Lowdex Eye Ear
Lowdex Eye Ear Uses, Dosage, Side Effects, Food Interaction and all others data.
Boric acid, also known as hydrogen borate, is a weak monobasic Lewis acid of boron with the chemical formula H3BO3. Boric acid is typically utilized in industrial processing and manufacturing, but is also used as an additive in pharmaceutical products, cosmetics, lotions, soaps, mouthwash, toothpaste, astringents, and eyewashes . It is known to exhibit some antibacterial activity against infections such as bacterial vaginosis and candidiasis .
Boric acid exhibits minimal bacteriostatic and antifungal activities . Boric acid is likely to mediate antifungal actions at high concentrations over prolonged exposures .
Dexamethasone is a synthetic glucocorticoid which decreases inflammation by inhibiting the migration of leukocytes and reversal of increased capillary permeability. It suppresses normal immune response.
Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Dexamethasone's duration of action varies depending on the route. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections.
Trade Name | Lowdex Eye Ear |
Generic | Borax + Boric Acid + Dexamethasone + Phenylmercuric Nitrate |
Weight | 0.06% |
Type | Drops |
Therapeutic Class | |
Manufacturer | |
Available Country | India |
Last Updated: | September 19, 2023 at 7:00 am |
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Uses
No FDA- or EMA-approved therapeutic indications on its own.
Endocrine disorders: Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy, mineralocorticoid supplementation is of particular importance). Acute adrenocortical insufficiency, pre operatively and in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful. Shock unresponsive to conventional therapy if adrenocortical insufficiency exists or is suspected congenital adrenal hyperplasia, nonsuppurative thyroiditis, hypercalcemia associated with cancer
Rheumatic disorders: As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in: post-traumatic osteoarthritis, synovitis of osteoarthritis, rheumatoid arthritis including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy), acute and sub-acute bursitis, epicondylitis, acute nonspecific tenosynovitis, acute gouty arthritis, psoriatic arthritis, ankylosing spondylitis.
Collagen diseases: During an exacerbation or as maintenance therapy in selected cases of Systemic lupus erythematosus and acute rheumatic carditis
Dermatologic diseases: Pemphigus,Severe erythema multiforme (Stevens-Johnson syndrome), Exfoliative dermatitis, Bullous dermatitis herpetiformis, Severe seborrheic dermatitis,Severe psoriasis, Mycosis fungoides
Allergic states: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in bronchial asthma, contact dermatitis, atopic dermatitis, serum sickness, seasonal or perennial allergic rhinitis, drug hypersensitivity reactions, urticarial transfusion reactions, acute non-infectious laryngeal edema (epinephrine is the drug of first choice)
Ophthalmic diseases: Severe acute and chronic allergic and inflammatory processes involving the eye, such as: herpes zoster ophthalmicus, iritis, iridocyclitis, chorioretinitis, diffuse posterior uveitis and choroiditis, optic neuritis, sympathetic ophthalmia, anterior segment inflammation, allergic conjunctivitis, keratitis, allergic corneal marginal ulcers.
Gastrointestinal diseases: To tide the patient over a critical period of the disease in ulcerative colitis (systemic therapy), regional enteritis (systemic therapy) Respiratory diseases Symptomatic sarcoidosis, berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate anti-tuberculous chemotherapy, Loeffler's syndrome not manageable by other means, aspiration pneumonitis.
Hematologic disorders: Acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura in adults (I.V. only: I.M administration is contraused), secondary thrombocytopenia in adults, erythroblastopenia (RBC anemia), congenital (erythroid) hypoplasticanemia
Neoplastic diseases: For palliative management of leukemias and lymphomas in adults, acute leukemia of childhood.
Edematous states: To induce diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus.
Miscellaneous: Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy,Trichinosis with neurologic or myocardial involvement
Cerebral Edema: Cerebral Edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Use in cerebral edema is not a substitute for careful neurosurgical evaluation and definitive management such as neurosurgery or other specific therapy.May also be useful in cystic tumors of an aponeurosis or tendon (ganglia).
