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Several studies on adrenal steroids with glucocorticoid activity have led to the synthesis of new molecules characterized by high anti-inflammatory potency and low incidence of side effects. Safety issues are particularly relevant in some populations on long-term therapy with corticosteroids, such as children and adolescents, in whom steroid therapy may result in growth retardation and behavioral disorders, as well as in somewhat "fragile" individuals such as politreated elderly patients.
Deflazacort is a recent synthetic glucocorticoid characterized by high efficacy and good tolerability, as demonstrated by several clinical studies that have evaluated its therapeutic efficacy and safety of use. In comparison to older corticosteroids, deflazacort shows a high anti-inflammatory and immunosuppressive activity, and a lower interference on glucose metabolism, on phosphocalcium metabolism hence, on growth and bone turnover , and on HPA axis functionality, as well as a minimal or absent sodium-retention effect.
These characteristics are favourable and suggest that deflazacort can be used safely even in pediatric and elderly populations. Furthermore, deflazacort shows a high dosage flexibility, due to its wide therapeutic index; in fact, the initial oral daily dosage of deflazacort in adults ranges from 6 to 90 mg, depending on the severity and progression of the specific disease to be treated.
The precise knowledge of the characteristics and physiological effects of corticosteroids can assist in the correct choice of the drug, avoiding potential problems due to its inappropriate use. Therefore, the exact quantification of the equipotency ratios between steroids is an important aspect to consider when using these drugs for long periods of time. At present there are few if any clinical reasons for preferentially using any steroid drug and therefore clinical experience, bioavailability and bio-pharmaceutical factors clearly affect choice of steroid for a given medical condition; however, knowing the relative potencies and equivalent doses of corticosteroids in clinical practice is useful.
We suggest that the new table for the conversion of corticosteroid doses presented in this paper, which for the first time includes deflazacort, could provide an aid to physicians when selecting the appropriate dosage of corticosteroids to be used in clinical practice.
The evaluation of deflazacort dose range and its therapeutic effectiveness in comparison with other corticosteroids could be improved by a specific meta-analysis; indeed, we hope that this paper could stimulate other Authors to conduct a meta-analysis on these topics.
Schimmer B, Parker K. Adrenocorticotropic hormone; adrenocortical steroids and their synthetic analogs; inhibitors of the synthesis and actions of adrenocortical hormones. New York: McGraw-Hill; Spectrophotometric and HPLC determination of deflazacort in pharmaceutical dosage forms.
Braz J Pharm Sci. Markham A, Bryson HM. A review of its pharmacological properties and therapeutic efficacy. Pharmacokinetics and metabolism of Deflazacort in the rat, dog, monkey and man. Adv Exp Med Biol. Luzzani F, Glasser A. Eur J Pharmacology. Deflazacort — Riassunto delle Caratteristiche del Prodotto. Accessed on 12 Sept Randomized, double-blind trial of deflazacort versus prednisone in juvenile chronic or rheumatoid arthritis: a relatively bone-sparing effect of deflazacort.
Long-term therapy with deflazacort in chronic sarcoidosis. Long term treatment of polymyalgia rheumatica with deflazacort. Ann Rheum Dis. Deflazacort modulates the fibrinolytic pattern and reduces uPA-dependent chemioinvasion and proliferation in rheumatoid arthritis synoviocytes. An Pediatr Barc. Effects of deflazacort versus prednisone on bone mass, body composition, and lipid profile: a randomized, double blind study in kidney transplant patients.
J Clin Endocrinol Metab. Effect of deflazacort versus methylprednisone on growth, body composition, lipid profile, and bone mass after renal transplantation. Pediatr Nephrol. Effects of long-term maintenance therapy with a new glucocorticoid, deflazacort, on mineral metabolism and statural growth.
Calcif Tissue Int. Change in glucose metabolism after long-term treatment with deflazacort and betamethasone. Eur J Clin Pharmacol. Comparison of growth retarding effects induced by two different glucocorticoids in prepubertal children: an interim long-term analysis. Calcif Tiss Int.
Glucose intolerance after short-term administration of corticosteroids in healthy subjects. Prednisone, deflazacort, and betamethasone. Arch Intern Med. Zoorob RJ, Cender D.
A Different Look at Corticosteroids. Am Fam Physician. Flinn M. Adrenal Cortical Steroids. In: Hebel SK, editor. Drug Facts and Comparisons. Louis: Facts and Comparisons, Inc.
