Hanall Biopharma


Full Prescribing Info
Hydrocortisone sodium succinate.
Each vial contains Hydrocortisone sodium succinate, USP 133.7 mg equivalent to 100 mg Hydrocortisone base.
Pharmacology: Pharmacodynamics: Hydrocortisone sodium succinate has the same metabolic and anti-inflammatory actions as hydrocortisone. When given parenterally and in equimolar quantities, the two compounds are equivalent in biologic activity.
Hydrocortisone is the principal glucocorticoid synthesized by the adrenal cortex in man. It influences carbohydrate, protein and lipid metabolism: In physiologic doses, its mineralocorticoid action is weak. Hydrocortisone's main therapeutic actions are its anti­-inflammatory and immunosuppressive effects. It inhibits the inflammatory response whatever the inciting agent, which is thought to be mediated by reduction in the formation of various vasoactive chemicals released during inflammation such as kinins, histamine, lyosomal enzymes, eicosanoids, and the complement system. Hydrocortisone inhibits the synthesis of prostaglandins through the synthesis of a family protein (lipocortin or macrocortin) that inhibits the activity of phospholipase A2. Lipocortin production also inhibits the synthesis of platelet activating factor. Hydrocortisone also modulates the immune response. The humoral response at therapeutic doses is inhibited only marginally. Cell mediated responses are not limited but their manifestations are prevented. These are affected by inhibition of macrophage production of tumor necrosis factor and IL-1, and response to IL-1, gamma­-interferon, migration inhibitory factor (MIF), and the T cell formation of IL-2.
Following intravenous administration demonstrable effects of hydrocortisone are evident within one hour and persist for a variable period.
Pharmacokinetics: Hydrocortisone sodium succinate is rapidly absorbed after parenteral administration.
After intramuscular injection. the absorption of the water soluble sodium succinate ester is rapid.
Hydrocortisone is extensively bound to plasma protein (90%) specifically, corticosteroid binding globulin (transcortin) and albumin.
Hydrocortisone is extensively metabolized in the liver and most body tissues to hydrogenated and degraded forms such as tetrahydrocortisone and tetrahydrocortisol. These are excreted in the urine, mainly conjugated as glucuronides, with a very small portion of unchanged hydrocortisone. Excretion of the administered dose is nearly complete within 12 hours. Hence, if constantly high blood levels are required, injection should be made every 4 to 6 hours. Negligible amounts are excreted in the bile; enterohepatic circulation does not occur. The metabolic clearance or hydrocortisone may be decreased in patients with hypothyroidism and increased in those with hyperthyroidism.
Endocrine Disorders: Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice: synthesis analogs like dexamethasone may be used in conjunction with mineralocorticoids where applicable; in infancy, mineralocorticoid supplementation is of particular importance; acute adrenocortical insufficiency (hydrocortisone or cortisone is the first choice mineralocorticoid supplementation may be necessary especially when synthetic analog are used); congenital adrenal hyperplasia; hypercalcemia associated w/ cancer; preoperatively and in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful; nonsuppurative thyroiditis.
Rheumatic Disorders: As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in: Post-traumatic osteoarthritis; rheumatoid arthritis including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy); ankylosing spondylitis; acute nonspecific tenosynovitis; psoriatic arthritis; temporal arteritis; synovitis or osteoarthritis; acute and subacute bursitis; acute gouty arthritis; epicondylitis.
Collagen Disorders: During exacerbation or as maintenance therapy in selected cases of systemic lupus erythematosus; systemic dermatomyositis (polymyositis); acute rheumatic carditis.
Dermatologic Disorders: Pemphigus; severe erythema multiforme (Stevens-Johnson syndrome); bullous dermatitis herpetiformis; mycosis fungoides; severe psoriasis; exfoliative dermatitis; severe seborrheic dermatitis.
Allergic States: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in adults and children with bronchial asthma; contact dermatitis; serum sickness; urticarial transfusion reactions; acute noninfectious laryngeal edema (epinephrine is the drug of choice); seasonal or perennial allergic rhinitis; atopic dermatitis; drug hypersensitivity reactions.
