Hydrocortisone Powder for Injection , Hydrocortisone Sodium
Succinate for Injection 100mg
Product : Hydrocortisone Sodium Succinate for Injection
Specification : 100mg,250mg, 500mg
Standard : BP, USP
Packing : 50vials/box
Hydrocortisone is a corticosteroid. It is commonly used to treat
inflammation of the skin, joints, lungs, and other organs. Common
conditions treated include asthma, allergies, and arthritis. It is
also used for other conditions, such as blood disorders and
diseases of the adrenal glands
Indications and Dosages :
➤➤To treat severe inflammation or acute adrenal insufficiency
oral suspension, tablets (hydrocortisone, hydrocortisone cypionate)
Adults. 20 to 240 mg daily as a single dose or in divided doses.
i.v. infusion or i.v., i.m., or subcutaneous injection
(hydrocortisone sodium phosphate); i.m. injection (hydrocortisone)
Adults. 15 to 240 mg daily as a single dose or in divided doses.
Usual: One-half to one-third the oral dose.
dosage adjustment Dosage increased to more than 240 mg daily if
needed to treat acute disease.
i.v. infusion; i.v. or i.m. injection (hydrocortisone sodium
Adults. 100 to 500 mg every 2, 4, or 6 hr.
➤➤To treat joint and tissue inflammation intra-articular injection
Adults. 25 to 37.5 mg injected into large joints or bursae as a
single dose, or 10 to 25 mg into small joints as a single dose.
intralesional injection (hydrocortisone acetate)
Adults. 5 to 12.5 mg injected into tendon sheaths as a single dose,
or 12.5 to 25 mg injected into ganglia as a single dose.
soft-tissue injection (hydrocortisone acetate)
Adults. 25 to 50 mg as a single dose. Sometimes a dose of up to 75
mg is needed.
➤➤As adjunct to treat ulcerative proctitis of the distal portion of
the rectum in patients who can’t retain hydrocortisone or other
rectal aerosol (hydrocortisone acetate)
Adult men. Initial: 1 applicatorful once or twice daily for 2 to 3
wk; then every other day thereafter. Maintenance: Highly
➤➤To treat ulcerative colitis
Adults. 100 mg every night for 2 to 3 wk or until condition
Route Onset Peak Duration
P.O.† Unknown 1 hr 1.25–1.5 days
P.O.|| Unknown 1–2 hr Unknown
I.V. ‡§ Rapid Unknown Unknown
I.M.† Unknown 4–8 hr Unknown
I.M.‡ Rapid 1 hr Unknown
I.M.§ Rapid 1 hr Variable
Other* Unknown 24–48 hr 3 days–4 wk
Hydrocortisone is the most important human glucocorticoid. It is
essential for life and regulates or supports a variety of important
cardiovascular, metabolic, immunologic and homeostatic functions.
Topical hydrocortisone is used for its anti-inflammatory or
immunosuppressive properties to treat inflammation due to
corticosteroid-responsive dermatoses. Glucocorticoids are a class
of steroid hormones characterised by an ability to bind with the
cortisol receptor and trigger a variety of important
cardiovascular, metabolic, immunologic and homeostatic effects.
Glucocorticoids are distinguished from mineralocorticoids and sex
steroids by having different receptors, target cells, and effects.
Technically, the term corticosteroid refers to both glucocorticoids
and mineralocorticoids, but is often used as a synonym for
glucocorticoid. Glucocorticoids suppress cell-mediated immunity.
They act by inhibiting genes that code for the cytokines IL-1,
IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most
important of which is the IL-2. Reduced cytokine production limits
T cell proliferation. Glucocorticoids also suppress humoral
immunity, causing B cells to express lower amounts of IL-2 and IL-2
receptors. This diminishes both B cell clonal expansion and
antibody synthesis. The diminished amounts of IL-2 also leads to
fewer T lymphocyte cells being activated.
Mechanism of action
Hydrocortisone binds to the cytosolic glucocorticoid receptor.
After binding the receptor the newly formed receptor-ligand complex
translocates itself into the cell nucleus, where it binds to many
glucocorticoid response elements (GRE) in the promoter region of
the target genes. The DNA bound receptor then interacts with basic
transcription factors, causing the increase in expression of
specific target genes. The anti-inflammatory actions of
corticosteroids are thought to involve lipocortins, phospholipase
A2 inhibitory proteins which, through inhibition arachidonic acid,
control the biosynthesis of prostaglandins and leukotrienes.
Specifically glucocorticoids induce lipocortin-1 (annexin-1)
synthesis, which then binds to cell membranes preventing the
phospholipase A2 from coming into contact with its substrate
arachidonic acid. This leads to diminished eicosanoid production.
The cyclooxygenase (both COX-1 and COX-2) expression is also
suppressed, potentiating the effect. In other words, the two main
products in inflammation Prostaglandins and Leukotrienes are
inhibited by the action of Glucocorticoids. Glucocorticoids also
stimulate the lipocortin-1 escaping to the extracellular space,
where it binds to the leukocyte membrane receptors and inhibits
various inflammatory events: epithelial adhesion, emigration,
chemotaxis, phagocytosis, respiratory burst and the release of
various inflammatory mediators (lysosomal enzymes, cytokines,
tissue plasminogen activator, chemokines etc.) from neutrophils,
macrophages and mastocytes. Additionally the immune system is
suppressed by corticosteroids due to a decrease in the function of
the lymphatic system, a reduction in immunoglobulin and complement
concentrations, the precipitation of lymphocytopenia, and
interference with antigen-antibody binding.