Google Scholar. Saviola G, Abdi. Ali L, Shams. Compared clinical efficacy and bone metabolic effects of low-dose deflazacort and methylprednisolone in male inflammatory arthropathies: a month open randomized pilot study. Nayak S, Acharjya B. Deflazacort versus other glucocorticoids: a comparison. Indian J Dermatol. Download references. You can also search for this author in PubMed Google Scholar.
Correspondence to Luca Parente. Reprints and Permissions. Parente, L. Deflazacort: therapeutic index, relative potency and equivalent doses versus other corticosteroids. BMC Pharmacol Toxicol 18 , 1 Complaint Form. Marketing Your Practice. Member-Only Marketing Resources. State Liaison Program. Apply to Become a State Liaison.
Position Statements. Action Center. Contact Your Legislators. Manage a Fellowship. Neuromuscular Medicine Fellowship Portal. Neurology 87, November 15, Submitted by Leigh Maria K. This was a phase III double blind placebo controlled study in 2 phases over the course of 52 weeks and included patients diagnosed with a dystrophinopathy either by genetic testing or muscle biopsy.
This multicenter trial initially had 4 groups to include a placebo group in the first phase of 12 weeks, then 3 treatment groups 1. Patients were between years old and could be either ambulatory or nonambulatory. The purpose of this study was to evaluate the safety and efficacy of deflazacort vs. The primary endpoint of this study was change from baseline of muscle strength based on the Medical Research Council scale.
The results demonstrated that in the first 12 weeks, compared to placebo, all three treatment arms demonstrated increased average muscle strength. The interval from weeks demonstrated a greater preservation of muscle strength of the high and low dose deflazacort arms compared to the prednisone arm. Overall, at week 52, there was greater preservation of muscle strength of the high and low dose deflazacort arms compared to the prednisone arm.
The actual glucocorticoid dosage was, in fact, much higher than the preplanned schedule, because physicians adjusted the dose visit after visit according to clinical status and creatinine levels to be on the safe side and to avoid a rejection crisis. Despite this individual dose adjustment, the daily and cumulative doses administered were strictly equivalent in both groups according to the 1. One can argue that the study lacks statistical power to be really conclusive.
Due to fewer graft donors than foreseen, the planned sample size of 60 could not be achieved. However, our results for bone density of the PRED group are perfectly consistent with previous studies of kidney transplant patients receiving that drug showing predominant bone loss at lumbar spine and relative bone preservation at limbs 5 , Julian et al.
In the present study, lumbar and whole body BMD decreased by 9. A bone-sparing effect of DEFLA at the level of lumbar spine has been described in various clinical situations. In a 1-yr double blind prospective study of patients with the nephrotic syndrome, bone loss induced by PRED at the lumbar spine was 1. In a randomized double blind prospective study of adult men with newly diagnosed rheumatoid arthritis, patients given DEFLA experienced spinal bone loss at one third the rate of that observed in the subjects receiving PRED at equivalent dosage Surprisingly, in our patients serum osteocalcin levels increased in both groups despite decreasing PTH levels.
This finding can be explained by cyclosporin A cotreatment, which is known to increase bone turnover Other researchers have claimed that some of the bone-sparing effect of DEFLA compared to that of PRED could be explained by a less impaired intestinal calcium absorption by the former Fat accumulation is a well known side-effect of glucocorticoid therapy as a consequence of peripheral resistance to insulin with decreased glucose tolerance and increased serum levels of triglycerides.
As a consequence, triglycerides increased less in the DEFLA-treated patients, although fasting blood glucose and hemoglobin A 1 c levels were similar in the treatment groups. In renal transplant patients, Elli et al. Lean body mass decreased early after grafting in both groups, probably due to a reduction in the degree of hydration of those patients 33 rather than to decreased muscle mass.
This hypothesis is supported by the lack of correlation between changes in lean body mass and those in creatinine excretion. It may also contribute to the prevention of coronary heart disease by lesser impairment of the lipid profile compared with PRED.
We thank Ms. Elisabeth Dijkhuis for her invaluable contribution as the coordinator of the study. This work was supported by a grant from Hoechst Marion Roussel, Inc. Sambrook PN , Jones G. Br J Rheum. Google Scholar. Harman JB. Olefsky JM , Kimmerling G. Am J Med Sci. Eur J Clin Invest. J Bone Miner Res. J Am Soc Nephrol. Int J Clin Pharmacol Res. Calcif Tissue Int. J Orthop Rheumatol. Gennari C , Imbimbo B. Arch intern Med. J Heart Lung Transplant. Am J Clin Nutr.
