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  • Hydrocortisone Panpharma 100 mg
    / Pharmalogic

    Active Ingredient
    Hydrocortisone (as sodium sucinate) 100 mg/dose

    Status in Israel

    Presentation and Status in Health Basket

    Presentation Basket Yarpa Pharmasoft


    25 X 100 mg

    not in the basket chart 84936 8371


    100 X 100 mg

    not in the basket chart 84935 8370


    This product may be administered by intravenous injection, by intravenous infusion or by intramuscular injection, the preferred method for initial emergency use being intravenous injection. Following the initial emergency period consideration should be given to employ a longer-acting injectable preparation or an oral preparation. Dosages usually range from 100 mg to 500 mg depending on severity of the condition, administered by intravenous injection over a period of one to ten minutes. This dose may be repeated at intervals of 2, 4 or 6 hours as indicated by the patient’s response and clinical condition. In general, high dose corticosteroid therapy should be continued only till the patient’s condition has stabilised – usually between 48– 72 hours. If hydrocortisone therapy must be continued beyond 48 to 72 hours hypernatremia may occur. Although adverse effects associated with high dose, short-term corticoid therapy are uncommon, peptic ulceration may occur. Prophylactic antacid therapy may be indicated. Patients subjected to severe stress following corticoid therapy should be observed closely for signs and symptoms of adrenocortical insufficiency. Corticosteroid therapy is an adjunct to and not a replacement for conventional therapy.
    Elderly patients: This product is primarily used in acute short-term conditions. There is no information to suggest that a change in dosage is warranted in the elderly. However, treatment in elderly patients should be planned bearing in mind the more serious consequences of the common sideeffects of corticosteroid in elderly patients and close clinical supervision is required.
    Children: While the dose may be reduced for infants and children, it is governed more by the severity of the condition and response of the patient than by the age or body weight but should not be less than 25 mg daily.


    Conditions responding to corticoid therapy.


    Systemic fungal infections unless specific anti-infective therapy is used.
    Idiopathic thrombocytopenic purpura.
    Intrathecal administration.
    Patients receiving immunosuppressive doses of corticosteroids.

    Special Precautions

    Undesirable effects may be minimised by using the lowest effective dose for the minimum period. Frequent patient observation is required to appropriately titrate the dose vs. disease activity. Adrenal cortical atrophy develops during prolonged therapy and may persist for months after stopping treatment. Withdrawal of corticosteroids after prolonged therapy must therefore always be gradual to avoid acute adrenal insufficiency, being tapered off over weeks or months according to the dose and duration of treatment. During prolonged therapy any intercurrent illness, trauma or surgical procedures will require a temporary increase in dosage; if corticosteroids have been stopped following prolonged therapy, they may need to be temporary re-introduced. Patients should carry “Steroid Treatment” cards which give clear guidance on the precautions to be taken to minimise risk and which provide details of prescriber, drug, dosage and the duration of treatment. Corticosteroids may mask some signs of infection and new infections may appear during their use. Suppression of the inflammatory response and immune function increases the susceptibility to fungal, viral and bacterial infections and their severity. The clinical presentation may often be atypical and may reach an advanced stage before being recognised. Chickenpox is of serious concern since this normally minor illness may be fatal in immunosuppressed patients. Patients (or parents of children) without a definite history of chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster and, if exposed, they should seek urgent medical attention. Passive immunization with varicella/zoster immunoglobulin (VZIG) is needed by exposed non-immune patients who are receiving systemic corticosteroids or who have used them within the previous 3 months; this should be given within 10 days of exposure to chickenpox. If a diagnosis of chickenpox is confirmed, the illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and the dose may need to be increased. Live vaccines should not be given to individuals with impaired immune responsiveness. The antibody response to other vaccines may be diminished. The use in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculosis regimen. If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis. Rarely, anaphylactoid reactions have been reported following parenteral therapy. Physicians using the drug should be prepared to deal with such a possibility. Appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of drug allergy. Care should be taken with patients receiving cardioactive drugs such as digoxin because of steroid induced electrolyte disturbance/ potassium loss. Particular care is required when considering the use of systemic corticosteroids in patients with the following conditions and frequent patient monitoring is necessary: osteoporosis (postmenopausal females are particularly at risk); hypertension or congestive heart failure; existing or previous history of severe affective disorders (especially previous steroid psychosis); diabetes mellitus (or a family history of diabetes). History of tuberculosis; glaucoma (or a family history of glaucoma); previous corticosteroidinduced myopathy; liver failure or cirrhosis; renal insufficiency; epilepsy, peptic ulceration; fresh intestinal anastomoses; predisposition to thrombophlebitis; abscess or other pyogenic infections; ulcerative colitis; diverticulitis; myasthenia gravis; ocular herpes simplex for fear of corneal perforation; hypothyroidism.
    Use in children: Corticosteroids cause growth retardation in infancy, childhood and adolescence, which may be irreversible. Treatment should be limited to the minimum dosage for the shortest possible time. The use of steroids should be restricted to the most serious indications.
    Use in the elderly: The common adverse effects of systemic corticosteroids may be associated with more serious consequences in old age, especially osteoporosis, hypertension, hypokalaemia, diabetes, susceptibility to infection and thinning of the skin. Close clinical supervision is required to avoid life-threatening reactions.