Ophthalmic Diseases: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa, such as herpes zoster ophthalmicus; chlorioretinitis; optic neuritis; anterior segment inflammation; keratitis; iritis, iridocyclitis; diffuse posterior uveitis and choroiditis; sympathetic ophthalmis; allergic conjunctivitis; allergic corneal marginal ulcers.
Gastrointestinal Diseases: To tide the patient over a critical period of the disease in: Ulcerative colitis (systemic therapy); Crohn's disease; regional enteritis (systemic therapy).
Respiratory Diseases: Symptomatic sarcoidosis. Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculosis chemotherapy; Loeffler's syndrome not manageable by other means; aspiration pneumonitis; idiopathic eosinophilic pneumonias; berylliosis; aspirations of gastric contents.
Hematologic Disorders: Idiopathic thrombocytopenic purpura in adults (IV only: IM administration is contraindicated); erythroblastopenia (RBC anemia; pure red cell aplasia); selected cases of secondary thrombocytopenia in adults; acquired (autoimmune) hemolytic anemia; congenital (erythroid) hypoplastic anemia (Diamond-Blackfan anemia); aspirations of gastric contents; idiopathic eosinophillic pneumonias.
Neoplastic Diseases: For palliative management of acute leukemia in children; leukemias and lymphomas in adults.
Edematous States/Renal Disorders: To induce diuresis or remission or proteinuria in nephrotic syndrome, without uremia, of the idiopathic type or due to lupus erythematosus.
Nervous System Disorders: Acute exacerbations of multiple sclerosis.
Medical Emergencies: Shock secondary to adrenocortical insufficiency or shock unresponsive to conventional therapy when adrenocortical insufficiency may be present;
acute allergic disorders (status asthmaticus, anaphylactic reactions, insect stings, etc.) following epinephrine.
Although there are no well controlled (double-blind, placebo) clinical trials, data from experimental animal studies indicate that corticosteroids may be useful in hemorrhagic, traumatic and surgical shock in which standard therapy (e.g., fluid replacement, etc.) has not been effective.
Other Uses: Tuberculosis meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculosis chemotherapy; trichinosis with neurologic or myocardial involvement.
Dosage/Direction for Use
Individualize dosage based on the condition being treated and the patient's response.
Corticosteroid therapy is an adjunct to, and not a replacement for conventional therapy.
This product may be administered by intravenous (IV) injection, IV infusion, or by intramuscular (IM) injection.
For initial emergency use IV injection is preferred. After the initial emergency period, consideration should be given to employing a longer-acting injectable preparation or an oral preparation.
Recommended Dose: Dosage usually ranges from 100 mg to 500 mg depending on the severity of the condition. Administer intravenously over a period of 30 seconds to 1 minute (e.g., 100 mg of hydrocortisone) to 10 minutes (e.g. 500 mg or more). The dose may be repeated at intervals of 2, 4 or 6 hours depending on the patient's response and clinical condition.
In general high-dose corticosteroid therapy should be continued only the patient's condition has stabilized usually not beyond 48 to 72 hours. Hypernatremia may result when high­-dose hydrocortisone therapy is administered beyond 48 to 72 hours: a corticoid product (e.g., methylprednisolone sodium succinate) which causes little or no sodium retention may be desirable.
Although adverse effects associated with high dose, short-term corticoid therapy are uncommon, peptic ulceration may occur. Prophylactic antacid therapy may be required.
Increased corticosteroid dosage is required in patients with adrenal insufficiency who are subjected to stress (eg., infection, surgery, trauma).
Patients subject to severe stress following corticosteroid therapy should be closely observed for signs and symptoms of adrenocortical insufficiency.
Treatment of Acute Exacerbations of Multiple Sclerosis: 800 mg per day of hydrocortisone for one week followed by 320 mg every other day for one month (see Precautions).
Use in Pediatric Patients: Hydrocortisone treatment should be based on seventy or the condition and response of the patient more than by age or body weight The range or initial doses is 0.56 to 8 mg/kg/day in three or four divided doses (20 to 240 mg/m2 BSA/day).
