Prednisone 20 mg para que es. Paciente em uso prolongado de corticoide oral: quando/como fazer a retirada gradual?
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- Prednisone 20 mg para que es
- Prednisone 20 mg para que es
This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine kinase may occur.
Clinical improvement or recovery after stopping corticosteroids may require weeks to years. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations.
Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored. Patients should be warned not to discontinue the use of corticosteroids abruptly or without medical supervision.
As prolonged use may cause adrenal insufficiency and make patients dependent on corticosteroids, they should advise any medical attendants that they are taking corticosteroids and they should seek medical advice at once should they develop an acute illness including fever or other signs of infection.
Following prolonged therapy, withdrawal of corticosteroids may result in symptoms of the corticosteroid withdrawal syndrome including, myalgia, arthralgia, and malaise. Persons who are on corticosteroids should be warned to avoid exposure to chickenpox or measles. Patients should also be advised that if they are exposed, medical advice should be sought without delay.
When corticosteroids are administered concomitantly with potassium-depleting agents e. In addition, there have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure. Concomitant use of anticholinesterase agents e. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. If concomitant therapy must occur, it should take place under close supervision and the need for respiratory support should be anticipated.
Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required.
Serum concentrations of isoniazid may be decreased. Since systemic steroids, as well as bupropion, can lower the seizure threshold, concurrent administration should be undertaken only with extreme caution; low initial dosing and small gradual increases should be employed. Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently.
Convulsions have been reported with this concurrent use. Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. Post-marketing surveillance reports indicate that the risk of tendon rupture may be increased in patients receiving concomitant fluoroquinolones e.
Tendon rupture can occur during or after treatment with quinolones. Drugs which inhibit CYP 3A4 e. Glucocorticoids are moderate inducers of CYP 3A4. Co-administration with other drugs that are metabolized by CYP 3A4 e.
In addition, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal. Concomitant use of aspirin or other nonsteroidal anti-inflammatory agents and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids; this could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn.
In post-marketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control.
Phenytoin has been demonstrated to increase the hepatic metabolism of corticosteroids, resulting in a decreased therapeutic effect of the corticosteroid. Increased doses of quetiapine may be required to maintain control of symptoms of schizophrenia in patients receiving a glucocorticoid, a hepatic enzyme inducer.
Co-administration with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use. Patients on corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. No adequate studies have been conducted in animals to determine whether corticosteroids have a potential for carcinogenesis or mutagenesis.
Steroids may increase or decrease motility and number of spermatozoa in some patients. Corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring. There are no adequate and well-controlled studies in pregnant women.
Corticosteroids should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Infants born to mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
Systemically administered corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Because of the potential for serious adverse reactions in nursing infants from corticosteroids, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
The efficacy and safety of corticosteroids in the pediatric population are based on the well-established course of effect of corticosteroids, which is similar in pediatric and adult populations. Other indications for pediatric use of corticosteroids, e.
Like adults, pediatric patients should be carefully observed with frequent measurements of blood pressure, weight, height, intraocular pressure, and clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.
Pediatric patients who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in their growth velocity. This negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of hypothalamic-pituitary-adrenal HPA axis suppression i.
Growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of HPA axis function. The linear growth of pediatric patients treated with corticosteroids should be monitored, and the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of treatment alternatives.
In order to minimize the potential growth effects of corticosteroids, pediatric patients should be titrated to the lowest effective dose. Clinical studies did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects.
Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. In particular, the increased risk of diabetes mellitus, fluid retention and hypertension in elderly patients treated with corticosteroids should be considered.
Cardiovascular System bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive heart failure, ECG changes caused by potassium deficiency, edema, fat embolism, hypertension or aggravation of hypertension, hypertrophic cardiomyopathy in premature infants, myocardial rupture following recent myocardial infarction see WARNINGS: Cardio-Renal , necrotizing angiitis, pulmonary edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis.
Endocrine Adrenal insufficiency-greatest potential caused by high potency glucocorticoids with long duration of action associated symptoms include; arthralgias, buffalo hump, dizziness, life-threatening hypotension, nausea, severe tiredness or weakness , amenorrhea, postmenopausal bleeding or other menstrual irregularities, decreased carbohydrate and glucose tolerance, development of cushingoid state, diabetes mellitus new onset or manifestations of latent , glycosuria, hyperglycemia, hypertrichosis, hyperthyroidism see WARNINGS: Endocrine , hypothyroidism, increased requirements for insulin or oral hypoglycemic agents in diabetics, lipids abnormal, moon face, negative nitrogen balance caused by protein catabolism, secondary adrenocortical and pituitary unresponsiveness particularly in times of stress, as in trauma, surgery or illness see WARNINGS: Endocrine , suppression of growth in pediatric patients.