Avioli LV. Br J Rheumatol. Curr Therapeutic Res. J Clin Endocrinol Metab. Analysis with monoclonal antibodies. Adv Exp Med Biol. J Rheumatol. N Engl J Med. Copenhagen: Osteopress; vol 2 : — Comparison of the effect of prednisone and deflazacort. Clin Rheumatol. Gennari C. Br J Radiol. Oxford University Press is a department of the University of Oxford.
It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Endocrine Society Journals. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Subjects and Methods. Journal Article. Kurt Lippuner , Kurt Lippuner.
Oxford Academic. Jean-Paul Casez. Fritz F. Philippe Jaeger. Revision received:.
Metrics details. Deflazacort is a synthetic corticosteroid characterized by a favourable pharmacokinetic profile, peculiar pharmacodynamic properties and a good safety profile. However, to the best of our knowledge, no dose-conversion table based on direct comparison of relative potencies between deflazacort and other main corticosteroids is currently available in scientific literature.
This paper, while reporting a brief review of deflazacort pharmacological properties, its efficacy and tolerability in different clinical areas, has been designed with the specific aim of providing a new dose-conversion table of corticosteroids, including for the first time also deflazacort.
We suggest that this new conversion table could be a useful tool for physicians who need to select the appropriate dose of deflazacort in their clinical practice. Peer Review reports. Corticosteroids are hormones with 21 carbon atoms; they are secreted by the adrenal cortex and are traditionally divided into two main groups: glucocorticoids and mineralocorticoids.
This distinction is based on their preferential biological activity, i. The main glucocorticoid produced by the adrenal cortex is cortisol also known as hydrocortisone ; the main mineralocorticoid hormone is aldosterone. The potency of corticosteroids on carbohydrate metabolism is closely related to their anti-inflammatory potency, as the activation of the same glucocorticoid receptor is responsible for both metabolic and anti-inflammatory effects.
However, classification of corticosteroids into glucocorticoids and mineralocorticoids should not be seen as a strict rule; for example, it has been shown that corticosteroids classified in one group can also perform, in addition to their specific biological activities, certain activities that are typical of the other group, although to a lesser extent.
Accordingly, some steroids predominantly classified as glucocorticoids, such as cortisol and prednisone a synthetic corticosteroidalso have a moderate, but significant, mineralocorticoid activity; similarly, fludrocortisone, a synthetic corticosteroid with a high mineralocorticoid potency, also exhibits a moderate glucocorticoid activity [ 1 ].
Furthermore, activation of glucocorticoid receptor or mineralocorticoid receptor in the human body does not rely only on the structure of the drugs, but also on additional factors, including drug metabolism by beta-hydroxydehydrogenase enzyme, which then can affect drug concentration both in the bloodstream and target tissues.
The anti-inflammatory action of corticosteroids is the main reason for their use as therapeutic agents. In its early stages, the scientific research on corticosteroids was oriented towards the synthesis of novel compounds characterized by a higher anti-inflammatory potency than cortisone, with a lower incidence of side effects.
This initially led to the development of synthetic glucocorticoids, such as prednisolone and prednisone, characterized by a higher anti-inflammatory potency than natural steroids, with a mineralocorticoid activity reduced approximately by a half. Subsequently, other corticosteroids were synthetized, including fluorinated glucocorticoids such as dexamethasone.
Even though these drugs are devoid of mineralocorticoid activity, some typical adverse events associated with their prolonged use have been reported. For example, safety issues are relevant in children and adolescents, where steroid therapy may result in behavioral disturbances and growth retardation due to a not yet fully understood mechanism, which probably involves abnormalities in GH releaseand in elderly patients, where the risk of steroid side effects may be enhanced by the frequent presence of comorbidities requiring pharmacological polytherapy.
More recently, other corticosteroids, including deflazacort, have been synthetized with the main aim of making available new agents that are better tolerated in each age group. Deflazacort is a heterocyclic corticosteroid, oxazoline-derivative of prednisolone [ 2 ], characterized by high efficacy and good tolerability, as demonstrated by the results of several clinical studies that have evaluated its therapeutic activity and safety in conditions where corticosteroid treatment is indicated.
