Chemicals / Complex Chemical Agents/ Chemical:

Dexamethasone (with special reference to Ruminants, Hedgehogs, Elephants, Bears, Lagomorphs, Ferrets, Great Apes and Cranes)

INFORMATION AVAILABLE

GENERAL CHEMICAL INFORMATION THERAPEUTIC INFORMATION [DOSE, FREQUENCY & ROUTE]

NUTRITIONAL INFORMATION

TOXICITY INFORMATION ENVIRONMENTAL INFORMATION
Information in this page has been entered to support the current volumes of Wildpro and further information will be added as new volumes are completed. This page is not intended to substitute for the manufacturer's data sheet and the information is not yet complete for all species, or for all contra-indications etc.

CAUTION: Before any pharmaceutical product is used, the manufacturer's data sheet, containing information on uses, dosage and administration, contra-indications, warnings etc., should always be consulted. It is important to remember that licensing of pharmaceutical products for use in a particular species/condition, as well as mandatory meat and milk withdrawal times for food-producing animals, varies between countries and changes with time. Withdrawal times also may vary between different pharmaceutical formulations and depending on route of administration. In the EU, the prescription cascade must be followed (see LCofC1.2H and W564.Apr05.w1); note that specific restrictions apply for food-producing animals. In the USA, FARAD may be consulted regarding residues and meat and milk withdrawal times.

General Chemical Information

Summary 
Glucocorticoid (steroidal) anti-inflammatory drug.  (B263)

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Names and Formulae
Type Synthetic glucocorticoid anti-inflammatory agent; immunomodulator, antineoplastic.(B263, W324)
Alternative Names
  • Dexamethasone sodium phosphate: 1.3 g is equivalent to 1g dexamethasone. (B263)
  • "9a-fluoro-16beta-methylprednisolone; 16beta-methyl-11beta,17a,21-trihydroxy-9a-fluoro-1,4-pregnadiene-3,20-dione; hexadecadrol; 9a-fluoro-16a-methyl prednisolone; 9a-fluoro-11beta,17a-21-trihydroxy-16a-methyl-1,4-pregnadiene-3,20-dione; 16a-methyl-9a-fluoro-1,4-pregnadiene-11beta,17a-21-triol-3,20-dione; Celestone cortisone; Cortone dexamethasone; Decadron; Dexameth; Hexadrol hydrocortisone; Solu-cortef methylprednisolone; Medrol; Depo-Medrol; Solu-medrol predn; (11beta,16alpha)-9-fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione; Superprednol; Calonat; Decasone; Decacortin; Deronil; Fluormone; Dekacort; Dexa-Cortisyl; Dinormon; Millicorten; Fortecortin; Anaflogistico; Spoloven; Luxazone; Dectancyl; Dexapos; Dexasone; Dexinoral; Gamma-corten; Dextelan; Policort; Dexacortal; Dexa-Manallet; Decalix; Dexacortin; Deseronil; Dergramin; Hexadrol; Deltafluorene; Oradexon; Dexa-Cortidelt; Aeroseb-D; Dexinolon; Decaderm; Dexafarma; Cortissumman; Dexasine; Loverine; Maxidex; Dexa-Scheroson; Pet Derm III; Isopto-Dex; 16alpha-Methyl-9alpha-fluoro-prednisolone; 1-Dehydro-16alpha-methyl-9alpha-fluorohydrocortisone; 16alpha-Methyl-9alpha-fluoro-delta-1-hydrocortisone; Lokalison F; Dexa-Mamallet; 9-fluoro-11-beta,17,21-trihydroxy-16-alpha-methylpregna-1,4-diene-3,20-dione; 16alpha-methyl-9alpha-fluoro-1-dehydrocortisol; 16alpha-methyl-9alpha-fluoro-delta(sup 1)hydrocortisone; delta(sup 1)-9alpha-fluoro-16alpha-methylcortisol; 9alpha-fluoro-16alpha-methyl-11beta,17,21-trihydroxypregna-1,4-diene-3,20-dione; 9alpha-fluoro-16alpha-methyl-1,4-pregnadiene-11-beta,17alpha,21-triol-3,20-dione; 9alpha-fluoro-11beta,17alpha,21-trihydroxy-16-alpha-methylpregna-1,4-diene-3,20-dione; 16alpha-methyl-9alpha-fluoro-11beta,17alpha,21-trihydroxypregna-1,4-diene-3,20-dione; 9-fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione; aeroseb-dex; aphtasolon; corsone; decaspray; desadrene; desametasone; desameton; desamethasone; DEXA; dexacort; dexadeltone; dexalona; dexamethasone alcohol; dexone; dezone; DXMS; mexidex; MK 125; sk-dexamethasone; dexapolcort; dexaprol; fluorocort; HL-DEX; prednisolone f; visumetazone; 9alpha-Fluoro-11beta,17alpha,21-trihydroxy-16alpha-methylpregn-1,4-diene-3,20-dione; Ak-Dex; Dalalone; Decadrol; Decaject; Decameth; Dexacen; Mymethsone; Solurex; Dexmethsone; Tobispray; 9-Fluoro-11,17,21-trihydroxy-16-a-methylpregna1,4diene-3,20-dione; Milli1) ten; Also available as Dexamethasone acefurate; Also available as Dexamethasone acetate; Also available as Dexamethasone dipropionate; Also available as Dexamethasone sodium phosphate;" (W324)
Chemical Formula C22H29FO5 (W324)
Chemical Structure --
Molecular Weight 392.4665. (W324)
Related Chemicals --

