Development Of Tophi Research Articles

Drugs for gout.

Drugs for gout are used to reduce the pain and inflammation of acute flares, decrease the frequency of exacerbations, and lower serum urate levels to prevent recurrent flares, development of tophi, and joint damage.

Characteristics, Comorbidities, and Potential Consequences of Uncontrolled Gout: An Insurance-Claims Database Study.

IntroductionGout is a common, progressive, systemic inflammatory arthritis caused by hyperuricemia. Current guidelines recommend that serum uric acid (sUA) levels be maintained below 6.0 mg/dl to minimize acute gout attacks, tophi development, and long-term joint and organ damage. This study examined the influence of uncontrolled gout on post-diagnosis comorbidities and medication use.MethodsThe Humana Research Database (2007–2016, commercial insurance and Medicare) was searched (PearlDiver tool) for patients who had a gout diagnosis code, claims data for at least 6 months before and after diagnosis, and at least 90 days of continuous urate-lowering therapy within 1 year of diagnosis. Patients with controlled (all sUA measurements < 6.0 mg/dl) and uncontrolled (all sUA measurements ≥ 8.0 mg/dl) gout were further examined and compared to better understand the influence of uncontrolled gout on post-diagnosis comorbidities, medication use, and reasons for seeking medical care.ResultsA total of 5473 and 1358 patients met inclusion and classification criteria for the controlled and uncontrolled groups, respectively. Identified comorbidities in both groups included hypertension, hyperlipidemia, diabetes, cardiovascular disease, and chronic kidney disease (CKD). However, the uncontrolled group was more likely to have diabetes, CKD, and cardiovascular disease (including heart failure and atrial fibrillation). Additionally, CKD tended to be more advanced in the uncontrolled gout population (Stage 4–5: 34.6 vs. 22.2%). Overall opioid use was higher in uncontrolled patients.ConclusionsThe current study identified differences between controlled and uncontrolled gout patients, including usage of medication, severity of CKD, and prevalence of CKD, diabetes, and heart disease.

Metabolic characteristics and renal dysfunction in 65 patients with tophi prior to gout.

Tophi typically occur many years after uncontrolled gout. Therefore, their development before gout remains unusual. Such patients might exhibit some characteristic differences compared with typical tophaceous gout patients. In this study, 65 tophaceous gout patients with tophi as the first sign of gout (tophi-first group) were enrolled. Their clinical characteristics were compared with those of 1421 patients whose tophi occurred after gout (tophi-after group). Compared with the tophi-after group, the tophi-first group had a significantly higher percentage of female patients and patients with elderly onset of disease and a lower percentage of patients with a positive family history; these patients had lower body mass indices, serum urate levels, and estimated glomerular filtration rates (eGFRs). Female sex and negative family history were identified as the principal determinants of tophi development before gout. The decreasing eGFR among the tophi-first group was not due to the group per se but was a result of older age, longer tophi duration, and hyperuricemia. The most common site of initial tophi occurrence in both groups was the toe. In the tophi-first group, the occurrence rates for initial tophi sites were significantly higher at the finger but were lower at the ankle. The tophi-first group exhibited distinct characteristics of age, gender, family history, BMI, serum urate levels, and initial tophi site. This group had fewer comorbidities but similar renal dysfunction compared with the tophi-after group. Thus, patients presenting with tophi should be treated promptly, even if they have no history of gout symptoms.

Limitations of the Current Standards of Care for Treating Gout and Crystal Deposition in the Primary Care Setting: A Review

PurposeThis article outlines several important issues regarding the management of patients with gout. The topics discussed include best practices for gout based on the most current guidelines, opportunities for improving gout management, and current and emerging therapies for gout. Methods[PubMed and Google Scholar databases] were search for all articles and trials published before 2016, using the key terms [hyperuricemia, gout, tophi, joint erosion, joint damage, treatment guidelines, American College of Rheumatology (ACR), European League Against Rheumatism (EULAR), flare, comorbidity, epidemiology, adherence, serum uric acid (sUA), monosodium urate (MSU), <6 mg/dL, MSU crystal formation, as well as individual drug names and classes of treatments of interest (allopurinol, febuxostat, colchicine, non-steroidal anti-inflammatories (NSAIDs)]. Studies were selected that presented data on gout treatment, including drugs under development, and on the management of gout from both the physician and patient perspectives. The reference lists of identified articles were searched manually for additional publications. FindingsGout, a progressive debilitating form of inflammatory arthritis, is caused by factors that elevate serum uric acid (sUA) levels, leading to hyperuricemia. Continued elevated sUA can result in monosodium urate crystal deposition in joints and soft tissues, causing acute and chronic inflammation. Crystal deposition can lead to chronic gout, with an increased number of flares, tophi development, and structural joint damage. The aims of gout treatment are to reduce the sUA level to <6 mg/dL, to inhibit the formation of new crystals, and to promote the dissolution of existing crystals. Gout is often poorly managed for several reasons, including a lack of adherence to treatment guidelines by health care providers, patients’ poor adherence to therapy, and differences between a provider’s and patient’s perspectives regarding treatment. ImplicationsPatients need to be educated about their diagnosis and management of the disease, such as the importance of compliance with long-term treatment. Gout treatment may also confounded by contraindications to current standards of therapy and the limitations of current treatment paradigms. Recently approved medications, as well as drugs under development, may provide new ways for reaching the sUA target and also “curing” the disease.

