View Full Version : Steroids: Prednisone vs Methylprednisolone

01-21-2011, 09:39 PM
So anyone up for primer on prednisone vs. methylprednisolone?

Vet Section of Drugs.com

Exceeding prednisolone in anti-inflammatory potency and having even less tendency than prednisolone to induce sodium and water retention, methylprednisolone offers the advantage over older corticosteroids of affording equally satisfactory anti-inflammatory effect with the use of lower doses and with an enhanced split between anti-inflammatory and mineralocorticoid activities. Estimates of the relative potencies of methylprednisolone and prednisolone range from 1.13 to 2.1, with an average of 1.5. In anti-inflammatory activity, as measured by the granuloma pouch assay, methylprednisolone is twice as active as prednisolone. In mineralocorticoid activity (ie, the capacity to induce retention of sodium and water in the adrenalectomized rat) methylprednisolone is slightly less active than prednisolone. The duration of plasma steroid levels following rapid intravenous injection in intact dogs is appreciably longer for methylprednisolone than for prednisolone, the respective “half-life” value for the two steroids being 80.9 ± 7.5 minutes for methylprednisolone and 71.3 ± 1.7 minutes for prednisolone.

While the effect of parenterally administered DEPO-MEDROL is prolonged, it has the same metabolic and anti-inflammatory actions as orally administered methylprednisolone acetate.


With therapeutically equivalent doses, the likelihood of occurrence of troublesome side effects is less with methylprednisolone than with prednisolone; moreover, side effects actually have been conspicuously absent during clinical trials with MEDROL Tablets in dogs and cats. However, methylprednisolone is similar to prednisolone in regard to kinds of side effects and metabolic alterations to be anticipated when treatment is intensive or prolonged. In animal patients with diabetes mellitus, use of methylprednisolone may be associated with an increase in the insulin requirement.

Negative nitrogen balance may occur, particularly in animals that require protracted maintenance therapy; measures to counteract persistent nitrogen loss include a high protein intake and the administration when indicated, of a suitable anabolic agent. Excessive loss of potassium, like excessive retention of sodium, is not likely to be induced by effective maintenance doses of MEDROL. However, these effects should be kept in mind and the usual regulatory measures employed as indicated. Ecchymotic manifestations, while not noted during the clinical evaluation in dogs and cats, may occur. If such reactions do occur and are serious, reduction in dosage or discontinuance of methylprednisolone therapy may be indicated. Concurrent use of daily oral supplements of ascorbic acid may be of value in helping to control ecchymotic tendencies.

The keystone of satisfactory therapeutic management with MEDROL Tablets, as with its steroid predecessors, is individualization of dosage in reference to the severity of the disease, the anticipated duration of steroid therapy, and the animal patient's threshold or tolerance for steroid excess. The prime objective of steroid therapy should be to achieve a satisfactory degree of control with a minimum effective daily dose.

The passage of blood from ruptured blood vessels into subcutaneous tissue, marked by a purple discoloration of the skin.

As with other orally administered corticosteroids, the total daily dose of MEDROL should be given in equally divided doses.

Average total daily oral doses for dogs and cats:
5 to 15 lb body wt 2mg
15 to 40 lb body wt 2 to 4 mg
40 to 80 lb body wt 4 to 8 mg

Jack weighs about 54 pounds and is on 8 mg once daily, I suspect to try to reduce the toxic effect per the information found elsewhere that once daily dosing is less toxic.

01-21-2011, 10:00 PM

Prednisone is activated by the patient's liver into Prednisolone.


Prednisone is rapidly converted in the liver to prednisolone. Except in cases of severe liver disease, the drugs are considered the same (equivalent).

