Rev Osteoporos Metab Miner. 2009; 1 (1): 31-3
Gout is a metabolic disease characterised by the deposition of monosodium urate crystals in the interior structures of the joints. Its prevalence is approximately 8.4 cases per 1000 individuals and is more frequent in middle-aged and older males1.
Although hyperuricemia is a necessary predispositional factor, its presence does not always imply the development of gout. In fact, the majority of hyperuricemic patients never develop gout2,3,4. Individual differences in the formation of the crystals or in the inflammatory response, or in both, could play a role in determining if a patient with hyperuricemia will develop gout. Unfortunately, there is not yet a satisfactory explanation for some of the clinical aspects of acute gout, including5,6,7,8 the precipitation of acute attacks by trauma or surgery, its predilection for the first metatarsal-phalangeal joint, and the spontaneous resolution of the attacks.
The clinical manifestations of gout include recurrent attacks of acute inflammatory arthritis, accumulation of monosodium urate crystals in the form of tophaceous deposits, nephrolithiasis caused by the uric acid and chronic nephropathy. Three classic stages are described in the natural history of the progressive deposition of monosodium urate, which includes acute gouty arthritis, an interval, or intercritical gout, and then chronic tophaceous gout.
Acute gouty arthritis generally occurs some years after a period of asymptomatic hyperuricemia. A typical attack, which is markedly inflammatory, consists of severe pain, reddening, swelling and functional impairment which reach their maximum intensity after a few hours. In general (80%), the initial attacks only affect a single joint, typically in the lower extremities, often at the base of the big toe (podagra), or the knee. The associated signs of inflammation frequently extend beyond the affected joint and at times, can affect a number of joints, with tenosinovitis, dactilitis and even celulitis also apparent.
Overall, it has been observed that 12-43% of patients with episodes of gout show normal or even reduced values of uric acid in the blood9,10,11.
Next, we present the radiological characteristics shown by a patient of 92 years of age with a history of arterial hypertension, which has developed over at least 5 years, a smoker until approximately 20 years ago, with packet–year index (IPA) of 150, diabetes mellitus type 2 which has developed for 5 years, being treated with oral anti-diabetics, dyslipidemia being treated with statins, chronic renal deficiency with levels of creatine habitually around 1.2-1.4 mg/dL, attributed initially to nephroangiosclerosis and diabetes mellitus, congestive cardiac failure diagnosed in the year 2005 and benign prostatic hyperplasia. The patient attended our service due to progressive dyspnea which had been developing over approximately 8 days until it practically became resting, and pleural effusion with characteristics of empyema was identified, which was treated with thoracic drainage and broad spectrum antibiotics.
The patient had a previous diagnosis of arthritis, troubling diffuse pain in multiple joints of several year’s evolution. What also stood out was the sausage-shaped swelling (dactilitis) (Figure 1), especially in the third finger of the hand, and gouty tophi on the toes. On the third day of admission the patient described her pain: in the right knee, in the big toe of the left foot, and in both hands accompanied by tumefaction, erythematous coloration in the affected zones, and fever (despite the broad spectrum antibiotic given for her empyema). The analysis carried out at that time revealed levels of uric acid of 12.8 mg/dL, along with a real elevation in acute phase reactants (leukocytes: 15,000/mm3 with 88% of neutrophiles, platelets: 1,096,000/mm3; VSG 105 mm/h; fibrogen: 842 mg/dL; albumin: 2.5g/dL; PCR 330.8 mg/L. Treatment was started with colchicin (I mg every 4 hours) and her symptoms gave way in 24 hours, the patient showing a good tolerance to the drug, with no secondary effects.
On the X-rays a reduction in the articular interline could be observed, resorption of the third distal phalanx in both hands, an increase in the soft tissues and lytic lesions, suggestive of gouty arthropathy (Figures 2.1 and 2.2).
In this case the attack of gout appeared in the context of a minor surgical procedure12, which is what a thoracic drainage is, and evolved satisfactorily, as is usual, 24 horas after starting treatment with colchicin.
1. Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 1998;41:778.
2. Hall AP, Barry PE, Dawber TR, McNamara PM. Epidemiology of gout and hyperuricemia: a long-term population study. Am J Med 1967;42:27.
3. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia: risks and consequences in the normative aging study. Am J Med 1987;82:421.
4. Zalokar J, Lellouch J, Claude JR, Kuntz D. Epidemiology of serum uric acid and gout in Frenchmen. J Chronic Dis 1974;27:59.
5. Craig MH, Poole GV, Hauser CJ. Postsurgical gout. Am Surg 1995;61:56.
6. Chakravarty K, Durkin CJ, al-Hillawi AH, Bodley R, Webley M. The incidence of acute arthritis in stroke patients, and its impact on rehabilitation. Q J Med 1993;86:819
7. Borstad GC, Bryant LR, Abel MP, Scroggie DA, Harris MD, Alloway JA. Colchicine for prophylaxis of acute flares when initiating allopurinol for chronic gouty arthritis. J Rheumatol 2004;31:2429.
8. Shoji A, Yamanaka H, Kamatani N. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum 2004;51:321.
9. Logan JA, Morrison E, McGill PE. Serum uric acid in acute gout. Ann Rheum Dis 1997;56:696.
10. Schlesinger N, Baker DG, Schumacher HR Jr. Serum urate during bouts of acute gouty arthritis. J Rheumatol 1997;24:2265.
11. Park YB, Park YS, Lee SC, Yoon SJ, Lee SK. Clinical analysis of gouty patients with normouricaemia at diagnosis. Ann Rheum Dis 2003;62:90.
12. Kundu AK, Chattopadhyay P, Biswas S. Martel’s Sign in Chronic Tophaceous Gout. J Assoc Physicians India. 2005 Sep;53: 782.