White Clay Drainage in Chronic Tophaceous Gout

Please cite this article as: Zapata Bonilla SA, Jaquez Nevarez MR, Lopez Reyes A, Rodriguez Henriquez P. Exudado en «arcilla blanca» en gota tofacea cronica. Reumatol Clin. 2015;11:328–329. ∗ Corresponding author. E-mail address: drszapatami@gmail.com (S.A. Zapata Bonilla). by destructive arthritis, often with degenerative changes, bone erosions and development of tophi. Acute attacks can become polyarticular, additive and ascending; with a tendency to increase in severity.3 Tophi area cardinal feature of this entity; their structure consists of a conglomerate of urate crystals surrounded by4 fibrosis and inflammatory tissue.

Gout nodulosis: report of a rare case and brief review

The development of tophi in the absence of prior episodes of gouty arthritis is unusual. We hereby present a case of a non-alcoholic, normoglycemic, and normotensive middle-aged man, who presented with multiple nodules distributed bilaterally over the dorsum of hands, feet, and elbow joints without any prior history of arthritis. Serum uric acid level was found to be normal. Histology was consistent with features of tophi. On the basis of clinical and histological findings, the nodules were diagnosed as gouty tophi and the patient was diagnosed with gouty nodulosis. Gouty nodulosis is a very rare presentation of gout and only a few reports exist in the medical literature.

Untreated tophaceous gout

Gout is associated with hyperuricemia and characterized by inflammatory arthritis induced by monosodium urate crystal deposition in synovial fluid and other tissues. Tophi can occur in soft and osseous tissue, ligaments, and different organs, either in presence or absence of gouty arthritis. If left untreated, hyperuricemic patients (serum urate level = 6.8 mg/dL or 400 mol/L) can evolve from intermittent arthritis to polyarticular tophaceous gout with symptoms between attacks. Lowering serum urate levels with xanthine oxidase inhibitors or uricosuric agents prevents acute flares and tophi development. Synovial fluid crystals slowly dissolve and can disappear after normalization of serum urate levels. Uricosuric agents are, generally, ineffective in patients with renal impairment. The recommended target serum uric acid concentration is <6 mg/dL (357 mol/L). Although controversial, recommendations have been made to achieve a target serum urate level <5 mg/dL (297 mmol/L) in severe chronic gout patients, as this concentration may be associated with greater depletion of synovial fluid crystals and a reduction in tophus size. Therapy is usually continued indefinitely. Several urate-lowering agents are currently under clinical investigation. These include uricase agents and inhibitors of renal urate transporter proteins. Interventions which enhance patient education and treatment adherence are considered important in improving gout management.

CaseBook Consults: Improving Outcomes in Gout (Multimedia Activity)

Gout is a chronic, potentially debilitating condition characterized by an inflammatory process in the joints or periarticular tissues that results from the deposition of monosodium urate crystals. Underdiagnosis and undertreatment can lead to the development of tophi and chronic arthropathy. A presumptive diagnosis of gout can be made on the basis of the clinical presentation as well as risk factors such as metabolic syndrome. Key conditions to rule out in the differential diagnosis are septic arthritis, calcium pyrophosphate deposition disease (pseudogout), fracture, and rheumatoid arthritis. Acute flares of gout should be managed with nonsteroidal antiinflammatory drugs (NSAIDs), colchicine, or corticosteroids. With a diagnosis of gout, if urate-lowering therapy (ULT) is required, prophylaxis should be considered with low-dose colchicine or an NSAID, followed by the addition of ULT. The goal of ULT is to reach a serum uric acid (SUA) level ≤6.0 mg/dL. Measurements of SUA should be obtained after resolution of an acute attack, then periodically to facilitate titration of the ULT dose to achieve the target SUA level. Studies have confirmed significant reductions in gout attacks among patients who have attained SUA levels ≤6.0 mg/dL with ULT. Patient education concerning the disease and its treatment is essential to ensure close adherence with recommended therapies. Patients should also understand that ULT is intended as long-term, and for most patients, lifelong therapy to maximize the prospects for control of the disease. Clinicians should feel confident in making a presumptive diagnosis and choosing a therapeutic regimen for gout while effectively communicating with and educating patients about their disease.