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Physical Properties / Chemistry
Appearance
  • Dexamethasone: white to off-white crystalline powder, odourless. (B263, W324)

  • Dexamethasone sodium phosphate: white to slightly yellow hygroscopic powder, odourless or with a slight odour. (B263)

Melting point 262 - 264C. (W324); about 250C, with some decomposition. (B263)
Boiling point  
Density  
Water solubility
  • Dexamethasone: <0.1 g/100 mL at 25C. (W324); practically insoluble. (B263)
  • Dexamethasone sodium phosphate: 1 g soluble in about 2 mL of water. (B263)
Other solubility Dexamethasone: sparingly soluble. (B263)
Acid/Base --

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Pharmacology & General Information
Pharmacology
  • Affects almost all cell types and systems. (B263)
  • Cells: glucocorticoids stabilise lysosome membranes; they inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitisation of lymphocytes and cellular response to inflammatory mediators. (B263)
  • Cardiovascular system: glucocorticoids can reduce capillary permeability, enhance vasoconstriction and increase blood pressure. May also be a clinically insignificant positive inotrophic effect. (B263)
  • Central nervous system and autonomic nervous system: glucocorticoids may lower seizure threshold, alter mood and behaviour, reduce response to pyrogens, stimulate appetite, maintain alpha rhythm. N.B. glucocorticoids are required for normal adrenergic receptor sensitivity. (B263)
  • Endocrine: In non-stressed animals exogenous glucocorticoids suppress release of ACTH from the anterior pituitary and thus reduce or prevent release of endogenous corticosteroids. The suppressing effects of exogenous glucocorticoids may sometimes be nullified by stress factors such as renal or liver disease or diabetes. Administration of glucocorticoids at pharmacological doses may reduce release of thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin and luteinizing hormone (LH), and may reduce conversion of thyroxine (T4) to triiodothyronine (T3), while plasma levels of parathyroid hormone may be increased. Osteoblast function may be inhibited. Activity of vasopressin (ADH) at the renal tubule is reduced; diuresis may occur. Binding of insulin to insulin receptors is inhibited and the post-receptor effects of insulin are inhibited. (B263)
  • Haematopoietic: glucocorticoids may increase circulating numbers of platelets, neutrophils and red blood cells; platelet aggregation is inhibited. Glucocorticoids may cause sequestration of peripheral lymphocytes, monocytes and eosinophils into the lungs and spleen and also decrease release of these cells from bone marrow, thus resulting in decreased amounts of circulating cells of these types. There may be reduced removal of old red blood cells. Lymphoid tissue involution may occur. (B263)
  • Gastro-intestinal and hepatic: glucocorticoids cause increased gastric acid, pepsin and trypsin secretion, alteration of mucin structure and a decrease in proliferation of mucosal cells. Absorption of iron salts and calcium are decreased; absorption of fat is increased. In the liver there may be increased deposition of fat and glycogen within hepatocytes, also serum levels of alanine aminotransferease (ALT) and gamma-glutamyl transpeptidase (GGT). There may be significant increases in serum alkaline phosphatase. There may be a minor increase in bromosulfophthalein (BSP) retention time. (B263)
