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Nombre de messages : 243
Localisation : Paris
Date d'inscription : 02/11/2005

MessageSujet: V the gout   Mer 7 Déc à 4:48

Holly Frisby, DVM, MS
Veterinary Services Department, Drs. Foster & Smith, Inc.

Gout is a common disease among reptiles, including snakes, iguanas, monitor lizards, and tortoises.

What Causes Gout?

Uric acid is one of the end breakdown products of dietary protein in certain animals, including terrestrial reptiles. The uric acid is removed from the blood by the kidneys and excreted in the urine. Gout can occur if the level of uric acid in the blood exceeds the ability of the kidneys to remove it. The uric acid may crystallize in the joints which is termed "articular gout". It may also be deposited in various organs ("visceral gout"), such as the liver, spleen, pericardial sac (the covering of the heart), kidneys, and lungs, and mucous membranes, such as the mouth. When the uric acid crystallizes in tissues it forms small, white nodules called "tophi."

There are two types of gout. In primary gout, the high uric acid level is a result of an abnormal breakdown of protein. Primary gout is thought to be hereditary in humans. In secondary gout, the high level is due to the inability of the kidneys to adequately excrete the uric acid. This can be caused by medications, chronic diseases, kidney disease, starvation, improper diet, decreased water intake or chronic dehydration, and other environmental factors which affect the kidneys' ability to eliminate uric acid. A common cause of gout is feeding animal proteins (e.g.; dog or cat food) to vegetarian reptiles, whose digestive systems cannot properly digest and metabolize animal-based protein. In these cases, large amounts of uric acid are produced and the kidneys cannot adequately eliminate them.

What Are the Signs of Gout and How Is It Diagnosed?

Tophi may be visible on the inside of the mouth in animals with gout. Joints may be enlarged, stiff, and painful. If there is renal failure or there are large deposits of uric acid in the kidneys, they may be enlarged.

After examining the animals and obtaining a thorough history of the diet, environment factors, availability of water, the temperature and humidity of the cage, and previous health problems and treatments, the veterinarian will suspect gout. Radiographs help to substantiate the diagnosis; the identification of uric acid crystals in joint fluid, biopsies, or tophi confirms it.

How Is Gout Treated?

Any underlying dietary or environmental cause will need to be remedied. Diets such as Hill's Canine u/d, which are low in those proteins which are metabolized into uric acid, may be used in carnivorous reptiles. Proper hydration is necessary and fluids may need to be administered. If arthritis from gout is severe, it is possible to surgically remove the uric acid crystals from the joint. Unfortunately, severe and sometimes irreversible damage to the joint may have already occurred. Medications such as allopurinol, probenecid, sulfinpyrazone, or colchicine may be used, but the exact dosage and safety of these drugs in reptiles have not been determined. Most reptiles will need to be treated for life or the condition will quickly reappear if therapy is discontinued.

Gout can be complicated by a secondary bacterial infection in the joints. If this occurs, antibiotics are added to the treatment regimen.

Information complémentaire:

Etude d'un cas chez varanus exanthematicus
Case presentation by Anne Keller, Christopher Pachel and Victori Ribeiro, Class of 2002. The pathologist was Dr. Arno Wann.

Signalment: Adult Savanna Monitor, a native of west African grassland

History: This zoo resident had signs of paralysis after the exhibit was treated with dichlorvos for mites. It died after exhibiting signs of joint pain and anorexia.

Necropsy gross findings: The general body condition was good. The joints of the forelimbs and the left stifle joint had marked white deposits within and around the joint capsules. Numerous similar foci were found in the musculature along the spine. Both kidneys were streaked with white deposits. There was a clear green gelatinous liquid in the coelom and subcutaneous edema in the ventral thorax/abdominal region. The liver was mildly enlarged and friable, reddish beige, with an accentuated lobular pattern. The tongue had multiple white plaque-like deposits.

Necropsy histologic findings: In the kidney there were urate crystals associated with histiocytic inflammation ("gouty tophi"), marked interstitial fibrosis, and diffuse mesangioproliferative glomerulonephritis.

Diagnosis and cause of death: Renal, visceral and articular gout; etiology unknown.

Comments: Gout is a result of a disturbance of the nucleic acid metabolism, (specifically of the purine metabolism) that leads to an increased blood concentration of the poorly soluble uric acid ("hyperuricemia"). The uric acids form salts with calcium or sodium that tend to precipitate in e.g. the kidneys, muscles, and soft tissues near or within joints. Most mammals, except for humans, primates and dalmatians, excrete allantoin via the kidneys as the end-product of the purine degradation thanks to the enzyme uricase (urate oxidase) that enables them to degrade uric acid further to allantoin. Gout is basically unknown in these species. Birds and terrestrial reptiles excrete uric acid as the endproduct of the purine metabolism and for unknown reasons (primary gout) or secondary to e. g. renal disease (secondary gout), the blood concentration increases over a threshold limit and uric acids precipitate as crystals in the aforementioned locations. The interstitial renal fibrosis and mesangioproliferative glomerulonephritis that were diagnosed histologically in the present case are thought to be a consequence of the renal gout. However, it cannot be excluded that these lesions were primary and may have predisposed the animal for the gout lesions. The differential diagnosis for gout with white chalky deposits in soft tissues and joints includes deposits of calcium salts (pseudogout), such as calcium hydroxylapatite or calcium pyrophosphate.

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