Chemicals / Complex Chemical Agents/ Chemical:

Hydrocortisone 

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 Glucocorticoid, also has mineralocorticoid actions. (B263)
Alternative Names Cortisol, compound F. (B263)
Chemical Formula --
Chemical Structure --
Molecular Weight --
Related Chemicals --

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Physical Properties / Chemistry
Appearance

White or nearly white crystalline powder; odourless. (B263)

  • Hydrocortisone acetate: white to practically white, crystalline powder; odourless.

  • Hydrocortisone cypionate: white to practically white, crystalline powder, odourless or with slight odour. (B263)

  • Hydrocortisone sodium phosphate: white to light yellow powder, odourless or practically odourless, and hygroscopic. (B263)

  • Hydrocortisone sodium succinate: white to nearly white, odourless, hygroscopic, amorphous solid. (B263)

Melting point --
Boiling point --
Density --
Water solubility
  • Very slightly soluble. (B263)
  • Hydrocortisone acetate: insoluble. 
  • Hydrocortisone cypionate: insoluble. (B263)
  • Hydrocortisone sodium phosphate: freely soluble. (B263)
  • Hydrocortisone sodium succinate: very soluble. (B263)
Other solubility
  • Sparingly soluble in alcohol. (B263)
  • Hydrocortisone acetate: slightly soluble in alcohol.(B263)
  • Hydrocortisone cypionate: soluble in alcohol. (B263)
  • Hydrocortisone sodium phosphate: slightly soluble in alcohol. (B263)
  • Hydrocortisone sodium succinate: very soluble in alcohol.  (B263)
Acid/Base --

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Pharmacology & General Information
Pharmacology
  • Effect on 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
  • Store at 15-30C (room temperature) and avoid freezing solutions or suspensions. (B263)
  • Hydrocortisone tablets: store in well-closed containers. (B263)
    Hydrocortisone cypionate oral suspension: store in tight, light resistant containers. (B263)
  • After reconstituting solutions, only use products that are clear should be used. (B263)
  • Unused solutions should be discarded after three days. (B263)
Legal Category (In UK) --

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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)
Referees Suzanne I. Boardman (V.w6)

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Therapeutic Information

Uses/Indications
Activity --
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)
Limitations --
Notes --

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Pharmacokinetics and Drug Interactions
Absorption /Bioavailability --
Distribution --
Plasma Protein binding / Storage --
Elimination Route --
Elimination half-life / Clearance Rate --
Drug Interactions
  • Administration of a glucocorticoid concurrently with amphoteracin 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 may decrease blood levels of salicylates. (B263)
  • Glucocorticoids may increase insulin requirements. (B263)
  • Metabolism of glucocorticoids may be increased in individuals administered ophenytoin, phenobarbital or rifampin. (B263)
  • Glucocorticoids administerd 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 of effects by administration with oestrogens. (B263)
  • Concurrent use of glucocorticoids with anticholinesterase agents in individuals with myesthenia gravis may result in profound muscle weakness. (B263)

Physical compatibilities and incompatibilities:

Hydrocortisone sodium phosphate solution for injection: reported to be compatible with: "10% fat emulsion, amikacin sulfate, amphotericin B (with or without heparin sodium), bleomycin sulfate, cephapirin sodium, metaraminol bitartrate, sodium bicarbonate, and verapamil HCl." (B263)

Hydrocortisone sodium succinate: reported to be compatible with: "dextrose-Ringer's injection combinations, dextrose-Ringer's lactate injection combinations, dextrose-saline combinations, dextrose injections, Ringer's injection, lactated Ringer's injection, sodium chloride injections, amikacin sulfate, aminophylline, amphotericin B (limited quantities), calcium chloride/gluconate, cephalothin sodium (not in combination with aminophylline), cephapirin sodium, chloramphenicol sodium succinate, clindamycin phosphate, corticotropin, daunorubicin HCl, dopamine HCl, erythromycin gluceptate, erythromycin lactobionate, lidocaine HCl, mephentermine sulfate, metronidazole with sodium bicarbonate, netilmicin sodium, penicillin G potassium/sodium, piperacillin sodium, polymyxin B sulfate, potassium chloride, prochlorperazine edisylate, sodium bicarbonate, thiopental sodium, vancomycin HCl, verapamil HCl and vitamin Bcomplex with C." (B263)

Hydrocortisone sodium succinate: reported to be incompatible with: "ampicillin sodium, bleomycin sulfate, colistemethate sodium, diphenhydrinate, diphenhydramine HCl, doxorubicin HCl, ephedrine sulfate, heparin sodium, hydralazine HCl, metaraminol bitartrate, methicillin sodium, nafcillin sodium, oxytetracycline HCl, pentobarbital sodium, phenobarbital sodium, promethazine HCl, secobarbital sodium and tetracycline HCl." (B263)

Note: compatibility is affected by factors such as pH, concentration, temperature and diluents used; specialized references should be consulted more specific information.