Presently, extensive clinical experience has been gained on the efficacy of deflazacort in rheumatic diseases in adults and children, as well as in respiratory, renal, and hematologic diseases. However, to the best of our knowledge, no complete dose-conversion table, based on direct comparisons of the relative potencies of deflazacort and other commonly used corticosteroids, is currently available in scientific literature.
In this paper, we briefly review some of the most relevant clinical trials on deflazacort, showing its efficacy and tolerability; furthermore, we propose a new table for the conversion of corticosteroid doses, elaborated from available literature data, including both deflazacort and other common steroids used in clinical practice. Deflazacort is a synthetic corticosteroid, characterized by the insertion of a methyl-oxazoline ring in the chemical structure of prednisolone acetate [ 3 ] Fig.
Chemical structures of prednisolone and deflazacort [ 3 ]. After oral administration, deflazacort is rapidly and completely absorbed in the intestinal tract peak plasma concentration is reached within 1—2 hours.
Subsequently, deflazacort is deacetylated at position 21 to form the main active metabolite, i. An almost complete elimination of deflazacort metabolites is reached within 24 hours, mainly through the kidneys [ 4 ].
Glucocorticoids have immunosuppressive and anti-inflammatory properties, both primarily related to the antagonism of specific leukocyte functions and to the inhibition of the synthesis of pro-inflammatory cytokines.
In vitro, deflazacort significantly inhibits both the proliferation of mononuclear cells derived from human peripheral blood, and the release of inflammatory cytokines by these cells. Deflazacort is also able to inhibit chemotaxis, superoxide anion generation and chemiluminescence of human polymorphonuclear leukocytes in vitro [ 3 ].
Studies carried out using different experimental models indicate that deflazacort is an effective inhibitor of the early exudative phase of inflammation, as well as of the development of chronic granulomatous inflammation.
Furthermore, deflazacort has been shown to inhibit experimentally-induced chronic inflammatory articular disease i. Studies carried out to evaluate glucocorticoids ability to induce glycogen deposition in the liver of surrenectomized rats have shown that deflazacort is able to increase gluconeogenesis and hepatic glycogen synthesis, with a potency of action about 10 times higher than prednisolone administered at equivalent doses. The anti-inflammatory potency of deflazacort is about 10—20 times higher than prednisolone and 40 times higher than cortisol hydrocortisone.
Furthermore, the duration of action of deflazacort anti-inflammatory effects is longer than other glucocorticoids administered at equivalent doses [ 6 ].
Deflazacort has proven to be effective in the treatment of various rheumatological disorders including: sarcoidosis, a chronic systemic disease of unknown etiology, characterized by the formation of granulomas in various organs [ 7 ]; juvenile chronic arthritis, a condition characterized by alternating periods of remission and exacerbation, where deflazacort use resulted in clinical improvements in a group of children with active disease [ 8 ]; polymyalgia rheumatica, which occurs predominantly in elderly patients with pain and stiffness in the shoulder girdle and pelvis, where deflazacort was able to induce a significant improvement of clinical outcome parameters pain intensity and duration of morning stiffness and laboratory parameters, e.
A clinical study, which evaluated deflazacort ability to exert a protective effect on bone erosion and joint damage, typical of RA, has shown that deflazacort is able to inhibit, in a dose-dependent manner, the invasiveness and the proliferation of synoviocytes collected both from patients with RA and healthy volunteers through differential modulation of single components of the fibrinolytic system [ 10 ].
Deflazacort is indicated in steroid treatment of bronchial asthma and in the exacerbations of Chronic Obstructive Pulmonary Disease COPDto control inflammation and increased bronchial reactivity, which are the basis of bronchospasm. The efficacy and tolerability of oral deflazacort in acute moderate asthma in children has been assessed in a prospective, randomized, parallel group trial of children aged 6 to 14 years with a diagnosis of asthma, who presented to the pediatric emergency department for moderate asthma exacerbation.
Patients were evaluated at the start of treatment visit 1on day 2 visit 2 and on day 7 visit 3. Two children out of the 54 enrolled were hospitalized on visit 2 one from each group. Further improvement was observed on visit 3, i. In summary, deflazacort and prednisolone demonstrated similar efficacy in improving pulmonary function and clinical symptoms in the treatment of children with moderate exacerbations of asthma [ 11 ].
