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A 53-year-old man presented with gouty arthritis. A physical examination and haematological and biochemical tests showed that he had chronic myeloid leukemia. He was treated with allopurinol, hydroxyurea and analgesics. The arthritis subsided completely within 2 weeks. He continues in haematologic remission (on interferon) with no further recurrence of the gout.
A 67-year-old man presented with acute monoarthritis of the right knee. Aspiration was carried out under aseptic precautions. This yielded a milky appearing fluid. Polarized microscopic examination confirmed uric acid crystals. The patient had a history of trauma to the joint. Acute monoarthritis of the knee can occur due to gout. Chylous effusions in the knee are rare. This combination of findings in the same joint has not been described in the literature. We emphasise the importance of history of trauma in acute monoarthritis. We discuss the unusual features of this case.
Renal function studies were performed in 524 gouty subjects, including follow-up studies at intervals up to 12 years in 112 of them. In 49 subjects, the glomerular filtration rate was less than 70 ml/min and Curate:glomerular filtration rate ratio tended to rise as the glomerular filtration rate decreased, reflecting a relatively stable urate excretion over varying filtered urate loads. The increment in Tsurate:glomerular filtration rate was small with spontaneous Purate between 7 and 9 mg/100 ml. It was modest with Purate up to 10 mg/100 ml. The increment in Tsurate:glomerular filtration rate became much higher beyond Purate of 10 mg/100 ml. Urinary urate levels above 800 mug/min, designated as excess urate excretion, occurred more commonly in subjects with Purate above 9 mg/100 ml, and with better preserved renal function. Tophi were more frequently observed in subjects with low glomerular filtration rate and proteinuria; but incidence of urolithiasis seemed to be less affected by a decrease in the glomerular filtration rate. Hyperuricemia alone had no deleterious effect on renal function as evidenced by follow-up studies over periods up to 12 years. Deterioration of renal function was largely associated with aging, renal vascular disease, renal calculi with pyelonephritis or independently occurring nephropathy. In only very few instances was diminished renal function ascribable to gout alone.
Erythrocyte adenosine kinase (AK) (EC 2.7.1.20) and guanosine monophosphate (GMP) reductase (EC 1.6.6.8) were measured in healthy male controls and primary gout subjects. Adenosine kinase activity in 19 controls and 26 gouty subjects was 0.717 +/- 0.176 and 0.615 +/- 0.128 nmol/mg protein/h, respectively. The difference was statistically significant (p less than 0.05). GMP reductase activity in 39 controls and 46 gouty subjects was 30.90 +/- 6.28 and 33.43 +/- 7.97 mumol/mg protein/h, respectively, without statistically significant difference.
AMP deaminase activity was undetectable by a sensitive spectrophotometric assay in the muscle biopsy of a 37-year-old man with gout and exercise-related cramps and myalgia. Venous ammonia failed to rise after ischemic exercise, but the diagnostic value of this test is uncertain because changes of plasma ammonia after exercise varied greatly in different normal individuals. In the patient, AMP deaminase activity was normal not only in erythrocytes, leukocytes and cultured fibroblasts but also in muscle cultures. Presence of AMP deaminase in muscle cultures was probably due to the expression of a fetal isoenzyme under separate genetic control from adult muscle AMP deaminase.
Patients with primary gout live as long as the nongouty male in the general population. Coronary heart disease is the leading cause of death in the gouty and nongouty population. There is a parallel decline in mortality particularly from coronary heart disease as that in the general population. This phenomenon is related to a number of specific and nonspecific factors. The changes in life styles and major risk factors may be counted as important influences. It is also clear that the impact of the disturbance of uric acid metabolism has not placed a particular individual in a category with any significantly inherent greater risk from intimately or remotely related causes of morbidity or mortality.
Entrapment neuropathy associated with gout is a rare occurrence. We report two cases of entrapment neuropathy of ulnar tunnel syndrome and carpal tunnel syndrome caused by gouty tophi. Problems related to its mechanism and treatment are discussed.
In a retrospective study we found that the incidence of gout in patients with Dupuytren's disease is 3.5%. The mean serum uric acid was 330 mumol/l. (5.5 mg./100 ml.) in men and 240 mumol./l. (4.0 mg./100 ml.) in women. The rate of hyperuricaemia was 7%. These are not significantly higher than the expected figures in Britain.
Severe, fulminating carpal tunnel compression due to gout has not previously been described. We report such a case.
We report a case of surgically proven tophaceous gout of the lumbar spine at the L5-S1 level that mimicked infectious spondylodiscitis and epidural abscess on magnetic resonance (MR) images in a 65-year-old woman. The spinal tophi were hypointense on T1-weighted images; focally and strongly hyperintense on T2-weighted images; and heterogeneously, marginally enhancing on contrast-enhanced T1-weighted images. The aim of this report is to emphasize the importance of considering this disease entity in the differential diagnosis of an epidural mass in a patient with chronic back pain.
A deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT; EC 2.4.2.8) is associated with a spectrum of disease that ranges from gouty arthritis (OMIM 300323) to the more severe Lesch-Nyhan syndrome (OMIM 300322). To date, all cases of HPRT deficiency have shown a mutation within the HPRT cDNA. In the present study of an individual with gout due to HPRT deficiency, we found a normal HPRT cDNA sequence. This is the first study to provide an example of HPRT deficiency which appears to be due to a defect in the regulation of the gene.
We report a case of cubital tunnel syndrome caused by tophaceous gout. The ulnar nerve was compressed by a tophus at the distal cubital tunnel. Surgical decompression relieved the symptoms.
Xanthine oxidase (xanthine: oxygen oxidoreductase EC 1.2.3.2) inhibitory activity was assayed from 26 species belonging to 18 families traditionally used for the treatment of gout and related symptoms by Indigenous people of northeastern North America. The degree of inhibition was determined by measuring the increase in absorbance at 295 nm associated with uric acid formation. Eighty-eight percent of the plants were found to have inhibitory activity at 100 microg/ml, with 20% having greater than 50% inhibition. Larix laricina exhibited the highest activity with an inhibition of 86.33%. Of the species with the highest activity, Lineweaver-Burk plots showed that inhibition mode was of linear mixed-type. Inhibitory activity of the plants correlated positively with their phenolic content (r = 0.52 P < 0.01) and tannin content (r = 0.59 P < 0.001).
A male patient with gout, complaining of wrist pain, in the absence of trauma, was found to have an avascular necrosis of the capitate bone. A scapho-luno-capitate arthrodesis was performed.
BACKGROUND: Oral desensitization with allopurinol presents a problem for patients with allopurinol hypersensitivity and gout that needs to be controlled rapidly. To our knowledge, only 1 case report of intravenous (i.v.) desensitization has been previously published. OBJECTIVE: To present a case report of a patient with cutaneous reactions to allopurinol who underwent i.v. allopurinol desensitization. METHODS: Intravenous infusion of allopurinol was performed using an escalating, 19-dose protocol. RESULTS: No adverse reactions were precipitated by 2 i.v., escalating dose procedures, allowing continuation of effective treatment of the patient's hyperuricemia. CONCLUSIONS: This case of safe and effective desensitization with allopurinol by the i.v. route should emphasize the need for a trial of this protocol in additional patients in whom rapid desensitization would be advantageous.
Gout secondary to lead-induced nephropathy is a long-term complication of occupational lead exposure. We report a case of this now-rare condition. The patient was a 63-year-old man who had been a miner from 1950 to 1970. Thirty years after cessation of his exposure to lead, he experienced onset of inflammatory symmetric polyarthritis with joint deformities. Hyperuricemia, moderately severe renal failure, and tubular acidosis were found, indicating gouty polyarthritis. Blood lead levels were high, establishing that the cause was lead poisoning. EDTA chelation therapy was effective. Lead poisoning is frequently under-recognized because the clinical manifestations are often minimal and the diagnosis difficult to establish. We suggest that lead bound to bone may result in continued exposure to lead after cessation of industrial or environmental exposure. Chelating agents are valuable for the diagnosis and can ensure a full recovery.
BACKGROUND: A 56-year-old white woman was referred to our institution with a 16-month history of severe, gouty, recurrent, acute polyarthritis involving the finger joints. She also had numerous small subcutaneous tophi in her hands. The patient was intolerant to allopurinol and had mild renal insufficiency attributed to uric-acid nephrolithiasis and interstitial nephropathy. INVESTIGATIONS: Physical examination, laboratory testing, X-rays of the hands, feet and pelvis, CT of the pelvis, microscopic analysis of an aspirate from a finger tophus. DIAGNOSIS: Tophaceous gout associated with urate nephropathy in a patient intolerant to allopurinol. MANAGEMENT: Acute polyarthritis was successfully managed by intravenous bolus methylprednisolone combined with codeine, diclofenac and low-dose colchicine. Rasburicase infusions combined with fenofibrate and sodium bicarbonate achieved to maintain serum acid uric below 360 micromol/l.
1. A method of measurement in vitro of purine biosynthesis de novo in human circulating blood lymphocytes is proposed. The rate of early reactions of purine biosynthesis de novo was determined by the incorporation of [14C]formate into N-formyl glycinamide ribonucleotide when the subsequent reactions of the metabolic pathway were completely inhibited by the antibiotic azaserine. 2. Synthesis of 14C-labelled N-formyl glycinamide ribonucleotide by lymphocytes was measured in healthy control subjects and patients with primary gout or hyperuricaemia secondary to renal failure, with or without allopurinol therapy. 3. The average synthesis was higher in gouty patients without therapy than in control subjects, but the values obtained overlap the normal range. In secondary hyperuricaemia the synthesis was at same value as in control subjects. 4. These results are in agreement with the inconstant acceleration of purine biosynthesis de novo in gouty patients as seen by others with measurement of [14C]glycine incorporation into urinary uric acid.