01-21-2011, 10:10 PM

Mineralocorticoids: Mineralocorticoids get their name from the fact that they have the responsibility of maintaining the levels of the minerals sodium and potassium in the body, and because they are produced by the cortex of the adrenal glands. Through their effect on sodium and potassium, as well as other actions, they conserve or maintain the body's concentration of water at a near constant level. Mineralocorticoids exert most of their effect on the kidneys, causing parts of these organs to selectively excrete excess potassium in the urine and at the same time conserve or retain sodium. These actions maintain the concentrations of these electrolytes (http://javascript<b></b>:popupWin1('/dictionary_term.cfm?term=electrolyte', 50, 50, 350, 300)) within a very narrow range that is compatible with life. The use of the mineralocorticoids or their synthetically produced imitations in veterinary medicine is much less common than the other two forms of steroids.

Glucocorticoids: The previously mentioned cortisol belongs to the glucocorticoid group. The members of this group get their name because they affect glucose metabolism and are produced by the cortex section of the adrenal glands. The glucocorticoids are the predominant steroids used in veterinary medicine. These naturally occurring steroids cause proteins (e.g., muscles) and lipids (e.g., body fats) to be chemically broken down and converted into glucose. This is why the glucocorticoids are also referred to as the "catabolic" steroids. Catabolism means to break down large molecules into smaller ones. Additionally, the glucocorticoids also cause carbohydrates (http://javascript<b></b>:popupWin1('/dictionary_term.cfm?term=carbohydrate', 50, 50, 350, 300)) stored in the form of glycogen to be converted back to glucose and deposited into the circulating blood. There it is available to all the body's tissues (http://javascript<b></b>:popupWin1('/dictionary_term.cfm?term=tissue', 50, 50, 350, 300)). To break down the proteins or fats of the body may seem harmful to the animal, but remember that glucose is the main energy source for all of the body's activities. The vast majority of the glucose that the body utilizes comes directly from the diet or stored glycogen, but in emergency situations it can be derived from its own protein and lipids. It is generally thought that the glucocorticoids only cause this to occur to a significant degree during periods of exceptional need.

Glucocorticoids also suppress inflammatory processes within the body. A bruise, bee sting, bacterial infection, or arthritis are just a few examples of inflammation within a pet's body. Inflammation is specifically defined as an area of the body characterized by redness, swelling, heat, and pain, often with impaired function. The warmth and redness seen in these affected tissues comes from an increase in the number and size of blood vessels within the area. The swelling (edema) is caused by free fluid within the tissues and also the engorged blood vessels. All of these changes are brought on by physical trauma and/or irritants within the tissues. The pain is caused by the swelling, by harmful substances putting pressure on, or by stimulating the local nerve fibers. The loss of function can be caused by pain or the simple inability of the body to move or act correctly.

An example of the inflammatory action of glucocorticoids is in their use in an animal that has ruptured a disc between the vertebrae in its back. The swollen, herniated disc puts pressure on the spinal cord and other nerve fibers in the area. This is painful and the pressure on the spinal cord prevents nerve impulses from passing between the brain and the rear part of the body. The animal may be unable to walk or control its colon or bladder. Severe damage to the spinal cord can lead to total paralysis or death. Although surgery is required in a small portion of these cases to relieve the pressure on the spinal cord, most of these dogs can be successfully handled with rest and steroids. The steroids, and this case it is often dexamethasone, are able to remove the swelling and fluids within the disc and surrounding tissues, thereby removing the pressure from the spinal cord. This allows the nerve fibers within it to function correctly. Given time, the disc shrinks back down and the steroids are slowly discontinued. Remember, the steroids do not 'heal' the disc; they only reduce the swelling while it slowly returns to its normal size and shape.

Increased water consumption and increased urination: are two of the most common side effects of glucocorticoid usage. Although it can be quite disconcerting to the owner of a pet that lives predominately in the home, it is not by itself a serious problem. Glucocorticoids increase the activity of the glomeruli, which are the filtration units of the kidneys. This causes the animal to excrete higher levels of urine. The loss stimulates thirst in an attempt to replace lost fluids. These actions may increase water consumption and urination to the point that the animal can control neither one. Such signs can be observed within hours of initiating steroid therapy if the initial dosages were too high for the individual animal to tolerate. When long-acting injectable forms are used at excessive levels, increased water consumption and urination can continue for several weeks.