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A number of sources on the subject of gout, and particularly its role in history, were consulted. Highlights are presented to illustrate popular conceptions of the social implications of gout. It is indicated that the consequences of this affliction may be disastrous to empires, yet are not always viewed as entirely negative for individual sufferers.
In a study designed to evaluate the radionuclide images in patients with gout, six (23%) of the 26 patients had clear evidence of Paget's disease of bone by technetium Tc 99m medronate imaging. A reference population consisting of 333 technetium Tc 99m medronate bone scans ordered for other reasons was reviewed, and only seven scans (2.1%) were found to have evidence of Paget's disease. This difference was found to be highly significant. All cases of Paget's disease were confirmed by independent radiologic evaluation. We conclude that there is a significant association between Paget's disease and gout, the basis for which is not yet known.
Colchicine is an effective and relatively specific treatment for acute gout and has a long, venerable history. Serious toxic reactions to colchicine could be prevented if guidelines for its use were followed strictly, but because of its relatively infrequent use and conflicting recommendations, considerable toxic effects might occur and still be undetected by passive surveillance. A review of a teaching hospital's four years' experience showed two deaths (2% incidence) due to inappropriate use. Colchicine has the smallest benefit-to-toxicity ratio of drugs that are effective for acute gout. This article gives specific recommendations for the use of colchicine in different clinical settings.
Two cases of coexistent gout and septic arthritis are presented. The known increased incidence of joint injections in patients with rheumatoid arthritis is contrasted with the relative rarity of this complication in persons with gouty arthritis. The reason for this dichotomy is not clear but it is suggested that an important factor may be the more episodic nature of the gouty process. For patients presenting with acute arthritis the possible concurrence of sepsis and gout should be considered.
The authors observed 10 patients from 4 families with hereditarily determined gout and detected some specific features in its course. The familial disease was sex-unrelated, its first signs manifested themselves early acquiring a subsequent severe course; purine metabolic derangement was of a metabolic type, a urolithic form of nephropathy was seldom observed. A morphological picture was characterized by a glomerular lesion looking like focal segmental mesangiocapillary or mesangioproliferative glomerulonephritis with noticeable changes in the tubules, stroma and vessels causing early renal insufficiency. Pathogenetic therapy with uricodepressants made it possible to improve the course of nephropathy. The authors described a pedigree of 3 generations of a family in which gout developed in its 10 out of 17 members, in 6 with chronic renal insufficiency.
This case report presents a successful nonoperative outcome of a type II odontoid fracture secondary to severe tophaceous gout. The patient presented with spastic quadriparesis and tophaceous involvement of the odontoid process with fracture and C1-C2 instability. He refused surgery. However, his odontoid process stabilized with the used of a collar, and he regained almost normal strength plus independence in self-care and ambulation, demonstrating that an unstable type II odontoid fracture secondary to tophaceous gout can stabilize with conservative management.
The result of our examinations was that there is a vast correspondence of the medium levels of serum uric acid as well as of the frequency of hyperuricaemia between children after the 10th year of age and the adults. In comparison to the average population children from families with a gout anamnesis revealed a twice as frequent disturbance of the purine metabolism. In a familial appearance of gout and/or in unclear renal as well as joint findings the paediatrician should think of the presence of a disturbance of the purine metabolism.
Hypertension was found in 18% of 65 patients with untreated gout, a lower prevalence than that previously reported. The clinical characteristics and renal function of these patients were compared with those of age matched groups of both normotensive gouty subjects and normouricaemic patients. The hypertensive patients had significantly greater body weights than their controls and also had a lower glomerular filtration rate. Other aspects of renal function were not significantly different between the three groups. The association of hypertension with gout and impaired renal function is complicated by many possible contributory factors and a simple cause and effect relationship is unlikely.
Allopurinol (4-hydroxypyrazolo (3,4-d)-pyrimidine) is a potent xanthine oxidase inhibitor which inhibits the oxidation of naturally occurring oxypurines, thus decreasing uric acid formation. The clinical and metabolic effects of this agent were studied in 80 subjects with primary and secondary gout and other disorders of uric acid metabolism. Allopurinol has been universally successful in lowering the serum uric acid concentration and uric acid excretion to normal levels, while not significantly affecting the clearance of urate or other aspects of renal function. Oxypurine excretion increased concomitantly with the fall in urine uric acid. The agent is particularly valuable in the management of problems of gout with azotemia, acute uric acid nephropathy and uric acid urolithiasis. The minor side effects, clinical indications and theoretical complications are discussed.
Acute gout may be associated with fever but activation of EP production by crystalline urate in vivo has not been previously reported. We found that crystalline urate or silica stimulated macrophages but not PMNs to produce EP, without mediation by lymphocytes. The activation process did not require ingestion of the urate crystals, was unaffected by colchicine, and was not due to incidental LPS. Additionally, the failure of ingested latex particles to stimulate EP release indicated that phagocytosis alone was not a sufficient stimulus for EP production. We suggest that since EP and IL 1 are probably the same, the known inflammatory effects of IL 1, apart from fever induction, may contribute to the pathogenesis of acute gout and other crystal-associated human diseases.