Fluid and Electrolyte Disturbances congestive heart failure in susceptible patients, fluid retention, hypokalemia, hypokalemic alkalosis, metabolic alkalosis, hypotension or shock-like reaction, potassium loss, sodium retention with resulting edema. Gastrointestinal abdominal distention, abdominal pain, anorexia which may result in weight loss, constipation, diarrhea, elevation in serum liver enzyme levels usually reversible upon discontinuation , gastric irritation, hepatomegaly, increased appetite and weight gain, nausea, oropharyngeal candidiasis, pancreatitis, peptic ulcer with possible perforation and hemorrhage, perforation of the small and large intestine particularly in patients with inflammatory bowel disease , ulcerative esophagitis, vomiting.
Gastric irritation may be reduced if taken before, during, or immediately after meals or with food or milk. The maximal activity of the adrenal cortex is between 2 am and 8 am, and it is minimal between 4 pm and midnight. Exogenous corticosteroids suppress adrenocorticoid activity the least when given at the time of maximal activity am for single dose administration. Therefore, it is recommended that prednisone be administered in the morning prior to 9 am and when large doses are given, administration of antacids between meals to help prevent peptic ulcers.
Multiple dose therapy should be evenly distributed in evenly spaced intervals throughout the day. Do not stop taking this medicine without first talking to your doctor. Avoid abrupt withdraw of therapy. The initial dosage of PredniSONE Tablets may vary from 5 mg to 60 mg per day, depending on the specific disease entity being treated. In situations of less severity lower doses will generally suffice, while in selected patients higher initial doses may be required.
The initial dosage should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period of time there is a lack of satisfactory clinical response, PredniSONE should be discontinued and the patient transferred to other appropriate therapy. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small increments at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response is reached.
It should be kept in mind that constant monitoring is needed in regard to drug dosage. Included in the situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient's individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment; in this latter situation, it may be necessary to increase the dosage of PredniSONE for a period of time consistent with the patient's condition.
If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly. In the treatment of acute exacerbations of multiple sclerosis daily doses of mg of prednisolone for a week followed by 80 mg every other day for 1 month have been shown to be effective.
Dosage range is the same for prednisone and prednisolone. Alternate day therapy is a corticosteroid dosing regimen in which twice the usual daily dose of corticoid is administered every other morning. The purpose of this mode of therapy is to provide the patient requiring long-term pharmacologic dose treatment with the beneficial effects of corticoids while minimizing certain undesirable effects, including pituitary-adrenal suppression, the Cushingoid state, corticoid withdrawal symptoms, and growth suppression in children.
The rationale for this treatment schedule is based on two major premises: a the anti-inflammatory or therapeutic effect of corticoids persists longer than their physical presence and metabolic effects and b administration of the corticosteroid every other morning allows for re-establishment of more nearly normal hypothalamic-pituitary-adrenal HPA activity on the off-steroid day.
A brief review of the HPA physiology may be helpful in understanding this rationale. Consult your doctor before breast-feeding. Drug interactions may change how your medications work or increase your risk for serious side effects. This document does not contain all possible drug interactions. Do not start, stop, or change the dosage of any medicines without your doctor's approval. If your doctor has directed you to take low-dose aspirin for heart attack or stroke prevention usually milligrams a day , you should continue taking it unless your doctor instructs you otherwise.
Ask your doctor or pharmacist for more details. This medication may interfere with certain laboratory tests including skin tests , possibly causing false test results. Make sure laboratory personnel and all your doctors know you use this drug. If someone has overdosed and has serious symptoms such as passing out or trouble breathing, call Otherwise, call a poison control center right away. US residents can call their local poison control center at Canada residents can call a provincial poison control center.
Consult your doctor for more details. This medication may cause bone problems osteoporosis when taken for an extended time. Lifestyle changes that may help reduce the risk of bone problems include doing weight-bearing exercise, getting enough calcium and vitamin D, stopping smoking, and limiting alcohol. Discuss with your doctor lifestyle changes that might benefit you. If you are taking this medication daily and miss a dose, take it as soon as you remember.
If it is near the time of the next dose, skip the missed dose. Take your next dose at the regular time. Do not double the dose to catch up. If you are taking this medication on a different schedule than a daily one such as every other day , ask your doctor ahead of time about what you should do if you miss a dose. Store at room temperature away from light and moisture. Do not store in the bathroom. Keep all medications away from children and pets.
