Body as a Whole: chest pain; abdominal pain; edema; chills; malaise Cardiovascular: atrial fibrillation; tachycardia; palpitations, and other cardiac arrhythmias; postural hypotension, orthostasis; hypotension; syncope Eye: toxic amblyopia; cystoid macular edema; ophthalmoplegia; eye irritation, blurred vision, progression of cataracts Gastrointestinal: activation of peptic ulcers and peptic ulceration; dyspepsia; vomiting; anorexia; constipation; flatulence, pancreatitis; hepatitis; fatty change in liver; jaundice; and rarely, cirrhosis, fulminant hepatic necrosis, and hepatoma, eructation, fatal and non-fatal hepatic failure Metabolic: gout, decreased glucose tolerance Musculoskeletal: muscle cramps; myopathy; rhabdomyolysis; arthralgia, myalgia Nervous: dizziness; insomnia; dry mouth; paresthesia; anxiety; tremor; vertigo; peripheral neuropathy; psychic disturbances; dysfunction of certain cranial nerves, nervousness, burning sensation/skin burning sensation, peripheral nerve palsy Psychiatric depression Skin: hyper-pigmentation; acanthosis nigricans; urticaria; alopecia; dry
Acute gout attacks can be managed with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids (intra-articular injection or systemic). All three agents are appropriate first-line therapy for acute gout. Therapy should be initiated within 24 hours of onset. The drug selection is dictated by the patient's tolerance of those medications and the presence of any comorbid diseases that contraindicates the use of a specific drug. For patients with severe or refractory gout attacks, practitioners can try combining agents. If all of these medications are contraindicated in a patient, narcotics may be used short term to relieve pain until the acute attack has resolved. Long-term use of narcotics should be avoided.