How long can a dog be on prednisone?

toomuchglassJanuary 19, 2011

I've had my dog on it since fall .Her scratching drove her crazy - so I got the first round. We assumed it was allergies. After that round - a couple weeks later she started itching again.We had our first frost - so I didn't think it was allergies any more - but it worked. It now Jan. & she's on her 3rd round. It works a miracle. Next time this itching starts - I'm taking her to the vet . What's next ? Blood tests ? More Prednisone. ? (Benedryl & Claritan don't help at all ) I've never dealt with this much itchiness before.

( PS -- I looked up every cause of itching on the web - and she doesn't fit any category.Her skin is clear,her coat is shiny-I'm at a loss )

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There are lots of reasons for pruitis in animals and some of them don't even have the skin as a primary reason. Insufficient kidney function for example can cause itchiness. I had a cat with constant itch and everything kept coming up negative until my vet had a hunch about a certain mite normally not causing systemic reactions in cats. Well, it did on my cat and he put her on revolution and it was history. I've kept old and terminal animals on pred since it was the lesser of evils and made their last days on earth more comfortable, but I am sure you would not like to make this a long-term treatment. Hope you find an answer.

    Bookmark   January 19, 2011 at 2:07PM
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That depends. How long do you want these side effects?

Note: Although separate entities, prednisone and prednisolone are often considered bioequivalent; most species rapidly convert prednisone to prednisolone in the liver. Horses, cats and patients in frank hepatic failure do not appear to either absorb or convert prednisone to prednisolone efficiently. Use either prednisolone or an alternative glucocorticoid in these patients when possible.

Prescriber Highlights
Classic glucocorticoids used for many conditions in many species. Antiinflammatory activity is 4X more potent than hydrocortisone; has some mineralocorticoid activity
Contraindications (relative): Systemic fungal infections
Caution: Active bacterial infections, corneal ulcer, Cushingoid syndrome, diabetes, osteoporosis, chronic psychotic reactions, predisposition to thrombophlebitis, hypertension, CHF, renal insufficiency
Goal of therapy is to use as much as is required & as little as possible for as short an amount of time as possible
Prednisone poorly absorbed after oral use in horses; prednisone may not be readily converted to prednisolone in cats. Prednisolone is preferred in these two species.
Primary adverse effects are "Cushingoid" in nature with sustained use
Many potential drug & lab interactions
Glucocorticoids have been used in an attempt to treat practically every malady that afflicts man or animal, but there are three broad uses and dosage ranges for use of these agents. 1) Replacement of glucocorticoid activity in patients with adrenal insufficiency, 2) as an antiinflammatory agent, and 3) as an immunosuppressive. Among some of the uses for glucocorticoids include treatment of: endocrine conditions (e.g., adrenal insufficiency), rheumatic diseases (e.g., rheumatoid arthritis), collagen diseases (e.g., systemic lupus), allergic states, respiratory diseases (e.g., asthma), dermatologic diseases (e.g., pemphigus, allergic dermatoses), hematologic disorders (e.g., thrombocytopenias, autoimmune hemolytic anemias), neoplasias, nervous system disorders (increased CSF pressure), GI diseases (e.g., ulcerative colitis exacerbations), and renal diseases (e.g., nephrotic syndrome). Some glucocorticoids are used topically in the eye and skin for various conditions or are injected intra-articularly or intra-lesionally. The above listing is certainly not complete.

In general, in using glucocorticoids, the following principles should be followed:

1. Glucocorticoids can mask disease! Try not to use them until you have a diagnosis.
2. Make a specific diagnosis!
3. Determine course from outset
4. Determine endpoint before you starting treating
5. Use the least potent form for the minimal time
6. Know where glucocorticoids inappropriate. (Behrend 2007)
Glucocorticoids have effects on virtually every cell type and system in mammals. An overview of the effects of these agents follows:

Cardiovascular System: Glucocorticoids can reduce capillary permeability and enhance vasoconstriction. A relatively clinically insignificant positive inotropic effect can occur after glucocorticoid administration. Increased blood pressure can result from both the drugs' vasoconstrictive properties and increased blood volume that may be produced.

