neopred - p eye susp

Uses

Prednisolone is a glucocorticoid used to treat adrenocortical insufficiency, inflammatory conditions, and some cancers.

Prednisolone is indicated to treat endocrine, rheumatic, and hematologic disorders; collagen, dermatologic, ophthalmic, respiratory, and gastrointestinal diseases; allergic and edematous states; and other conditions like tuberculous meningitis.

neopred - p eye susp is also used to associated treatment for these conditions: Acne Rosacea, Acute Gouty Arthritis, Allergic Bronchopulmonary Aspergillosis, Allergic Contact Dermatitis, Allergic corneal marginal ulcers, Alveolitis, Extrinsic Allergic, Anal Fissures, Ankylosing Spondylitis (AS), Aspiration Pneumonitis, Atopic Dermatitis (AD), Bell's Palsy, Berylliosis, Bullous dermatitis herpetiformis, Burns, Chorioretinitis, Choroiditis, Chronic Obstructive Airways Disease Exacerbated, Congenital Adrenal Hyperplasia (CAH), Congenital Hypoplastic Anemia, Conjunctivitis, Corneal Inflammation, Corneal injuries, Corneal ulceration, Crohn's Disease (CD), Cyclitis, Dermatitis exfoliative generalised, Dermatitis, Contact, Dermatomyositis, Dermatosis of the Ear Canal, Drug hypersensitivity reaction, Edema of the cerebrum, Epicondylitis, Erythroblastopenia, Exacerbation of asthma, Eye inflammation caused by Cataract Surgery, Eye inflammation caused by Infection, Herpes Zoster Keratitis, Hot Water Burns (Scalds), Hypercalcemia of Malignancy, Idiopathic Pulmonary Fibrosis (IPF), Idiopathic Thrombocytopenic Purpura, Inflamed External Hemorrhoid, Inflamed Hemorrhoids, Internal, Inflammatory Reaction caused by susceptible Bacterial Infections, Iridocyclitis, Iritis, Itching caused by susceptible Bacterial Infections, Leukemia, Acute, Loeffler's syndrome, Malignant Lymphomas, Multiple sclerosis exacerbation, Mycosis Fungoides (MF), Ocular Inflammation, Ophthalmia, Sympathetic, Optic Neuritis, Otic Eczema, Pemphigus, Perennial Allergic Rhinitis (PAR), Pericarditis, Pneumocystis Jirovecii Pneumonia, Pneumonia, Aspiration, Polymyalgia Rheumatica, Post-traumatic Osteoarthritis, Proctitis, Proteinuria, Pruritus, Pruritus Ani, Psoriatic Arthritis, Pulmonary Tuberculosis (TB), Pure Red Cell Aplasia, Rash, Rejection, Transplant, Relapsing Polychondritis, Rheumatoid Arthritis, Rheumatoid Arthritis, Juvenile, Seasonal Allergic Conjunctivitis, Seasonal Allergic Rhinitis, Secondary Adrenal Insufficiency, Secondary thrombocytopenia, Serum Sickness, Severe Asthma, Sjögren's Syndrome, Skin Infections, Bacterial, Stevens-Johnson Syndrome, Superficial punctate keratitis, Synovitis, Systemic Lupus Erythematosus (SLE), Trichinosis, Tuberculosis (TB), Tuberculous Meningitis, Ulcerative Colitis, Uveitis, Vasculitis, Acquired immune hemolytic anemia, Acute Bursitis, Acute Rheumatic heart disease, unspecified, Acute Tenosynovitis, Allergic skin manifestations, Anal eczema, Exfoliative erythroderma, Idiopathic Bronchiolitis obliterans with organizing pneumonia, Idiopathic eosinophilic pneumonias, Non-suppurative Thyroiditis, Primary adrenocoritical insufficiency, Severe Psoriasis, Severe Seborrhoeic dermatitis, Severe alcoholic liver disease, Steroid-responsive inflammation of the eye, Subacute Bursitis, Susceptible Bacterial Infections, Symptomatic Sarcoidosis, Varicella-zoster virus acute retinal necrosis

How neopred - p eye susp works

The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.

Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10.

Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.

Toxicity

The intraperitoneal LD₅₀ in rats is 2g/kg and 65mg/kg in mice. The subcutaneous LD₅₀ in rats is 147mg/kg and >3500mg/kg in mice. The oral LD₅₀ in mice is 1680mg/kg. In humans, the oral TDLO in men is 9mg/kg/2W and in women is 14mg/kg/13D.

Patients experiencing an overdose of prednisolone may present with gastrointestinal disturbances, insomnia, and restlessness. Overdose of oral prednisolone may be treated by gastric lavage or inducing vomiting if the overdose was recent, as well as supportive and symptomatic therapy. Chronic overdosage may be treated by dose reduction or treating patients on alternate days. An overdose by the ophthalmic route is not expected to cause problems.

Volume of Distribution

A 0.15mg/kg dose of prednisolone has a volume of distribution of 29.3L, while a 0.30mg/kg dose has a volume of distribution of 44.2L.

Elimination Route

Oral prednisolone reaches a C_max of 113-1343ng/mL with a T_max of 1.0-2.6 hours. Oral prednisolone is approximately 70% bioavailable.

Half Life

Prednisolone has a plasma half life of 2.1-3.5 hours. This half life is shorter in children and longer in those with liver disease.

Clearance

A 0.15mg/kg dose of prednisolone has a clearance of 0.09L/kg/h, while a 0.30mg/kg dose has a clearance of 0.12L/kg/h.

Elimination Route

Prednisolone is over 98% eliminated in urine.

Innovators Monograph

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