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Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Gout is a disease that results from an overload of uric acid in the body. This overload of uric acid leads to the formation of tiny crystals of urate that deposit in tissues of the body, especially the joints. When crystals form in the joints, it causes recurring attacks of joint inflammation (arthritis). Gout is considered a chronic and progressive disease. Chronic gout can also lead to deposits of hard lumps of uric acid in the tissues, particularly in and around the joints and may cause joint destruction, decreased kidney function, and kidney stones (nephrolithiasis).
Gout has the unique distinction of being one of the most frequently recorded medical illnesses throughout history. It is often related to an inherited abnormality in the body's ability to process uric acid. Uric acid is a breakdown product of purines that are part of many foods we eat. An abnormality in handling uric acid can cause attacks of painful arthritis (gout attack), kidney stones, and blockage of the kidney-filtering tubules with uric acid crystals, leading to kidney failure. On the other hand, some people may only develop elevated blood uric acid levels (hyperuricemia) without having manifestations of gout, such as arthritis or kidney problems. The state of elevated levels of uric acid in the blood without symptoms is referred to as asymptomatic hyperuricemia. Asymptomatic hyperuricemia is considered a precursor state to the development of gout. The term gout refers the disease that is caused by an overload of uric acid in the body, resulting in painful arthritic attacks and deposits of lumps of uric acid crystals in body tissues.
Gouty arthritis is typically an extremely painful attack with a rapid onset of joint inflammation. The joint inflammation is precipitated by deposits of uric acid crystals in the joint fluid (synovial fluid) and joint lining (synovial lining). Intense joint inflammation occurs as the immune system reacts, causing white blood cells to engulf the uric acid crystals and chemical messengers of inflammation to be released, leading to pain, heat, and redness of the joint tissues. As gout progresses, the attacks of gouty arthritis typically occur more frequently and often in additional joints.
Approximately 5 million people in the United States suffer from gout. (Did you know that none other than Benjamin Franklin had terribly painful gouty arthritis?) Gout is nine times more common in men than in women. It predominantly attacks males after puberty, with a peak age of 75. In women, gout attacks usually occur after menopause.
While an elevated blood level of uric acid may indicate an increased risk of gout, the relationship between hyperuricemia and gout is unclear. Many patients with hyperuricemia do not develop gout (asymptomatic hyperuricemia), while some patients with repeated gout attacks have normal or low blood uric acid levels. In fact, the blood level of uric acid often lowers during an acute attack of gout. Among the male population in the United States, approximately 10% have hyperuricemia. However, only a small portion of those with hyperuricemia will actually develop gout.
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