Hydrocortisone Sodium Succinate

Treatment of a wide variety of diseases and conditions principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic systems in the palliative treatment of various diseases. When used for anti-inflammatory and immunosuppressant properties, synthetic glucocorticoids that have minimal mineralocorticoid activity are preferred.

Treatment of a wide variety of diseases and conditions principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic systems in the palliative treatment of various diseases. When used for anti-inflammatory and immunosuppressant properties, synthetic glucocorticoids that have minimal mineralocorticoid activity are preferred.

No contraindications information is recorded for this medicine yet.

No side effects information is recorded for this medicine yet.

May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression and anxiety, and personality changes to frank psychoses. Use may aggravate emotional instability or psychotic tendencies. Use with caution in patients with myasthenia gravis receiving anticholinesterase therapy. Serious, potentially permanent, and sometimes fatal adverse neurologic events (e.g., spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke, seizures, nerve injury, brain edema) reported rarely, often within minutes to 48 hours following epidural glucocorticoid injection given either with or without fluoroscopic guidance. FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use. When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency). The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy. Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy. Withdraw hydrocortisone very gradually following long-term therapy with pharmacologic dosages. Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods. Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma) and replacement therapy may be required. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered. If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal. Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients. Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained. May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease). 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; reactivation of latent infections may occur. Infections may be mild, but they can be severe or fatal, and localized infections may disseminate. Do not use, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives. Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children. Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids. If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., VZIG, IG). Prolonged use of systemic corticosteroids in patients with COVID-19 † may increase risk of reactivation of latent infections (e.g., HBV, herpesvirus, strongyloidiasis, tuberculosis). Risk of reactivation of latent infections following a 10-day course of dexamethasone (6 mg once daily) or equivalent corticosteroid therapy (e.g., hydrocortisone) not well established. When initiating hydrocortisone in patients with COVID-19, consider appropriate screening and treatment to reduce the risk of Strongyloides hyperinfection in those at high risk (e.g., patients from tropical, subtropical, or warm, temperate regions or those engaged in agricultural activities) and reduce the risk of fulminant reactivation of HBV. May exacerbate fungal infections and should not be used in the presence of such infection unless needed to control drug reactions to amphotericin B; however, cases of cardiac enlargement and CHF have been reported with concomitant use of hydrocortisone and amphotericin B. Not effective and can have detrimental effects (prolongation of coma, higher incidence of pneumonia and GI bleeding) in the management of cerebral malaria. Can reactivate tuberculosis. Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy. Observe closely for evidence of reactivation. Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate chemoprophylaxis. Can reactivate latent amebiasis. Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy. Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids. These adverse effects may be especially serious in geriatric or debilitated patients. A high-protein diet may help to prevent adverse effects associated with protein catabolism. An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium). Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy. The American College of Rheumatology (ACR) has published guidelines on prevention and treatment of glucocorticoid-induced osteoporosis. Recommendations are made according to a patient's risk of fracture. Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur with average or large doses of hydrocortisone. Edema and CHF (in susceptible patients) may occur. Dietary salt restriction is advisable and potassium supplementation may be necessary. Increased calcium excretion and possible hypocalcemia. Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased IOP which may result in glaucoma or may occasionally damage the optic nerve. May enhance the establishment of secondary fungal and viral infections of the eye. Cortical blindness has occurred following epidural glucocorticoid injection. Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation. Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties. Corticosteroids have also been reported to increase or decrease motility and number of sperm in some men. May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus. If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary. Exaggerated response to the glucocorticoids in hypothyroidism. Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested. Anaphylactic and hypersensitivity reactions. Certain tablet formulations contain the dye tartrazine (FD&C yellow No. 5), which may cause allergic reactions including bronchial asthma in susceptible individuals. Although the incidence of tartrazine sensitivity is low, it frequently occurs in patients who are sensitive to aspirin. Some commercially available formulations contain sulfites that may cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals. Overall prevalence of sulfite sensitivity in the general population is unknown but probably low; appears to occur more frequently in asthmatic than in nonasthmatic individuals. Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, blood pressures, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients. Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease. During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and blood pressure evaluations. Increased or decreased motility and number of sperm in some men. Corticosteroids should be used with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses. Use with caution in patients with active or latent peptic ulcer. Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids. Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids. Various dermatologic effects (i.e., impaired wound healing, skin atrophy and thinning, acne, increased sweating, hirsutism, facial erythema, striae, petechiae, ecchymoses, easy bruising) are associated with systemic glucocorticoids. Kaposi’s sarcoma reported in patients receiving glucocorticoids; discontinuance may result in clinical remission. Category C. Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants. Discontinue nursing (in mothers taking pharmacologic doses) because of potential risk to nursing infants. The effects of glucocorticoids on the pathophysiology and course of diseases considered to be similar in adults and children. Evidence of safety and efficacy of corticosteroids in pediatric patients is based on treatment of nephrotic syndrome (in patients >2 years of age) and aggressive leukemias and lymphomas (in patients >1 month of age). Evidence of safety and efficacy in other pediatric indications (e.g., severe asthma and wheezing) is based on controlled trials in adults. Adverse effects in pediatric patients are similar to those in adults. As in adults, perform periodic evaluations of height, weight, IOP, and BP. Children, like adults, also should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis. With long-term use, may delay growth and maturation in children and adolescents. Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy. Titrate dosage to the lowest effective level. Alternate-day therapy may minimize growth suppression and should be instituted if growth suppression occurs. Some commercially available injections contain benzyl alcohol as a preservative. Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (when large amounts administered [100–400 mg/kg daily]), although causal relationship not established. Some manufacturers state that benzyl alcohol-containing injectable preparations are contraindicated in premature infants and use should be avoided whenever possible; AAP states that presence of small amounts in a commercially available injection should not proscribe its use when the medication is indicated in neonates and comparable benzyl alcohol-free preparations are not available. Safety and efficacy of dexamethasone and other corticosteroids (e.g., hydrocortisone) for COVID-19 † treatment not fully evaluated in pediatric patients. Use caution when extrapolating recommendations for adults with COVID-19 to pediatric patients <18 years of age. The NIH COVID-19 Treatment Guidelines Panel recommends use of dexamethasone for hospitalized pediatric patients with COVID-19 who are receiving high-flow oxygen, noninvasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation (ECMO); dexamethasone not routinely recommended for pediatric patients who require only low levels of oxygen support (i.e., nasal cannula only). If dexamethasone not available, the NIH panel states that alternative corticosteroids (e.g., hydrocortisone) at equivalent dosages may be considered. Use of corticosteroids for treatment of severe COVID-19 in pediatric patients who are profoundly immunocompromised not evaluated to date and may be harmful; therefore, the NIH panel states consider such use only on a case-by-case basis. IV corticosteroids have been used as first-line therapy in pediatric patients with multisystem inflammatory syndrome in children (MIS-C); however, the NIH panel recommends consultation with a multidisciplinary team when considering and managing immunomodulating therapy for children with this condition. Optimal choice and combination of immunomodulating therapies for children with MIS-C not definitely established. Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19. With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur. May be especially serious in geriatric or debilitated patients. Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis. Use with caution in patients with osteoporosis. Patients with cirrhosis show an exaggerated response to glucocorticoids. Use with caution.

