Arthritis Clinic
Dr. Jacob Aelion and Dr. Satish Odhav are board certified in rheumatology and in internal medicine. They founded the Arthritis Clinic, at 371 North Parkway, two years ago. Appointments are taken by referral.
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The Famous — and Gout
Throughout history, gout has struck many famous people. One well known sufferer, King Henry VIII, at left, was notorious for making rash decisions during gout flareups.
Others in history who had gout include Mongolian emperor Kublai Khan; Nostradamus, a French prophesier; poets John Milton and Alfred Lord Tennyson; Sir Issac Newton, English physicist and mathematician; English writers Henry Fiedling and Samuel Johnson; Pablo Neruda, a Nobel Prize winning writer; King George IV; John Hancock, whose signature is famous on the Declaration of Independence; President Thomas Jefferson; British Prime Minister Benjamin Disraeli; and even Benjamin Franklin, an inventor and U.S. Ambassador.
Roman poet Ennius even attributed his success to gout, writing “I only write poetry when I suffer from gout.”
Other stories with our doctors…
• Doctors note unusual side effects with anti-TNF medications
• Annual Arthritis Walk raises money for research
• Scardiosis: Doctors share new findings with peers
Gout: New treatments for an age-old disease
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Gout — long recognized as a source of human misery — is the most common inflammatory arthritis in the United States.
The number of people with gout has increased over the past few decades. The estimated total gout population in this country is more than seven million — about the same number of people who have activity-limiting back pain. In contrast, the number of people affected by rheumatoid arthritis and fibromyalgia is two and five million respectively.
Until recently, however, gout management has lagged behind the rising tide. Fortunately, we now have a better understanding of the disease and new medications for its treatment and prevention.
The condition has been considered a source of misery throughout human history. The word gout can be traced to the Latin guta (a drop), which has its origin in the belief that the disease was caused by a poisonous chemical falling drop by drop into the joint.
Egyptians first identified the disease in 2640 B.C., and, indeed, evidence of gouty arthritis was found in the great toe of an Egyptian mummy. The distinctive clinical features of the disease were described by Hippocrates in the fifth century B.C. In the first century A.D., Celsus recognized that gouty arthritis often afflicted the rich and powerful.
King Henry VIII of England was rumored to have made several misguided personal and matters of state decisions when afflicted by acute gouty flares. It was only in the mid 18th century that the British physician Alfred Garrod demonstrated an increased amount of uric acid in the blood of gouty patients and went on to delineate the cause and effect relationship of urate deposition and gouty inflammation.
Misconceptions about gout are quite common to this day. People usually associate the condition only with acute flares, but in reality, gout is a chronic, progressive disease, and disease progression continues even in the absence of acute flares. Another misconception is that gout affects only the joints. Uric acid crystals, however, can deposit in soft tissues other than joint lining and cause a variety of medical problems ranging from the skin to the kidneys.
To understand gout, we must first understand uric acid, one of the “waste products” that the body excretes through the kidneys.
An elevated blood uric acid level or hyperuricemia is a necessary precursor to gout. (In physiologic terms it is defined as a serum uric acid level in excess of 6.8 mg/dL at a temperature of 37C.)
Above this level, urate crystals may begin to form and precipitate in joints and soft tissues. Lower temperatures decrease the solubility of uric acid, which may explain the peripheral distribution of gouty arthritis and why, for example, the disease affects the big toe more commonly than it does the shoulder.
Besides low temperature, other physical factors affecting urate crystal formation are low pH (acidity), trauma or exercise and dehydration. Hyperuricemia can be due to overproduction of uric acid (about 10% of patients) or renal under excretion (about 90% of patients). Sometimes it can be due to both. An elevated blood uric acid level can remain silent for several years before triggering health problems.
The typical gout patient is an elderly male or post-menopausal female with other medical problems, such as hypertension, cardiovascular disease, chronic kidney disease, diabetes and hypercholesterolemia. They tend to be obese, have a diet rich in meat and seafood, have high alcohol intake and are frequent consumers of high-fructose corn syrup. They commonly use medications such as thiazide diuretics, low dose aspirin and nicotinic acid that negatively impact the renal handling of uric acid.
Treating patients with gout is simple if both the physician and the patient have a good grasp of what causes the disease and a good line of communication. If the patient has an acute flare of gout, treatment should be eliminated to stop the acute painful attack first. Once that is done, treatment should concentrate on preventing future flares and, in those patients with longstanding disease, preventing and reversing the complications of chronic urate deposition in joints, kidneys or other involved sites.
Acute flares are resolved with anti-inflammatory agents, including nonsteroidal anti-inflammatory drugs, colchicine and corticosteroids. Treatment is tailored to the individual patient. For chronic management, the physician should start urate-lowering therapy to achieve a serum uric acid level of less than 6 mg/dL. This therapy usually starts two weeks after the acute event has resolved because initiation of urate-lowering therapy may result in a “mobilization” flare, which occurs when urate moves from tissue deposits. For the same reason, anti-inflammatory prophylaxis is recommended for several months after starting such therapy.
Between 1965 and early 2009 not a single new drug was approved for gout. Now treatment is poised for a transformation with new drugs on the market and others in clinical development.
The new therapeutic options are for all stages of the disease. One of them, Febuxostat (Uloric) has been available for clinical use since 2009. Others, in phase two or three clinical trials, include Rilonacept and Canakinimab for resolving acute attacks by neutralizing IL-1; Pegloticase, a pegylated uricase that enzymatically breaks down uric acid; and RDEA594, which increases renal excretion of uric acid.