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We describe a 34-year-old man in whom non-union of a patellar fracture led to an unrecognized diagnosis of gout. He presented with a mass in the superolateral quadrant of the patella, which had the radiographic appearance of a non-united fracture. In the operating room, a gouty tophus was found. Although patellar tophi are uncommon, gout should be included in the differential diagnosis of non-united patellar fractures.
The identification of monosodium urate crystals in synovial fluid is essential for the definite diagnosis of gout. Neutrophils interact with urate crystals to produce inflammatory reactions associated with acute arthritis. Crystals activate monocyte-macrophages and synoviocytes to produce high levels of proinflammatory cytokines, like TNF alpha und interleukin-1 and different chemokines. High levels of interleukin-8, a powerful neutrophil attractant with activating properties, were demonstrated in the synovial fluid of patients with acute gout arthritis.
We studied purine metabolism in gouty patients from three categories: primary gout, familial juvenile hyperuricaemic nephropathy (FJHN) and partial HPRT deficiency.
We recently encountered a destructive case of tophaceous gout in a 57-year-old patient. Despite perfect therapy compliance, the patient failed in the conventional urate-lowering treatment, accounting for the ongoing urate retention and accumulation with progressive tophaceous bulky disease. Application of an experimental scheme of uricolytical therapy on this patient was able to reduce bulky disease significantly. In modern medicine, potent urate-debulking medication with urate oxidase (uricase) derivatives is at our disposal, and it is a challenge for rheumatologists to install the right strategy including innovative approaches with potent uricolytic therapy on the right patient at the right time.
A case of gout and secondary amyloid is described. This rare association is described and the literature is reviewed.
The manifestations of gout can be abolished permanently by lifelong urate-lowering therapy maintaining serum urate levels under 360 mmol/l, as this ensures dissolution of pathogenic crystals of monosodium urate monohydrate. Benzbromarone has been withdrawn from the market, leaving allopurinol as the only urate-lowering drug readily available in France. Allopurinol may induce unacceptable side effects, and in patients with dose-limiting renal failure it may not be sufficiently effective. Because allopurinol can induce serious side effects when given concomitantly with purine antimetabolites, it is contraindicated in organ transplant recipients. In patients who cannot tolerate allopurinol, dietary treatment, discontinuation of diuretic agents, and use of losartan or fenofibrate to treat concomitant hypertension or dyslipidemia, respectively, may ensure adequate control of serum urate levels. Desensitization to allopurinol can be attempted in patients with mild cutaneous hypersensitivity reactions but is difficult to perform and rarely used. Uricosuric agents may be helpful in patients with normal or diminished urate excretion. Probenecid is available in France from hospital pharmacies, and benzbromarone can be prescribed via a time-limited authorization procedure. Rasburicase, an Aspergillus urate oxidase produced by genetic engineering, is indicated to prevent acute hyperuricemia induced by chemotherapy for hematological malignancies. Factors that limit the use of rasburicase include the absence of a marketing authorization, the need for parenteral administration, and the absence of validated treatment schedules. Patients with renal failure precluding the use of effective allopurinol dosages are good candidates for benzbromarone therapy. Organ transplant recipients can be given benzbromarone, within the current restrictions to its use; alternatively, mycophenolate mofetil can be substituted for calcineurin inhibitors, which elevate serum urate levels, or for azathioprine, which contraindicates the use of allopurinol.
Gout is a group of diseases characterized by arthritis and results from a disturbance of urate metabolism with the deposition of monosodium urate crystals in the joints and soft tissues. Often, but not invariably, the serum urate levels are elevated as a result of overproduction or underexcretion of uric acid. Clinical manifestations include acute and chronic arthritis, tophaceous deposits, interstitial renal disease, and uric acid nephrolithiasis. The diagnosis is based on the identification of uric acid crystals in joints, tissues, or body fluids. Acute episodes are treated with colchicine, NSAIDs, or steroids. Long-term management includes treatment with uricosuric agents or xanthine oxidase inhibitors.
Colchicine myoneuropathy is a rare and often underdiagnosed disease. It often presents as painless subacute muscle weakness. We present a case of painful colchicine myoneuropathy in a 76-year-old man with chronic renal failure and gout. Published work about clinical presentations of colchicine myoneuropathy in gouty arthritis patients are reviewed. During the previous year, the patient had a drug regimen of colchicine 0.5 mg three times per day for a 3 day course each month. He developed bilateral lower leg weakness and severe myalgia. His serum creatinine level was 680.7 micromol/L and creatinine kinase was 959 IU/L on admission. Laboratory findings included decreasing amplitude of motor and sensory nerve conduction velocity and an electromyogram showed small amplitude, short duration polyphasic waves over the right biceps. A muscle biopsy disclosed vacuolar changes in the cytoplasm. These results all supported a diagnosis of colchicine myoneuropathy. After cessation of colchicine, the creatinine kinase level decreased approximately 50% in 6 days, myalgia subsided and his muscle weakness improved gradually over the next 2 weeks.
