Vidarabine or 9-β-D-arabinofuranosyladenine (ara-A, trade name Vira-A) is a synthetic purine nucleoside analog with in vitro and in vivo inhibitory activity against herpes simplex virus types 1 (HSV-1), 2 (HSV-2), and varicella-zoster virus (VZV). The inhibitory activity of Vidarabine is highly selective due to its affinity for the enzyme thymidine kinase (TK) encoded by HSV and VZV. This viral enzyme converts Vidarabine into Vidarabine monophosphate, a nucleotide analog. The monophosphate is further converted into diphosphate by cellular guanylate kinase and into triphosphate by a number of cellular enzymes. in vitro, Vidarabine triphosphate stops replication of herpes viral DNA. When used as a substrate for viral DNA polymerase, Vidarabine triphosphate competitively inhibits dATP leading to the formation of 'faulty' DNA. This is where Vidarabine triphosphate is incorporated into the DNA strand replacing many of the adenosine bases. This results in the prevention of DNA synthesis, as phosphodiester bridges can longer to be built, destabilizing the strand.

Betamethasone and its derivatives, betamethasone sodium phosphate and betamethasone acetate, are synthetic glucocorticoids. Used for its antiinflammatory or immunosuppressive properties, betamethasone is combined with a mineralocorticoid to manage adrenal insufficiency and is used in the form of betamethasone benzoate, betamethasone dipropionate, or betamethasone valerate for the treatment of inflammation due to corticosteroid-responsive dermatoses. Betamethasone and clotrimazole are used together to treat cutaneous tinea infections. Betamethasone is a glucocorticoid receptor agonist. This leads to changes in genetic expression once this complex binds to the GRE. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. 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. Betamethasone binds to plasma transcortin, and it becomes active when it is not bound to transcortin.Betamethasone is used for: treating certain conditions associated with decreased adrenal gland function. It is used to treat severe inflammation caused by certain conditions, including severe asthma, severe allergies, rheumatoid arthritis, ulcerative colitis, certain blood disorders, lupus, multiple sclerosis, and certain eye and skin conditions.

Dexamethasone is an anti-inflammatory agent that is FDA approved for the treatment of many conditions, including rheumatic problems, a number of skin diseases, severe allergies, asthma, chronic obstructive lung disease, croup, brain swelling and others. Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. Adverse reactions are: Glaucoma with optic nerve damage, visual acuity and field defects; cataract formation; secondary ocular infection following suppression of host response; and perforation of the globe may occur; muscle weakness; osteoporosis and others. Aminoglutethimide may diminish adrenal suppression by corticosteroids. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance.

Dexamethasone is an anti-inflammatory agent that is FDA approved for the treatment of many conditions, including rheumatic problems, a number of skin diseases, severe allergies, asthma, chronic obstructive lung disease, croup, brain swelling and others. Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. Adverse reactions are: Glaucoma with optic nerve damage, visual acuity and field defects; cataract formation; secondary ocular infection following suppression of host response; and perforation of the globe may occur; muscle weakness; osteoporosis and others. Aminoglutethimide may diminish adrenal suppression by corticosteroids. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance.

Dexamethasone is an anti-inflammatory agent that is FDA approved for the treatment of many conditions, including rheumatic problems, a number of skin diseases, severe allergies, asthma, chronic obstructive lung disease, croup, brain swelling and others. Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. Adverse reactions are: Glaucoma with optic nerve damage, visual acuity and field defects; cataract formation; secondary ocular infection following suppression of host response; and perforation of the globe may occur; muscle weakness; osteoporosis and others. Aminoglutethimide may diminish adrenal suppression by corticosteroids. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance.

Dexamethasone is an anti-inflammatory agent that is FDA approved for the treatment of many conditions, including rheumatic problems, a number of skin diseases, severe allergies, asthma, chronic obstructive lung disease, croup, brain swelling and others. Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. Adverse reactions are: Glaucoma with optic nerve damage, visual acuity and field defects; cataract formation; secondary ocular infection following suppression of host response; and perforation of the globe may occur; muscle weakness; osteoporosis and others. Aminoglutethimide may diminish adrenal suppression by corticosteroids. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance.

Prednisolone hemisuccinate is a prodrug of a glucocorticoid agonist prednisolone, which is marketed under trade name Prednisolut in Germany and Austria. Prednisolone hemisuccinate is used in emergency medicine to treate shock due to allergic reaction, insect and snake bites, in neurology to treat brain edema and meningitis, in transplantation medicine to reduce risk of organ refection after kidney transplane, in pneumology to treat acute asthma attack, pulmonary edema, in severe or life-threatening situation in rheumatic diseases.

Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. 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. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). Hydrocortisone is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

Phosphate is a major intracellular anion in mammals. Hydrogen phopshate is a protonated form of phosphate. In serum, phosphate exists in two forms, dihydrogen phosphate (H2PO4) and its salt, mono-hydrogen phosphate (HPO4). At the physiologic pH of 7.40, the pK of H2PO4 is 6.8 and the ratio of HPO4 to H2PO4 is 4:1. Altered level of phosphate can be an indicator of various disorders, such as chronic renal failure, hypoparathyroidism, familial intermittent hyperphosphatemia, endocrine disorders, hyperthyroidism, acromegaly, juvenile hypogonadism, etc. These disorders may lead to either hyper- or hypophosphatemia, which can be caused by cellular shifts of phosphate. Patients with hypophosphatemia can be treated with dietary phosphate supplements (potassium phosphate, for example).

Phosphate is a major intracellular anion in mammals. Hydrogen phopshate is a protonated form of phosphate. In serum, phosphate exists in two forms, dihydrogen phosphate (H2PO4) and its salt, mono-hydrogen phosphate (HPO4). At the physiologic pH of 7.40, the pK of H2PO4 is 6.8 and the ratio of HPO4 to H2PO4 is 4:1. Altered level of phosphate can be an indicator of various disorders, such as chronic renal failure, hypoparathyroidism, familial intermittent hyperphosphatemia, endocrine disorders, hyperthyroidism, acromegaly, juvenile hypogonadism, etc. These disorders may lead to either hyper- or hypophosphatemia, which can be caused by cellular shifts of phosphate. Patients with hypophosphatemia can be treated with dietary phosphate supplements (potassium phosphate, for example).