  • Immune: many effects are seen only at high or very high doses; there are species differences. Glucocorticoid administration may cause decreases in circulating T-lymphocytes, inhibit lymphokines, inhibit migration of neutrophils, macrophages and monocytes, reduce interferon production, inhibit phagocytosis, chemotaxis and antigen processing and decrease intracellular killing. Nonspecific immune responses are affected to a greater degree than are specific immune responses. The complement cascade may be antagonised and the clinical signs of infection may be masked. Decreases in mast cell number and suppression of histamine synthesis may also occur. (B263)
  • Metabolic: gluconeogenesis is stimulated by glucocorticoids. There is enhancement of lipogenesis in some areas of the body such as the abdomen and there may be a redistribution of adipose tissue from the limbs to the trunk. Fatty acid mobilisation from tissues, and their oxygenation, is increased. There are increases in plasma levels of triglycerides, cholesterol and glycerol. Protein is mobilised from many areas but not from the liver. (B263)
  • Musculoskeletal: Muscular weakness may result from glucocorticoids, also atrophy and osteoporosis may occur. Via inhibition of growth hormone and somatomedin, increased excretion of calcium and inhibition of the activation of vitamin D, bone growth may be inhibited. Bone resorption may be enhanced. Growth of fibrocartilage is inhibited also. (B263)
  • Ophthalmic: prolonged systemic or topical ocular use of corticosteroids may lead to increased intraocular pressure, glaucoma, cataracts and exophthalmos. (B263)
  • Reproductive: glucocorticoids are probably required for normal fetal development and may be needed for adequate production of surfactant, and development of myelin, retina, pancreas and mammary tissues. Teratogenic effects may be seen if glucocorticoids are administered early in pregnancy. In the later stages of pregnancy of horses and ruminants, administration of exogenous steroids may result in induction of parturition. Glucocorticoids which are not bound to plasma proteins will enter milk; high doses or prolonged administration to the nursing mother may potentially inhibit growth of nursing newborns. (B263)
  • Renal/Fluids: glucocorticoids may increase excretion of potassium and calcium, resorption of sodium and chloride, and intracellular fluid volume. Rarely may result in hypokalaemia and/or hypocalcaemia. Diuresis may occur when glucocorticoids are administered. (B263)
  • Skin: glucocorticoid therapy may lead to thinning of dermal tissue and atrophy of skin, also hair follicles may become extended and alopecia may be seen. (B263)
Storage / Stability
  • Heat labile: store at room temperature 15-30C. (B263)
  • Store dexamethasone tablets in tight containers. (B263)
  • Store dexamethasone sodium phosphate injection protected from light. (B263)
  • Light sensitive. (W324)
Legal Category (In UK) POM (B266)

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References

Associated Techniques

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ORGANISATIONS

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ELECTRONIC LIBRARY
(Further Reading)
Click image for full contents list of ELECTRONIC LIBRARY

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Authors Debra Bourne (V.w5); Gracia Vila-Garcia (V.w67)
Referees Suzanne I. Boardman (V.w6); Becki Lawson (V.w26); Susan Mikota (V.w72)