20 patients with an attack of acute gout participated in this double-blind study, ten patients received N-(2,6-dichloro-m-tolyl)anthranilic acid, sodium salt (meclofenamate sodium, Meclomen) and ten indometacin. The median time interval between onset of attack and onset of treatment was 11 h in the meclofenamate sodium group and 14 h in the indometacin group; medication was started with a dose of 200 mg meclofenamate sodium or 25 mg indometacin followed by 100 mg meclofenamate sodium or 25 mg indometacin every 4 h for the first 24 h. Thereafter patients received 100 mg meclofenamate sodium or 50 mg indometacin at 8-h intervals for 6 days. Similar improvement of intensity of spontaneous pain, swelling, tenderness of touch and degree of limitation of function was noted in patients of both treatment groups. This improvement could already be noted after 24 h of treatment and was sustained throughout the medication period and follow-up period. Adverse reactions were reported by 2 patients in the meclofenamate sodium group and by 5 patients in the indometacin group. The results of this double-blind study indicate that meclofenamate sodium in the dose administered was equally effective in relieving pain and inflammation and restoring restricted function in patients with acute gout as indometacin when used in the generally recommended dose for this indication. Meclofenamate sodium, even at these high dosage levels, was better tolerated than indometacin.
Ten patients with gout, hypertension, and mild to moderate renal insufficiency were studied for possible lead nephropathy by measuring stimulated urinary lead excretion. Seven had a history of lead exposure, 5 from illegal alcohol and 2 from industrial sources. Occult lead was assessed by 24 h urine collection measurements over a 72 h period after intramuscular administration of calcium disodium EDTA. Two patients with a history of lead exposure excreted 707 and 687 micrograms Pb/72 h, respectively, and a 3rd excreted 506 micrograms Pb/72 h. The remainder had a normal response, with mean urinary lead excretion of 251 +/- 42 micrograms Pb/72 h. Since we were unable to demonstrate that lead was important to the pathogenesis of the renal we were unable to demonstrate that lead was important to the pathogenesis of the renal failure in 7 patients despite a positive history of lead exposure in 2, we suggest that factors other than lead may be the cause of renal failure in most patients with gout and renal disease.
Investigations were made on a total of 92 patients with gout and hyperuricemia. 30% had no clinical signs of spinal involvement. The remaining 70% were examined radiologically and by xero-radiography. Examination revealed signs of erosion of vertebral bodies, spondylodiscitis, osteopenia, manifestations of Forestier's disease and changes on sacroiliac joints. In 35% of subjects there were polytopic hyperostoses including an increased incidence of calcifications around the large joints and periosteal appositions at the periphery, particularly on the finger and toe tips. The hypothesis was raised that massive calcifications and manifestations of hyperostosis and ossification of the ligaments and tendons (osteodesmosis) in gout may correlate with a latent glycide metabolism disorder like in Forestier's disease.
Two observations of gout with typical articular changes but different variants of renal involvement are presented. One of the cases had typical gouty kidneys, the other had moderate changes typical of gout but with the prevalence of membranous and proliferative processes in the glomeruli with glomerulosclerosis as the end point. Examination of materials from this case in polarized light showed the presence of urate crystals not only in tubules but also in glomeruli.
Platelet aggregation and adhesion were measured in twelve male patients with gout. Tests were performed with the patients off all treatment for six weeks and after the serum uric had been lowered with allopurinol. Results of aggregation and adhesion tests were normal and not influenced by the uric acid level. The increased cardiovascular disease risk in gout is unlikely to be due to an increased thrombotic tendency.
Gout may be a primary or a secondary disorder. In both types of gout, overproduction or underexcretion of uric acid, or a combination of these abnormalities, may be the underlying mechanism. Controversy exists over the need for treatment of asymptomatic hyperuricemia. Treatment of tophi requires use of both uricosurics and allopurinol. A xanthine oxidase inhibitor is the drug of choice for patients with uric acid stones and for those with renal insufficiency.
Intrasynovial deposits of monourate crystals in the presence of serum hyperuricaemia, and calcium pyrophosphate dihydrate (CPPD) crystals, are responsible for gout and pseudogout respectively. Identification of these by synovial fluid analysis is described. The clinical features, minimum investigations, history-taking, management and drug regimes of gout and pseudogout are discussed. Periodic review of the patient is stressed. Other intrasynovial crystals are briefly outlined.
A large family with medullary cystic disease is described to show that juvenile nephronophthisis and medullary cystic disease should not be differentiated by age of onset and type of inheritance. The age at diagnosis of six family members with medullary cystic disease ranged from 4-32 years, and age at death from renal failure or commencement of dialysis from 7-48 years. A mother of two children with renal failure in early childhood has histological evidence of medullary cystic disease with normal renal function. We suggest that juvenile nephronophthisis and medullary cystic disease are the same conditions and that the disease be classified as medullary cystic disease, autosomal dominant or recessive form. When undertaking genetic counselling in the parents of children with medullary cystic disease, we suggest that renal biopsy may need to be considered even if their renal function is normal. Three patients presented with gout, and the possibility of an association with medullary cystic disease should be considered when more than one member of a family develops gout. Two patients died of status epilepticus, and epilepsy is probably an added association of medullary cystic disease.