• Decreased production of prostaglandins, cytokines, and interleukins.
• Decreased proliferation and migration of lymphocytes and macrophages.

• Rapidly and promptly absorbed from the gastrointestinal tract due to its lipophilic character.
• Half-life varies between 2 to 5 hours.
• Highly bound to plasma proteins.
• Prednisone is metabolized in the liver to its active form, prednisolone.
• Liver and kidneys are the major sites of inactivation.
• Inducers of hepatic drug metabolism such as phenytoin may accelerate biotransformation of prednisone in the liver and higher doses of prednisone may be required.

• Multiple sclerosis. Results of a retrospective analysis suggest that oral prednisone taper, often used for the treatment of relapses in multiple sclerosis following treatment with intravenous methylprednisolone for a relapse, does not lead to improved neurologic outcome after 12 months compared with treatment with intravenous methylprednisolone only (14).

• Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy.

• Trichinosis with neurologic involvement.

• Concomitant with albendazole treatment of neurocysticercosis.

• Neurosarcoidosis.

• Susac syndrome.

• Cerebral vasculitis.

• Optic neuritis.

• Duchenne muscular dystrophy. Of all the therapeutic drugs studied in Duchenne muscular dystrophy, only prednisone seems to have the potential for providing interim functional improvement for patients with this disease and delaying the progression while they wait for a cure with gene or cell therapy. A retrospective analysis of data of patients with Duchenne muscular dystrophy who were treated with prednisone 0.75 mg/kg per day intermittently (10 days on, then 10 days off) showed that this approach has few side effects and extends the period of improvement by 1 year compared to historical controls (17). A double-blind, randomized study has provided Class I evidence that weekend prednisone dosing is as safe and effective as daily prednisone in preserving muscle strength and preventing increase of body mass index in boys with Duchenne muscular dystrophy over a 1-year period (06). Alternating prednisone regimen (10 days on/10 days off) has no apparent adverse effects on weight and height in children with Duchenne muscular dystrophy who are ambulant (19).

• Low-dose prednisone with gradual dose escalation was shown to be safe, well-tolerated, and effective in treating ocular myasthenia gravis in a randomized clinical trial (03).

• Treatment of myelopathy in Sjögren syndrome with a combination of prednisone and cyclophosphamide.

• Prednisone therapy is considered a safe and effective adjunctive treatment for epilepsy for older children with intractable generalized epilepsy who have failed conventional antiepileptic therapy.

• In a comparative study on children with intractable epilepsy, intravenous immune globulin was more effective than prednisone and had less adverse effects. This response was independent of epilepsy type, etiology, and duration, suggesting different mechanisms of action between intravenous immune globulin and prednisone despite a common, reversible, immune-mediated pathway to intractability of epilepsy (18).

• Temporal arteritis.

• Polyneuropathy and myositis in idiopathic hypereosinophilic syndrome.

• Vestibular neuritis

• Intratympanic dexamethasone is effective in preventing the progression of sensorineural hearing loss in Ménière disease (13). This is preferable to the use of oral high-dose prednisone for the recovery of hearing loss, which can have adverse effects.

• Episodic cluster headache

• High-dose prednisone has been used successfully in the treatment of infantile spasms in China (20). There is immune dysfunction in infantile spasms as evidenced by the rise in serum levels of inflammatory cytokines such as interleukin-8 and tumor necrosis factor alfa. Prednisone can control seizures in children with infantile spasms, possibly by regulating and improving immune dysfunction as evidenced by lowering levels of cytokines (04).

• In a patient with post-stroke central pain in whom first-line agents were contraindicated due to comorbidities, the choice was limited to low-dose gabapentin, but prednisone taper as adjunct medication led to significant pain relief with eventual resolution (02).

• Bell palsy. Several studies have reported significant improvement in recovery of function in complete idiopathic facial nerve palsy following treatment with corticosteroids. It is usually used in combination with acyclovir or valacyclovir.

• Pain associated with herpes zoster

• Endocrine disorders: primary or secondary adrenocortical insufficiency. Hydrocortisone or cortisone is the first choice, but synthetic analogs may be used in conjunction with mineralocorticoids where applicable.

• Rheumatic disorders: as adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation).

• Collagen diseases: eg, during an exacerbation or as maintenance therapy in selected cases of systemic lupus erythematosus.

• Skin disorders such as severe erythema multiforme.

• Allergic states: eg, allergic rhinitis, bronchial asthma, and drug hypersensitivity reactions.

• Respiratory diseases: eg, aspiration pneumonitis.

• Hematological disorders: eg, idiopathic thrombocytopenic purpura in adults.