Preparation of Solution: Whenever solution and container permit, inspect the solution for particulate and discoloration before administration.
Similar to other steroid formulations, this product is sensitive to heat. Therefore, the product should not be autoclaved when it is desirable to sterilize the exterior of the vial.
For IV or IM Injection: Prepare solution by aseptically adding not more than 2 mL of Bacteriostatic Water for Injection or Bacteriostatic Sodium Chloride Injection to the contents of one vial.
For IV Infusion: Prepare solution by aseptically adding not more than 2 mL of Bacteriostatic Water for Injection or Bacteriostatic Sodium chloride Injection to the contents of one vial. This solution may then be added to 100 to 1000 mL of the following 5% dextrose in water (or isotonic saline solution or 5% dextrose in isotonic saline solution if patient is not on sodium restriction).
After reconstitution, hydrocortisone sodium succinate injection has a pH of 7-8.
The reconstituted solution should be stored at temperatures not exceeding 30°C. Protect light. Use solution only if it is clear and any unused solution should be discarded after 3 days.
As the clinically effective dose of corticosteroids vary according to the infections and requirements of individual patient, it is difficult to define "excessive" dosage of corticosteroids. Reports of acute toxicity and/or death resulting from corticosteroids overdosage are rare. However, continued use of large doses of corticosteroids (which are often necessary to elicit a clinical response) without proper dose reduction, leads to exaggeration of usual corticosteroid-related problems and aggravate pre-existing disease states (i.e., ulcerations of the gastrointestinal tract, electrolyte disturbances, infections, diabetes, and edema).
Cushingoid state results after doses (daily or several times per week) over a protracted period. The dose of hydrocortisone should be gradually reduced over a period of time to minimized the risk of developing adrenal insufficiency.
There is no known specific antidote available. Treatment of acute overdose is symptomatic and supportive (including respiratory and cardiovascular function). In case of chronic toxicity, closely monitor fluids and electrolytes levels, serum levels are not clinically useful.
Hydrocortisone is dialyzable.
Hypersensitivity to hydrocortisone or to any component of the product.
Bacterial infections unless specific anti-infective is given, systemic fungal and viral infections (due to immunosuppressing action, infection can be exacerbated).
Patients with herpes simplex, herpes zoster and chicken pox.
Patients with articular cavity infection or peritonitis/tenosynovitis (infection may be exacerbated by immunosuppression effect).
Patients with articular cavity instability.
Administration of live or live attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Intramuscular administration of corticosteroid is contraindicated for idiopathic thrombocytopenic purpura.
Intrathecal administration is contraindicated. Reports of severe medical events have been associated with this route of administration.
Special Precautions
General: Anaphylactoid reactions have occurred rarely in patients receiving corticosteroid therapy.
The lowest effective corticosteroid dose should be used to control the condition being treated. Gradual reduction of dosage is recommended whenever possible.
Complications of corticosteroid treatment are highly variable between patients as are durations of treatment. Dose and duration of treatment should be individually determined based on assessment of risk/benefit.
Kaposi's sarcoma has been seen mostly in patients receiving corticosteroids for chronic conditions. Clinical improvement may be observed upon discontinuation of corticosteroids.
Abrupt withdrawal of corticosteroids after prolonged therapy may result in corticosteroid withdrawal syndrome with symptoms such as fever, myalgia, arthralgia, and malaise.
Although recent studies have not been conducted with hydrocortisone or other­ corticosteroids, studies of methylprednisolone in septic shock suggest that increased mortality may occur in some subgroups of patients at higher risk (i.e., elevated creatinine­ greater than 2 mg/dL or with secondary infections).
Injection site reactions: Infection with hydrocortisone may result in demand and/or subdermal changes forming depression in the skin at the infection site. Care must be taken not be exceed the recommended doses in order to minimize the incidence of dermal and subdermal atrophy.