    Side Effects

    Depending on steroid, dose and length of treatment, glucocorticoid and mineralocorticoid side effects may be seen. These include suppression of growth in children, hypertension, sodium retention, GI effects, CNS disturbances, water retention, potassium loss, muscle weakness, aseptic necrosis of femoral and humeral heads, cushingoid changes, hyperglycemia, osteoporosis, depression, euphoria, peptic ulceration, posterior subcapsular cataracts, impaired wound healing, glaucoma with optical nerve damage, altered sperm motility, skin thinning, other skin reactions.
    For full details see prescribing information.

    Drug interactions

    Convulsions have been reported with concurrent use of corticosteroids and cyclosporin. Since concurrent administration of these agents results in a mutual inhibition of metabolism, it is possible that convulsions and other adverse effects associated with the individual use of either drug may be more apt to occur. Drugs that induce hepatic enzymes, such as rifampicin, rifabutin, carbamazepine, phenobarbitone, phenytoin, primidone and aminoglutethimide enhance the metabolism of corticosteroids and its therapeutic effects may be reduced. Drugs such as erythromycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance. Steroids may reduce the effects of anticholinesterases in myasthenia gravis. The desired effects of hypoglycaemic agents (including insulin), antihypertensives and diuretics are antagonised by corticosteroids and the hypokalaemic effects of acetazolamide, loop diuretics, thiazide diuretics and carbenoxolone are enhanced. The efficacy of coumarin anticoagulants may be enhanced by concurrent corticosteroid therapy and close monitoring of the INR or prothrombin time is required to avoid spontaneous bleeding. The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may result in salicylate intoxication. Salicylates and non-steroidal anti-inflammatory agents should be used cautiously in conjunction with corticosteroids in hypothrombinaemia. Steroids have been reported to interact with neuromuscular blocking agents such as pancuronium with partial reversal of the neuromuscular block.

    Pregnancy and Lactation

    Corticosteroids cross the placenta. There may be a very small risk of cleft palate and intrauterine growth retardation in the fetus; there is evidence of harmful effects on pregnancy in animals. Neonates of mothers who received such therapy during pregnancy should be observed for signs of hypoadrenalism and appropriate measures instituted if such signs exist. When corticosteroids are essential, however, patients with normal pregnancies may be treated as though they were in the non-gravid state. Patients with pre-eclampsia or fluid retention require close monitoring. Because prednisolone is excreted in breast milk, it is reasonable to assume that all corticosteroids are. Infants of mothers taking pharmacological doses of steroids should be monitored carefully for signs of adrenal suppression.


    There is no clinical syndrome of acute overdose with this product. Hydrocortisone is dialysable.

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