Gout affects around 1% of people in the UK, most aged over 45 years. The condition, which is five times more common in men than women, usually presents as a painful inflammatory monoarthritis, which can be diagnosed clinically and successfully treated with a high dose of an NSAID. Problems arise when the features are atypical or when high doses of an NSAID are inappropriate. Also; there is no robust evidence to guide when to start prophylactic therapy or what advice to give on lifestyle changes. Here we review current practice and offer advice on managing patients with this increasingly common condition, concentrating on approaches to be taken by the non-specialist.
Gout and calcium pyrophosphate deposition disease are two common causes of inflammatory joint disease. Despite differences underlying their pathogenesis, their clinical presentation and treatment share some common features. Optimal treatment for both requires prompt resolution of acute synovitis, reduction of chronic joint damage and management of associated conditions. Available therapeutic interventions and future strategies are reviewed in this article.
Treatment for gouty arthritis should be individualized to address the patient's other medical problems and the likelihood that gout will become chronic. We present a typical case and review the options, explaining their utility for this and other patients.
Speakers at the course were given vignettes describing one or more clinical scenarios on which to base their talks, selected because they represent common but challenging problems likely to be encountered by any physician practising in general internal medicine. Three of the subjects covered--weird thyroid function tests, difficult gout, and dementia--are presented here.
Gout is a disease resulting from the deposition of urate crystals caused by the overproduction or underexcretion of uric acid. The disease is often, but not always, associated with elevated serum uric acid levels. Clinical manifestations include acute and chronic arthritis, tophi, interstitial renal disease and uric acid nephrolithiasis. The diagnosis is based on the identification of uric acid crystals in joints, tissues or body fluids. Treatment goals include termination of the acute attack, prevention of recurrent attacks and prevention of complications associated with the deposition of urate crystals in tissues. Pharmacologic management remains the mainstay of treatment. Acute attacks may be terminated with the use of nonsteroidal anti-inflammatory agents, colchicine or intra-articular injections of corticosteroids. Probenecid, sulfinpyrazone and allopurinol can be used to prevent recurrent attacks. Obesity, alcohol intake and certain foods and medications can contribute to hyperuricemia. These potentially exacerbating factors should be identified and modified.
We report a 29 years old woman with a chronic tophaceous gout, whose disease started at the age of 18. On clinical examination, the blood pressure was elevated. The laboratory assessment showed a serum uric acid of 15 mg/dl, a urinary uric acid of 155 mg/24 h, a creatinine clearance of 59 ml/min/1.73 m2 and a uric acid excretion fraction off 1.3% (normal 7 to 12%). The clinical and laboratory features of this patient suggest the diagnosis of a familial juvenile gouty nephropathy.
A 65-year old man had gout and a secondary infection of a tophus with Pseudomonas at the metatarsophalangeal joint of the right first toe.
An 89-year-old woman was admitted for high fever and debilitating pelvic pain, notably in the pubic area. Physical examination revealed multiple gouty tophi in her hands and feet. Laboratory investigation revealed severe leukocytosis and a sharply increased C-reactive protein level. The patient was treated with broad-spectrum antibiotics in view of the possibility of a serious bacterial infection, but there was no clinical effect. CT of the pelvis revealed an osteolytic process and a mass anterior to the pubic symphysis. Histological investigation of a biopsy revealed an inflammatory infiltrate with signs of gout. Culture of the biopsy specimen was negative. The diagnosis was confirmed by the finding ofneedle-like urate crystals under the polarizing microscope. After treatment with colchicine and later with prednisone, the symptoms disappeared. She was given uric acid-lowering therapy with allopurinol as a preventive measure.
With students such as Hippocrates, Galen, Paracelsus, Sydenham, Herberden, Harvey, Cheyne, Boerhaave and Paŕe, the history of "The Gout" (L. gutta-drop), more than any other disorder, parallels the history of Western medicine. It also played important parts in modifying American and European culture and history. Such was the fear and honor it commanded in the last 3,000 years, that over a score of saints and holy men are credited with its cure. Long stated to be a disease of the upper class, at one time, it was considered so stylish that it was said that the only thing worse than having it was to be cured.
Uricaemia-lowering treatment is indicated when hyperuricaemia is pronounced (90 mg/L or more) or when it is expressed by uric acid stones and/or gout. The drugs which lower plasma uric acid levels are presented according to their mode of action: uric acid inhibitors (allopurinol and tisopurine), uric acid excretors (probenecid, benzbromarone) and the uric acid lyser (urate-oxidase). The pharmacological and pharmaceutical data needed to understand the respective indications and applications of these drugs are given. These indications and those of adjuvant therapies are presented as answers to the following questions: when should a uricaemia-lowering treatment be initiated? What are the general rules to be obeyed? Which indications or contraindications must be borne in mind?