A-Hydrocort Side Effects
Generic Name: hydrocortisone
Note: This page contains information about the side effects of hydrocortisone. Some of the dosage forms included on this document may not apply to the brand name A-Hydrocort.
Not all side effects for A-Hydrocort may be reported. You should always consult a doctor or healthcare professional for medical advice. Side effects can be reported to the FDA here.
For the Consumer
Applies to hydrocortisone: oral tablet
Other dosage forms:
Get emergency medical help if you have any of these signs of an allergic reaction while taking hydrocortisone (the active ingredient contained in A-Hydrocort) hives; difficulty breathing; swelling of your face, lips, tongue, or throat.
Call your doctor at once if you have any of these serious side effects:
problems with your vision;
swelling, rapid weight gain, feeling short of breath;
severe depression, unusual thoughts or behavior, seizure (convulsions);
bloody or tarry stools, coughing up blood;
pancreatitis (severe pain in your upper stomach spreading to your back, nausea and vomiting, fast heart rate);
low potassium (confusion, uneven heart rate, extreme thirst, increased urination, leg discomfort, muscle weakness or limp feeling); or
dangerously high blood pressure (severe headache, blurred vision, buzzing in your ears, anxiety, confusion, chest pain, shortness of breath, uneven heartbeats, seizure).
Less serious side effects of hydrocortisone may include:
sleep problems (insomnia), mood changes;
acne, dry skin, thinning skin, bruising or discoloration;
slow wound healing;
headache, dizziness, spinning sensation;
nausea, stomach pain, bloating; or
changes in the shape or location of body fat (especially in your arms, legs, face, neck, breasts, and waist).
This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects.
For Healthcare Professionals
Applies to hydrocortisone: compounding powder, injectable powder for injection, injectable solution, injectable suspension, oral suspension, oral tablet, rectal foam with applicator, rectal suspension
Corticosteroid complications are primarily dose and duration of therapy dependent. Adverse effects have occurred less frequently at physiologic or lower pharmacologic dosages.
Adverse effects associated with duration of corticosteroid therapy include those occurring during short-term therapy (up to three weeks) or those occurring during long-term therapy (greater than three weeks).
Short-term effects have included sodium retention-related weight gain and fluid accumulation, hyperglycemia and glucose intolerance, hypokalemia, gastrointestinal upset and ulceration, reversible depression of the hypothalamus-pituitary-adrenal axis, and mood changes including mild euphoria and insomnia, nervousness, restlessness, mania, catatonia, depression, delusions, hallucinations, and violent behavior.
Long-term effects have included hypothalamus-pituitary-adrenal activity suppression, Cushingoid appearance, hirsutism or virilism, impotence, menstrual irregularities, peptic ulcer disease, cataracts and increased intraocular pressure/glaucoma, myopathy, osteoporosis, and vertebral compression fractures.
Cardiovascular effects such as hypertension and congestive heart failure due to long-term fluid retention as well as direct vascular effects have occurred during corticosteroid therapy.
Corticosteroid therapy may induce glucose intolerance by reducing the utilization of glucose in tissues and increasing hepatic glucose output. Diabetes mellitus requiring diet modifications and hypoglycemic agents has developed in some patients.
Adrenal suppression can persist for up to twelve months after long-term corticosteroid therapy. Giving corticosteroids once a day or once every other day may reduce adrenal suppression. After corticosteroid therapy has been tapered, supplemental corticosteroid therapy during times of physical stress may be required.
Endocrine effects such as decreased glucose tolerance and hyperglycemia resulting in diabetes-like symptoms have occurred. Hypothalamus-pituitary-adrenal activity has been suppressed up to 12 months following long-term corticosteroid administration. Cushingoid appearance commonly has occurred with chronic therapy. Hirsutism or virilism, impotence, and menstrual irregularities may occur.