Gout Is on the Rise; Improved Treatments Needed

Sharon Worcester is with the Southeast bureau of Elsevier Global Medical News. DESTIN, FLA. — The incidence of gout is on the rise, and lifestyle factors are largely to blame, according to Dr. N. Lawrence Edwards, professor and vice chairman of the department of medicine at the University of Florida, Gainsville. For example, one study showed that between 1977–1978 and 1995–1996, the annual rate of primary gout more than doubled, from about 16 cases/100,000 population to nearly 42 cases/100,000 population. Factors that appear to play a role in this incidence spike are greater longevity, widespread diuretic and aspirin use, hypertension incidence, obesity, metabolic syndrome, and dietary trends, Dr. Edwards said at the annual Rheumatology on the Beach. Certain dietary factors affect the risk for gout (high consumption of meat, seafood, and beer increase risk, and high intake of dairy is protective, for example); other risk factors are modifiable (such as obesity and hypertension). However, despite the association between lifestyle factors and risk, their modification will not eliminate existing gout. Weight reduction, decreased alcohol consumption, and reduced intake of purine-rich foods (which have been linked with gout) will reduce urate levels only by about 1 mg/dL. Urate-lowering therapy, which 15 years ago was reserved for use only in patients with chronic gout, now is considered warranted following the first one or two acute attacks, he noted. Treatment goals for gout include termination of the attack as rapidly as possible, prevention of future attacks by reducing the chance of crystal-induced inflammation, and long-term correction of metabolic problems with a goal of lowering serum urate to below 6 mg/dL to allow depletion of the total body uric acid pool. Uricosuric agents, such a probenecid, and the xanthine oxidase inhibitor allopurinol are used for this purpose. These agents are used for reducing urate levels—the most common physiologic abnormality found in gout patients—but uricosuric agents increase the risk of uric acid crystallization in the urine and associated stone formation. A number of other agents, such as ampicillin, penicillin, cephradine, heparin, and rifampicin, can potentially affect the action of uricosuric agents, Dr. Edwards said. Allopurinol, which is a purine analog that is both a substrate and inhibitor of xanthine oxidase, is effective both for people who overproduce and for those who underexcrete xanthine oxidase. The drug also has the convenience of single daily dosing, and it can be efficacious in patients with renal insufficiency. However, allopurinol isn't always effective for achieving target serum urate levels. In one study of patients treated daily with a 300-mg dose, only about half achieved a serum urate level of 6 mg/dL, and in an observational study of nearly 6,000 patients, median serum urate levels decreased from 8.7 mg/dL to 7.1 mg/dL. Although dosing up to 800 mg/day is acceptable, concerns about intolerance based on reports of severe hypersensitivity syndrome, rash, gastrointestinal problems, increases in liver enzymes, and rare bone marrow suppression, tend to scare physicians away from prescribing higher doses, he noted. As with uricosuric agents, drug-drug interactions also are a problem with allopurinol. Keys to effective treatment with this drug include dosing allopurinol to achieve a serum urate level between 5.0 and 6.0 mg/dL, which allows reduction of total body urate pool and mobilization of deposited crystals, Dr. Edwards said, stressing the need to start at a low dose of 50–100 mg/day, with close monitoring of escalation. If the target serum urate level is reached, therapy should be ongoing; intermittent therapy or withdrawal will lead to recurrence of acute attacks within 6 months, and development of tophi within a few years. Allopurinol shouldn't be started during an acute attack and shouldn't be stopped in those already on treatment. Also keep in mind that these medications will not control the pain of gout, and pain medications will do nothing to reduce serum urate, he advised. New urate-lowering agents that improve compliance and are useful in those with allopurinol intolerance and renal failure are needed, as are options for those taking other drugs that interact with allopurinol and uricosuric agents, he concluded.

Tophi as the Initial Manifestation of Gout

The development of tophi in the absence of prior episodes of gouty arthritis is unusual. We present six such cases and review 26 previously published cases. These patients differ from those with typical gout in that they were older, more likely to be women, and usually had predominant or exclusive finger involvement. Most had renal insufficiency and many were receiving an anti-inflammatory or diuretic. Although several possibilities for the lack of gouty arthritis in the presence of tophi exist, usually no clear explanation is found.

Misdiagnosis of Rheumatoid Arthritis in an Elderly Woman with Gout

Polyarticular gout may be misdiagnosed in the elderly. This reflects the confusing clinical presentation of "diuretic gout" in the elderly, characterized by polyarticular onset, subacute symptoms, hand involvement, and early development of tophi. A misdiagnosis of rheumatoid arthritis can lead to poor treatment of gout, failure to recognize underlying renal insufficiency, and associated cardiac risks. Hyperuricemia may reflect systemic ATP depletion in acutely ill patients and thus represents a predictor for mortality. Medical treatment of polyarticular gout in elderly patients with compromised cardiac and renal function requires recognition of the clinical profile and consideration of the increased toxicity from standard therapies.

Gout and Gouty Arthritis

According to these two eminent specialists, proper treatment of this destructive disease can prevent its extension or reverse its morbid changes. Gout is a metabolic defect which results in the deposition of urates in the organs and soft tissues. In the arthritic phase, the patient has agonizing joint pain. The tophaceous stage produces joint damage, destruction, and deformity. The aim of uricosuric therapy is to prevent the development of tophi or effect their resorption.