Hier kun je al je vragen en problemen kwijt met betrekking tot de gezondheid. Raadpleeg uw dierenarts bij twijfel of urgente zaken.

Moderator: Lizzy

Door Heidi
#3266906
We weten sinds woensdag dat onze reu, een Briard van 4 jaar, koperstapelingsziekte heeft. Op dit moment wordt nog onderzocht welke waarde hij heeft maar uit eerste onderzoek bleek het wel in hoge mate te zijn dat behandeling met medicatie en speciale brokken nodig zijn.
Hij heeft nog nergen last van gelukkig, is nog actief vrolijk en fit. De speciale brokken krijgen we aankomende week. Echter lees ik van veel mensen dat honden daar eigenlijk maar weinig energie uithalen en ook spierkracht verliezen. Wij zouden onze hond dus graag naast de brok bijvoeren met vers. Hoe kunnen we dit het beste aanpakken? Wat wel geven en wat niet. Kunnen alle groentes en aardappels of havermout en het vlees zoals kip kunnen we dat gewoon rauw geven of moet het gekookt worden ? Dacht ik ergens iets van gelezen te hebben namelijk.
En is het nog verstandig om iets van zink supplementen erbij naast te geven?
Heel veel vragen dus, hopelijk kan iemand ons een beetje op weg helpen.
Door Lizzy
#3267174
Koperstapeling komt ook bij dalmatische honden voor. Ik heb er zelf (Godzijdank) nog geen ervaring mee maar ik weet een zeer goede facebook groep en daar doen ze ook aanbevelingen mbt voeding. Bij mijn weten staat er een heel groepje Dalmatiërs gewoon op BARF. Aangepast, veel lager in koper. Ik ga ook even lezen over zink, daar staat ook veel over op deze groep (is voor dalmatiers dus daar heb je niet zoveel aan).
Door Lizzy
#3267177
Copper is not a nutrient that many owners contemplate, until it is associated with disease. In health, copper plays a role in the formation of a dog’s bones, connective tissue, collagen, and myelin (the protective covering of nerves). Copper also helps the body absorb iron, making it an important part of red blood cell function. It also acts as an antioxidant, is a part of many enzymes, and is necessary for the formation of melanin, the pigment that darkens hair and skin.

Copper is found in meat, liver, fish, whole grains, and legumes and is typically added as a supplement to commercially prepared foods. Copper deficiency is extremely unlikely if a dog eats a nutritionally balanced diet. Problems are most often associated with copper excess, not generally from an improperly formulated diet but instead due to inborn errors of metabolism that eventually cause too much copper to accumulate in the liver. At excessively high levels, copper results in oxidative stress, inflammation, and eventually to liver scarring (cirrhosis) and failure.
Liver disease associated with abnormal copper metabolism has a strong genetic component and is seen most frequently in Bedlington Terriers, West Highland White Terriers, Skye Terriers, Dalmatians, Labrador retrievers, and possibly Doberman Pinschers. Symptoms can include loss of appetite, weight loss, depression, jaundice, vomiting, diarrhea, increased thirst and urination, accumulation of fluid within the abdomen, and behavioral changes. Liver disease can usually be diagnosed based on the results of blood work but determining that copper is responsible requires liver biopsies that are evaluated using special stains

Treatment for this type of liver disease centers on reducing the amount of copper that gets stored in the liver. Chelating agents like trientine or D-penicillamine bind to copper and aid in its excretion from the body. Zinc changes the way in which copper is absorbed and metabolized and ameliorates its toxic effects. Zinc supplements are often prescribed for maintenance after a dog has been decoppered (I love that word) with chelating agents. Generalized liver support is also important and can include antioxidants like Vitamin E and S-Adenosylmethionine.

Dietary therapy plays an important role in managing copper associated liver disease. The ideal food is low in copper, high in zinc, high in B-vitamins (which are often deficient with liver disease), and contains adequate but not excessive amounts of high quality protein since eating too much protein can adversely affect brain function in dogs with liver disease. The diets should be tasty enough to encourage dogs to eat and nutrient dense so that pets with marginal appetites don’t have to take in large volumes. Feeding multiple meals throughout the day is often necessary to maintain a dog’s body condition.

Prescription “liver diets” are available that meet most if not all of these parameters. Homemade diets prepared according to a recipe designed by a veterinary nutritionist familiar with the dog’s case are another good option, particularly for dogs with poor appetites. It is also important to avoid feeding these dogs foods that are high in copper, including shellfish, liver, and mineral supplements that have not been prescribed by the pet’s veterinarian.

Van de website: http://www.petmd.com/blogs/nutritionnug ... ease-30744

=====

Ik weet niet hoe je Engels is? Maar als je bovenstaande leest is zink toevoegen een prima plan maar is er niks op tegen om gewoon zelf te blijven samenstellen. Met verstand. Dieet moet natuurlijk aangepast worden. Ik ben nog steeds zoekende naar hoeveel koper je hond maximaal per dag binnen mag krijgen enzo.
Door Lizzy
#3267210
Op de website wordt zelfs aangeraden om vooral geen brok te gaan voeren omdat deze juist veel koper bevatten. Als je al brok voert, moet het een lever-dieet-brok zijn.

Dit gaat over de Bedlington Terriers. Ik heb vet gemaakt wat ik zeer opvallend vond. Ik denk dat dit voor alle rassen met CSF geldt.