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Therapeutic Information

Uses/Indications
Activity
  • Suppression of inflammatory reactions. (B201.7.w7)
    • In general may provide symptomatic relief but not treat the underlying cause. (B201.1.w1)
    • May reduce clinical signs of hypersensitivity disorders.
Appropriate Use Glucocorticoids may be used in the treatment of:
  • Adrenal insufficiency. (B263)
  • Arthritis. (B263)
  • Systemic lupus. (B263)
  • Allergic reactions including asthma. (B263)
  • Dermatological conditions: pemphigus and allergic dermatoses. (B263)
  • Thrombocytopaenia. (B263)
  • Autoimmune haemolytic anaemia. (B263)
  • Neoplasias. (B263)
  • Increased cerebrospinal fluid pressure. (B263)
  • Exacerbations of ulcerative colitis. (B263)
  • Nephrotic syndrome. (B263)
  • Topically (some glucocorticoids) topically - eye, skin, intra-articular, intra-lesion. (B263)

Dexamethasone is used in the treatment of:

  • Shock or acute circulatory failure (together with intravenous fluid therapy). (B201.7.w7)
  • Inflammatory and allergic disorders. (B201.7.w7)
  • Ketosis. (B201.7.w7)
  • Induction of parturition in cattle. (B201.7.w7)
  • Hypoadrenocorticism. (B201.7.w7)
  • Horses: chronic granulomatous enteritis. (B201.7.w7)
Limitations
  • Avoid use of high dose dexamethasone in the treatment of acute spinal cord injuries. (B201.7.w7)
Notes --

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Pharmacokinetics and Drug Interactions
Absorption /Bioavailability --
Distribution Cattle:
  • Following intravenous administration of 0.1 mg/kg dexamethasone 21-isonicotinate in dairy cows, the volume of distribution Vd was 1.31 L/kg. Distribution into milk was rapid; the drug was detected in four of five cows when sampled at 15 minutes after administration, the concentration in milk peaked at 20.6 +/- 1.47 ng/mL at 30 minutes and then declined at a similar rate to plasma concentration. (J295.65.w1)
Plasma Protein binding / Storage --
Elimination Route Urine:
  • Following intramuscular administration of 60 g/kg of either a crystalline suspension of dexamethasone or a mixture containing dexamethasone sodium phosphate (short-acting) plus the long-acting phenylpropionate ester of dexamethasone, urine contained 6.2 to 21.2 ng/mL urine, and were at least five times higher than levels in milk over the same period. (J289.20.w3)
  • Following intramuscular administration of 60 g/kg of a crystalline suspension of dexamethasone milk contained 2.0 to 6.8 ng/mL at the first milking (seven to 13 hours after injection) and levels were at least five times lower than levels in urine over the same period. With the crystalline dexamethasone suspension levels declined rapidly: within 48 hours the concentration was less than 1.0 ng/mL and within 72 hours it was less than 0.5 ng/mL. In cows given a preparation containing dexamethasone sodium phosphate (short-acting) plus the long-acting dexamethasone phenylpropionate, also at 60 g/kg intramuscularly, one animal developed a peak residue in milk of nearly 3.0 ng/mL at six hours; levels in this and another cow remained above the detection limit (0.23 ng/mL) and above the recommended maximum residue limit (0.3 ng/mL) throughout the monitoring period (72 hours after drug administration). (J289.20.w3)
Elimination half-life / Clearance Rate Plasma half-life:
  • Dog: 119-136 hours. (B263)
  • Human: 200-300 hours or more. (B263)

Cattle:

