Gout is an inflammatory disease characterized by episodic acute and chronic arthritis, due to deposition of monosodium urate monohydrate crystals in and around synovial joints1. It is a metabolic disease most often affecting middle-aged to elderly men and postmenopausal women. It is the result of an increased body pool of urate with hyperuricemia.
The prevalence of gout varies between populations but is approximately 1-2%, with greater than 5:1 male preponderance. Women represent only 5–20% of all patients with gout.
Lifestyle factors, such as a diet with high-purine foods, obesity and excessive alcohol use – especially heavy beer consumption – can contribute to development of hyperuricemia and gout. In over 90% of patients, the main abnormality is reduced uric acid excretion by the renal tubules, which impairs the body`s ability to respond to a purine load. In many cases this is genetically determined and recent studies have identified polymorphisms in several genes that are associated with gout.
The classical presentation is with an acute mono arthritis, which in over 50% of cases affects the first MTP joint. Other common sites are ankle, mid-foot, knee, small joints of hands, wrist and elbow. The axial skeleton and large proximal joints are rarely involved. Usually, only one joint is affected initially, but polyarticular acute gout can occur in subsequent episodes. Inflamed Heberden's or Bouchard's nodes may be a first manifestation of gouty arthritis.
Other typical features are Rapid onset, reaching maximum severity in 2-6 hours, and often waking the patient in the early morning.Marked swelling with overlying red, shiny skin; Self-limiting over 5-14 days ,with complete resolution
During the attack, the joint shows signs of marked synovitis, swelling and erythema. There may be accompanying fever, malaise and even confusion. As the attack subsides, pruritus and desquamation of overlying skin are common. The main differential diagnosis is septic arthritis, infective cellulitis or reactive arthritis. Some people never have a second episode after an acute attack. In others, several years may elapse before the next attack. In many, however, a second attack occurs within one year and may progress to chronic gout, with chronic pain and joint damage, and occasionally severe deformity and functional impairment. Patients with uncontrolled hyperuricaemia who suffer multiple attacks of acute gout may also progress to chronic gout.
Crystals may be deposited in the joints and soft tissues to produce irregular firm nodules called tophi. These have a predilection for the extensor surfaces of fingers, hands, forearm, elbows, achilles tendon and sometimes the helix of the ear. Tophi have a white colour and can ulcerate, discharging white gritty material, become infected or induce a local inflammatory response, with erythema and pus in the absence of secondary infection. They are usually a feature of long standing gout but can sometimes develop within 12 months in patients with chronic renal failure. The diagnosis of gout can be confirmed by the identification of urate crystals in the aspirate from a joint, bursa or tophus.
A biochemical screen, including renal function, uric acid, glucose and lipid profile, should be performed because of the association with metabolic syndrome. Although hyperuricaemia is usually present, this does not confirm the diagnosis. Conversely, normal uric acid levels during attacks do not exclude gout, as serum urate falls during the acute phase response. Elevated ESR and CRP and neutrophelia are typical of acute gout, and they return to normal as the attack subsides.
The mainstay of treatment during an acute attack is the administration of anti-inflammatory drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or glucocorticoids. Ultimate control of gout requires correction of the basic underlying defect, the hyperuricemia. Attempts to normalize serum uric acid to <300–360 mol/L (5.0–6.0 mg/dL) to prevent recurrent gouty attacks and eliminate tophaceous deposits entail a commitment to long-term hypouricemic regimens and medications that generally are required for life. Hyperuricemia cannot be corrected by simple means (control of body weight, low-purine diet, and increase in liquid intake, limitation of ethanol use and avoidance of diuretics). Urine volume must be maintained by ingestion of 1500 mL of water every day.
Ayurvedic classical description of the etiopatogenesis and clinical features of Vatarakta can be correlated to the description of gouty arthritis and on critical analysis of the signs and symptoms it may be diagnosed as pittadhika vatarakta. Vatarakta is a spectrum of diseases which are having involvement of musculo skeletal structures. The etiological factors of the clinical condition are mainly related to the lifestyle of the person especially physiological and dietary habits that leads to metabolic disturbances. On analyzing the pathogenesis of the disease it may be seen that the vitiated raktha dhathu obstructs the movement of vata dosha and leads to the localization of toxic materials in asthisandhis. The description of the signs and symptoms of vatarakta is more or less similar to the clinical features of gout.
The line of treatment in Vatarakta associated with Pitta and Rakta are managed with Virechana (Purgation), Ghrithapana (Intake of pitta/ rakthahara processed ghee), Vasti (Enema – eg: ksheera vasthi) and Sheetanirvapana (Application of pitta/ rakthahara dravya in the form of paste in the affected regions). Rakthamokshana like jaloukavacharana are very effective in treating gout. Other symptomatic treatment such as lepa, upanaha, abhyanga, various types of pindasweda, pizhichil, dhara etc are also having significant action according to the stage of the disease and condition of the patient. However pathyahara vihara are important factors being observed to avoid the recurrence of the complaints.
In the present social status of the society, especially the food habits and the lifestyle are major contributory factors for the high rate of incidence of Gout. Ayush Ayurveda hospital has developed a special treatment programme based on Ayurvedic principles with modified life style for the effective management of this disease.
This is an Article by our Chief Consultant,Dr.P.K Sudarsanan Nair. View Profile
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