Cells: Glucocorticoids inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitization of lymphocytes, and the cellular response to mediators of inflammation. Glucocorticoids stabilize lysosomal membranes.

CNS/Autonomic Nervous System: Glucocorticoids can lower seizure threshold, alter mood and behavior, diminish the response to pyrogens, stimulate appetite, and maintain alpha rhythm. Glucocorticoids are necessary for normal adrenergic receptor sensitivity.

Endocrine System: When animals are not stressed, glucocorticoids will suppress the release of ACTH from the anterior pituitary, thereby reducing or preventing the release of endogenous corticosteroids. Stress factors (e.g., renal disease, liver disease, diabetes) may sometimes nullify the suppressing aspects of exogenously administered steroids. Release of thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin and luteinizing hormone (LH) may all be reduced when glucocorticoids are administered at pharmacological doses. Conversion of thyroxine (T4) to triiodothyronine (T3) may be reduced in glucocorticoids and plasma levels of parathyroid hormone increased. Glucocorticoids may inhibit osteoblast function. Vasopressin (ADH) activity is reduced at the renal tubules and diuresis may occur. Glucocorticoids inhibit insulin binding to insulin-receptors and the post-receptor effects of insulin.

Hematopoietic System: Glucocorticoids can increase the numbers of circulating platelets, neutrophils, and red blood cells, but platelet aggregation is inhibited. Decreased amounts of lymphocytes (peripheral), monocytes, and eosinophils are seen as glucocorticoids can sequester these cells into the lungs and spleen and prompt decreased release from the bone marrow. Removal of old red blood cells is diminished. Glucocorticoids can cause involution of lymphoid tissue.

GI Tract and Hepatic System: Glucocorticoids increase the secretion of gastric acid, pepsin, and trypsin. They alter the structure of mucin and decrease mucosal cell proliferation. Iron salts and calcium absorption are decreased while fat absorption increases. Hepatic changes can include increased fat and glycogen deposits within hepatocytes, increased serum levels of alanine aminotransferase (ALT), and gamma-glutamyl transpeptidase (GGT). Significant increases can be seen in serum alkaline phosphatase levels. Glucocorticoids can cause minor increases in BSP (bromosulfophthalein) retention time.

Immune System (also see Cells and Hematopoietic System): Glucocorticoids can decrease circulating levels of T-lymphocytes; inhibit lymphokines; inhibit neutrophil, macrophage, and monocyte migration; reduce production of interferon; inhibit phagocytosis and chemotaxis; antigen processing; and diminish intracellular killing. Specific acquired immunity is affected less than nonspecific immune responses. Glucocorticoids can also antagonize the complement cascade and mask the clinical signs of infection. Mast cells are decreased in number and histamine synthesis is suppressed. Many of these effects only occur at high or very high doses and there are species differences in response.

Metabolic effects: Glucocorticoids stimulate gluconeogenesis. Lipogenesis is enhanced in certain areas of the body (e.g., abdomen) and adipose tissue can be redistributed away from the extremities to the trunk. Fatty acids are mobilized from tissues and their oxidation is increased. Plasma levels of triglycerides, cholesterol, and glycerol are increased. Protein is mobilized from most areas of the body (not the liver).

Musculoskeletal: Glucocorticoids may cause muscular weakness (also caused if there is a lack of glucocorticoids), atrophy, and osteoporosis. Bone growth can be inhibited via growth hormone and somatomedin inhibition, increased calcium excretion and inhibition of vitamin D activation. Resorption of bone can be enhanced. Fibrocartilage growth is also inhibited.

Ophthalmic: Prolonged corticosteroid use (both systemic or topically to the eye) can cause increased intraocular pressure and glaucoma, cataracts, and exophthalmos.

Reproductive Tract, Pregnancy, & Lactation: Glucocorticoids are probably necessary for normal fetal development. They may be required for adequate surfactant production, myelin, retinal, pancreas, and mammary development. Excessive dosages early in pregnancy may lead to teratogenic effects. In horses and ruminants, exogenous steroid administration may induce parturition when administered in the latter stages of pregnancy. Glucocorticoids unbound to plasma proteins will enter milk. High dosages or prolonged administration to mothers may potentially inhibit the growth of nursing newborns.