Do not flush medications down the toilet or pour them into a drain unless instructed to do so. Properly discard this product when it is expired or no longer needed. Consult your pharmacist or local waste disposal company. Your condition can cause complications in a medical emergency. This information does not assure that this product is safe, effective, or appropriate for you. This information is not individual medical advice and does not substitute for the advice of your health care professional.
Always ask your health care professional for complete information about this product and your specific health needs. This copyrighted material has been downloaded from a licensed data provider. The above information is intended to supplement, not substitute for, the expertise and judgment of your health care professional. You should consult your health care professional before taking any drug, changing your diet, or commencing or discontinuing any course of treatment.
Want to stay signed on? We are unable to switch you to this area of care. Pero hay ciertos factores que pueden aumentar el riesgo de adquirirla. La probabilidad de tener gota es mayor si la han tenido otras personas en la familia. Este medicamento puede ser:. Este resumen fue preparado por el John M. Personas con gota aportaron sus opiniones sobre este resumen.
Internet Citation: Consumer Summary: Control de la gota. Content last reviewed November Effective Health Care Program. Search small Search. Control de la gota.
Son los estudios sobre el tema publicados hasta marzo de La gota es un tipo de artritis. Pero puede volver a ocurrir un ataque. Alrededor de ocho millones de personas tienen gota en Estados Unidos. No se conoce la causa exacta de la gota. Pero hay ciertos factores que pueden aumentar el riesgo de adquirirla. La probabilidad de tener gota es mayor si la han tenido otras personas en la familia.
Este medicamento puede ser:. Este resumen fue preparado por el John M. Personas con gota aportaron sus opiniones sobre este resumen. Internet Citation: Consumer Summary: Control de la gota. Content last reviewed November Effective Health Care Program. Search small Search. Control de la gota.
Download PDF files for this report here. Table of Contents. La colchicina reduce el dolor del ataque de gota. De hecho, estos medicamentos pueden aumentar el riesgo de un ataque de gota cuando empiezan a tomarse por primera vez.
Topic Initiated. Research Protocol Archived. Systematic Review Archived. Consumer Summary Archived. Clinician Summary Archived. Manejo del insomnio. Tratamientos no invasivos para el dolor lumbar. Programas conductuales para ayudar a controlar la diabetes tipo 1. Page last reviewed November Back to Top. Tomar colchicina en una cantidad mayor que la prescrita puede causar sobredosis y muerte.
En casos muy raros, el alopurinol y el febuxostat causan reacciones graves de la piel que pueden poner en peligro la vida.
Prednisone part mg que el sirve medicamento lowest prices on. Price $ for One dose prednisone 5 mg and increases blood flow. Para que sirve la medicina prednisone 20 mg best. Buy secure from $ x dose prednisone 40 mg without a rx. Para que sirve el jarabe bersen prednisone 20 mg. Effects of from $ for dose prednisone 20 mg non prescription. Learn about prednisone, potential side effects, proper use and dosing, Pricing based on most commonly-filled versions: 10 tablets of prednisone 20mg. prednisone 20 mg tablet. Color: white. Shape: round. Imprint: PD This medicine is a white, round, scored. No se conoce la causa exacta de la gota.If you are a consumer or patient please visit this version. Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract. Prednisone is a white to practically white, odorless, crystalline powder. It is very slightly soluble in water; slightly soluble in alcohol, chloroform, dioxane, and methanol.
The chemical name for prednisone is pregna-1,4-diene-3,11,trione monohydrate,17,dihydroxy-. The structural formula is represented below:. Inactive ingredients: 1 mg — colloidal silicon dioxide, lactose monohydrate, magnesium stearate, pregelatinized starch, sodium starch glycolate; 2. Naturally occurring glucocorticoids hydrocortisone and cortisone , which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states.
Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli. Prednisone tablets are contraindicated in systemic fungal infections and known hypersensitivity to components. Increased dosage of rapidly acting corticosteroids is indicated in patients on corticosteroid therapy subjected to any unusual stress before, during and after the stressful situation.
Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary.
All corticosteroids increase calcium excretion. Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction; therefore, therapy with corticosteroids should be used with great caution in these patients.
Corticosteroids can produce reversible hypothalamic-pituitary adrenal HPA axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment. Adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage.
This type of relative insufficiency may persist for up to 12 months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. If the patient is receiving steroids already, dosage may have to be increased.
Metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased in hyperthyroid patients. Changes in thyroid status of the patient may necessitate adjustment in dosage.
Patients who are on corticosteroids are more susceptible to infections than are healthy individuals. There may be decreased resistance and inability to localize infection when corticosteroids are used.
