Increase in thyroid stimulating hormone levels in patients with gout treated with inhibitors of xanthine oxidoreductase.

Increase in thyroid stimulating hormone (TSH) levels over the upper normal limit has been reported in a small percentage of patients treated with febuxostat in clinical trials, but a mechanistic explanation is not yet available. In an observational parallel longitudinal cohort study, we evaluated changes in TSH levels in patients with gout at baseline and during urate-lowering treatment with febuxostat. Patients to be started on allopurinol who had a measurement of TSH in the 6-month period prior to baseline evaluation were used for comparison.

Renal clearance of uric acid is linked to insulin resistance and lower excretion of sodium in gout patients.

Inefficient renal excretion of uric acid is the main pathophysiological mechanism for hyperuricemia in gout patients. Polymorphisms of renal tubular transporters linked with sodium and monosaccharide transport have yet to be demonstrated. We intended to evaluate the impact of insulin resistance, evaluated with the homeostasis model assessment (HOMA), through a transversal study of non-diabetic patients with gout, with normal renal function, not treated with any medication but colchicine as prophylaxis.

Clinical manifestations and diagnosis of gout.

Gout has been academically considered to be a step-up disease consisting of different stages: acute gout, intercritical gout, and chronic gout. This simple approach may lead to misinterpretation and misdiagnosis. In clinical practice, we should consider gout as a single disease with either or both acute (most commonly, episodes of acute inflammation) and persistent clinical manifestations, but not restricted to chronic synovitis.

Canakinumab for gout: a specific, patient-profiled indication.

The role of interleukin-1 (IL-1) in inflammation induced by crystals, and especially by monosodium urate crystals (MSUCs), has raised much interest in both basic and clinical investigation. Several drugs have been developed, and more are still in development, to block IL-1 driven inflammation, though to date only canakinumab (blocking IL-1β) has been labelled, yet limited to the European Union, with a restricted indication to treat episodes of acute inflammation (EAIs) in patients with gout in whom other therapeutic choices are unacceptable. Other medications developed for IL-1 blocking, such as anakinra and rilonacept, have been tested in gout patients in clinical trials, but lack label approval and may be further restricted to orphan indication in gout.

Tophaceous gout and high level of hyperuricaemia are both associated with increased risk of mortality in patients with gout.

Background: While several studies have reported a link between the presence of gout and adverse cardiovascular (CV) events in the general population, none has addressed the question of whether the mortality risk of patients with gout is influenced by disease severity.

Methods: We applied survival analysis methodology to prospectively collected data on clinical and radiographic measures of disease severity and mortality in a specialty clinic based cohort of 706 patients with gout (1992-2008). Standardised mortality ratios (SMR) were calculated to assess the magnitude of excess mortality among patients with gout compared with the underlying general population.

Evaluation and treatment of gout as a chronic disease.

Gout is a disease caused by deposition of monosodium urate crystals in tissues. One of the limitations for successful treatment of gout is to consider it as an intermittent disease rather than a chronic inflammatory disease which, if improperly treated, leads to chronic clinical manifestations. In addition, gout is linked to increased cardiovascular morbidity and mortality.

A two-stage approach to the treatment of hyperuricemia in gout: the "dirty dish" hypothesis.

Objective: It is commonly accepted that the target serum urate level in patients receiving urate-lowering therapy for dissolution of urate crystals in hyperuricemia of gout is <6 mg/dl, and that patients with gout should continue urate-lowering therapy for the rest of their lives. This study was undertaken to reevaluate whether this stringent therapeutic target to dissolve crystals must be maintained lifelong to prevent new crystal formation.

Methods: In a prospective cohort of 211 patients with gout, urate-lowering therapy was withdrawn after 5 years if no tophus was present at baseline, or 5 years after resolution of the last tophus.

Risk factors associated with renal lithiasis during uricosuric treatment of hyperuricemia in patients with gout.

Objective: To find factors associated with the development of renal colic during uricosuric therapy.

Methods: We performed a prospective cohort followup study of patients with gout and no previous history of kidney stones who had been treated with uricosurics. Clearance of creatinine and urate, 24-hour urinary uric acid (UA), undissociated urinary UA concentration, 24-hour undissociated urinary UA, and pH and urine sediment were obtained.

[Influence of the natural history of disease on a previous diagnosis in patients with gout].

The clinical diagnosis of gout can be quite precise in clinically typical forms. However, in chronic or atypical forms, such precision tends to be diminished in clinical practice. A cohort of 248 patients with a diagnosis of urate crystal arthropathy was studied, sent with a definite clinical evaluation, and data such as severity of the disease, joint distribution and the presence of tophi were gathered.

Long-term efficacy of hyperuricaemia treatment in renal transplant patients.

Background: Although hyperuricaemia and gout are frequently found in renal transplant recipients, little has been published on the efficacy of urate-lowering therapy (ULT) in this patient population. We therefore examine the effects of allopurinol and benziodarone therapy in a cohort of renal transplant patients.

Methods: We reviewed files from a cohort of 1328 patients that received renal transplantation.

Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout.

Objective: The optimal serum urate levels necessary for elimination of tissue deposits of monosodium urate in patients with chronic gout is controversial. This observational, prospective study evaluates the relationship between serum urate levels during therapy and the velocity of reduction of tophi in patients with chronic tophaceous gout.

Method: Sixty-three patients with crystal-confirmed tophaceous gout were treated with allopurinol, benzbromarone, or combined therapy to achieve serum uric acid levels less than the threshold for saturation of urate in tissues.