Renal, Fluid, & Electrolytes: Glucocorticoids can increase potassium and calcium excretion; sodium and chloride reabsorption and extracellular fluid volume. Hypokalemia and/or hypocalcemia occur rarely. Diuresis may occur following glucocorticoid administration.

Skin: Thinning of dermal tissue and skin atrophy can be seen with glucocorticoid therapy. Hair follicles can become distended and alopecia may occur.

Plasma half-life is not meaningful from a therapy standpoint when evaluating systemic corticosteroids. Prednisolone and prednisone are intermediate acting corticosteroids with a biologic "half-life" of 12�36 hours.

Systemic use of glucocorticoids is generally considered contraindicated in systemic fungal infections (unless used for replacement therapy in Addison's), when administered IM in patients with idiopathic thrombocytopenia, and those hypersensitive to a particular compound. Sustained-released injectable glucocorticoids are considered contraindicated for chronic corticosteroid therapy of systemic diseases.

Animals that have received glucocorticoids systemically, other than with "burst" therapy, should be tapered off the drugs. Patients who have received the drugs chronically should be tapered off slowly as endogenous ACTH and corticosteroid function may return slowly. Should the animal undergo a "stressor" (e.g., surgery, trauma, illness, etc.) during the tapering process or until normal adrenal and pituitary function resume, additional glucocorticoids should be administered.

Adverse Effects
Adverse effects are generally associated with long-term administration of these drugs, especially if given at high dosages or not on an alternate day regimen. Effects generally are manifested as clinical signs of hyperadrenocorticism. When administered to young, growing animals, glucocorticoids can retard growth. Many of the potential effects, adverse and otherwise, are outlined above in the Pharmacology section.

In dogs, polydipsia (PD), polyphagia (PP), and polyuria (PU) may all be seen with short-term "burst" therapy as well as with alternate-day maintenance therapy on days when giving the drug. Adverse effects in dogs can include: dull, dry haircoat, weight gain, panting, vomiting, diarrhea, elevated liver enzymes, pancreatitis, GI ulceration, lipidemias, activation or worsening of diabetes mellitus, muscle wasting, and behavioral changes (depression, lethargy, viciousness). Discontinuation of the drug may be necessary; changing to an alternate steroid may also alleviate the problem. With the exception of PU/PD/PP, adverse effects associated with antiinflammatory therapy are relatively uncommon. Adverse effects associated with immunosuppressive doses are more common and potentially more severe.

Cats generally require higher dosages than dogs for clinical effect, but tend to develop fewer adverse effects. Occasionally, polydipsia, polyuria, polyphagia with weight gain, diarrhea, or depression can be seen. Long-term, high dose therapy can lead to "Cushingoid" effects, however.

Reproductive/Nursing Safety
Corticosteroid therapy may induce parturition in large animal species during the latter stages of pregnancy. In humans, the FDA categorizes this drug as category C for use during pregnancy (Animal studies have shown an adverse effect on the fetus, but there are no adequate studies in humans; or there are no animal reproduction studies and no adequate studies in humans.) In a separate system evaluating the safety of drugs in canine and feline pregnancy (Papich 1989), this drug is categorized as class C (These drugs may have potential risks. Studies in people or laboratory animals have uncovered risks, and these drugs should be used cautiously as a last resort when the benefit of therapy clearly outweighs the risks.)

Use with caution in nursing dams. Glucocorticoids unbound to plasma proteins will enter milk. High dosages or prolonged administration to mothers may potentially inhibit growth, interfere with endogenous corticosteroid production or cause other unwanted effects in nursing offspring. In humans, however, several studies suggest that amounts excreted in breast milk are negligible when prednisone or prednisolone doses in the mother are less than or equal to 20 mg/day or methylprednisolone doses are less than or equal to 8 mg/day. Larger doses for short periods may not harm the infant.

Overdosage/Acute Toxicity
Glucocorticoids when given short-term are unlikely to cause harmful effects, even in massive dosages. One incidence of a dog developing acute CNS effects after accidental ingestion of glucocorticoids has been reported. Should clinical signs occur, use supportive treatment if required.