  • Following intravenous administration of 0.1 mg/kg dexamethasone 21-isonicotinate in dairy cows, the half-life of elimination t1/2β was 4.54 h in plasma and 3.00 h in milk. Clearance ClB was 0.2 L/kg/h. By 12 hours after administration the concentration in milk was too low for detection and was calculated from the regression line to be 1.46 ng/mL. (J295.65.w1)
Drug Interactions
  • Administration of a glucocorticoid such as dexamethasone concurrently with amphotericin B or with potassium-depleting diuretics such as furosamide and thiazide diuretics may result in hypokalaemia. (B263)
    • In individuals receiving digitalis glycosides, in the event of hypokalaemia from the above combinations, there is an increased risk of digitalis toxicity. (B263)
  • Administration of glucocorticoids such as dexamethasone may decrease blood levels of salicylates. (B263)
  • Glucocorticoids such as dexamethasone may increase insulin requirements. (B263)
  • Metabolism of glucocorticoids such as dexamethasone may be increased in individuals administered phenytoin, phenobarbital or rifampin. (B263)
  • Glucocorticoids administered concurrently with cyclosporin may result in the blood levels of both drugs being increased due to mutual inhibition of hepatic metabolism; the significance of this effect is unclear. (B263)
  • Glucocorticoids may inhibit the hepatic metabolism of cyclophosphamide; this may require adjustment of the dosage. (B263)
  • Steroid metabolism may be altered by mitotane such that increased dose of the steroid may be required for treatment of mitotane-induced adrenal insufficiency. (B263)
  • In individuals receiving immuno-suppressive doses of corticosteroids, live attenuated virus vaccines should not generally be given as virus replication may be increased. (B263)
  • In individuals receiving immuno-suppressive doses of glucocorticoids, responses to vaccination, toxoids or bacterins may be decreased. (B263)
  • Possibility of potentiation by administration with oestrogens. (B263)
  • Concurrent use of glucocorticoids with anticholinesterase agents in individuals with myesthenia gravis may result in profound muscle weakness. (B263)
  • Dexamethasone sodium phosphate injection incompatibility reported with: daunorubicin hydrochloride, doxorubicin hydrochloride, metaraminol bitartrate, vancomycin. (B263)
  • Dexamethasone sodium phosphate injection compatibility reported with: amikacin sulphate, aminophylline, bleomycin sulphate, cimetidine hydrochloride, glycopyrrolate, lidocaine hydrochloride, nafcillin sodium, netilmicin sodium, prochlorperazine edisylate, verapamil. (B263)
  • Compatibility depends of factors such as pH, concentration, temperature and diluents. (B263)

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Administration
Formulations available
  • Dexamethasone 1 mg = dexamethasone acetate 1.1 mg = dexamethasone isonicotinate 1.3 mg = dexamethasone sodium phosphate 1.3 mg = dexamethasone trioxaundecanoate 1.4 mg (approximates). (B201.7.w7)
  • Dexamethasone sodium phosphate injection 4 mg/mL is approximately equivalent to dexamethasone 3mg/mL. (B263)

UK: 

USA:

  • Injection, oral powder. (B263)
Doses / Administration Routes / Frequencies Erinaceus europaeus - West European Hedgehog: Atelerix albiventris - Four-toed hedgehog:
  • 0.1-1.5 mg/kg; up to 5 mg/kg for shock. (J204.59.w1)

"Hedgehog" (species not distinguished between Atelerix albiventris - Four-toed hedgehog or Erinaceus europaeus - West European Hedgehog):

  • 0.1-1.5 mg/kg intramuscularly. For inflammation and allergies. (B267)
  • 5.0 mg/kg intramuscularly. For shock. (B267)

In Elephants:

Loxodonta africana - African Elephant

  • 20 mg was given to one 12-year old elephant and 100 mg was given to another, 13-year-old elephant as part of treatment for acute salmonellosis. (J4.185.w1)
  • 200 mg intramuscularly one daily for three days in a six year old elephant as part of treatment of an atypical salmonellosis. (P1.1985.w3)
  • 8,000 mg as a single dose intravenously was given in an adult 3,600 kg elephant for treatment of inflammation and respiratory signs. For further details see Interstitial Pulmonary Fibrosis in Elephants. (J4.189.w5)

In Bears:

  • In general: "Domestic dog drugs and dosages are used to treat bears." (B336.51.w51)
  • 4 mg intramuscularly followed by 10 mg orally once daily (in a donut) as initial treatment for Ruptured Intervertebral Disk in a Bear. Post surgery, 0.22 mg/kg bodyweight three times daily intramuscularly (discontinued on the fourth day post surgery). (J4.177.w3)
Lagomorphs - Oryctolagus cuniculus domesticus - Domestic rabbit:
  • 0.5 - 2.0 mg/kg subcutaneously, intramuscularly or intravensouly. (B373.Guide.w41)
  • 1 - 2 mg/kg intramuscular or intravenous injection. As an anti-inflammatory.. (B600.4.w4)
  • 1.0 - 2.0 mg/kg intramuscularly or intravenously. (B603.5.w5)
  • Note: In general, inflammation in rabbits should be treated using a NSAID, not a corticosteroid. a single intravenous bolus may be useful in treatment of shock or acute inflammation (e.g. Encephalitozoonosis in Lagomorphs (Parasitic Disease)). Corticosteroids may be useful in the management of neoplasia, particularly lymphoproliferative disorders, and may be useful in allergic or autoimmune disorders. (B603.5.w5)
  • 0.6 mg/kg intramuscularly as an inflammatory agent. (B263)
  • 0.2 - 0.6 mg/kg subcutaneously, intravenously or intramuscularly every 24 hours. (B546)
  • In the treatment of shock, 2 mg/kg intravenously or intramuscularly once only. (B546)
    • [For dogs and cats, use of the sodium phosphate salt is specified for the shock dose]. (B546)
  • 0.5 - 2.0 mg/kg intravenously, intramuscularly or subcutaneously. Shock dose in the treatment of enterotoxaemia. (B601.15.w15)
  • 0.5 - 2.0 mg/kg orally or subcutaneously every 12 hours. (B602.41.w41)

Ferrets - Mustela putorius furo - Ferret:

  • 0.5 - 2.0 mg/kg subcutaneously, intramuscularly or intravenously. (B602.41.w41)
  • For shock: 
    • Dexamethasone sodium phosphate 5 - 10 mg/kg subcutaneously or intramuscularly. (B626.App.w22)
    • Dexamethasone 0.5 mg/kg orally, subcutaneously, intramuscularly or intravenously. (B626.App.w22)
  • 1.0 mg/kg subcutaneously or intramuscularly following adrenalectomy. (B631.21.w21)

Great Apes

  • Adult Pan troglodytes - Chimpanzee: 2 mg/kg intravenously, intramuscularly or orally. d(W768.Jun2012.w1)
  • Primates:
    • As an anti-inflammatory 0.25 - 1.0 mg/kg intramuscularly or orally once daily. (D425.3.15.w3o)
    • For shock 2 - 8 mg/kg intravenously once. (D425.3.15.w3o)
    • For treatment of cerbral oedema 2 mg/kg intravenously or subcutaneously once, then 1 mg/kg three times daily. (D425.3.15.w3o)

Cranes

  • 2 - 8 mg/kg intramuscularly, intravenously or subcutaneously, once or twice daily. In the treatment of shock, trauma, endotoxaemia, capture myopathy. (B12.56.w14, B115.8.w4)
    • Reduce the dose for long-term treatment. (B115.8.w4) Reducing the dosage over time . (B12.56.w14)
  • Dexamethasone was given at 1-2 mg/kg subcutaneously every 12 hours for 1-2 days in the successful treatment of cranes with Capture Myopathy. (B703.10.w10)
Monitoring parameters --

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Withdrawal period / Withholding time
Notes

USA:

  • Cattle: Dexamethasone injection, 2 mg/mL; various manufacturers: "there are no withdrawal times required when used in cattle. A withdrawal period has not been established for this product in preruminal calves; do not use in veal calves." (B263)