Cardio-Renal: Sodium retention resulting in edema, potassium loss, hypokalemic alkalosis, and hypertension may occur in patients receiving glucocorticoids. Congestive heart failure may occur in susceptible patients. These mineralocorticoid effects occur mostly with average and large doses of hydrocortisone or cortisone and occur less frequently with synthetic corticosteroids. However, these effects may occur when synthetic corticosteroids are used in high dosage for prolonged periods. Dietary salt restriction and potassium supplementation may be advised when necessary. All corticosteroids increase calcium excretion which may result in hypocalcemia.
Use corticosteroid with caution in patients with hypertension, congestive heart failure, or renal insufficiency.
Use corticosteroid with caution in patients who have experienced a recent myocardial infarction since corticosteroid use is associated with ventricular free wall rupture in these patients.
Endocrine: Acute adrenal insufficiency may occur if corticosteroids are abruptly withdrawn since hypothalam1c-p1tu1tary adrenal (HPA) suppression 1s dependent on dose and duration of treatment. In some cases, withdrawal symptoms may stimulate a clinical relapse of the
disease for which the patient has been under treatment and therefore withdrawal of corticosteroids should be gradual.
Withdraw corticosteroids gradually following long-term (more than 3 weeks) use to minimize drug-induced secondary adrenocortical insufficiency. Since drug-induced adrenocortical insufficiency may persist for months after discontinuation of therapy, reinstitute hormone therapy in any situation of stress occurring during that period. Dosage may have to be increased in patients already receiving corticosteroid therapy. Administer a salt and/or mineralocorticoid concurrently since mineralocorticoid secretion may also be impaired.
Metabolic clearance of corticosteroids may be altered in hypothyroid (decreased clearance) or hyperthyroid (increased clearance) patients. Dosage adjustment based on thyroid status may be necessary for these patients.
Use with caution in patients with diabetes mellitus since corticosteroids may cause an increase in blood sugar or steroid-induced diabetes. This usually resolves when the steroid is discontinued.
Gastrointestinal: An increase risk of perforation has been shown in active or latent peptic ulcers, diverticulitis, fresh intestinal anastomoses, and non specific ulcerative colitis and therefore caution in the use of steroids is recommended. Manifestations of peritoneal irritation following gastrointestinal perforation may not be seen or is minimal in patients receiving corticosteroids.
Musculoskeletal: Hydrocortisone's effect in calcium regulation and its capacity to inhibit osteoblast formation may cause a decrease in bone formation and an increase in bone resorption. These catabolic effects may lead to osteoporosis at any age and inhibition of bone growth in children and adolescents. Since postmenopausal women and geriatric or debilitated patients are especially prone to osteoporosis, special consideration must be given to these patients prior to initiation of corticosteroid therapy.
Vaccination: Do not administer live or live-attenuated vaccines (including small pox vaccine) in patients receiving corticosteroids. Although killed or inactivated vaccines may be administered in patients on corticosteroids, response to such vaccines cannot be predicted.
Patients who are receiving corticosteroids as replacement therapy, e.g. for Addison's disease, may be immunized.
Infections: Glucocorticoids (especially in large doses) suppress the immune system and increase susceptibility to or mask symptoms of infection. Corticosteroid may cause decreased resistance and inability to localize infection. Infections caused by any pathogen including viral, bacterial fungal protozoan or helminthic infections in any location of the body may be
associated with corticosteroids alone or in combination with other immunosuppressive agents. These infections may be mild to severe and occur more frequently with increasing doses of corticosteroid.
If corticosteroid have to be used in the presence of fungal or bacterial infections, administer appropriate anti-infective therapy.
Viral Infections: Viral infections such us chicken pox or measles can be more serious or even fatal in non-immunized children or adults on corticosteroid. Patients who have not had these diseases should particularly care to avoid exposure. Prophylaxis with varicella zoster immune globulin (VZIG) may be indicated if exposed to chicken pox, while prophylaxis with immunoglobulin (IG) may be indicated if exposed to measles. Consider treatment with antiviral agents if chicken pox develops.
Fungal Infections: Systemic fungal infections may be exacerbated by corticosteroids. Do not use corticosteroids in the presence of such infections unless they are needed to control life-threatening drug reactions. Cardiac enlargement and congestive heart failure have been reported with concomitant use of amphotericin B and hydrocortisone.