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Administration
Formulations available Various formulations are available for topical use. (B263)
Doses / Administration Routes / Frequencies
  • Hydrocortisone acetate: administration by intraarticular, intrabursal, intralesional, intrasynovial or soft tissue injection. (B263)
  • Hydrocortisone cypionate: oral administration. (B263)
  • Hydrocortisone sodium phosphate: administered by intramuscular, subcutaneous or intravenous injection. (B263)
  • Hydrocortisone sodium succinate: administered by intravenous or intramuscular injection. (B263)

Great Apes

Monitoring parameters --

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Withdrawal period / Withholding time
Notes USA: A tolerance of 10 ppb has been established for hydrocortisone (as the succinate or acetate) in milk. (B263)

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Toxic Information

Toxic effects of Pharmaceutical Products
Contraindications / Precautions
  • Prolonged treatment with glucocorticoids may suppress the hypothalamic-pituitary-adrenal axis (HPA) and result in atrophy of the adrenal glands. (B201.7.w7)
    • Prolonged therapy should be avoided if possible, to minimise the risk of precipitating signs of adrenal insufficiency in the event of superimposed stress or when therapy ceases. (B201.7.w7)
  • Use corticosteroids with caution during pregnancy due to the risk of causing fetal abnormalities and abortion. (B201.7.w7)
  • In horses: use of corticosteroids is contraindicated for treatment of laminitis. (B201.7.w7)
  • Glucocorticoids and vaccines should not be administered concurrently with one another. (B201.7.w7)
  • If the course of therapy lasts for longer than two weeks, the dose of prednisolone should not be stopped abruptly but reduced gradually. (B201.7.w7)
  • For prolonged treatment, the dose should be tapered to the lowest level clinically acceptable for maintenance of the required effect then a gradual transition made to give twice this dose on alternate days. In dogs the dose should be given in the morning to minimise suppression of the HPA axis; for cats evening medication has been suggested (however the diurnal rhythm of the HPA in cats is uncertain). (B201.7.w7)
Adverse Effects / Side Effects / Warnings
  • In horses: use of corticosteroids may induce laminitis. (B201.7.w7)
  • Long term administration of glucocorticoids may cause iatrogenic hyperadrenocorticism. (B201.7.w7)
  • Administration of corticosteroids may cause hepatomegaly and a concurrent rise in serum levels of hepatic enzymes. (B201.7.w7)
  • Administration of glucocorticoids may change the required dosage of insulin in diabetic patients and may unmask diabetes in individuals not previously diagnosed as diabetic. (B201.7.w7)
  • Glucocorticoid treatment may cause gastric and colonic ulceration. (B201.7.w7)
  • The immunosuppression and modification of inflammatory processes by glucocorticoids may facilitate progression of infectious disease. (B201.7.w7)
    • If glucocorticoids are used in an individual with a known infection, an appropriate antimicrobial drug should be administered concurrently. (B201.7.w7)
  • Glucocorticoids have catabolic effects including: muscle wasting, cutaneous atrophy, telogen arrest of hair follicles, delay in healing of wounds, suppression of both corneal stroma repair and epithelial repair in cases of corneal ulceration. (B201.7.w7)

Reported side effects from glucocorticoid treatment include effects on blood cells and blood chemistry, central nervous system, endocrine system, gastro-intestinal system, renal system, musculoskeletal system and skin, as well as reduction in growth, redistribution of body fat, increased risk of infection, enhanced spread of infection and poor wound healing. (B270.33.w33)

Operator Warnings --
Overdose / Acute Toxicity --

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Detailed Toxicological Information
Classification --
Acute Toxicity --
Chronic Toxicity --
Reproductive effects --
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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