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Toxic Information

Toxic effects of Pharmaceutical Products
Contraindications / Precautions
  • Except in emergencies, contraindicated in individuals with renal impairment, diabetes mellitus, chronic nephritis, congestive heart failure, osteoporosis, viral infections (during the viraemic stage), pregnant animals (except to induce parturition in cattle/sheep), laminitis. (B201.7.w7)
  • Systemic glucocorticoids are considered contraindicated in individuals with systemic fungal infections, except when used as replacement therapy in Addison's. (B263)
  • Systemic glucocorticoids are contraindicated for intramuscular injection in individuals with ideopathic thrombocytopaenia. (B263)
  • Contraindicated in individuals known to be hypersensitive to the drug. (B263)
  • Sustained-release injectable glucocorticoids are considered contraindicated for chronic corticosteroid therapy of systemic diseases. (B263)
  • Except in "burst" therapy, systemic glucocorticoid use should be tapered off gradually and additional glucocorticoids may be required in the event of stress. (B263)
  • Large animals: use of corticosteroids late in pregnancy may induce parturition. (B263)
Adverse Effects / Side Effects / Warnings
  • Effects generally manifest as signs of hyperadrenocorticism. (B263)
  • Growing animals: may retard growth. (B263)
  • Poldipsia, polyuria, polyphagia, hypokalaemia, calcinotis cutis, immunosuppression, delay in wound healing, gastro-intestinal ulceration. (B201.7.w7)
  • May cause iatrogenic Cushing's syndrome (iatrogenic hyperadrenocorticism). (B201.7.w7)
  • Dogs:
    • Polydipsia, polyuria and polyphagia may be seen even with short-term "burst" therapy. (B263)
    • Side effects may include a dull, dry coat, weight gain, panting, vomiting, diarrhoea, liver enzyme elevation, pancreatitis, gastro-intestinal ulceration, lipidaemia, diabetes mellitus (activation, or worsening of an existing condition), muscle wasting, behavioural changes: depression, lethargy, viciousness. (B263)
    • When used for anti-inflammatory therapy, side effects are relatively uncommon except for polyuria, polydipsia and polyphagia. (B263)
    • When used in immunosuppressive doses side effects are more common and may be more severe. (B263)
  • Cats: 
    • Generally develop fewer adverse effects than do dogs. (B263)
    • Occasional signs of polydipsia, polyuria, polyphagia with weight gain, diarrhoea or depression. (B263)
    • "Cushingoid" effects may be seen with long-term high-dose treatment. (B263)
  • Horses: use of dexamethasone may play a role in development of laminitis. (B263); may induce laminitis. (B201.7.w7)
  • Cattle: 
    • In lactating cows, milk yield may decrease. (B201.7.w7)
    • If used to induce parturition, may increase risk of retained placenta. (B201.7.w7)
  • For induction of parturition: do not give until after day 260 (cattle) or 138 (sheep) to avoid premature offspring. (B201.7.w7)
Operator Warnings --
Overdose / Acute Toxicity --

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Detailed Toxicological Information
Classification --
Acute Toxicity --
Chronic Toxicity --
Reproductive effects
  • In laboratory animals, administration of glucocorticoids, particularly in the first third of pregnancy, has resulted in fetal abnormalities. (B201.7.w7)
  • Use late in pregnancy may induce parturition. (B201.7.w7)
Teratogenic effects --
Mutagenic effects --
Carcinogenic effects

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Organ toxicity --
Bird Toxicity --
Aquatic organism activity --
Other organism toxicity --

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Nutrient Information

Nutritional Data
Sources --
Biological Use --
Recommended Daily Allowance / Recommended level in food --
Stability in food (Storage time) --
Interactions --

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External / Environmental Information

External / Environmental Uses
Use --
Formulation --
Application method --
Application Concentration --
Persistence of Effect / Frequency of Application --

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Sources in the Environment
Natural sources --
Human-associated sources --

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Effects on the Environment
Effects in the aquatic environment

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Effects on land --

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Persistence in the Environment
Breakdown in soil and groundwater

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Breakdown in water --
Breakdown in vegetation --

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