Lowdex Eye Ear is also used to associated treatment for these conditions: Acne, Asthenopia, Ocular Irritation, Skin Mycoses, Eye discomfort, Skin disinfection, Irrigation of the ocular surface therapyAcne Rosacea, Acute Gouty Arthritis, Acute Otitis Externa, Acute Otitis Media, Adrenal cortical hypofunctions, Adrenocortical Hyperfunction, Alopecia Areata (AA), Ankylosing Spondylitis (AS), Anterior Segment Inflammation, Aspiration Pneumonitis, Asthma, Atopic Dermatitis (AD), Berylliosis, Bullous dermatitis herpetiformis, Bursitis, Chorioretinitis, Choroiditis, Congenital Adrenal Hyperplasia (CAH), Congenital Hypoplastic Anemia, Conjunctivitis, Conjunctivitis allergic, Corneal Inflammation, Cushing's Syndrome, Dermatitis, Dermatitis exfoliative generalised, Dermatitis, Contact, Diabetic Macular Edema (DME), Discoid Lupus Erythematosus (DLE), Drug hypersensitivity reaction, Edema of the cerebrum, Epicondylitis, Episcleritis, Erythroblastopenia, Eye Infections, Eye allergy, Eye swelling, Glaucoma, Hypercalcemia, Idiopathic Thrombocytopenic Purpura, Infection, Inflammation, Inflammation of the External Auditory Canal, Intraocular Inflammation, Iridocyclitis, Iritis, Keloid Scars, Leukemia, Acute, Lichen Planus (LP), Lichen simplex chronicus, Loeffler's syndrome, Macular Edema, Malignant Lymphomas, Middle ear inflammation, Mucosal Inflammation of the eye, Multiple Myeloma (MM), Muscle Inflammation caused by Cataract Surgery of the eye, Mycosis Fungoides (MF), Necrobiosis lipoidica diabeticorum, Noninfectious Posterior Uveitis, Ocular Infections, Irritations and Inflammations, Ocular Inflammation, Ocular Inflammation and Pain, Ocular Irritation, Ophthalmia, Sympathetic, Optic Neuritis, Otitis Externa, Pemphigus, Perennial Allergic Rhinitis (PAR), Phlyctenular keratoconjunctivitis, Post-traumatic Osteoarthritis, Postoperative Infections of the eyes caused by susceptible bacteria, Regional Enteritis, Rheumatoid Arthritis, Rheumatoid Arthritis, Juvenile, Sarcoidosis, Scleritis, Seasonal Allergic Conjunctivitis, Seasonal Allergic Rhinitis, Secondary thrombocytopenia, Serum Sickness, Severe Seborrheic Dermatitis, Stevens-Johnson Syndrome, Synovitis, Systemic Lupus Erythematosus (SLE), Trichinosis, Tuberculosis (TB), Tuberculosis Meningitis, Ulcerative Colitis, Uveitis, Vernal Keratoconjunctivitis, Acquired immune hemolytic anemia, Acute nonspecific tenosynovitis, Acute rheumatic carditis, Corticosteroid-responsive dermatoses, Ear infection-not otherwise specified caused by susceptible bacteria, Granuloma annulare lesions, Non-suppurative Thyroiditis, Ocular bacterial infections, Severe Psoriasis, Steroid-responsive inflammation of the eye, Varicella-zoster virus acute retinal necrosis, Watery itchy eyes
How Lowdex Eye Ear works
Information regarding the mechanism of action of boric acid in mediating its antibacterial or antifungal actions is limited. Boric acid inhibits biofilm formation and hyphal transformation of Candida albicans, which are critical virulence factors . In addition, arrest of fungal growth was observed with the treatment of boric acid .
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.
Dosage
Lowdex Eye Ear dosage
Intraarticular-
Inflammatory joint diseases:
- Adult: 0.8-4 mg depending on the size of the affected joint. For soft-tissue inj, 2-6 mg may be used. May repeat inj every 3-5 days to every 2-3 wk.
