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HYDROCORTISONE BUTYRATE
Overview
What is Locoid?
LOCOID (hydrocortisone butyrate) Lotion, 0.1% contains hydrocortisone butyrate, a non-fluorinated hydrocortisone ester, for topical use. The chemical name of hydrocortisone butyrate is Pregn-4-ene-3,20-dione, 11,21,-dihydroxy-17-[(1-oxobutyl)oxy(11β)-]. It has the following structural formula:
Hydrocortisone butyrate is a white to off-white powder with a molecular weight of 432.56, and a molecular formula of CHO. It is practically insoluble in water, slightly soluble in ether, soluble in methanol, in alcohol, and in acetone, and freely soluble in chloroform.
Each gram of LOCOID Lotion contains 1 mg of hydrocortisone butyrate in a white to off-white lotion base consisting of anhydrous citric acid, ceteth-20, cetostearyl alcohol, butylated hydroxytoluene (BHT), butylparaben, light mineral oil, propylparaben, purified water, safflower oil, sodium citrate, and white petrolatum.
What does Locoid look like?
What are the available doses of Locoid?
Lotion, 0.1% (1 mg/g) supplied in bottles of 2 fl. oz. and 4 fl. oz. ()
What should I talk to my health care provider before I take Locoid?
How should I use Locoid?
LOCOID Lotion is indicated for the topical treatment of mild to moderate atopic dermatitis in patients 3 months of age and older.
Apply a thin layer to the affected skin areas two times daily and rub in gently. Do not apply LOCOID Lotion in the diaper area unless directed by a physician.
Discontinue therapy when control is achieved. If no improvement is seen within 2 weeks, reassessment of the diagnosis may be necessary. Before prescribing for more than 2 weeks, any additional benefits of extending treatment to 4 weeks should be weighed against the risk of HPA axis suppression and local adverse events. The safety and efficacy of LOCOID Lotion has not been established beyond 4 weeks of use .
Do not use LOCOIDLotion with occlusive dressings unless directed by a physician. Avoid use in the diaper area, as diapers or plastic pants may constitute occlusive dressings.
LOCOID Lotion is not for oral, ophthalmic, or intravaginal use.
What interacts with Locoid?
Sorry No Records found
What are the warnings of Locoid?
Sorry No Records found
What are the precautions of Locoid?
Sorry No Records found
What are the side effects of Locoid?
Sorry No records found
What should I look out for while using Locoid?
None.
What might happen if I take too much Locoid?
Sorry No Records found
How should I store and handle Locoid?
Store at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F) LOCOID Lotion, 0.1% is white to off-white in color and supplied in bottles of 2 fl. oz. (NDC 16781-392-02) and 4 fl. oz. (NDC 16781-392-04).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature]. Protect from freezing.LOCOID Lotion, 0.1% is white to off-white in color and supplied in bottles of 2 fl. oz. (NDC 16781-392-02) and 4 fl. oz. (NDC 16781-392-04).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature]. Protect from freezing.
Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
Topical corticosteroids share anti-inflammatory, antipruritic, and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical corticosteroids is unclear. However, corticosteroids are thought to act by the induction of phospholipase A inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A.
Non-Clinical Toxicology
None.Furosemide may increase the ototoxic potential of aminoglycoside antibiotics, especially in the presence of impaired renal function. Except in life-threatening situations, avoid this combination.
Furosemide should not be used concomitantly with ethacrynic acid because of the possibility of ototoxicity. Patients receiving high doses of salicylates concomitantly with furosemide, as in rheumatic disease, may experience salicylate toxicity at lower doses because of competitive renal excretory sites.
There is a risk of ototoxic effects if cisplatin and furosemide are given concomitantly. In addition, nephrotoxicity of nephrotoxic drugs such as cisplatin may be enhanced if furosemide is not given in lower doses and with positive fluid balance when used to achieve forced diuresis during cisplatin treatment.
Furosemide has a tendency to antagonize the skeletal muscle relaxing effect of tubocurarine and may potentiate the action of succinylcholine.