Special Pathogens: Corticosteroids may cause activation of latent diseases or exacerbation of intercurrent infections due to pathogens including Candida, Mycobacterium, Amoeba, Toxoplasma, Pneumocystis, Cryptococcus, Nocardia, etc.
As corticosteroids may also activate latent amoebiasis rule out intent or active amoebiasis before initiating corticosteroid therapy in patients who have spent time in the tropics or with unexplained diarrhea.
In patients with known or suspected Strongyloides (threadworm) infestation, corticosteroid­ induced immunosuppression may lead to Strongyloides hyperinfection dissemination with widespread larval migration which is often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia. Use with great care in these patients.
Do not use corticosteroid in cerebral malaria.
Tuberculosis: Use hydrocortisone in active tuberculosis only in fulminating or disseminated cases in which corticosteroids are used with appropriate antituberculous regimen.
Since reactivity to the disease may occur in patients with lalent tuberculosis or tuberculin reactivity, observe these patients closely and administer chemoprophylaxis during prolonged corticosteroid therapy.
Ophthalmic: Prolonged use or corticosteroid may cause posterior subcapsular and nuclear cataracts (particularly in children), exophthalmus or increased intraocular pressure which may result in glaucoma or may occasionally damage the optic nerve. Monitor intraocular pressure if steroid therapy is continued for more than 6 weeks. Development of secondary fungal and viral infections of the eye may be enhanced in patients receiving corticosteroids.
Do not use corticosteroids in active ocular herpes simplex to avoid corneal perforation.
Neuro-Psychiatric: Although corticosteroids have shown to be effective in speeding the resolution acute exacerbations of multiple sclerosis, data do not show that corticosteroids affect the ultimate outcome or natural history of the disease. Relatively high doses of corticosteroids are necessary to demonstrate a significant effect.
Acute myopathy which occurs most frequently in patients with disorders of neuromuscular transmission such as myasthenia gravis, or in patients receiving therapy with neuromuscular blocking agents such as pancuronium has been observed with use of high doses of corticosteroid. Acute myopathy, which may result in quadriparesis, is generalized and may involve ocular and respiratory muscles. Elevation of creatinine kinase may also be observed.
Clinical improvement or recovery may need weeks to years of stopping corticosteroid therapy.
Corticosteroid may lead to mental disturbances including euphoria, mood swings, depression and anxiety, personality changes, and frank psychoses. Corticosteroids may also aggravate emotional instability or psychotic tendencies.
Use in children: The efficacy and safety of corticosteroids are considered to be similar in adults and children.
Evidence of efficacy and safety in children for the treatment of nephrotic syndrome (>2 years old), and aggressive lymphomas and leukemias (>1 month old) have been in clinical studies
However, some of these conclusions and other indications for pediatric use of corticosteroid (e.g., severe asthma and wheezing) are based on adequate and well-controlled trials conducted in adults on the assumption that the course of the disease and their pathophysiology are considered to be substantially the same in both populations.
Periodically evaluate height, weight, ocular pressure, and blood pressure of children receiving corticosteroids. As in adults, children should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.
As much as possible, avoid long-term administration of pharmacologic doses of corticosteroids in children since these drugs may retard bone growth. Closely monitor growth and development of infants and children if prolonged therapy is necessary. Carefully weigh the potential effects on growth against the clinical benefits and the availability of alternative therapy. Minimize the potential effects of corticosteroids on by titrating to the lowest effective dose.
Use in elderly: There have been no clinical studies with sufficient number of patients (65 years old and above) to establish whether elderly patients respond differently from younger population. Although some reports have not seen any difference in responses between the elderly and younger patients, the incidence of corticosteroid-induced side effects may be increased since these patients have a greater frequency of decreased hepatic, renal, or cardiac function, and or concomitant disease or other drug therapy.
Use in pregnancy & lactation: During pregnancy the clinical benefit and possible risks of corticosteroid treatment should be considered.