Intravenous-
Prophylaxis of nausea and vomiting associated with cytotoxic therapy:
- Adult: Prevention: 10-20 mg 15-30 minutes before admin of chemotherapy on each treatment day. For continuous infusion regimen: 10 mg every 12 hr on each treatment day. For midly emetogenic regimen: 4 mg every 4-6 hr.
Unresponsive shock:
- Adult: As phosphate: Initially, 40 mg or 1-6 mg/kg as a single IV inj, may repeat every 2-6 hr. Continue high-dose treatment only until patient's condition has stabilised and not to be continued beyond 48-72 hr.
Bacterial meningitis:
- Adult: 0.15 mg/kg 4 times daily, to be given 10-20 min before or with the 1st dose of anti-infective treatment. Treatment should be given for the first 2-4 days of the anti-infective treatment.
- Child: As phosphate: 2 mth-18 yr: 150 mcg/kg every 6 hr for 4 days, starting before or with 1st dose of antibacterial treatment.
Cerebral oedema caused by malignancy:
- Adult: As phosphate: 10 mg IV followed by 4 mg IM every 6 hr until response is achieved, usually after 12-24 hr. May reduce dosage after 2-4 days then gradually discontinued over 5-7 days. In severe cases, an initial dose of 50 mg IV may be given on day 1, with 8 mg every 2 hr, reduced gradually over 7-13 days. Maintenance dose: 2 mg 2-3 times daily.
- Child: As phosphate: 35 kg: Initially 25 mg, then 4 mg every 2 hr for 3 days, then 4 mg every 4 hr for 1 day, then 4 mg every 6 hr for 4 days, then decrease by 2 mg daily. Doses are given via IV inj.
Oral-
Anti-inflammatory:
- Adult: 0.75-9 mg daily in 2-4 divided doses; may also be given via IM/IV admin.
- Child: 1 mth-18 yr: 10-100 mcg/kg daily in 1-2 divided doses via oral admin, adjusted according to response; up to 300 micrograms/kg daily may be used in emergency situations.
Screening test for Cushing's syndrome:
- Adult: 0.5 mg every 6 hr for 48 hr after determining baseline 24-hr urinary 17-hydroxycorticosteroid (17-OHCS) concentrations. During the second 24 hr of dexamethasone admin, urine is collected and analysed for 17-OHCS. Alternatively, after a baseline plasma cortisol determination, 1 mg may be given at 11 pm and plasma cortisol determined at 8 am the next morning. Plasma cortisol and urinary output of 17-OHCS are depressed after dexamethasone admin in normal individuals but remain at basal levels in patients with Cushing's syndrome.
Acute exacerbations in multiple sclerosis:
- Adult: 30 mg daily for 1 wk followed by 4-12 mg daily for 1 mth.
- Child: 1 mth-12 yr: 100-400 mcg/kg daily in 1-2 divided doses; 12-18 yr: Initially 0.5-24 mg daily. Max. 24 mg daily.
Side Effects
Dexamethasone is generally well tolerated in standard low doses, Nausea, vomiting, increased appetite, and obesity may occur. Higher doses may result behavioral personality changes. Following adverse reactions have been associate with prolonged systemic glucocorticoid therapy, endocrine & metabolic disturbances, fluid & electrolyte disturbances, musculo-skeletal effects like osteoporosis etc; GI effects like ulcer, bleeding, perforation; Opthelmic effects like Glaucoma, increased intraocular pressure etc; immunosuppressive effects like increased susceptibility to infection etc.
Toxicity
Acute oral LD50 is 2660 mg/kg in rat . Individuals are likely to be exposed to boric acid from industrial manufacturing or processing. Local tissue injury from boric acid exposure is likely due to caustic effects. Systemic effects from boric acid poisoning usually occur from multiple exposures over a period of days and involve gastrointestinal, dermal, CNS, and renal manifestations. Gastrointestinal toxicity include persistent nausea, vomiting, diarrhea, epigastric pain, hematemesis, and blue-green discoloration of the feces and vomit . Following the onset of GI symptoms, a characteristic intense generalized erythroderma follows . Management of mild to moderate toxicity should be supportive. In case of severe toxicity, dialysis may be required in addition to supportive treatment.