May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression and anxiety, and personality changes to frank psychoses. Use may aggravate emotional instability or psychotic tendencies. Use with caution in patients with myasthenia gravis receiving anticholinesterase therapy. Serious, potentially permanent, and sometimes fatal adverse neurologic events (e.g., spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke, seizures, nerve injury, brain edema) reported rarely, often within minutes to 48 hours following epidural glucocorticoid injection given either with or without fluoroscopic guidance. FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use. When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency). The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy. Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy. Withdraw hydrocortisone very gradually following long-term therapy with pharmacologic dosages. Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods. Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma) and replacement therapy may be required. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered. If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal. Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients. Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained. May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease). 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; reactivation of latent infections may occur. Infections may be mild, but they can be severe or fatal, and localized infections may disseminate. Do not use, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives. Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children. Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids. If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., VZIG, IG). Prolonged use of systemic corticosteroids in patients with COVID-19 † may increase risk of reactivation of latent infections (e.g., HBV, herpesvirus, strongyloidiasis, tuberculosis). Risk of reactivation of latent infections following a 10-day course of dexamethasone (6 mg once daily) or equivalent corticosteroid therapy (e.g., hydrocortisone) not well established. When initiating hydrocortisone in patients with COVID-19, consider appropriate screening and treatment to reduce the risk of Strongyloides hyperinfection in those at high risk (e.g., patients from tropical, subtropical, or warm, temperate regions or those engaged in agricultural activities) and reduce the risk of fulminant reactivation of HBV. May exacerbate fungal infections and should not be used in the presence of such infection unless needed to control drug reactions to amphotericin B; however, cases of cardiac enlargement and CHF have been reported with concomitant use of hydrocortisone and amphotericin B. Not effective and can have detrimental effects (prolongation of coma, higher incidence of pneumonia and GI bleeding) in the management of cerebral malaria. Can reactivate tuberculosis. Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy. Observe closely for evidence of reactivation. Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate chemoprophylaxis. Can reactivate latent amebiasis. Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy. Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids. These adverse effects may be especially serious in geriatric or debilitated patients. A high-protein diet may help to prevent adverse effects associated with protein catabolism. An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium). Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy. The American College of Rheumatology (ACR) has published guidelines on prevention and treatment of glucocorticoid-induced osteoporosis. Recommendations are made according to a patient's risk of fracture. Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur with average or large doses of hydrocortisone. Edema and CHF (in susceptible patients) may occur. Dietary salt restriction is advisable and potassium supplementation may be necessary. Increased calcium excretion and possible hypocalcemia. Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased IOP which may result in glaucoma or may occasionally damage the optic nerve. May enhance the establishment of secondary fungal and viral infections of the eye. Cortical blindness has occurred following epidural glucocorticoid injection. Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation. Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties. Corticosteroids have also been reported to increase or decrease motility and number of sperm in some men. May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus. If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary. Exaggerated response to the glucocorticoids in hypothyroidism. Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested. Anaphylactic and hypersensitivity reactions. Certain tablet formulations contain the dye tartrazine (FD&C yellow No. 5), which may cause allergic reactions including bronchial asthma in susceptible individuals. Although the incidence of tartrazine sensitivity is low, it frequently occurs in patients who are sensitive to aspirin. Some commercially available formulations contain sulfites that may cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals. Overall prevalence of sulfite sensitivity in the general population is unknown but probably low; appears to occur more frequently in asthmatic than in nonasthmatic individuals. Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, blood pressures, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients. Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease. During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and blood pressure evaluations. Increased or decreased motility and number of sperm in some men. Corticosteroids should be used with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses. Use with caution in patients with active or latent peptic ulcer. Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids. Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids. Various dermatologic effects (i.e., impaired wound healing, skin atrophy and thinning, acne, increased sweating, hirsutism, facial erythema, striae, petechiae, ecchymoses, easy bruising) are associated with systemic glucocorticoids. Kaposi’s sarcoma reported in patients receiving glucocorticoids; discontinuance may result in clinical remission. Category C. Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants. Discontinue nursing (in mothers taking pharmacologic doses) because of potential risk to nursing infants. The effects of glucocorticoids on the pathophysiology and course of diseases considered to be similar in adults and children. Evidence of safety and efficacy of corticosteroids in pediatric patients is based on treatment of nephrotic syndrome (in patients >2 years of age) and aggressive leukemias and lymphomas (in patients >1 month of age). Evidence of safety and efficacy in other pediatric indications (e.g., severe asthma and wheezing) is based on controlled trials in adults. Adverse effects in pediatric patients are similar to those in adults. As in adults, perform periodic evaluations of height, weight, IOP, and BP. Children, like adults, also should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis. With long-term use, may delay growth and maturation in children and adolescents. Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy. Titrate dosage to the lowest effective level. Alternate-day therapy may minimize growth suppression and should be instituted if growth suppression occurs. Some commercially available injections contain benzyl alcohol as a preservative. Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (when large amounts administered [100–400 mg/kg daily]), although causal relationship not established. Some manufacturers state that benzyl alcohol-containing injectable preparations are contraindicated in premature infants and use should be avoided whenever possible; AAP states that presence of small amounts in a commercially available injection should not proscribe its use when the medication is indicated in neonates and comparable benzyl alcohol-free preparations are not available. Safety and efficacy of dexamethasone and other corticosteroids (e.g., hydrocortisone) for COVID-19 † treatment not fully evaluated in pediatric patients. Use caution when extrapolating recommendations for adults with COVID-19 to pediatric patients <18 years of age. The NIH COVID-19 Treatment Guidelines Panel recommends use of dexamethasone for hospitalized pediatric patients with COVID-19 who are receiving high-flow oxygen, noninvasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation (ECMO); dexamethasone not routinely recommended for pediatric patients who require only low levels of oxygen support (i.e., nasal cannula only). If dexamethasone not available, the NIH panel states that alternative corticosteroids (e.g., hydrocortisone) at equivalent dosages may be considered. Use of corticosteroids for treatment of severe COVID-19 in pediatric patients who are profoundly immunocompromised not evaluated to date and may be harmful; therefore, the NIH panel states consider such use only on a case-by-case basis. IV corticosteroids have been used as first-line therapy in pediatric patients with multisystem inflammatory syndrome in children (MIS-C); however, the NIH panel recommends consultation with a multidisciplinary team when considering and managing immunomodulating therapy for children with this condition. Optimal choice and combination of immunomodulating therapies for children with MIS-C not definitely established. Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19. With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur. May be especially serious in geriatric or debilitated patients. Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis. Use with caution in patients with osteoporosis. Patients with cirrhosis show an exaggerated response to glucocorticoids. Use with caution.

No adult dosage information is recorded for this medicine yet.

No child dosage information is recorded for this medicine yet.

No neonatal dosage information is recorded for this medicine yet.

No drug interactions information is recorded for this medicine yet.

No storage information is recorded for this medicine yet.