Chronic usage of glucocorticoids can lead to serious adverse effects. Refer to Adverse Effects above for more information.

From Plumb's drug handbook 6th edition

    Bookmark   January 19, 2011 at 6:20PM
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Holy cow ..what a reply ! ..

In all honesty - if I understood all that - I'd already be a vet ! I'm not the brightest crayon in the box when it comes to medical stuff. Can you give me the Readers Digest condensed version in easy to understand terms ? LOL

Thanks for taking the time to post it for me .


    Bookmark   January 19, 2011 at 10:36PM
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The most important sentence in that whole post is this:

Goal of therapy is to use as much as is required & as little as possible for as short an amount of time as possible.

    Bookmark   January 20, 2011 at 12:15PM
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Well - now THAT makes perfect sense. That's my goal .Stop the itch ,but do no harm in the process.

    Bookmark   January 20, 2011 at 4:34PM
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The longer or more often or pred, the more likely you can have bad side effects. Prednisone destroys muscle (including the heart), suppresses the immune system, can ulcerate the stomach to the point of rupturing, cause diabetes, cause thin skin, weakens ligaments and tendons (which may cause surgical disease), causes panting, can cause hair loss, extreme hunger and thirst, dilutes the urine making your pet have to pee all the time (dose dependent) and more.

There is no way to give pred without having some degree of all of the side effects. It's not usually enough to be noticeable but the more the pet is on pred, the more likely to run into trouble.

    Bookmark   January 20, 2011 at 7:44PM
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Thanks again Meghane !

    Bookmark   January 21, 2011 at 1:57PM
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A way to mitigate the bad effects is to take the drug every other day - that way the body does not quit making its' own prednisolone.

It's powerful and cheap but is a bad guy in the long run.

    Bookmark   January 21, 2011 at 5:43PM
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Good post. My golden was on pred for about 2.5 mths...and has now been off for about 2 mths, but she has not lost the weight that she gained...her appetite is back to normal so no reason for the weight to stay on.....also, she has developed a growth on her lower eyelid...could this be a side effect. She will be going to the vets next month for her follow up...not rushing her in for the growth because it is small and does not seem to affect her in any way......the strange thing is that our little yorkie keeps licking it and trying to bite it off the golden....humm

    Bookmark   January 25, 2011 at 2:10PM
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Is there any chance that an ingredient in her food might be bothering her?

    Bookmark   January 25, 2011 at 10:44PM
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My dog was on it for hot spots - she licked holes into her legs - we had just stopped her third round of prednisone when we felt desperate knowing that she really couldn;t live on that stuff forever - we finally decided on our own to change her dog food - know we are not financially invested in this product- we took her off the Purina and put her on Orijen and within three weeks she completely stopped licking at the hot spots.

This dog food costs more and isnt as easy to buy because grocery stores don't carry it (high end dog food store here carries it), but if you are willing to put your dog on this and allow your dog to eat ONLY THIS FOOD OR TREATS MADE WITH NO GRAINS/FILLERS for three weeks or so, then you might find that your dog's problems are over or so greatly reduced that it's finally controllable.

It is very important that the dog eats only the food because if you feed him dog treats from the grocery store, you are defeating the whole point of finding out if it's a food allergy - the allergy would most likely be from the junk put in common dog food products such as fillers and grains. No people food - this is very important that your dog eat ONLY the chicken/turkey Orijen or similar high end brand dog food product.

We began to see results within a week or so but for some dogs it takes longer if it's a food allergy that is the problem.

A person at the store told us to put our dog on the chicken/turkey Orijen because chicken/turkey is the least likely for the dog to have allergies but there is also beef, other meats offered but were I you, I'd stick to the chicken/turkey since it's best allergy wise since some allergies can be aggravated by other meats. If you get cookies for your dog, look in the same area as the dog food and find some in chicken/turkey with no grains/ fillers and you should be safe. Our dog eats less of this dog food because she is filled up faster with decent food and fillers and that helps with the difference in price.

