Albet G

Uses

The topical treatment of corticosteroid responsive dermatoses when complicated by secondary infection caused by organisms sensitive to gentamicin or when the possibility of such infection is suspected. The cream is recommended for wet, oozing primary infections, and greasy, secondary infections such as pustular acne or infected seborrheic dermatitis. The ointment helps retain moisture and has been useful in infection on dry eczematous or psoriatic skin.

Albet G is also used to associated treatment for these conditions: Acute Gouty Arthritis, Adrenal cortical hypofunctions, Alopecia Areata (AA), Ankylosing Spondylitis (AS), Berylliosis, Blepharitis allergic, Blepharoconjunctivitis, Bullous dermatitis herpetiformis, Bursitis, Congenital Adrenal Hyperplasia (CAH), Congenital Hypoplastic Anemia, Conjunctivitis, Corneal Inflammation, Dermatitis, Eczematous, Dermatomyositis, Dermatosis, Discoid Lupus Erythematosus (DLE), Edema of the cerebrum, Epicondylitis, Episcleritis, External ear inflammation, Eye allergy, Hypercalcemia of Malignancy, Inflammatory Reaction of the ear, Iridocyclitis, Iritis, Itching caused by Allergies, Keloid Scars, Keratitis interstitial, Keratoconjunctivitis, Leukemias, Lichen Planus (LP), Lichen simplex chronicus, Lupus Erythematosus, Malignant Lymphomas, Multiple sclerosis exacerbation, Mycosis Fungoides (MF), Necrobiosis lipoidica diabeticorum, Nephrotic Syndrome, Ocular Inflammation, Ocular injuries, Ophthalmia, Sympathetic, Pemphigus, Plaque psoriasis of the body, Plaque psoriasis of the scalp, Polymyositis, Post-Surgical Ocular Inflammation, Pruritus, Psoriasis, Psoriasis Vulgaris (Plaque Psoriasis), Psoriatic Arthritis, Psoriatic plaque, Pulmonary Tuberculosis (TB), Pure Red Cell Aplasia, Regional Enteritis, Rheumatoid Arthritis, Rheumatoid Arthritis, Juvenile, Scleritis, Secondary thrombocytopenia, Severe Asthma, Severe Atopic Dermatitis, Skin Infections, Stevens-Johnson Syndrome, Systemic Lupus Erythematosus (SLE), Temporal Arteritis, Trichinosis, Tuberculous Meningitis, Ulcerative Colitis, Uveitis, Verrucous Lichen Planus (LP), Acquired immune hemolytic anemia, Acute nonspecific tenosynovitis, Acute rheumatic carditis, Bacterial blepharitis, Corticosteroid-responsive dermatoses, Eczematous rash, Exfoliative erythroderma, Granuloma annulare lesions, Idiopathic eosinophilic pneumonias, Non-suppurative Thyroiditis, Ocular bacterial infections, Severe Allergic rhinitis, Severe Contact dermatitis, Severe Serum sickness, Severe Transfusion Reactions, Severe drug hypersensitivity reactions, Superficial ocular infections, Symptomatic Sarcoidosis, Synovitis of osteoarthritisBacterial Conjunctivitis, Bacterial Infections, Bacterial Peritonitis, Bacterial dacryocystitis, Blepharoconjunctivitis, Central Nervous System Infections, Conjunctivitis allergic, Corneal infection, Dermatitis infected, Ecthyma, Eczematous dermatitis infected, Folliculitis, Furunculosis, Gram-negative enteric bacilli neonatal sepsis, Impetigo contagious, Inflammation, Keratitis bacterial, Keratoconjunctivitis, Meibomianitis, Meningitis, Bacterial, Ocular Inflammation, Pustular Psoriasis (PP), Pustular acne, Pyoderma Gangrenosum, Seborrheic Dermatitis, Septicemia gram-negative, Skin Infections, Skin Infections, Bacterial, Skin and Subcutaneous Tissue Bacterial Infections, Sycosis barbae, Bacterial blepharitis, Bacterial corneal ulcers, Bacterial dermatoses, Complicated Bacterial Urinary Tract Infections, Complicated Respiratory tract infection bacterial, Corticosteroid-responsive dermatoses, Ocular bacterial infections, Severe Endocarditis enterococcal, Severe Infection Pseudomonas aeruginosa, Severe Staphylococcal infection

How Albet G works

Glucocorticoids inhibit neutrophil apoptosis and demargination, and inhibit NF-Kappa B and other inflammatory transcription factors. They also inhibit phospholipase A2, leading to decreased formation of arachidonic acid derivatives. In addition, glucocorticoids promote anti-inflammatory genes like interleukin-10.

