Here's some wonderful info on shar-pei related health info and link's to some great site's this site will be updated often.

         Health Issues of the Shar-Pei ·
 If your veterinarian requires more information about the Chinese Shar-Pei, send the name and address of your veterinarian (for overseas orders, send $2.00 in U.S. funds for postage) to: Jeff Vidt, DVM210 S. Park StreetWestmont, IL 60559-1940·

Entropion:
This is where the eyelid rolls in towards the eye, rubbing against the cornea and irritating this sensitive structure. Watery eyes, infection, even a corneal ulcer, can occur. Surgical correction is required. Dogs with this condition should not be bred, as a genetic component is suspected. ·

Hypothyroidism
The thyroid glands secrete a hormone which controls the basic metabolic rate of the entire body. Inadequate hormone levels reset the body to function at a lower metabolic level. In that case, dogs fatten easily on a normal diet, become sluggish, and are easily chilled. Hair changes are most noticeable and include loss of hair from the flanks and back, increased pigmentation of the skin, scaling and seborrhea (an abnormality in the production of skin cells.) Secondary bacterial infection of the skin is common. The ears may also be affected, filling with thick, yellow greasy material which may predispose the dog to ear infections. Blood tests will determine the level of thyroid function and administration of thyroid hormone can treat the condition. ·

Familial Shar-Pei Fever
       Familial Shar-Pei fever also known as "Swollen Hock Syndrome" (SHS) typically may include the following symptoms: Swelling of the hock joint and sometimes other joints can be affected. Reluctance to move. Sometimes a swollen painful muzzle. Abdominal pain, vomiting, diarrhea, and shallow breathing. "Familial Shar-Pei Fever (FSF) is an episodic fever disorder. Shar-Pei with this disorder have one or more bouts of unexplained fever, usually 103-107 degrees but rare cases may go higher. Fevers usually start when they are less then 18 months old but sometimes the first attack is not until they are adults. Fever episodes usually become less frequent with age. Fevers last 24-36 hours in most cases without treatment". The disorder is "thought to result from an inability to regulate the immune system. Dogs suffering from this disorder are at risk of dying from a related disorder, amyloidosis.

· Demodectic Mange
The mite, Demodex canis, starts off as small dry areas on the head, chest, and legs of the Shar-Pei. Because the dog scratches to relieve the intense itching, the skin becomes red and raw with a leathery look about it. Check with your veterinarian for prescribed medication, shampoos, and other appropriate treatment. ·

Seborrhea
OleosaSevere rancid body odor which comes from raw, scaly, bloody skin. Could be caused by hypothyroidism, yeast infections, and or food allergies. This situation should be immediately discussed with a veterinarian and the appropriate shampoos and medication can effectively treat this condition.

· MalocclusionOverbites
      This can occur due to the misplacement of the incisors causing an overcrowding. Extraction at a young age can prevent the adult canines from cutting into the hard palate.

· Tight Lip
This is where the excess flesh from the lower lip covers the teeth making it difficult for the Shar-Pei to chew. This excess flesh also traps food and is usually associated with an overbite. ·

 · Nose
- Stenotic NaresThese dogs snore because of excess flesh. If the dog is unable to pass air with ease, surgery to the alar folds of the nostril may be necessary. An "elongated soft palate" is likely to be the cause of "respiratory distress."

· Carpal Laxity
This is a weakness is the carpal ligaments which causes instability and bowing forward in young puppies. Decrease the protein level and exercise on a non-slippery surface. In severe cases soft wraps will be in order. · Patellar LuxationIs where the knee cap slips out of its socket. Any Shar-Pei with this condition should not be bred.

· Hip Dysplasia A
dysplastic dog has an abnormal hip joint where the femur and acetabulum are misaligned. This can range in severity from mild (controllable) pain to dogs in such agony they must be put down. Make sure the parents of any puppy you consider has been cleared of Hip Dysplasia through the Orthopedic Foundation for Animals. ·

Megaesophagus
Megaesophagus and or diaphramatic hernias may not be detected until the dog is much older when they will appear underweight or emaciated with a history of vomiting. This is a developmental defect possibly a delayed maturation of the esophageal nueromuscular system. Mild cases in young dogs can improve with careful feeding." ·

Cutaneous Mucinosis
"Mucin is the substance in the Shar-Pei skin that causes all the wrinkling. It is clear and stringy and acts like glue in fight wounds." Some Shar-Pei have an excess of Mucin causing it to form clear bubbles on the skin that may rupture and ooze. May be associated with possible allergies and can be treated by a alternate day steriod therapy. · Torsion/BloatBeing one of many deep chested breeds, bloat can occur in Shar-Pei. Can also be caused by the way you roll your dog. Although similar to colic in horses, "bloat and torsion occur when the stomach swells with gas and then twists and cuts off its blood supply. Without timely surgical intervention the condition is fatal". The dog must see a veterinarian as soon as possible. ·

Chronic Inflammatory
Bowel DiseaseOften complicated by food allergies and or Chronic stress diarrhea. Usually responds to a strict hypoallergenic diet. · AllergiesSome Shar-Pei can be susceptible to allergies caused by food, grass, plants (indoor and outdoor), flea-bite dermatitis an allergy-based condition where the dog develops an itchy rash in reaction to flea saliva after being bitten. Try to keep the dog's living quarters and play area as flea-free as possible. Other allergies are "Inhalant allergies" that causes the dog to lick his/her paws, scratch, and rub its muzzle. "Eliminating the allergy's cause, using the correct type of shampoo and administering antihistamines or cortisone are common forms of treatment".

