Prednisone

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Keep container tightly closed in a dry and well-ventilated place.

Prednisone tablets should be stored in well closed containers at a temperature less than 40 °C, preferably between 15-30 °C. Prednisone syrup should be stored in tight containers. Prednisone oral solution and oral concentrate solution should be stored in tight containers at 15-30 °C.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminate area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter.

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Impervious clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Concomitant use of anticholinesterase agents (e.g., neostigmine, pyridostigmine) and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. If concomitant therapy must occur, it should take place under close supervision and the need for respiratory support should be anticipated. /Corticosteroids/

Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. /Corticosteroids/

Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. /Corticosteroids/

Cholestyramine may increase the clearance of corticosteroids. /Corticosteroids/

For more Interactions (Complete) data for PREDNISONE (25 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 110(SRC), determined from a structure estimation method(2), indicates that prednisone is expected to have high mobility in soil(SRC). Volatilization of prednisone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.8X10-10 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Prednisone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.8X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2016).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 110(SRC), determined from a structure estimation method(2), indicates that prednisone is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.8X10-10 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 4(SRC), from its log Kow of 1.46(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2016).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), prednisone, which has an estimated vapor pressure of 3.8X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase prednisone may be removed from the air by wet and dry deposition(SRC). Prednisone contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Adverse effects are common in patients receiving glucocorticoids in high doses or over a long period. Regimens involving prednisone administration of ≥40 mg daily are considered "high-dose." The primary adverse effects associated with prednisone therapy include hyperglycemia, insomnia, increased appetite, hypertension, osteoporosis, edema, adrenal suppression, cataracts, delayed wound healing, skin fragility, weight gain, increased risk of infections, and fractures. Potential cardiovascular and metabolic effects include hypertension, hyperglycemia, and dyslipidemia.

Readily absorbed from the gastrointestinal tract. Rayos, the delayed-release formulation, has a 4-hour release time. To compare, the delayed-release formulation has a Tmax of 6.0 - 6.5 hours in healthy male subjects, whereas the immediate-release formulation has a Tmax of 2.0 hours. The rate of absorption, Cmax, and exposure is comparable between formulations.

IDENTIFICATION AND USE: Prednisone is white crystalline powder with a persistent bitter after-taste. It is glucocorticoid, anti-inflammatory agent and antineoplastic agent. HUMAN EXPOSURE AND TOXICITY: Prednisone causes profound and varied metabolic effects when used at therapeutic doses, given on a continuous basis. When given in large doses it can induce cardiac complications. In addition, it modifies the body's immune response to diverse stimuli; among the changes that occur are lymphopenia, monocytopenia and suppression of delayed hypersensitivity skin tests. Fluid and electrolyte disturbances may occur, including sodium and fluid retention, which may lead to congestive heart failure and hypertension. With large doses, potassium loss, hypokalemic alkalosis, and increased calcium excretion may occur. Glucocorticoids may cause fetal damage when administered to pregnant women. One retrospective study of 260 women who received pharmacologic dosages of glucocorticoids during pregnancy revealed 2 instances of cleft palate, 8 stillbirths, 1 spontaneous abortion, and 15 premature births. Another study reported 2 cases of cleft palate in 86 births. No chromosomal damage was detected in peripheral lymphocytes of patients treated with 3 mg/kg bw per day prednisone alone for 28 days and then with 0.5-1 mg/kg bw per day for 18-120 months. ANIMAL STUDIES: Carcinogenicity studies have been conducted in rats and mice. Of treated males, 7/20 developed tumors, among which were 3 pituitary tumors and 1 tumor of the breast; 16/18 female rats developed tumors, 8 of the breast, 5 of the pituitary, 2 of the adrenal and 1 of the liver. The overall tumor incidence in females was 1.5-2-fold higher than that in controls. However in mice, the tumor incidence in treated males was 4/19 (21%), with 2 lymphosarcomas and 2 lung tumors, and that in treated females was 8/27 (30%), with 4 lung tumors, 2 lymphosarcomas and 2 uterine tumors. These incidences were not significantly greater than those in controls. Prednisone given to rats from the 11th day of pregnancy until parturition at daily doses of 2.5 or 5 mg was reported to inhibit the growth of the fetal thymus and spleen. Prednisone was not mutagenic in Escherichia coli, and it caused no chromosomal damage when administered to rats. ECOTOXICITY STUDIES: The rotifer Brachionus calyciflorus and two crustaceans, the cladoceran Daphnia magna and the anostracan Thamnocephalus platyurus, were used to perform acute toxicity tests. Chronic toxicity tests have been performed on the alga Pseudokirchneriella subcapitata and the crustacean Ceriodaphnia dubia. The results showed low acute and chronic toxicity of prednisone. Some of the photoproducts had high toxic effects on C. dubia.