Corticosteroids like betamethasone can act through nongenomic and genomic pathways. The genomic pathway is slower and occurs when glucocorticoids activate glucocorticoid receptors and initiate downstream effects that promote transcription of anti-inflammatory genes including phosphoenolpyruvate carboxykinase (PEPCK), IL-1-receptor antagonist, and tyrosine amino transferase (TAT). On the other hand, the nongenomic pathway is able to elicit a quicker response by modulating T-cell, platelet and monocyte activity through the use of existing membrane-bound receptors and second messengers.

There are 3 key phases of aminoglycoside entry into cells. The first “ionic binding phase” occurs when polycationic aminoglycosides bind electrostatically to negatively charged components of bacterial cell membranes including with lipopolysaccharides and phospholipids within the outer membrane of Gram-negative bacteria and to teichoic acids and phospholipids within the cell membrane of Gram-positive bacteria. This binding results in displacement of divalent cations and increased membrane permeability, allowing for aminoglycoside entry. The second “energy-dependent phase I” of aminoglycoside entry into the cytoplasm relies on the proton-motive force and allows a limited amount of aminoglycoside access to its primary intracellular target - the bacterial 30S ribosome. This ultimately results in the mistranslation of proteins and disruption of the cytoplasmic membrane.[A233320] Finally, in the “energy-dependent phase II” stage, concentration-dependent bacterial killing is observed. Aminoglycoside rapidly accumulates in the cell due to the damaged cytoplasmic membrane, and protein mistranslation and synthesis inhibition is amplified. The necessity of oxygen-dependent active transport explains why aminoglycosides are ineffective against anaerobic bacteria. Hence, aminoglycosides have both immediate bactericidal effects through membrane disruption and delayed bactericidal effects through impaired protein synthesis; observed experimental data and mathematical modeling support this two-mechanism model. Inhibition of protein synthesis is a key component of aminoglycoside efficacy. Structural and cell biological studies suggest that aminoglycosides bind to the 16S rRNA in helix 44 (h44), near the A site of the 30S ribosomal subunit, altering interactions between h44 and h45. This binding also displaces two important residues, A1492 and A1493, from h44, mimicking normal conformational changes that occur with successful codon-anticodon pairing in the A site.[A232324, A232329] Overall, aminoglycoside binding has several negative effects including inhibition of translation, initiation, elongation, and ribosome recycling. Recent evidence suggests that the latter effect is due to a cryptic second binding site situated in h69 of the 23S rRNA of the 50S ribosomal subunit.[A232329, A232339] Also, by stabilizing a conformation that mimics correct codon-anticodon pairing, aminoglycosides promote error-prone translation.[A232344] Mistranslated proteins can incorporate into the cell membrane, inducing the damage discussed above.

Dosage

Albet G dosage

A sufficient quantity of the cream or ointment should be applied to cover completely the affected area and should be massaged gently and thoroughly into the skin. The usual frequency of application is twice daily although some patients may be maintained adequately with less frequent application.

Side Effects

The following local adverse skin reactions have been reported with the use of topical steroids: dryness, itching, burning, local irritation, striae, skin atrophy, hypertrichosis, change in pigmentation and secondary infection. Adrenal suppression has also been reported following topical corticosteroid therapy. Posterior subcapsular cataracts have been reported following systemic use of corticosteroids.

Toxicity

Chronic high doses of glucocorticoids can lead to the development of cataracts, glaucoma, hypertension, water retention, hyperlipidemia, peptic ulcer, pancreatitis, myopathy, osteoporosis, mood changes, psychosis, dermal atrophy, allergy, acne, hypertrichosis, immune suppression, decreased resistance to infection, moon face, hyperglycemia, hypocalcemia, hypophosphatemia, metabolic acidosis, growth suppression, and secondary adrenal insufficiency. Overdose may be treated by adjusting the dose or stopping the corticosteroid as well as initiating symptomatic and supportive treatment.

As with other aminoglycosides, nephrotoxicity and ototoxicity are associated with gentamicin. Signs of nephrotoxicity include an increase in plasma creatinine and urea, while signs of ototoxicity include issues with balance, nausea, tinnitus, and hearing loss. It is important to note that aminoglycoside-induced nephrotoxicity is typically reversible, while ototoxicity is more likely to be permanent. The risk of both toxicities increases with long-term gentamicin therapy. Gentamicin is considered to be more vestibulotoxic than cochleotoxic compared to other aminoglycosides. Unfortunately, gentamicin-related ototoxicity does not correlate with cumulative dosing, peak and trough levels, or dosing schedule. The unpredictability of ototoxicity supports close monitoring of the patient throughout treatment. In cases of toxicity or overdose, the medication should be discontinued immediately; hemodialysis may be initiated to lower gentamicin serum concentrations.