• Neoplastic diseases: eg, palliative management of leukemia and lymphoma in adults.

• Known hypersensitivity to components of prednisone tablets.
• Systemic fungal infections.

• Patients on corticosteroid therapy subjected to unusual stress. Increased dosage of rapidly acting corticosteroids before, during, and after the stressful situation is indicated.

• Corticosteroids may mask some signs of infection.

• Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. Because mineralocorticoid secretion may be impaired, salt or a mineralocorticoid or both should be administered concurrently.

• Persons who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure to COVID-19.

• There is an enhanced effect of corticosteroids in patients with hypothyroidism and in those with cirrhosis.

• Steroids should be used with caution in myasthenia gravis. Patients at risk of developing treatment-resistant myasthenia-associated ophthalmoplegia may have inadequate endogenous levels of complement regulatory protein protection in their extraocular muscle in response to prednisone, which increases their susceptibility to complement-mediated damage (01). In patients with generalized myasthenia, adjuvant therapy with intravenous immunoglobulin when starting prednisone for the first time is safe and effective in preventing prednisone-induced exacerbation (05). A clinical trial has shown that thymectomy is useful for patients with myasthenia gravis by increasing the likelihood of achieving sustained minimal manifestation status with complete withdrawal of prednisone (10).

• Drugs that induce hepatic enzymes, such as phenobarbital, phenytoin, and rifampin, may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response.

• Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and, thus, decrease their clearance. Therefore, the dose of corticosteroid should be titrated to avoid steroid toxicity.

• Corticosteroids may increase the clearance of chronic, high-dose aspirin. This could lead to decreased salicylate serum levels or increased risk of salicylate toxicity when the corticosteroid is withdrawn. Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering from hypoprothrombinemia.

• The effect of corticosteroids on oral anticoagulants is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effect.

• Convulsions have been reported with concurrent use of methylprednisolone and cyclosporin. Because concurrent use of these agents results in a mutual inhibition of metabolism, it is possible that adverse events associated with the individual use of either drug may be more apt to occur.

• Psychic disorders: These may appear when corticosteroids are used and range from euphoria, insomnia, mood swings, personality changes, and severe depression to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. Switching from a regimen of intravenous methylprednisolone in an inpatient to outpatient setting is without problems in patients with multiple sclerosis, but rare psychotic reactions to treatment are unpredictable (12).

• Neurologic: increased intracranial pressure with papilledema (pseudotumor cerebri) usually after treatment; convulsions, vertigo, or headache.

• Musculoskeletal: muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fracture of long bones

• Gastrointestinal: peptic ulcer with possible perforation and hemorrhage.

• Cardiovascular: Patients receiving high-dose corticosteroid therapy are at increased risk of developing atrial fibrillation.

• Impaired wound healing.

• Fluid and electrolyte disturbances: sodium retention and hypertension.

• Leukocytosis: The degree of leukocytosis is related to the dosage administered. It reaches maximal values within 2 weeks in most cases, after which the white blood cell count decreases, albeit not to pretreatment levels. There is predominantly a rise in the polymorphonuclear white blood cells and coincides with monocytosis, eosinopenia, and a variable degree of lymphopenia.

• Diabetes: Manifestations of latent diabetes mellitus and increased requirements for insulin or oral hypoglycemic agents in diabetics may occur. Even low doses of prednisone for 1 week impair insulin sensitivity in a dose-dependent manner, which is clinically relevant in individuals predisposed to develop glucose intolerance (09). Patients on long-term prednisone therapy should be monitored by blood HbA1c test for detection of pre-diabetes.

• Prolonged use of prednisone can lead to negative nitrogen balance due to protein catabolism.

• Addison-like adrenal insufficiency may manifest if prednisone is discontinued after prolonged use. The adrenocorticotrophic hormone stimulation test is the most specific test for diagnosing adrenal insufficiency. Blood cortisol levels are measured before and after a synthetic form of adrenocorticotrophic hormone is given by injection. If the measurement of cortisol levels shows no response to adrenocorticotrophic hormone stimulation, the patient may need to remain on a low dose of prednisone for prevention of an Addisonian crisis, eg, 5 mg per day.

• Ophthalmic: posterior subcapsular cataracts, increased intraocular pressure, glaucoma, exophthalmos.

• Urticaria and other allergic, anaphylactic, or hypersensitivity reactions.

• Malignancies: Kaposi sarcoma has been reported to occur in patients receiving corticosteroid therapy. Discontinuation of corticosteroids may result in clinical remission.

• Miscellaneous side effects: These include skin atrophy, menstrual irregularities, osteoporosis, fatty liver, and growth inhibition in children.