Signs and Symptoms of Overdose

Prednisone is a glucocorticoid receptor agonist. It is first metabolized in the liver to its active form, prednisolone. Prednisolone crosses cell membranes and binds with high affinity to specific cytoplasmic receptors. The result includes inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisone can stimulate secretion of various components of gastric juice. Suppression of the production of corticotropin may lead to suppression of endogenous corticosteroids. Prednisone has slight mineralocorticoid activity, whereby entry of sodium into cells and loss of intracellular potassium is stimulated. This is particularly evident in the kidney, where rapid ion exchange leads to sodium retention and hypertension.

/AQUATIC SPECIES/ Solar simulator irradiation of an aqueous suspension of prednisone, a widely prescribed drug, produces seven photochemical derivatives. The compounds have been identified on the basis of their physical features. All the chemicals have been tested to evaluate their toxic effects on freshwater organisms from different trophic levels. The rotifer Brachionus calyciflorus and two crustaceans, the cladoceran Daphnia magna and the anostracan Thamnocephalus platyurus, were used to perform acute toxicity tests. Chronic toxicity tests have been performed on the alga Pseudokirchneriella subcapitata (formerly known as Selenastrum capricornutum) and the crustacean Ceriodaphnia dubia. The results showed low acute and chronic toxicity of prednisone. Some of the photoproducts had high toxic effects on C. dubia.

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of October 28, 2016: http://actor.epa.gov/dashboard/]

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Short-Term Toxicity Studies," "Long-Term Carcinogenicity Studies," and "Genetic Toxicology Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from: http://ntp.niehs.nih.gov/testing/status/agents/ts-10936-e.html]

Prednisone concentration in sewage influent samples in the Ebre, Ter and Llobregat Rivers, Tarragona area, Spain ranged from 21-285 ng/L(1). Prednisone was detected in 23 of 37 water samples collected from the River Wenyu and tributaries, Beijing China between Aug 9-12, 2006 at concentrations ranging from not detected to 0.25 ng/L. No farms or livestock areas were located within the sampling area(2).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of prednisone can be estimated to be 110(SRC). According to a classification scheme(2), this estimated Koc value suggests that prednisone is expected to have high mobility in soil

/SIGNS AND SYMPTOMS/ Prednisone causes profound and varied metabolic effects when used at therapeutic doses, given on a continuous basis. When given in large doses it can induce cardiac complications. In addition, it modifies the body's immune response to diverse stimuli; among the changes that occur are lymphopenia, monocytopenia and suppression of delayed hypersensitivity skin tests. Fluid and electrolyte disturbances may occur, including sodium and fluid retention, which may lead to congestive heart failure and hypertension. With large doses, potassium loss, hypokalemic alkalosis, and increased calcium excretion may occur.

/SIGNS AND SYMPTOMS/ Moderate- to high-dose glucocorticoid therapy is associated with loss of bone and an increased risk of fracture. There also is evidence that long-term, low-dose (e.g., mean of 5.6 mg of prednisone daily) glucocorticoid therapy is associated with a risk of bone loss. Thus, while the American College of Rheumatology (ACR) previously considered patients who received at least 7.5 mg of prednisone (or its equivalent) daily for 6 months or longer to be at risk for glucocorticoid-induced osteoporosis, they currently consider patients receiving or planning to receive at least 5 mg of prednisone daily for 3 months or longer to be at risk for such bone loss. Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone. The adverse skeletal effects of glucocorticoids appear to be both dose and duration dependent, with prednisone dosages of at least 7.5 mg daily for 6 months or longer often resulting in clinically important bone loss and increased fracture risk.