Amyloidosis
Amyloidosis is the deposition of an abnormal substance called amyloid in the tissues of the body. These amyloid deposits are composed of protein fibrils formed by the polymerization of protein subunits forming a specific pattern called the beta-pleated sheet.
The specific biophysical arrangement of this sheet gives the amyloid deposits their unique staining and optical properties. Due to this structure amyloid is insoluble and can be thought of as "wax". It is also important to realize that amyloidosis is not a single disease, but can be the end point of many diseases. The structure of amyloid also is responsible for the characteristic green color after staining with Congo red.   In Shar-Pei amyloidosis is a reactive amyloidosis. This form of systemic amyloidosis usually occurs with chronic inflammatory diseases and is characterized by the presence of amyloid protein AA. Amyloid protein AA is derived from an acute phase protein called serum amyloid A protein (SAA) produced by the liver. There are many other acute phase proteins produced by the liver which have important roles in the inflammatory process and in tissue repair after injury. It is important to understand that amyloid protein AA is a normal protein and that it's production is a normal response to tissue injury and inflammation. It is also important to realize that many diseases, traumatic injuries, cancer disorders, stresses, etc. can stimulate the production of the acute phase proteins. There appears to be a balance between the production of SAA and the degradation and excretion of SAA from the body. It is not known whether the development of amyloidosis in the Shar-Pei is due to prolonged excessive SAA production by the liver which overwhelms the degradation mechanisms or a defect in the degradation process itself, or a combination of both. We do know that Familial Shar-Pei Fever is an inflammatory process which does stimulate the synthesis and release of acute phase proteins from the liver. That this occurs can be surmised from the changes seen on the hemogram and biochemical profiles of Shar-Pei during, or shortly after, an FSF episode. It certainly appears that the cause of amyloidosis in Shar-Pei has a genetic basis.  Reactive amyloidosis results in extracellular deposition of amyloid protein in tissues. This means the "waxy" amyloid is surrounding the cells and slowly crushes them as well as interfering with nutrition of the cells. These cells die and the structures they make up are replaced by fibrous, nonfunctional scar tissue. There are species differences as to which tissues amyloid will accumulate in. In dogs, the kidney is the primary organ involved with the spleen and liver affected less often. The kidney is especially vulnerable due to its decreased ability to replace damaged cells and ultimately, when a certain number of cells have been irreparably damaged, kidney failure with its accompanying clinical signs develops. Once amyloid is deposited in the tissues it appears that nothing can remove it.  Why does amyloidosis have so many different clinical presentations? Why does it occur in some Shar-Pei at 2 years of age and in others at 10 years of age? Why do some Shar-Pei develop amyloidosis and others don't? Why is it a genetic disease in Shar-Pei? There are many questions which have no answers at this time. I think several theories are plausible to explain the variations we see:  The underlying basis of amyloidosis in Shar-Pei is Familial Shar-Pei Fever (FSF). It is quite possible that FSF has variable age of onset and variable degrees of severity in terms of the inflammatory disease it causes. This may result in a variable rate of progression in the development of amyloidosis in different individuals. For example, the response of the liver to FSF and the synthesis and release of the acute phase proteins, especially SAA, may be more acute in some dogs resulting in a more rapid deposition of amyloid. In other individuals, the response to FSF may be more chromic and result in slower deposition of amyloid. In effect, there may be milder forms and more severe forms of the same disease. The exact mechanism of amyloid deposition may be different in different individuals. There may be other effects of FSF on the body which are additive with the amyloidosis. As an example, we know Shar-Pei are more susceptible to disseminated intravascular coagulation (internal blood clotting) during an episode of FSF and blood clots in the kidneys may cause more kidney damage than just amyloid deposition itself. Some dogs may have other disease processes going on which can be additive with the effects of amyloidosis.  These are just some ideas on why we see different presentations of the same disease. One fact remains - any amyloid deposits found in a Shar-Pei have to be regarded as related to FSF and genetic until proven otherwise. It really doesn't matter whether a little or a large amount of amyloid is found. Another point to keep in mind is that the mechanisms initiating amyloid deposition are normal protective responses seen in any breed of dog. It appears in our breed that the mechanisms, which regulate the inflammatory response, don't work properly allowing this normal response to go out of control and cause disease.
 

Always consult a Shar-Pei knowledgeable veterinarian for proper treatment and care.