All homozygous affected dogs (two abnormal genes) should be treated for their entire lifetime. There is some controversy regarding the appropriate treatment for affected dogs. Copper chelating agents and zinc are the two treatments that are proposed. No large follow-up studies in dogs are published on either treatment. Advice for owners is based largely upon studies in human patients with genetic copper storage disease (Wilson's Disease), and upon anecdotal evidence from dog breeders and veterinarians. The copper chelating agents are somewhat expensive and sometimes are difficult to obtain, but appear to be the more effective in extending the life of affected dogs. Copper chelating agents remove copper from the liver very slowly and affected dogs will require lifetime treatment. Affected dogs that are acutely ill from liver failure will not benefit from chelation therapy since the drugs work so slowly to remove excess copper.

The zinc treatment is relatively new. Zinc has been shown to be effective in managing human patients with copper storage disease once the hepatic copper concentration has been lowered by chelation therapy. This same effect has not yet been substantiated for dogs through scientific publications. Also, there is evidence that zinc therapy will prevent the copper accumulation in affected human patients if the therapy is started very early in life. Again, this has not yet been substantiated for Bedlington terriers with CT.

Dietary manipulation will not prevent CT or cure an affected dog. All natural dietary ingredients contain copper and all diets contain more copper than the body can utilize. Normal genes are necessary in order for an animal to excrete the normal excess of daily intake of dietary copper. Therefore, any Bedlington terrier with two abnormal genes will accumulate excess hepatic copper regardless of the diet that is fed.

In summary, copper toxicosis (CT) is an inherited disease in Bedlington terriers. The specific gene that causes the disease has not yet been discovered. As of December 2002 the most accurate diagnosis is made through the quantitative copper analysis of a liver biopsy from a dog that is at least 12 months old. At 12 months of age the homozygous affected dog (two abnormal genes) will commonly have a liver copper concentration greater than 2000 ppm dw while the homozygous normal dog and the heterozygous carrier dog will have hepatic copper concentrations less than 400 ppm dw. The majority of affected dogs will die from liver disease by 4 to 6 years of age if left untreated. The majority of heterozygous carrier dogs (one normal gene and one abnormal gene) will have a normal liver copper concentration at 12 months of age. However, a rare heterozygous carrier will have a mild elevation in the hepatic copper at 12 months (and throughout its lifetime), but heterozygous carriers never accumulate enough copper to suffer liver damage.
For more information on Copper Toxicosis please visit the VetGen website. You may also check the website for the Veterinary Diagnostic Center.
Door Lizzy
#3267211
THERAPEUTIC STRATEGIES: COPPER STORAGE DISEASE

Irrespective of cause, dogs with excessive hepatic copper stores should have restricted copper
intake. Tissues Cu concentrations > 1,000 ppm should bechelated with d-penicillamine for at least
2–6 months. Only tissue biopsy can confirm the extent of tissue Cu removal after protracted chelation
therapy. However, liver enzymes (ALT activity) function as a surrogate marker. Typically after the first
month of treatment, enzyme activity notably declines.

Summary of Therapeutic Strategies: Copper Storage Disease
1. Copper chelation (removes copper from tissues or
blood):
a. D-Penicillamine (gold standard, first line Rx) or
Trientine (see below)
b. Do NOT combine zinc treatment with D-Penicillamine
chelation: zinc uptake by chelator

c. Supplement pyridoxine with D-penicillamine (25
mg/day B6)
2. Reduce systemic Cu uptake:
a. Limit dietary Cu intake: use prescription diets with
known low copper content or home cook using Cu
food content in USDA food tables
b. Limit water Cu intake: < 0.1 ppm
c. Zinc supplementation: chronic therapy AFTER chelation
removal of Cu; efficacy not proven

3. Glucocorticoids: Only for dogs with crisis hepatocellular
necrosis / hemolysis
4. Avoid Vitamin C supplementation: May augment
transition metal induced tissue injury
5. Antioxidants:
a. Vitamin E 10 IU/kg / day PO
b. SAMe (as DenosylTM) 20 mg/kg PO / day on an empty
stomach
6. Ursodeoxycholic acid: If cholestatic injury / high bile
acids: 10–15 mg/kg/day, divided BID with food
So....If liver biopsy of a dog or cat with chronic hepatitis suggests abnormal stain uptake for copper,
a quantitative measurement of the tissue copper concentration is needed to strategize best therapy.
Tissue copper concentrations of ≥ 1,000 ug/gm (1.0 mg/gm) tissue are very abnormal. Sometimes
the results are provided as ppm (parts per million); 1 ug/gm = 1 ug/1,000,000 ug or 1 ppm.
Door Heidi
#3267524
Wauw! Super super bedankt voor alle informatie! Ik had geen bericht gekregen dat ik reacties had vandaar late reactie van mij, sorry.
Morgen met m'n frisse hoofd zal ik alles even goed doorlezen. Hij staat nu iig sinds gisteren op speciale brok, maar naar mijn idee zijn die speciale brokken al helemaal niet goed voor een hond. Misschien wel voor het probleem maar niet voor het lichamelijk gestel van de hond.
 Terug naar “Vragen en Problemen over gezondheid”

Barfplaats wordt gesponsord door