Lithium generally should not be given with diuretics because they reduce lithium's renal clearance and add a high risk of lithium toxicity.
Furosemide combined with angiotensin converting enzyme inhibitors or angiotensin II receptor blockers may lead to severe hypotension and deterioration in renal function, including renal failure. An interruption or reduction in the dosage of furosemide, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers may be necessary.
Potentiation occurs with ganglionic or peripheral adrenergic blocking drugs.
Furosemide may decrease arterial responsiveness to norepinephrine. However, norepinephrine may still be used effectively.
Simultaneous administration of sucralfate and furosemide tablets may reduce the natriuretic and antihypertensive effects of furosemide. Patients receiving both drugs should be observed closely to determine if the desired diuretic and/or antihypertensive effect of furosemide is achieved. The intake of furosemide and sucralfate should be separated by at least two hours.
In isolated cases, intravenous administration of furosemide within 24 hours of taking chloral hydrate may lead to flushing, sweating attacks, restlessness, nausea, increase in blood pressure, and tachycardia. Use of furosemide concomitantly with chloral hydrate is therefore not recommended.
Phenytoin interferes directly with renal action of furosemide. There is evidence that treatment with phenytoin leads to decrease intestinal absorption of furosemide, and consequently to lower peak serum furosemide concentrations.
Methotrexate and other drugs that, like furosemide, undergo significant renal tubular secretion may reduce the effect of furosemide. Conversely, furosemide may decrease renal elimination of other drugs that undergo tubular secretion. High-dose treatment of both furosemide and these other drugs may result in elevated serum levels of these drugs and may potentiate their toxicity as well as the toxicity of furosemide.
Furosemide can increase the risk of cephalosporin-induced nephrotoxicity even in the setting of minor or transient renal impairment.
Concomitant use of cyclosporine and furosemide is associated with increased risk of gouty arthritis secondary to furosemide-induced hyperurecemia and cyclosporine impairment of renal urate excretion.
High doses (> 80 mg) of furosemide may inhibit the binding of thyroid hormones to carrier proteins and result in transient increase in free thyroid hormones, followed by an overall decrease in total thyroid hormone levels.
One study in six subjects demonstrated that the combination of furosemide and acetylsalicylic acid temporarily reduced creatinine clearance in patients with chronic renal insufficiency. There are case reports of patients who developed increased BUN, serum creatinine and serum potassium levels, and weight gain when furosemide was used in conjunction with NSAIDs.
Literature reports indicate that coadministration of indomethacin may reduce the natriuretic and antihypertensive effects of furosemide in some patients by inhibiting prostaglandin synthesis. Indomethacin may also affect plasma renin levels, aldosterone excretion, and renin profile evaluation. Patients receiving both indomethacin and furosemide should be observed closely to determine if the desired diuretic and/or antihypertensive effect of furosemide is achieved.
Systemic effects of topical corticosteroids may include reversible HPA axis suppression, manifestations of Cushing’s syndrome, hyperglycemia, and glucosuria.
Studies conducted in pediatric subjects demonstrated reversible HPA axis suppression after use of LOCOID Lotion. Pediatric patients may be more susceptible than adults to systemic toxicity from equivalent doses of LOCOID Lotion due to their larger skin-surface-to-body-mass ratios
Patients applying a topical corticosteroid to a large surface area or to areas under occlusion should be considered for periodic evaluation of the HPA axis. This may be done by using cosyntropin (ACTH1-24) stimulation testing (CST).
Minimize systemic corticosteroid effects by mitigating the risk factors for increased systemic absorption and using LOCOIDLotion as recommended [].
If HPA axis suppression is noted, the frequency of application should be reduced or the drug should be withdrawn, or a less potent corticosteroid should be substituted. Signs and symptoms of glucocorticosteroid insufficiency may occur, requiring supplemental systemic corticosteroids
The following adverse reactions are discussed in greater detail in other sections of the labeling:
Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
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