Adverse effect is proven in animal experiments. Sufficient data is not available for a safe application in human pregnancy (possibility of cleft-palate formation and foetus growth retardation are low). Signs of hypo-adrenalism should be monitored in case of newborn whose mother has received corticosteroid treatment during pregnancy. In such case signs are observed, the appropriate treatment should be applied.
Prednisolone, is proven to be excreted in mother milk, which is most probably the case for other corticosteroids as well.
No data is available for hydrocortisone sodium succinate.
The benefit/risk ratio should be considered carefully, when treatment is to be applied during pregnancy and lactation and in case women in conceptive age.
Corticosteroids delay growth during infancy, childhood and adolescence. Treatment should be applied for the shortest possible time and for the most severe indications only.
Use In Pregnancy & Lactation
Use in Pregnancy: Category C: Corticosteroids may cause fetal damage when administered to pregnant women. Women who are pregnant or planning on becoming pregnant while receiving should inform their physician. Hydrocortisone and other corticosteroids should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus.
Hydrocortisone readily cross the placenta. Carefully monitor infants born to women who received corticosteroids during pregnancy for symptoms of adrenal insufficiency. There are no known effects of corticosteroids on labor and delivery.
Use in Lactation: Corticosteroids may be excreted in breast milk. Although hydrocortisone doses up to 160 mg daily are unlike to cause systemic effects in the infant, infants of mothers taking higher doses than this may have a degree of adrenal suppression. It may also suppress growth, interfere with endogenous corticosteroid production, or cause untoward effects. Hydrocortisone and other corticosteroids should be administered to breastfeeding mothers only if the potential benefits outweigh the potential risk to the infant.
Adverse Reactions
Gastrointestinal Effects: Dyspepsia, esophagitis, peptic ulcer with possible perforation and hemorrhage, abdominal distention, esophageal ulceration, esophageal candidiasis, pancreatitis, perforation of bowel, gastric hemorrhage, of the small and large bowel particularly in patients with inflammatory bowel disease, ulcerative esophagitis, hepatomegaly, nausea.
Evaluation of serum liver enzyme levels (alanine transaminase, aspartate transaminase and alkaline phosphatase) which are usually reversible upon discontinuation have also occurred.
Musculoskeletal Effects: Proximal myopathy, steroid myopathy, osteoporosis, pathological fracture of long bones, compression fractures, avascular osteonecrosis, tendon rupture, aseptic necrosis of femoral and humeral heads. Charcot-like arthropathy, muscle weakness, steroid myopathy, aseptic necrosis, loss of mass, and tendon rupture (particularly of the Achilles tendon).
Dermatological Effects: Impaired wound healing (usually at high doses), petechiae, and ecchymosis, thin fragile skin, facial erythema, skin atrophy, bruising, striae, increased sweating, telangiectasia, acne, burning or tingling (especially in the perineal area, after intravenous injection), dry scaly skin, impaired wound healing, rash and allergic dermatitis. Reports of Kaposi's sarcoma occurrence in patients receiving corticosteroid therapy; discontinuation of corticosteroids may result in clinical remission.
Endocrine-Metabolic Effects: Suppression of hypothalamo-pituitary-adrenal axis; growth suppression in infants, children and adolescents, menstrual irregularities and amenorrhea, development of cushingoid state, glycosuria, hyperglycemia. hirsutism, hypertrichosis, weight gain, decreased carbohydrate tolerance, increased requirements for insulin or oral hypoglycemic agents in diabetes, negative nitrogen and calcium balance due to protein catabolism, increased appetite manifestations of latent diabetes mellitus, secondary adrenocortical and pituitary unresponsiveness particularly in times of stress as in trauma, surgery or illness.
Neuro-Psychiatric Effects: Irritability, emotional instability, euphoria, depression, suicidal thoughts, mania, delusions, hallucinations, aggravation of schizophrenia, behavioral disturbances, anxiety, sleep disturbances, cognitive dysfunction, seizures, convulsions, confusion, amnesia, increased intracranial pressure with papilledema (pseudo cerebri) usually after discontinuation of treatment, psychic disorders insomnia, mood swings, neuritis, neuropathy, paresthesia, personality changes, exacerbation of pre-existing emotional instability or psychotic tendencies, headache, and vertigo.