Gastrointestinal effects of corticosteroid therapy have included gastrointestinal upset, nausea, vomiting, and peptic ulcer disease. Pancreatitis, ulcerative esophagitis, gastrointestinal perforation and hemorrhage have also been reported.
Gastrointestinal effects most commonly occurring during corticosteroid therapy have included nausea, vomiting, dyspepsia, and anorexia. Peptic ulcer disease has been associated with long-term corticosteroid therapy, but is relatively uncommon. Routine prophylactic therapy is not warranted in all individuals. Aluminum/magnesium-containing antacids generally have been used to manage GI complaints without significant drug interactions.
Metabolic adverse effects including hypernatremia (rare), hypokalemia, fluid retention, negative nitrogen balance and increased blood urea nitrogen concentration have occurred during corticosteroid therapy. Glucocorticoids have been reported to decrease the secretion of thyrotropin (TSH).
Musculoskeletal effects of corticosteroid therapy including myopathy, osteoporosis, vertebral compression fractures, tendon rupture (particularly the Achilles tendon), and aseptic necrosis of bone have been reported. Aseptic necrosis has been reported most often to affect the femoral head.
Corticosteroid myopathy has presented as weakness and wasting of the proximal limb and girdle muscles and generally has been reversible following cessation of therapy.
Corticosteroids inhibit intestinal absorption and increase urinary excretion of calcium leading to bone resorption and bone loss. Postmenopausal females are at risk of loss of bone density. Sixteen percent of elderly patients treated with corticosteroids for 5 years may experience vertebral compression fractures.
Immunologic effects of corticosteroid therapy have included impairment in cell-mediated immunity and increased susceptibility to bacterial, viral, fungal and parasitic infections. Immune response to skin tests may be suppressed.
Hepatic effects such as reversible increases in serum transaminase and alkaline phosphatase concentrations have occurred during corticosteroid therapy.
Hematologic effects have included thrombocytopenia, lymphopenia, and platelet alterations resulting in thrombolic events.
Dermatologic effects occurring during corticosteroid therapy have included increased ease in bruising, ecchymosis, petechiae striae, delayed wound healing, and acne.
Ocular changes with corticosteroid therapy have included increased intraocular pressure, glaucoma, and posterior subcapsular cataracts.
Psychiatric effects including psychoses, personality or behavioral changes, and pseudotumor cerebri have occurred/been exacerbated during corticosteroid therapy.
Bronchospasm after intravenous hydrocortisone (the active ingredient contained in A-Hydrocort) has been reported in some patients with aspirin-sensitive respiratory disease. A challenge study with oral aspirin followed with 100 mg hydrocortisone (IV) resulted in respiratory reactions to aspirin in 45 of 53 patients. These 45 patients then received a hydrocortisone challenge. No naso-ocular, dermal, or respiratory reactions were noted in 44 of 45 patients administered hydrocortisone. One aspirin-sensitive patient experienced bronchospasm and naso-ocular reactions to hydrocortisone and naso-ocular with minimal bronchospasm with methylprednisolone. Following aspirin desensitization and while on maintenance aspirin therapy, this patient again reacted with similar symptoms to hydrocortisone.
Case reports of hypersensitivity reactions to corticosteroids have been relatively uncommon. Side effects have included bronchospasm, shock, urticaria, and angioedema. Cross-reactivity between aspirin and hydrocortisone in patients with aspirin-sensitive respiratory disease has been suggested as the mechanism in patients with asthma, however data are controversial. Anaphylaxis has been most frequently associated with rapid injection or infusion of a high dose of corticosteroid. Reactions may be mediated by an immune or nonimmune mechanism.
Pseudorheumatism or glucocorticoid-withdrawal syndrome not related to adrenal insufficiency has occurred on withdrawal of corticosteroids. Patients experienced anorexia, nausea, vomiting, lethargy, headache, fever, arthralgias, myalgias, and postural hypotension. Symptoms resolved when corticosteroid therapy was reinstated.
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