Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Rheum Dis Clin North Am [journal]
- Gout and crystal arthropathies. [Editorial]
- Rheum Dis Clin North Am 2014 May; 40(2):xv-xvi.
- Gout and crystal arthropathies. [Editorial]
- Rheum Dis Clin North Am 2014 May; 40(2):xiii.
- Emerging Therapies for Gout. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):375-387.
Over the past decade much has been learned about the mechanisms of crystal-induced inflammation and renal excretion of uric acid, which has led to more specific targeting of gout therapies and a more potent approach to future management of gout. This article outlines agents being developed for more aggressive lowering of urate and more specific anti-inflammatory activity. The emerging urate-lowering therapies include lesinurad, arhalofenate, ulodesine, and levotofisopam. Novel gout-specific anti-inflammatories include the interleukin-1β inhibitors anakinra, canakinumab, and rilonacept, the melanocortins, and caspase inhibitors. The historic shortcomings of current gout treatment may, in part, be overcome by these novel approaches.
- Long-Term Management of Gout: Nonpharmacologic and Pharmacologic Therapies. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):357-374.
Gout is a common disorder with clinical signs and symptoms resulting from inflammatory responses to monosodium urate crystals deposited in tissues from extracellular fluids saturated for urate. Long-term management of gout focuses on nonpharmacologic and pharmacologic means to achieve and maintain serum urate levels in a subsaturating range. Despite a firm understanding of gout pathophysiology, means to achieve certain diagnosis, and a variety of effective therapies, treatment outcomes remain suboptimal. In this review, available nonpharmacologic and pharmacologic therapies for chronic gout are discussed and a framework is provided for successful achievement and maintenance of goal-range serum urate levels.
- Nonpharmacologic and Pharmacologic Management of CPP Crystal Arthritis and BCP Arthropathy and Periarticular Syndromes. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):343-356.
Calcium crystal arthritis is often unrecognized, poorly managed, and few effective therapies are available. The most common types of calcium crystals causing musculoskeletal syndromes are calcium pyrophosphate (CPP) and basic calcium phosphate (BCP). Associated syndromes have different clinical presentations and divergent management strategies. Acute CPP arthritis is treated similarly to acute gouty arthritis, whereas chronic CPP and BCP arthropathy may respond to strategies used for osteoarthritis. Calcific tendonitis is treated with a variety of interventions designed to dissolve BCP crystals. A better understanding of the causes and larger well-planned trials of current therapies will lead to improved care.
- Treatment of Acute Gout. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):329-341.
This article presents an overview of the treatment of acute gout. Nonpharmacologic and pharmacologic treatments, monotherapy versus combination therapy, suggested recommendations, guidelines for treatment, and drugs under development are discussed.
- The Structural Consequences of Calcium Crystal Deposition. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):311-328.
Calcium pyrophosphate dihydrate and basic calcium phosphate (BCP) crystals are the most common calcium-containing crystals associated with rheumatic disease. Clinical manifestations of calcium crystal deposition include acute or chronic inflammatory and degenerative arthritides and certain forms of periarthritis. The intra-articular presence of BCP crystals correlates with the degree of radiographic degeneration. Calcium crystal deposition contributes directly to joint degeneration. Vascular calcification is caused by the deposition of calcium hydroxyapatite crystals in the arterial intima. These deposits may contribute to local inflammation and promote further calcification, thus aggravating the atherosclerotic process. Calcium crystal deposition results in substantial structural consequence in humans.
- Structural Joint Damage in Gout. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):291-309.
This article summarizes the structural damage that is observed in advanced gout and current understanding of the mechanisms by which this damage occurs. Interactions between monosodium urate crystals and cells within the joint are described as well as knowledge gained from imaging studies. Future research directions and potential therapeutic strategies for the prevention and treatment of joint damage in gout are also discussed.
- The Genetic Basis of Gout. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):279-290.
Gout results from deposition of monosodium urate (MSU) crystals. Elevated serum urate concentrations (hyperuricemia) are not sufficient for the development of disease. Genome-wide association studies (GWAS) have identified 28 loci controlling serum urate levels. The largest genetic effects are seen in genes involved in the renal excretion of uric acid, with others being involved in glycolysis. Whereas much is understood about the genetic control of serum urate levels, little is known about the genetic control of inflammatory responses to MSU crystals. Extending knowledge in this area depends on recruitment of large, clinically ascertained gout sample sets suitable for GWAS.
- Comorbidities in Patients with Crystal Diseases and Hyperuricemia. [REVIEW]
- Rheum Dis Clin North Am 2014 May; 40(2):251-278.
Crystal arthropathies are among the most common causes of painful inflammatory arthritis. Gout, the most common example, has been associated with cardiovascular and renal disease. In recent years, evidence for these associations and those involving other comorbidities, such as the metabolic syndrome, have emerged, and the importance of asymptomatic hyperuricemia has been established. In this review, an update on evidence, both experimental and clinical, is presented, and associations between hyperuricemia, gout, and several comorbidities are described. Causality regarding calcium pyrophosphate arthropathy and associated comorbidities is also reviewed.