/SIGNS AND SYMPTOMS/ Children with acute lymphoblastic leukemia (ALL) receive as part of induction therapy a 4-week course of high-dose glucocorticoid, which is either abruptly discontinued or shortly tapered. The aim of this study was to evaluate the signs and symptoms of steroid withdrawal syndrome and performance status (according to Lansky scale) during the 9-day tapering period and 1 week after withdrawal of the steroid in 63 children randomly allocated to receive prednisone or dexamethasone as part of induction treatment according the AIEOP ALL 2000 protocol. Twenty of 28 (75%) patients on dexamethasone versus 18 of 35 (51.4%) on prednisone (P < 0.05) developed at least one steroid withdrawal symptom during the study period. Three or more symptoms were observed in 39.3% (11/28) of the dexamethasone group and 8.6% (3/35) of the prednisone group (P < 0.05). Dexamethasone patients developed clinical signs earlier (within 3 days from the steroid tapering) than symptomatic prednisone patients. In the prednisone group, the symptoms were less severe and the performance status was higher (P < 0.05). ...

/SIGNS AND SYMPTOMS/ Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection. Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents. These infections may be mild, but they can be severe or fatal, and localized infections may disseminate. Patients who become immunosuppressed while receiving glucocorticoids have increased susceptibility to infections compared with healthy individuals. Some infections such as varicella (chickenpox) and measles can have a more serious or even fatal outcome in such patients, particularly in children. /Corticosteroids/

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including prednisone, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Prednisone is included on this list.

Implantation or injectable dosage form new animal drugs. Sterile prednisone suspension. ... Indications for use: It is used /in horses, dogs and cats/ for conditions requiring an anti-inflammatory agent. ... Do not use in horses intended for human consumption. Federal law restricts this drug to use by or on the order of a licensed veterinarian.

MEDICATION

MEDICATION (VET)

Anti-Inflammatory Agents; Antineoplastic Agents, Hormonal; Glucocorticoids

Use (kg) in Switzerland (2009): >100

For the treatment of drug-induced allergic reactions, perennial or seasonal allergic rhinitis, serum sickness, giant cell arteritis acute rheumatic or nonrheumatic carditis, systemic dermatomyositis, systemic lupus erythematosus, atopic dermatitis, contact dermatitis, exfoliative dermatitis, bullous dermatitis herpetiformis, severe seborrheic dermatitis, severe (Stevens-Johnson syndrome) erythema multiforme, mycosis fungoides, pemphigus, severe psoriasis, acute adrenocortical insufficiency, Addison's disease, secondary adrenocortical insufficiency, congenital adrenal hyperplasia, hypercalcemia associated with neoplasms, nonsuppurative thyroiditis, ulceratice colitis, Crohn's disease, acquired hemolytic anemia, congenital hypoplastic anemia, erythroblastopenia, adult secondary thrombocytopenia, adult idiopathic thrombocytopenia purpura, acute or subacute bursitis, epicondylitis, acute nonspecific tenosynovitis, acute or chronic lymphocytic leukemia, Hodgkin's or non-Hodgkin's lynphomas, Waldenstrom's macroglobulinemia, primary brain tumors (adjunct), nephrotic syndrome, tuberculous meningitis, multiple sclerosis, myasthenia gravis. cerebral edema, chorioretinitis, diffuse posterior choroiditis, aleergic conjunctivitis, Herpes zoster ophthalmicus, anterior segment inflammation, iridocyclitis, iritis, keratitis, optoc neuritis, sympathetic ophthalmia, corneal marginal allergic ulcers, symptomatic sarcoidosis, Loeffler's syndrome not manageable by other means, berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy and aspiration pneumonitis.

Chemical synthesis of prednisone was first reported by introduction of the two double bonds in ring A by 2,4-dibromination of the 3-ketone and dehydrobromination, but the yields were only 10-15%. Prednisone is prepared more efficiently microbiologically by the dehydrogenation of cortisone: a pure culture of Corynebacterium simplex is grown in a sterilized nutrient medium of yeast extract, and cortisone is added. The C. simplex selectively dehydrogenates the cortisone. When the reaction is complete, the fermentation broth is extracted and purified to give prednisone in good yield.

Preparation: Oliveto, Gould, United States of America patent 2897216 (1959 to Schering); Microbiological preparation: ... Nobile, United States of America patents 2837464 and 3134718 (1958, 1964 both to Shering).

Prednisolone (alcohol oxidation)

Oral: 1 mg, 2 mg, 5 mg, Rayos

Table: Prednisone Preparations [Table#4483]

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

Pharmaceuticals

Pharmaceuticals -> Alimentary tract and metabolism -> Glucocorticoides

Pregna-1,4-diene-3,11,20-trione, 17,21-dihydroxy-: INACTIVE

Generic name for an analog of cortisone.

Solar simulator irradiation of an aqueous suspension of prednisone, a widely prescribed drug, produces seven photochemical derivatives. ...