Update: November 20, 2006

Draft proposal for a total EU ban on cat and dog furs!
The effort was worth it! We crossed the first hurdle, as a consequence of the abundant protests and petitions sent to the EU Commissioner Markos against the horrible and unimaginable cruelty inflicted on cats and dogs for their pelts. Yesterday, the European Commission adopted a proposal to ban the import, export, and sale of cat and dog fur throughout the EU. We only hope that the European Parliament and the Council of Ministers will now enact this initiative into law across the EU. Below is the press release on this dated November 20, 2006.

Ibiza, November 22, 2006
Hanspeter Kobold

Amyloidosis / AA amyloidosis!

What is amyloidosis?
Rudolf Virchow was the first to coin the term amyloidosis for the field of human medicine – as early as 1854 – when he discovered an atypical substance in livers of the deceased. Although this disease has been known for over three centuries, we have we only been able to research how amyloidosis affects the growth and structure of protein in the last 25 years. Amyloidosis itself is not a disease, but rather an abnormal deposition process that can be triggered by various metabolic disorders like Shar-Pei Fever. Depending on the organs affected, this can lead to many chronic diseases.

The underlying cause of amyloidosis is a protein metabolic disorder, resulting in extra-cellular deposition and accumulation of abnormal proteins in body tissue. Also known as corpora amylacea or amyloid, these are insoluble microscopic fibrils. If the blood serum protein concentration rises (in a blood test, for instance), the proteins will be deposited in the surrounding tissue as well. Enzymes attack these proteins, synthesizing insoluble microscopic fibers that are deposited in the organs. Episodes of high fever between 41°C and 42°C (acute phases) can stimulate such a reaction. These fibers are resistant to the body’s defense mechanism and cannot be removed, but scientists currently believe that the precursor proteins of these fibrils or can be reduced!

The following is an excerpt of the article, Generalized Amyloidosis in a Shar-Pei Bitch, by Dr. K. Kamenica and Prof. Dr. W. Hermanns, Ludwig-Maximilians University, Munich {© Schattauer GmbH}.

“Amyloidosis is a syndrome of extra-cellular deposits of proteins with a beta-pleated pattern. One of its most common forms is characterized by the presence of amyloid protein AA, which is derived from an acute phase protein produced by the liver, called serum amyloid A protein (SAA). Such amyloidosis can occur with chronic inflammatory or cancerous disorders, and is thus referred to as secondary or reactive amyloidosis. It appears that primary AA amyloidosis also occurs without any basic symptoms. This has been reported in the literature, for instance, in Chinese Shar-Pei of US ancestry. Although one observes generalized changes, the renal deposits are the key and ultimately lead to death of the animal through kidney failure.”  

I am not sure as to where this eight-year-old bitch suffering from generalized amyloidosis was bred. However, I can certainly say that she is NOT from the Shar-Pei kennel [vom Oekonom].

What is AA Amyloidosis?
AA amyloidosis or secondary amyloidosis is a progressive and deadly disease. It appears in increasing numbers of Shar-Pei with chronic inflammations like Shar-Pei Fever. Amyloid develops from the degradation of excessive acute phase serum amyloid A protein, which can form due to acute fever episodes. Amyloid symptoms usually appear throughout the body, particularly affecting the kidneys, spleen, liver, and adrenal glands. The kidney is especially vulnerable, with the abnormal proteins collecting around the finest capillary vessels or in vessels leading in and out. This invariably results in damaged kidney, and ultimately renal insufficiency.

Clinical symptoms only give an indication of generalized AA amyloidosis, and a biopsy is needed for proper diagnosis. A tissue sample is frequently taken from the most vulnerable organ, the kidney. Hereditary amyloidosis in Shar-Pei appears as excessive deposits of amyloid in the kidney’s medulla, with comparatively little impact on the glomerulus. Shar-Pei dogs are reported to suffer from very painful swelling of the tarsal joints and intermittent fever of unknown causes (Familial Shar-Pei Fever or FSF). Please see my report on FSF.

The following excerpt is from the article Generalized Amyloidosis in a Bred Shar-Pei Bitch, by Dr. K. Kamenica and Prof. Dr. W. Hermanns, Tierärztl Praxis Kleintiere (Small Animal Clinic), 2006 34-2, pp. 108-11, {© Schattauer GmbH}.

“Suspected renal amyloidosis can be confirmed clinically by a histological renal biopsy. It should be noted that familial amyloidosis in Shar-Pei appears mostly in the medulla. This means that renal cortical biopsies of this breed could be falsely negative, if amyloid deposits do not show up in histology of the glomerulus. The etiology and pathogenesis of familial amyloidosis in Shar-Pei are still not fully understood. Current debate focuses on deviations in the amino acid sequence of the acute phase protein SAA, the precursor of the amyloid protein AA that leads to multiplication of the beta-pleated molecular structure (12). In contrast, Revas et al (21) found high serum levels of interleukin 6 in Shar-Pei canines suffering from intermittent fever and renal amyloidosis. They postulate a cytokine induced synthesis of SAA as the underlying cause of familial amyloidosis.”

Current research has undoubtedly proven that FSF and SHS (Shar-Pei Swollen Hock Syndrome or painful deposits in the joints) are polyarthritic and associated with progressive amyloidosis. The phenotypes of the genetic transfer of protein metabolic disorders are often related to a form of autosomal disorder.

The diagnosis is frequently possible only through an autopsy. Hence, owners should (rather must) request a necropsy of their pets, which involves an anatomicopathologic and histologic examination. This officially identifies the most serious renal changes, especially damage to the medulla and other organs. The purpose of an autopsy, however, should not be to just collect more data and identify the cause of death of the Shar-Pei.

At present, veterinary medicine still lacks an effective therapy to treat or cure AA amyloidosis. As far as I am aware, the majority of all canines afflicted with this disease die shortly after the diagnosis. My experience, research, and conclusions suggest that so far certain preventive measures plus medical treatment can only slow the onset and progress of the underlying illness, chronic infection, or inflammatory amyloidosis!  

In the case of the Shar-Pei, early preventive treatment of the basic disease, FSF, can markedly improve renal amyloidosis if the serum creatine levels are normal. It is critical to measure and lower the temperature of Shar-Pei suffering from FSF. In my opinion, it really makes a difference if the animal is given an antipyretic and palliative medication at the first signs of typical symptoms. As mentioned earlier, amyloid develops from the degradation of excessive acute phase serum amyloid A protein, which can arise from acute fever episodes. If the fever is very high, 41°C to 42°C, administering aspirin, metacam, rimadyl, or similar medications is effective. I personally prefer metacam for my Chilly, since it drops her fever rapidly.

Feeding ampules of calcium, as recommended by the frequently mentioned breeder, is one of this person’s big white lies. This recommendation has hindered the incomprehensibly gullible puppy buyers and forum members from immediately administering the necessary antipyretic and palliative medication. And it has clearly harmed rather than helped the animals!

Shar-Pei pets that tend to have fewer episodes of FSF are being increasingly treated in the US, and more commonly in Europe too, with colchicine as a prophylactic against renal amyloidosis. Colchicine does not help if the animal already has fever, but it can lower the tendency to get fever, and thus increase the interval between fever episodes. Colchicine must be taken lifelong everyday, but it can be effective in slowing down or preventing the onset of amyloidosis. Unfortunately, I am also aware that colchicine is suspected of causing bone cancer!


To reiterate: “The hereditary disease FSF marked by much suffering and premature death can be suppressed only through an unrelenting effort at selective breeding.”  

The damage has already been done to our baby, the beloved Shar-Pei!

Hanspeter Kobold
Glashütten, December 2006

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