Glucocorticoid Comparison Table
Pharmacology - 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 by 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 is increased. 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.
Uses/Indications - Glucocorticoids have been used in attempts to treat practically every malady that afflicts man or animal. Among some of the uses for glucocorticoids are: endocrine (adrenal insufficiency), rheumatic (arthritis), collagen diseases (systemic lupus), allergic states, respiratory diseases (asthma), dermatologic diseases (pemphigus, allergic dermatoses), hematologic (thrombocytopenias, autoimmune hemolytic anemias), neoplasias, nervous system (increased CSF pressure), GI (ulcerative colitis exacerbations) and renal (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. For specific dosages and indications refer to the Doses section for each glucocorticoid drug monograph.
Contraindications/Precautions - Systemic use of glucocorticoids are generally considered to be contraindicated in systemic fungal infections (unless used for replacement therapy in Addison’s), when administered IM in patient’s with idiopathic thrombocytopenia and in patient’s hypersensitive to a particular compound. Use of sustained-release injectable glucocorticoids are considered to be contraindicated for chronic corticosteroid therapy of systemic diseases.
Animals who 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.
Corticosteroid therapy may induce parturition in large animal species during the latter stages of pregnancy.
Adverse Effects/Warnings - 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 symptoms 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 the drug is given. 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 “Cushinoid” effects, however.
Administration of dexamethasone or triamcinolone may play a role in the development of laminitis in horses.
Overdosage - 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 symptoms occur, use supportive treatment if required.
Chronic usage of glucocorticoids can lead to serious adverse effects. Refer to Adverse Effects above for more information.
Drug Interactions - Amphotericin B or potassium-depleting diuretics (furosemide, thiazides) when administered concomitantly with glucocorticoids may cause hypokalemia. When these drugs are used concurrently with digitalis glycosides, an increased chance of digitalis toxicity may occur should hypokalemia develop. Diligent monitoring of potassium and digitalis glycoside levels are recommended. Glucocorticoids may reduce salicylate blood levels. Insulin requirements may increase in patients taking glucocorticoids. Phenytoin, phenobarbital, rifampin may increase the metabolism of glucocorticoids. Concomitant administration of glucocorticoids and cyclosporin may increase the blood levels of each, by mutually inhibiting the hepatic metabolism of each other. The clinical significance of this interaction is not clear. Glucocorticoids may also inhibit the hepatic metabolism of cyclophosphamide. Dosage adjustments may be required. The hepatic metabolism of methylprednisolone may be inhibited by erythromycin. Mitotane may alter the metabolism of steroids; higher than usual doses of steroids may be necessary to treat mitotane-induced adrenal insufficiency.
Patients taking corticosteroids at immunosuppressive dosages should generally not receive live attenuated-virus vaccines as virus replication may be augmented. A diminished immune response may occur after vaccine, toxoid, or bactrin administration in patients receiving glucocorticoids. Administration of ulcerogenic drugs (e.g., non-steroidal antiinflammatory drugs) with glucocorticoids may increase the risk of gastrointestinal ulceration.
The effects of hydrocortisone, and possibly other glucocorticoids, may be potentiated by concomitant administration with estrogens. In patients with myasthenia gravis, concomitant glucocorticoid and anticholinesterase agent (e.g., pyridostigmine, neostigmine, etc.) administration may lead to profound muscle weakness. If possible, discontinue anticholinesterase medication at least 24 hours prior to corticosteroid administration.
Drug/Laboratory Interactions - Glucocorticoids may increase serum cholesterol and urine glucose levels. Glucocorticoids may decrease serum potassium. Glucocorticoids can suppress the release of thyroid stimulating hormone (TSH) and reduce T3 & T4 values. Thyroid gland atrophy has been reported after chronic glucocorticoid administration. Uptake of I131 by the thyroid may be decreased by glucocorticoids. Reactions to skin tests may be suppressed by glucocorticoids. False-negative results the nitroblue tetrazolium test for systemic bacterial infections may be induced by glucocorticoids.
Monitoring Parameters - Monitoring of glucocorticoid therapy is dependent on its reason for use, dosage, agent used (amount of mineralocorticoid activity), dosage schedule (daily versus alternate day therapy), duration of therapy, and the animal’s age and condition.The following list may not be appropriate or complete for all animals; use clinical assessment and judgement should adverse effects be noted:
1) Weight, appetite, signs of edema
2) Serum and/or urine electrolytes
3) Total plasma proteins, albumin
4) Blood glucose
5) Growth and development in young animals
7) ACTH stimulation test if necessary
Client Information - Clients should carefully follow the dosage instructions and should not discontinue the drug abruptly without consulting with veterinarian beforehand. Clients should be briefed on the potential adverse effects that can be seen with these drugs and instructed to contact the veterinarian should these effects become severe or progress.
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