Infection with any pathogen viral, bacterial, fungal, protozoan or helminthic in any location of the body may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect cellular immunity, humoral immunity, or neutrophil function. With increasing doses of corticosteroids, the rate of occurrence of infectious complications increases.
Corticosteroids may exacerbate systemic fungal infections and therefore should not be used in the presence of such infections unless they are needed to control life-threatening drug reactions. Latent disease may be activated or there may be an exacerbation of intercurrent infections due to pathogens, including those caused by Amoeba, Candida, Cryptococcus, Mycobacterium, Nocardia, Pneumocystis, Toxoplasma.
It is recommended that latent amebiasis or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent time in the tropics or any patient with unexplained diarrhea. Similarly, corticosteroids should be used with great care in patients with known or suspected Strongyloides threadworm infestation. In such patients, corticosteroid-induced immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.
The use of prednisone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for management of the disease in conjunction with an appropriate antituberculous regimen.
If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis. Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Killed or inactivated vaccines may be administered. However, the response to such vaccines may be diminished and cannot be predicted.
Indicated immunization procedures may be undertaken in patients receiving nonimmunosuppressive doses of corticosteroids as replacement therapy e. Chickenpox and measles can have a more serious or even fatal course in pediatric and adult patients on corticosteroids. In pediatric and adult patients who have not had these diseases, particular care should be taken to avoid exposure. How the dose, route and duration of corticosteroid administration affect the risk of developing a disseminated infection is not known.
If exposed to chickenpox, prophylaxis with varicella zoster immune globulin VZIG may be indicated. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin IG may be indicated. If chickenpox develops, treatment with antiviral agents may be considered. Use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to bacteria, fungi or viruses.
The use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. Corticosteroids should not be used in active ocular herpes simplex because of possible corneal perforation. The lowest possible dose of corticosteroids should be used to control the condition under treatment. When reduction in dosage is possible, the reduction should be gradual. Discontinuation of corticosteroids may result in clinical improvement. As sodium retention with resultant edema and potassium loss may occur in patients receiving corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for up to 12 months after discontinuation of therapy following large doses for prolonged periods; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. Steroids should be used with caution in active or latent peptic ulcers, diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative colitis, since they may increase the risk of a perforation.
Signs of peritoneal irritation following gastrointestinal perforation in patients receiving corticosteroids may be minimal or absent. There is an enhanced effect due to decreased metabolism of corticosteroids in patients with cirrhosis. Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation i. This, together with a decrease in the protein matrix of the bone secondary to an increase in protein catabolism, and reduced sex hormone production, may lead to inhibition of bone growth in pediatric patients and the development of osteoporosis at any age.
Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed. Special consideration should be given to patients at increased risk of osteoporosis e. Inclusion of therapy for osteoporosis prevention or treatment should be considered. To minimize the risk of glucocortoicoid-induced bone loss, the smallest possible effective dosage and duration should be used.
Lifestyle modification to reduce the risk of osteoporosis e. Calcium and vitamin D supplementation, bisphosphonate e. Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, they do not show that they affect the ultimate outcome or natural history of the disease.
The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect. An acute myopathy has been observed with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission e.
This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored. Patients should be warned not to discontinue the use of corticosteroids abruptly or without medical supervision. As prolonged use may cause adrenal insufficiency and make patients dependent on corticosteroids, they should advise any medical attendants that they are taking corticosteroids and they should seek medical advice at once should they develop an acute illness including fever or other signs of infection.
Following prolonged therapy, withdrawal of corticosteroids may result in symptoms of the corticosteroid withdrawal syndrome including, myalgia, arthralgia, and malaise. Persons who are on corticosteroids should be warned to avoid exposure to chickenpox or measles. Patients should also be advised that if they are exposed, medical advice should be sought without delay.
When corticosteroids are administered concomitantly with potassium-depleting agents e. In addition, there have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure. Concomitant use of anticholinesterase agents e.
If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. If concomitant therapy must occur, it should take place under close supervision and the need for respiratory support should be anticipated. Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports.
Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required.
Serum concentrations of isoniazid may be decreased. Since systemic steroids, as well as bupropion, can lower the seizure threshold, concurrent administration should be undertaken only with extreme caution; low initial dosing and small gradual increases should be employed. Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently.
Convulsions have been reported with this concurrent use. Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. Post-marketing surveillance reports indicate that the risk of tendon rupture may be increased in patients receiving concomitant fluoroquinolones e. Tendon rupture can occur during or after treatment with quinolones. Drugs which inhibit CYP 3A4 e.
Glucocorticoids are moderate inducers of CYP 3A4.
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