder is an advanced form of this pathology, associated with rotator cuff arthropathy. Oxalate crystal deposition disease is seen rarely, in patients with primary hyperoxaluria and in patients with end-stage renal disease. Therefore ultrasonography is useful in characterize the articular and juxta-articular alterations in crystal related diseases.

Avram Z, Krishnan E. · Division of Rheumatology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA. · Rheumatology (Oxford). · Pubmed #18443007 No free full text.

Abstract: Rheumatologists care for patients with gouty arthritis, a condition caused by chronic and uncontrolled hyperuricaemia. Hyperuricaemia, gout and renal dysfunction are often bedfellows, raising the possibility of the former causing the latter. We sought the answer to the question 'Among patients with normal measures of glomerular filtration, does hyperuricaemia predict future renal disease'? We identified prospective cohort studies evaluating the relationship between serum uric acid and chronic kidney function from the past 20 yrs, through MEDLINE, Cochrane Library and EMBASE searches and bibliography cross-referencing. Nine cohort studies that met the selection criteria were found. Because of the extreme heterogeneity, a statistical meta-analysis was not performed. Most (eight out of nine) studies found an independent risk factor for deterioration of kidney function. Nearly all published prospective studies support the role of hyperuricaemia as an independent risk factor for renal dysfunction. In the absence of large randomized controlled trials of uric acid reduction, it remains uncertain if this relation is causal or merely an epiphenomenon. Regardless, our review suggests that hyperuricaemia is a useful, inexpensively measured, widely available and useful early marker for chronic kidney disease.

Akahoshi T. · Department of General Medicine, Kitasato University School of Medicine. · Nippon Rinsho. · Pubmed #18409519 No free full text.

Abstract: Gout is a disease caused by the deposition of monosodium urate monohydrate (MSU) crystals. Precise mechanisms underlying the initiation of acute gout, however, are not known. Recent investigations provided novel evidence in the pathology of acute gout. A number of studies indicated that MSU crystals can act as a "danger signal" which resembles exogenous adjuvants, and toll-like receptor(TLR)-mediated pathways and/or MyD88-dependent IL-1 receptor pathways are involved in acute gout. Up-regulation of the triggering receptor expressed on myeloid cells 1(TREM-1) in phagocytes by the stimulation with MSU crystals has been demonstrated. Furthermore, pathological significance of NALP 3 inflammasome in gout has been also demonstrated. These findings provide a new insight into the mechanisms underlying the initiation of MSU crystal-induced acute inflammation.

Kalliolias GD, Liossis SN. · Hospital for Special Surgery, Arthritis and Tissue Degeneration Program, Department of Medicine, New York, NY 10021, USA. · Expert Opin Investig Drugs. · Pubmed #18321234 No free full text.

Abstract: BACKGROUND: IL-1 receptor antagonist (IL-1Ra) is a naturally occurring IL-1RI-binding molecule that blocks the biologic effects of the proinflammatory cytokine IL-1. A recombinant form of human IL-1Ra, anakinra (Kineret), has been approved for use in rheumatology initially to manage rheumatoid arthritis (RA) patients that are refractory to more conventional forms of treatment. OBJECTIVE: This review summarizes the experience with anakinra in the treatment of patients with rheumatic diseases emphasizing its beneficial effects in novel applications. METHODS: English-language trials of anakinra were searched using MEDLINE and abstracts from rheumatology scientific meetings. RESULTS/CONCLUSIONS: In the treatment of patients with RA anakinra is effective but inferior to TNF-alpha blocking agents. Over the last few years it has become increasingly evident that anakinra is highly effective and safe in patients with systemic-onset juvenile idiopathic arthritis, adult-onset Still's disease, hereditary autoinflammatory syndromes, Schnitzler's syndrome and recently in gouty attacks.

Schlesinger N. · Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903-0019, USA. · Drugs. · Pubmed #18318560 No free full text.

Abstract: It is important to distinguish between therapy used to reduce acute inflammation in gout and therapy used to manage hyperuricaemia in patients with chronic gouty arthritis. This article discusses treatments for acute gout, emphasizing the use of corticotrophin (adrenocorticotropic hormone; ACTH) and the evidence on which we base our treatment of acute gout. There are no formal guidelines for the treatment of acute gout and only a few randomized controlled trials have been conducted to evaluate the efficacy of the various treatments for acute gout. The options available for the treatment of acute attacks of gout are NSAIDs, colchicine, corticosteroids, corticotropin and intra-articular corticosteroids. Most rheumatologists practicing in the US use combination therapy to treat acute gout, a practice that merits study. In a patient without complications, NSAIDs are the preferred therapy. The most important determinant of therapeutic success is not which NSAID is chosen, but rather how soon NSAID therapy is initiated. Exciting new research shows that corticotropin acts peripherally by activation of the melanocortin type 3 receptor, and this could be responsible, at least in part, for its efficacy in acute gout. Hopefully, this will lead to renewed interest in corticotropin as a treatment for acute gout.