Ophthalmic Effects: Glaucoma, increased intraocular pressure, posterior subcapsular cataracts (associated with prolonged, high dose systemic therapy), exophthalmos, papilledema with possible damage to the optic nerve, cataracts, corneal or sclera thinning, exacerbation or ophthalmic viral or fungal disease.
Cardiovascular Effects: Myocardial rupture following recent myocardial infarction, bradycardia. cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, fat embolism, cardiomyopathy in premature infants, pulmonary edema, syncope, tachycardia, thromboembolism, thrombophlebitis, and vasculitis.
Immune System Effects: Masking of infections, latent infections becoming active, including of tuberculosis and opportunistic infections, allergic reactions including anaphylactoid reactions, anaphylaxis, and angioedema; may suppress reactions to skin tests.
Parenteral corticosteroid therapy may also induce hyperpigmentation or hypopigmentation, subcutaneous and cutaneous atrophy, sterile abscess, anaphylactoid reaction (e.g., bronchospasm, laryngeal edema, urticaria).
Fluid and Electrolyte Disturbances: Congestive heart failure in susceptible patients, hypertension, hypokalemic alkalosis, fluid retention, potassium loss, sodium retention, and increased calcium excretion.
Others: Abnormal fat deposits, decreased resistance to infection hiccups, increased or motility and number of spermatozoa, injection site infections following non-sterile administration, malaise, moon face, weight gain.
Drug Interactions
Barbiturates phenytoin, carbamazepine, rifampicin and other drugs that stimulate hepatic metabolism. These drugs may enhance hydrocortisone metabolism, shorten its plasma half-life and lead to decreased effect of hydrocortisone. Increased hydrocortisone dosage may be required.
CYP 3A4 inhibitors such as troleandomycin, ketoconazole and macrolide antibiotics: May increase plasma concentrations of corticosteroids. Ketoconazole decreases the metabolism of certain corticosteroid by up to 60% leading to an increased risk of corticosteroids side effects.
Oral contraceptives and estrogen: Can cause alterations in plasma protein binding and metabolism of corticosteroids which can result in exposure of women to increased levels of the unbound corticosteroids for long periods of time.
Aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs): Concomitant use results in increased risk of gastrointestinal adverse effects. Use aspirin cautiously in conjugation with corticosteroid. The clearance of salicylates may be increased with concomitant use of corticosteroids.
Warfarin: Coadministration of corticosteroids and warfarin usually results in decreased response to warfarin, although there have been conflicting results. Monitor coagulation indices frequently to maintain the desired anticoagulant effect.
Potassium-depleting agents such as diuretics and amphotericin-B: Observe patient closely for the development of hypokalemia. In addition, there have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure.
Anticholinesterase agents: Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, withdraw anticholinesterase agents at least 2 hours before initiating corticosteroids therapy.
Insulin and Oral antidiabetic Agents: Concomitant administration of dexamethasone and insulin generally requires higher doses or insulin. Dosage adjustment of antidiabetic agents may be required because corticosteroids may increase blood glucose concentrations.
Aminoglutethimide: May diminish adrenal suppression of hydrocortisone.
lsoniazid: Serum concentrations of isoniazid may be decreased when used concomitantly.
Cholestyramine: May increase the clearance of hydrocortisone.
Ciclosporin: Increased activity of both ciclosporin and corticosteroids may occur when the two are used concomitantly. Convulsions have been reported with concomitant use.
Digitalis Glycosides: Patients may be at increased risk of arrhythmias due to hypokalemia.
Other interactions: Toxoids and five or inactivated vaccines: Patients on prolonged corticosteroid therapy may exhibit diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. If possible, postpone routine administration of vaccines or toxoids until corticosteroids therapy is discontinued.
Skin tests: Corticosteroids may suppress reactions to skin tests.
Store at temperature not exceeding 30°C.
ATC Classification
H02AB09 - hydrocortisone ; Belongs to the class of glucocorticoids. Used in systemic corticosteroid preparations.
Inj (vial) 100 mg (white to pale yellow, sterile lyophilized powder) x 10's.
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