The dog food costs more but it's worth it and the poops are much less and much firmer. You want to keep the dog treats as close to the dog food as is possible. Those cookies will be more expensive too, but it's worth it.
It must be delicious, our dog loves it right from the first bite, obviously so since she danced around her bowl asking for seconds, please.

It can't hurt to try this and very well might help - food allergies are a huge problem for dogs due to the crappy dog food ingredients used as fillers and the huge amount of grain thrown in to fill up the dog.

We are so glad we did this and she has not had a single hot spot problem since we put her on the Orijen a year ago. I hear that some product with the main word "California" used in the brand name is very very good too - I'm sure in a high end pet food store you can ask for help and they will guide you to a good brand, but I swear by the Orijen because that is what worked for our dog so well and so quickly.

Best of luck to your little buddy and to you also. It's hard to see your dog in such constant, steady discomfort, I know.

    Bookmark   January 26, 2011 at 12:37AM
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My little girl bichon has Cushing's disease and we are a member of k9cushings website. There are a number of people on that site whose dogs developed Cushing's disease from overuse or misuse of prednisone. If you post your question there, you will receive answers from people who have experienced this firsthand.
All 3 of my dogs were serious lickers, scratchers and biters. I changed their diet. It all stopped.
Hope this helps.

    Bookmark   February 7, 2011 at 7:19PM
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My rottweiler, Ray, is approximatly 7 years old. In September he was diagnosed with osteosarcoma after visitng the vet for a slight limp. His back left leg was amputated September 24 and we went through 4 chemo treatments over the winter. Post surgery he took a few weeks to recover. After his recovery he got back to his old self, he could run, play, go on walks, was capable of most thinks prior to his surgey. In February we noticed a bit of a slow down, but it was a tough winter, lots of snow, we thought perhaps either he was over tired because of the extra work moving around on snowy ground or just the cold was getting to him. Then one day in February he woke up in the morning and could not walk on his back leg at all - it seemed to happen overnight. We thought injury to his back leg or back initially, but all x-rays are negative. He went on 10mg of prednisone. This got him moving enough to go outside to the bathroom and move a round the house a bit, but not at the strength he once had. Since February he has regressed more, he is now on 40mg of prednisone a day to maintain enough mobility to go outside to do his business and limited movement around the house. We have tried to begin dialing back the dosage, but he regresses back to extreme difficulty moving around. My question is 1- How much danager is my dog in being on this prolonged usage of prednisone. 2- has anyone had success with altenate drugs? I should also mentiong that he is also on some herbal supplements, weekly accupuncture, and a boiled chicken and veggy diet.

Thank you

    Bookmark   April 11, 2011 at 11:57AM
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mw1590, my dog is going through the same thing right now! Fritzy is a mutt, 10 years old, and last fall, he was diagnosed with osteosarcoma after a slight limp. His back left leg was also amputated and he went through 6 months of chemo. Then, he was fine for a month, and all of a sudden, he woke up in the morning, squealed, and then couldn't walk. He's now on 10mg pred, robaxin, and a pain killer. And he seems to be regressing, with the latest symptom being episodes of crying, cramping, panting, and shaking usually starting 15 mins after eating and lasting hours at times. I'm at a loss. Not sure what to do. He's been to every doctor in the book. What happened with Ray? Fritzy's seems to be on the identical path, and this is the first time I've seen an identical story!! Please share.

    Bookmark   July 27, 2012 at 8:36PM
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I'm sorry to hear of your dog's illness and urge you to have a serious talk with your vet about his condition and prognosis.
As you know, robaxin is a muscle relaxant and you can read the side effects at this site:
If your dog is having difficulty getting up, some of it may be due to the robaxin, but the symptoms you've described go beyond the side effects of robaxin.

Did your vet examine your dog for possible spinal problems, and what has he said about the cancer returning?
I don't mean to sound uncaring, but personally, if I had a dog crying, panting, shaking and cramping (all signs of pain) and the vet was unable to find the problem, I would have the vet ease his pain by euthanasia.

Please read the link below about Osteosarcoma and it's overall prognosis.

Here is a link that might be useful: Osteosarcoma

    Bookmark   July 27, 2012 at 10:23PM
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