Precaution

Gentamicin is not effective against fungi, yeasts or viruses. Patients with superficial fungus or yeast infections also must receive specific therapy and the use of the drug may have to be discontinued. The use of such topical preparations may result in an overgrowth of non-susceptible organisms.

Suitable precautions should be taken in using topical corticosteroids in patients with stasis dermatitis and other skin diseases with impaired circulation.

Prolonged use of corticosteroid preparations may produce striae or atrophy of the skin or s.c. tissue. If this occurs, treatment should be discontinued.

Causal factors should be sought and eliminated whenever possible and the sensitivity of an infecting organism to gentamicin should be verified.

Patients should be advised to inform subsequent physicians of the prior use of corticosteroids.

While no systemic effects have been observed following the topical application of gentamicin, toxic systemic concentrations can cause permanent impairment of vestibular function in the presence of renal insufficiency or existing 8th cranial nerve damage.

Caution should be exercised if gentamicin is used in individuals who are known to be sensitive to topically applied antibacterials. If irritation or sensitization develops, treatment should be discontinued.

Application over extensive lesions may result in significant systemic absorption producing hypercortisonism manifesting itself by adrenal suppression, moon face, striae and suppression of growth in children.

Patients should be followed up regularly, and the product should be discontinued when the infection has cleared.

Occlusive dressing should not be used.

Interaction

Increased hyperglycaemia and hypokalaemia with thiazide diuretics. Increased incidence of peptic ulcer or GI bleeding with concurrent NSAIDs admin. Response to anticoagulants altered. Dose of antidiabetics and antihypertensives needs to be increased. Decreases serum concentration of salicylates and antimuscarinic agents.

Potentially Fatal: Reduced efficacy with concurrent use of carbamazepine, phenytoin, primidone, barbiturates and rifampicin. Enhanced effect in women taking oestrogens or oral contraceptives.

None has been reported so far with topical and Eye/Ear drops.

Volume of Distribution

In a study that included Indian women of reproductive age, the volume of distribution following a single intramuscular dose of betamethasone phosphate was 94,584±23,539 mL(s).

Elimination Route

The absorption and potency of any topical corticosteroid including betamethasone depends on the vehicle in which the steroid is delivered. For example, betamethasone dipropionate 0.05% ointment is classified as a highly potent topical steroid, while betamethasone dipropionate 0.05% cream or lotion is considered to be moderately potent.

There are several structural modifications that can determine the potency of a topical corticosteroid. For example, corticosteroids containing a halogen at specific carbons, or that contain esters are more potent due to enhanced lipophilicity. As such, there is a marked difference between topical products containing betamethasone dipropionate vs. betamethasone valerate. Betamethasone dipropionate contains 2 esters which enhances its potency, while betamethasone valerate has only one ester and is less potent.

It should be noted that the use of occlusive dressings with topical steroids significantly increases the absorption, increasing the risk for adverse effects.

Half Life

In a study that included Indian women of reproductive age, the half-life following a single intramuscular dose of betamethasone phosphate was 10.2 ± 2.5 hours.

One study assessing the pharmacokinetics of gentamicin in children and adults reported a mean half-life of 75 minutes after intravenous administration. The mean half-life associated with intramuscular administration was about 29 minutes longer. Fever and anemia may result in a shorter half-life although dose adjustments are not usually necessary. Severe burns are also associated with a shorter half-life and may result in lower gentamicin serum concentrations.

Clearance

In a study that included Indian women of reproductive age, the CL/F following a single intramuscular dose of betamethasone phosphate was 6,466 ± 805 mL/hour.

The renal clearance of gentamicin is comparable to individual creatinine clearance.

Elimination Route

Corticosteroids are eliminated predominantly in the urine.

Gentamicin is excreted primarily by the kidneys. In patients with normal renal function, 70% or more of an initial gentamicin dose can be recovered in the urine within 24 hours. Excretion of gentamicin is significantly reduced in patients with renal impairment.

Pregnancy & Breastfeeding use

Since safety of topical corticosteroid use in pregnant women has not been established, drugs of this class should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Drugs of this class should not be used extensively in large amounts or for prolonged periods of time in pregnant patients. Since it is not known whether topical administration of corticosteroids can result in sufficient systemic absorption to produce detectable quantities in breast milk, a decison should be made to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. This drug should not be used in or near the eyes since the vehicle is not formulated for ophthalmic use.

Contraindication

Viral diseases including vaccinia, varicella, herpes simplex, fungal infections, tuberculosis of the skin and hypersensitivity to any of the components.

Acute Overdose

Symptoms: Excessive prolonged use of topical corticosteroids can suppress pituitary-adrenal function leading to secondary adrenal insufficiency.

Treatment: Correct electrolyte imbalance, if needed. Slow withdrawal of corticosteroids may be needed.

Storage Condition

Store between 2-30° C.

Innovators Monograph

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