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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 51-year-old male patient who had been suffering from gouty arthritis and podagra with relapsing attacks of severe pain for the last 10 years. We treated two tophaceus deposits on the left heel with the CO2 laser and conventional enucleating surgery. These tophi had immobilized the patient for months and it had not been possible to control them by conservative therapy.
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PMID:[Ulcerating gout tophi. Surgical therapy in a patient with hyperuricemia, hyperlipidemia and alcohol abuse]. 193

We describe the clinical, radiographic and histological features of skeletal involvement in four patients with end-stage renal failure due to primary oxalosis. The clinical features were unrelenting bone pain, and in two patients multiple fractures. Radiographic features were, in chronological order: (1) radiodense metaphyses and other red marrow bone; (2) cortical defects in metaphyses; (3) spontaneous fracture-separations of epiphyses of long limb bones which healed poorly. The fractures occurred through crystal deposits, and fracture displacement was associated with extrusion of crystalline material from bone. On histological examination crystals were found to replace metaphyseal bone. Pericrystalline giant cell granulomata replaced bone marrow. Erosion surfaces near granulomas were increased. Subperiosteal and intra-osseous tophi of calcium oxalate were seen. Calcium oxalate appears to precipitate with greater facility than does physiological mineral. Bone showed the features of mixed uraemic osteodystrophy in all four patients. We conclude that: (1) the fractures occurred through heavy crystal deposits; (2) ununited fractures and intra-osseous and subperiosteal tophi contributed to the pain; (3) spontaneous fractures are of poor prognostic significance. We recommend that unstable fractures be internally fixed.
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PMID:Skeletal manifestations of primary oxalosis. 203 34

Today hyperuricaemia and gout are likewise seen in every population of the western industrial world and have been increasing since the fifties. As known from number of studies hyperuricaemia often occurs in connection with hyperlipoproteinaemia, obesity, diabetes mellitus, arterial hypertension and atherosclerosis. Up to now it was not clear whether one disease caused the other. In 1988 Abbot could prove that among men, those afflicted by gout as compared to those without gout experienced a 60% excess of coronary heart disease. Therefore, patients with gout should receive a regular thorough cardiovascular evaluation. Furthermore risk factor levels which predispose to coronary heart disease, arterial hypertension and gout should be reduced. There is a significant positive correlation between the plasma uric acid levels and the prevalence of attacks of gouty arthritis and nephrolithiasis. It is possible to avoid gouty arthritis, tophi and nephrolithiasis with a consequent diet and medical treatment. Unfortunately, many patients interrupt therapy during intervals free of pain. The consequence is that even today the complications of hyperuricaemia cause days of inability to work and to earn one's living, despite of modern therapy. Hyperuricaemia not sufficiently treated reduces the quality of life through attacks of gout, chronic gout and nephrolithiasis as well as life expectancy caused by nephropathy, arterial hypertension and atherosclerosis. This is of special importance because of the frequency of gout and hyperuricaemia in our population. An early diagnosis, a consistent therapy and a thorough monitoring could stop an increase of this disease and prolong life expectancy for those who have gout and the other attendant diseases.
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PMID:[Hyperuricemia--does modern therapy improve life expectancy?]. 227 73

A 33-yr-old male ran 10 miles, drank some beer, and developed pain in his left knee and ankle. He took some leftover antibiotics but was no better after 6 d, when a heart murmur and an aortic valve nodule were discovered. He was presumed to have endocarditis with septic arthritis and was started on intravenous antibiotics. On the second hospital day, synovial fluid analysis revealed acute gout, and the patient improved very rapidly on anti-gout therapy. The valvular nodule remained unexplained, but one very rare cause of valvular heart nodules is visceral gout. An unsuccessful attempt to resorb the nodule was made by using allopurinol. This patient demonstrates several points about gout in endurance athletes: 1) acute gout can mimic infectious endocarditis, 2) misdiagnosed or undertreated gout often leads to multiple joint involvement and sometimes to visceral tophi, and 3) athletes who exercise in warm weather and quench their thirst with cold beer are at risk for acute gout.
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PMID:Runner with gout and an aortic valve nodule. 767 64

A 57-year-old man with severe gouty arthritis for over 20 years was admitted because of persistent back and leg pain and neurogenic claudication. Lumbar spinal stenosis from the L4 to L5 level was diagnosed after admission and decompressive laminectomy was done. However, about 10 months later, another surgery with laminectomy of L2 and L3 and postero-lateral fusion was performed due to post-laminectomy instability with recurrence of stenosis. The pathology of the resected ligmentum flava had tophi deposition. At the one-year follow-up examination after the second operation, the patient was pain free and had resumed daily activity.
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PMID:Recurrent spinal stenosis caused by tophaceous gout: a case report and review of literature. 892 48

