Cortisol - Glucocorticosteroid. Inhibits the function of leukocytes and tissue macrophages. The migration of leukocytes in the area of inflammation. Impair the capacity of macrophages to phagocytosis and the formation of interleukin-1. Contributes to the stabilization of lysosomal membranes, thereby reducing the concentration of proteolytic enzymes in the field of inflammation. Decreases capillary permeability due to histamine release. Inhibits activity of fibroblasts and collagen formation.
Inhibits the activity of phospholipase A2 which leads to suppression of the synthesis of prostaglandins and leukotrienes. Suppresses the release of COX (mainly COX-2), which also helps to reduce production of prostaglandins.
Reduces the number of circulating lymphocytes (T-and B-cells), monocytes, eosinophils and basophils as a result of their displacement from the vascular bed to lymphoid tissue, suppresses the formation of antibodies.
hydrocortisone suppresses the release of pituitary ACTH and beta-lipotropin but does not reduce the level of circulating beta-endorphin. Inhibits the secretion of TSH and FSH.
With direct application of the receptacles has a vasoconstrictor effect.
hydrocortisone has a pronounced dose-dependent effect on the metabolism of carbohydrates, proteins and fats. Stimulates gluconeogenesis, promotes the capture of amino acids by the liver and kidneys and increases the activity of enzymes of gluconeogenesis. In the liver of hydrocortisone increases glycogen deposition by stimulating the activity of glycogen synthase and synthesis of glucose from the products of protein metabolism. Increased blood glucose activates the secretion of insulin.
hydrocortisone suppresses the seizure of glucose by fat cells that leads to activation of lipolysis. However, due to increased secretion of insulin is stimulation of lipogenesis which leads to the accumulation of fat.
This medication has catabolic effect in lymphoid and connective tissue, muscle, adipose tissue, skin, bone tissue; to a lesser extent than the mineralocorticoid affects the processes of water and electrolyte metabolism: promotes the excretion of potassium ions and calcium, delay in the body of sodium and water. Osteoporosis and Itsenko-Cushing's syndrome are the main factors limiting the long-term therapy of GCS. As a result of catabolic actions may suppress growth in children.
In high doses hydrocortisone may increase the excitability of brain tissue and contributes to lowering the threshold of convulsive readiness. It stimulates the excessive production of hydrochloric acid and pepsin in the stomach that promotes the development of peptic ulcers.
For systems use therapeutic activity of hydrocortisone caused by anti-inflammatory, anti-allergic, immunosuppressive and antiproliferative action. When external and local application the therapeutic activity of hydrocortisone is due to anti-inflammatory, anti-allergic and antiexudative (due to vasoconstrictor effect) action. For anti-inflammatory activity this medicine is 4 times weaker than prednisolone, at mineralocorticoid activity is superior to other GCS.
Cortisol 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.
Indication: For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.
Clobetasol propionate is a corticosteroid used to treat various skin disorders including eczema and psoriasis. It is also highly effective for contact dermatitis caused by exposure to poison ivy/oak.
Indications: Atopic eczema.
Allergic contact dermatitis.
Primary irritant dermatitis.
Psoriasis of face, flexures.
Hypertrophied scars, keloids.
Psoriasis of palm, sole, elbow, knee.
A combination of steroid with proper antibiotic cover may also be
Used for: Impetigo, furunculosis, secondary infected dermatoses, napkin rash, otitis externa, intertriginous eruptions.