The oral LD50 in female mice was 6.5g/kg and 794mg/kg via the intravenous route.
Overdoses are not expected with otic formulations. Chronic high doses of glucocorticoids can lead to the development of cataract, 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.
Precaution
The lowest possible dose of corticosteroids should be used to control the conditions under treatment. Dexamethasone should be used with caution in patient with cardiomyopathy, heart failure, hypertension, or renal insufficiency, drug induced secondary adrenocortical insufficiency, peptic ulcer, diverticulitis, intestinal anastomosis, ulcerative colitis, osteoporosis, & latent tuberculosis etc.
Interaction
Drug interaction can be occurred with following drugs:Diuretics, cardiac glycosides, antidiabetics, NSAIDs, anticoagulants, antacids etc. Besides, if patients undergo long-term therapy of glucororticoids with concomitant salicylates, any reduction in glucocorticoid dosage should be made with caution, since salicylate intoxication has been reported in such cases.
Volume of Distribution
Volume of distribution ranges from 0.17 to 0.5 L/kg in humans, where large amounts of boric acid are localized in brain, liver, and kidney .
A 1.5mg oral dose of dexamethasone has a volume of distribution of 51.0L, while a 3mg intramuscular dose has a volume of distribution of 96.0L.
Elimination Route
Boric acid is well absorbed from the gastrointestinal tract, open wounds, and serous cavities but displays limited absorption in intact skin . Following intraperitoneal injection in mice, the peak concentration was reached in about 1.0-1.5 hr in the brain whereas the value was 0.5 hr in other tissues .
Absorption via the intramuscular route is slower than via the intravenous route. A 3mg intramuscular dose reaches a Cmax of 34.6±6.0ng/mL with a Tmax of 2.0±1.2h and an AUC of 113±38ng*h/mL. A 1.5mg oral dose reaches a Cmax of 13.9±6.8ng/mL with a Tmax of 2.0±0.5h and an AUC of 331±50ng*h/mL. Oral dexamethasone is approximately 70-78% bioavailable in healthy subjects.
Half Life
According to human cases of poisoning, the elimination half-life of boric acid ranges from 13 to 24 hours .
The mean terminal half life of a 20mg oral tablet is 4 hours. A 1.5mg oral dose of dexamethasone has a half life of 6.6±4.3h, while a 3mg intramuscular dose has a half life of 4.2±1.2h.
Clearance
A case report of acute boric acid poisoning following oral ingestion of 21 g of boric acid presents the total body clearance of 0.99 L/h before hemodialysis .
A 20mg oral tablet has a clearance of 15.7L/h. A 1.5mg oral dose of dexamethasone has a clearance of 15.6±4.9L/h while a 3.0mg intramuscular dose has a clearance of 9.9±1.4L/h.
Elimination Route
Regardless the route of administration, boric acid predominantly undergoes rapid renal excretion of >90% of total administered dose as unchanged form. Small amounts are also excreted into sweat, saliva, and feces. Following administration as ointment, urinary excretion of boric acid accounted for only 1% of the administered dose .
Corticosteroids are generally eliminated predominantly in the urine. However, dexamethasone is 15
Pregnancy & Breastfeeding use
Pregnancy Category C. There are no adequate and well-controlled studies in pregnant women. Corticosteroids should be used during pregnancy only if the potential benefit justifies. Glucocorticoids appear in breast milk, Mothers taking high dosages of corticosteroids should be advised not to breast-feed.
Contraindication
In case of adrenal insufficiency, no absolute contraindications are applicable. In the treatment of non endocrine diseases where pharmacological doses are more likely to be used, the contraindications have to be considered carefully.
Relative contraindications include the followings: patient with Cushing’s syndrome, Osteoporosis, Diabetes mellitus, renal insufficiency, gastrointestinal ulcers, systemic fungal infection & acute infection.
Acute Overdose
Overdose is unlikely; however, treatment of overdose is by supportive and symptomatic therapy.
Storage Condition
Store at 15-30° C.
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