A 51-year-old immigrant from the Caucasus had had chronic tophaceous gout for over 20 years, but had never been treated with anti-hyperuricemic drugs. He had developed large, multiple tophi in many locations, including both ankles and feet. The enormous size and unique location of the tophi caused considerable pain, and difficulty in standing and on walking. Since surgical removal of the tophi was refused by the patient, a course of allopurinol, 300 mg/day, was begun.
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PMID:[Chronic tophaceous gout]. 922 16

Aim of this paper is to describe and discuss, on the basis of the available current literature, the case of a female patient affected by a tophaceous gout associated with plurimetabolic syndrome. Hyperuricemia and gout may be seen today in all the populations of developed countries, with increasing frequency on the last fifty years. Increased production or reduced urinary excretion of uric acid (and hypoxanthine and xanthine) are the most important pathogenetic mechanisms of primary or secondary hyperuricemia. Gout is an acute rheumatic disorder (characterized by a limited range of manifestations) which occurs in humans in connection with deposition of crystals of monosodium urate (the final product of purine metabolism) in the articular and soft periarticular tissues. Hyperuricemia and/or gout are often associated with hyperinsulinemia, obesity, diabetes mellitus, hyperlipemia, hypertension and atherosclerosis to form the syndrome called "Plurimetabolic syndrome" or "Syndrome X". Here we report the clinical case of a 64-year-old female patient who had android obesity, type 2 diabetes mellitus, hypertension, dyslipidemia and hyperuricemia and had been suffering (over many years) from intermittent episodes of severe pain and inflammatory joint swelling (first metacarpo- and metatarso-phalangeal joints) with development of pronounced multiple tophi in bone articular and soft periarticular tissues. Hyperuricemia and acute episodes had never been treated with anti-hyperuricemic drugs because gouty arthritis had never been diagnosed. This severe tophaceous gout associated to multiple metabolic disorders prompted us to present knowledge on gout and to focus on the interrelationships between hyperuricemia and/or gout and plurimetabolic syndrome, important risk factors for coronary heart disease.
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PMID:[Tophaceous gout in plurimetabolic syndrome]. 1021 66

Gout, like diabetes mellitus, is a common metabolic disorder. Typically affecting the distal joint of the appendicular skeleton, its occurrence in the spine is rare. We report the case of a 68-year-old male with a long history of diabetes mellitus and hyperuricemic gout. Neck pain developed over two weeks with subsequent quadriparesis, with concomitant subcutaneous deposition of gouty tophi in the right elbow. Magnetic resonance image of the cervical spine revealed multiple segmental narrowing of the thecal sac at the C3-6 levels due to hypertrophic spurs and bulging discs. Anterior discectomies of C3-4 and C4-5 were performed, with a chalky-white, granular material noted in the C4-5 disc space. Histological examination of the surgical specimen revealed deposits of needle-like crystals surrounded by histiocytes and multinucleated giant cells, with the appearance compatible with gout. The patient was ambulatory with the assistance of a walking frame six months after the operation. We emphasize that gouty tophi can be deposited in the spine over a relatively short time, subsequently precipitating a variety of symptoms, from pain to cord compression. The regular administration of antihyperuricemia drug treatment for hyperuricemic gout is necessary to prevent this deposition. If neurological defects are found, surgical decompression can provide satisfactory results.
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PMID:Cervical myelopathy due to gouty tophi in the intervertebral disc space. 1186 23

Gouty arthritis, a common source of pain and disability, is the most common form of inflammatory arthritis affecting older people. The authors review the epidemiology and pathogenesis of hyperuricemia and gout, as well as the clinical forms of gouty arthritis. Gout is part of a clinical spectrum of conditions (obesity, diabetes mellitus, hyperlipidemia, coronary artery disease) and need for better patient education on management of these associated conditions is emphasized. The general algorithm of gout management is presented. Clinical particularities of gout presentation in older patients (increased incidence in women, polyarticular onset with hand involvement, earlier development of tophi, association with use of diuretics) are reviewed. Barriers against an optimal control of gout include lack of patient education, presence of comorbid conditions, particularly renal impairment, use of multiple drugs such as diuretics, and cognitive decline. Gout management in older adults remains unsatisfactory.
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PMID:Gouty arthritis. A primer on late-onset gout. 1602 79

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.
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PMID:Gout: an update. 1869


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