Schlesinger N. · Division of Rheumatology, Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, One Robert Wood Johnson Pl., New Brunswick, NJ 08903-0019, USA · Minerva Med. · Pubmed #18299687 No free full text.

Abstract: Acute gouty arthritis typically presents with rapid development of severe joint pain, swelling, and tenderness that reaches its maximum within just 6-12 h, especially with overlying erythema, most classically in the first metatarsophalangeal joint. Demonstrating the presence of monosodium urate (MSU) crystals in the joint fluid or tophus has been the gold standard for the diagnosis of gout. However, many physicians do not perform synovial fluid analysis. In the absence of demonstrating the presence of MSU crystals in aspirated joint fluid or tophus clinical, radiological and laboratory criteria are helpful. This paper presents an overview of the various classification criteria, clinical presentations, laboratory and radiological studies needed to make the diagnosis of gout.

Kuo CF, Tsai WP, Liou LB. · Division of Rheumatology, Allergy and Immunology, Chang-Gung Memorial Hospital, Kwei-san Hsiang, Tao-Yuan County, Taiwan. · Clin Rheumatol. · Pubmed #18064397 No free full text.

Abstract: Copresent rheumatoid arthritis (RA) and gout is seldom reported. This study summarizes the findings of eight cases of copresent RA and gout and compares them with 31 pure RA cases. Additional reported cases were retrieved from the current literature by Medline search. Patients with copresent RA and gout were older (p = 0.014) and predominantly male (p < 0.01). Synovial fluid, positive for urate crystals, was aspirated most frequently from the knee (five out of eight), followed by the first metatarsophalangeal joint (three out of eight). Serum creatinine and urate levels in the copresent group were significantly higher (p < 0.01, both), and serum hemoglobin was lower (p = 0.04) than those with pure RA. Copresent subjects had much lower percentage of positive rheumatoid factor (RF) tests than patients with pure RA (37.5 vs 80.6%). Only one copresent subject had both RF and anti-cyclic citrullinated peptide antibody. Of copresent subjects, 75% had gouty arthritis before diagnosis of RA, which is consistent with earlier reports. Seven copresent subjects had gout attacks under disease-modifying antirheumatic drug use. This study revealed that polyarthritis negative for RF in a previously gouty patient may be RA and vice versa. This combination occurs more frequently in males. Moreover, anti-CCP antibody examination is not helpful for this diagnosis. Therefore, physicians must obtain synovial fluid for analysis in joints with intense swelling, especially in old RA subjects with renal insufficiency or involvement of lower extremities. Conversely, RA must be considered in gouty patients with polyarticular involvement.

Mikuls TR. · Department of Internal Medicine, Section of Rheumatology and Immunology, University of Nebraska Medical Center, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, USA. · Clin Exp Rheumatol. · Pubmed #18021516 No free full text.

Abstract: Gout is a growing health problem, affecting approximately 7% of men and 3% of women over the age of 65 years. Although effective therapies for gout management exist, quality in gout care has been too frequently characterized as being "suboptimal." This review examines issues pertinent to quality of care in gouty arthritis with a focus on initial reports examining suboptimal care, subsequent efforts to develop quality of care indicators for gout management, more recently published evidence-based recommendations for gout diagnosis and treatment, and an ongoing international initiative to develop core outcome measures for acute and chronic gout. "If you can not measure it, you can not improve it" - Lord Kelvin.

So A. · Service de Rhumatologie, Departement de Médicine, CHU Vaudois, University of Lausanne, 1011, Lausanne, Schweiz. · Z Rheumatol. · Pubmed #17924125 No free full text.

Abstract: Gout is caused by the deposition of monosodium urate crystals (MSU) in tissue and provokes a local inflammatory reaction. It is the most common form of inflammatory arthritis in the elderly. The formation of MSU crystals is facilitated by hyperuricemia. In the last two decades, both hyperuricemia and gout have increased markedly and similar trends in the epidemiology of the metabolic syndrome have been observed. Recent studies provide new insights into uric acid metabolism in the kidneys as well as possible links between hyperuricemia and hypertension. MSU crystals provoke inflammation by activating leukocytes to produce inflammatory cytokines and other inflammatory mediators. The uptake of MSU crystals by monocytes involves interactions with Toll-like receptors (TLR-2 and TLR-4) and CD14, components of the innate immune system. Intracellularly, MSU crystals activate inflammasomes to activate pro-IL-1 (interleukin 1) processing to yield mature IL-1beta. The inflammatory effects of MSU are IL-1-dependent and can be blocked by IL-1 inhibitors. These advances provide new therapeutic targets to treat hyperuricemia and gout.

Eggebeen AT. · University of Pittsburgh Arthritis Institute, Pittsburgh, Pennsylvania 15261, USA. · Am Fam Physician. · Pubmed #17910294 links to  free full text

Abstract: Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.

Pope RM, Tschopp J. · Northwestern University Feinberg School of Medicine, and the Jesse Brown VA Medical Center, Chicago, Illinois 60611, USA. · Arthritis Rheum. · Pubmed #17907163 links to  free full text

This publication has no abstract.