You are in: eMedicine Specialties > Ophthalmology > METABOLIC DISORDERS GoutArticle Last Updated: Jun 22, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Andrew A Dahl, MD, Director of Ophthalmology Teaching, Mid-Hudson Family Practice Institute; Assistant Professor of Surgery (Ophthalmology), New York College of Medicine Andrew A Dahl is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, and Wilderness Medical Society Editors: Richard W Allinson, MD, Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center, Scott and White Clinic; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; R Christopher Walton, MD, Professor, Director of Uveitis and Ocular Inflammatory Diseases Service, Assistant Department of Ophthalmology, Assistant Dean for Graduate Medical Education and Continuing Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital; Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri; Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences Author and Editor Disclosure Synonyms and related keywords: uric acid, urate crystals, ocular tissue, kidneys, kidney stones, urinary collecting system, joint inflammation, tophus, tophi, alcohol, uric acid salts INTRODUCTIONSection 2 of 10
  Background"Drink wine, and have the gout; drink none, and have the gout." Thomas Cogan, The Haven of Health (1584) Gout is one of the oldest diseases in medical literature and has been characterized as a condition caused by indiscretions of diet and alcohol. Since the time of the Greeks, many authors have written about gout as the result of personal excess. However, among the abstinent was John Milton, who lived a life of rigorous self-discipline and yet, to his anger and despair, suffered from what commonly was regarded as just punishment of the dissolute. Gout, the king of diseases and the disease of kings, is an illness that produces signs and symptoms secondary to elevated levels of uric acid salts in the serum and the resulting deposition of these salts within target organs, primarily the joints of the extremities, the kidneys, and the urinary collecting system. Rarely, gout can produce significant ocular findings. The incidence of age-related macular degeneration (ARMD) is higher in patients with gout. FrequencyUnited StatesUnknown InternationalUnknown Mortality/MorbidityDuring an attack, the patient is incapacitated by pain in the affected area. RaceNo racial predilection is known. SexMales are affected more commonly than females. AgeOnset of this condition generally occurs in patients aged 30-50 years. CLINICALSection 3 of 10
HistoryWith joint involvement, patients experience pain in the distal extremities. With kidney stones, patients experience acute flank pain. PhysicalThe classic attack of acute primary gouty arthritis occurs in a portly middle-aged man and produces fairly sudden inflammation of a single joint, most commonly the metatarsal-phalangeal joint of the great toe, resulting in intense pain, tenderness, and swelling. The folklore surrounding gout also has involved the eye, and, prior to the 20th century, a myriad of common and unusual ocular symptoms falsely were ascribed to the gout. All manifestations of gout in the eye are secondary to deposition of urate crystals within ocular tissue.
CausesAttacks are caused by the deposition of monosodium urate monohydrate within the joint space. Precipitating factors can include emotional stress, dehydration, surgery, and thiazide diuretics. Attacks tend to be recurrent and usually are self-limited. Recurrent attacks of acute gouty arthritis can result in chronic arthritis with limitation of joint mobility. Uric acid levels may be elevated as a result of primary gout. Primary gout is an autosomal dominant error of metabolism. It can occur secondarily from increased production of uric acid or decreased excretion of uric acid. The latter is seen in chronic renal disease.
Other causes of secondary gout include chronic lead poisoning, polycystic kidney disease, systemic cyclosporine therapy, various antimitotic chemotherapeutic agents, sarcoidosis, psoriasis, and hyperparathyroidism. DIFFERENTIALSSection 4 of 10
Keratopathy, Band
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| Drug Name | Colchicine |
|---|---|
| Description | Decreases leukocyte motility and phagocytosis in inflammatory responses. |
| Adult Dose | 1-1.2 mg PO qd for acute attacks of gouty arthritis; 0.5-0.6 mg PO qd as maintenance dose |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; severe renal, hepatic, GI, or cardiac disorders; blood dyscrasias |
| Interactions | Sympathomimetic agent toxicity and effect of CNS depressants are significantly increased with colchicine |
| Pregnancy | X - Contraindicated in pregnancy |
| Precautions | Risk of renal failure, hepatic failure, permanent hair loss, bone marrow suppression, numbness or tingling in hands and feet, disseminated intravascular coagulopathy, and decreased sperm count |
Inhibit renal tubular reabsorption of urates, causing increase in urinary excretion of urates.
| Drug Name | Probenecid |
|---|---|
| Description | The generic name is 4-[(dipropylamine) sulfonyl)] benzoic acid. Inhibits tubular secretion of penicillin, and usually increases penicillin plasma levels by any route the antibiotic is given. A 2-fold to 4-fold elevation has been demonstrated for various penicillins. Used in treatment of hyperuricemia associated with gout and gouty arthritis. Also used as an adjuvant to therapy with penicillin or ampicillin, methicillin, oxacillin, cloxacillin, or nafcillin, for elevation and prolongation of plasma levels by whichever route the antibiotic is given. |
| Adult Dose | 0.5 g PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; known blood dyscrasia or uric acid kidney stones; coadministration of ketorolac as levels/toxicity of ketorolac are significantly increased |
| Interactions | Salicylates at high dosages, and nitrofurantoin, may decrease effects of probenecid; probenecid increases levels/toxicity of methotrexate, beta-lactam antibiotics, acyclovir, thiopental, clofibrate, dyphylline, pantothenic acid, ketorolac, benzodiazepines, rifampin, sulfonamide, dapsone, zidovudine, sulfonylureas |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Crosses placental barrier; use of any drug in women of childbearing potential requires anticipated benefit be weighed against possible hazards; caution in history of peptic ulcer |
| Drug Name | Allopurinol (Zyloprim) |
|---|---|
| Description | Inhibit xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. Reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines. |
| Adult Dose | 200-400 mg/d PO in divided doses |
| Pediatric Dose | <10 years: 10 mg/kg/d PO divided bid/tid; not to exceed 400 mg/d >10 years: 200-400 mg/d PO |
| Contraindications | Documented hypersensitivity |
| Interactions | Alcohol decreases effects; increases incidence of skin rash when used concurrently with ampicillin and amoxicillin; large amounts of vitamin C acidify urine and may cause kidney stone formation; allopurinol inhibits metabolism of azathioprine and mercaptopurine |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Not for use in asymptomatic hyperuricemia; reduce dose in renal insufficiency; monitor liver function and perform complete blood counts before initiating therapy and periodically thereafter |
Article Last Updated: Jun 22, 2006