Some clinical trials, conducted both in adult and pediatric populations, have evaluated the use of deflazacort in patients undergoing renal transplantation and in patients with nephrotic syndrome. A randomized, double-blind study compared the effects of treatment with deflazacort versus prednisone on Bone Mineral Density BMDon body composition and on lipid profile in 24 adult patients with end-stage renal disease, over a follow-up period of 78 months after kidney transplantation.
Lean body mass decreased by approximately 2. The study concluded that, in kidney-transplanted patients, the use of deflazacort is associated with lesser loss of lumbar spine BMD and whole body BMD compared to prednisone; deflazacort also helps to prevent fat accumulation and lipid profile worsening [ 12 ]. Another randomized, double-blind study compared the effects of treatment with deflazacort 0. The results of this study showed that the maintenance therapy with deflazacort, in comparison with methylprednisone maintenance therapy, is associated with an improved linear growth and also prevents excessive bone loss and fat accumulation in the population of pre-puberal patients [ 13 ].
Nephrotic syndrome, characterized by hypoproteinaemic edema in association with extensive proteinuria, may occur as a result of several underlying kidney diseases, the most common of which are minimal lesion glomerulonephritis and membranous glomerulonephritis. It is known that corticosteroid therapy increases the rate of spontaneous remission in patients with minimal lesion nephrotic syndrome, and has beneficial effects also in focal and segmental glomerulosclerosis.
Clinical trials have demonstrated the efficacy of deflazacort treatment in both adult and pediatric patients with nephrotic syndrome. Two clinical trials found that deflazacort was at least as effective as prednisone in adult patients with idiopathic nephrotic syndrome during a 3-month crossover study as well as in patients with minimal change, membranoproliferative, focal segmental or membranous glomerulonephritis during a month double-blind parallel study [ 3 ].
A clinical complication of nephrotic syndrome is hypogammaglobulinemia due to increased catabolism and urinary loss of immunoglobulin which is associated with a higher risk of infections, mainly caused by encapsulated bacteria. In this respect, some evidence indicate that IgG2-subclass antibodies are protective against this type of microorganisms, so that their loss in nephrotic syndrome is a risk factor for infection. In both treatment groups, a similar return to normal levels of total IgG and IgG1 was observed, but only those patients treated with deflazacort showed a significant improvement in the IgG2 and IgG3 subclasses values [ 14 ].
Another distinctive feature of deflazacort is its smaller influence on carbohydrate metabolism than other glucocorticoids, as demonstrated in both studies conducted on animal models [ 4 ] and in clinical trials [ 1718 ]. Furthermore, the risk of sodium retention and hypokalemia, related to the mineralocorticoid activity of the drug, is greatly reduced with deflazacort in comparison with older synthetic steroids [ 3 ]. Because of its low liposolubility, only a small part of desacetyl-deflazacort, biologically active metabolite of deflazacortcrosses the blood—brain barrier [ 5 ].
Thus, when compared with older corticosteroids, deflazacort has a smaller suppressive effect on hypothalamic-pituitary-adrenal HPA axis, a system that modulate the physiologic response to stressors and regulate glucose and phosphocalcium metabolism and electrolyte balance. Furthermore, given the minor impact of deflazacort on the HPA axis, a reduced risk of behavioral disorders compared to other corticosteroids has been hypothesized.
Deflazacort safety in children is a clinically relevant issue. In fact, when using corticosteroids in pediatric patients, and especially after long-term treatment, one of the most alarming adverse event is linear growth retardation; such event could be due to several mechanisms, the main of which seems to be the inhibition of Growth Hormone GH release from the pituitary gland.
In children receiving long-term steroid treatment after kidney transplantation, the substitution of methylprednisolone mean dose, 0. Deflazacort therapeutic indications include a number of pathological conditions, i. The initial daily dosage of deflazacort in adults may range from 6 to 90 mg, depending on the severity and evolution of the specific disease, and should remain unchanged, or be modified as appropriate, until a satisfactory clinical response is observed.
It should be emphasized that corticosteroid requirements vary from patient to patient, so the dosage should be individualized taking into account the nature of the disease and the patient's therapeutic response. The maintenance dose should always be the minimum dose required to control the symptoms in order to minimize the risk of side effects; in any case, the dose should be reduced gradually [ 6 ].
Corticosteroids were initially introduced in clinical practice in the late '40s, when they began to be used for the treatment of rheumatoid arthritis; since then, corticosteroid therapeutic indications have expanded to various medical areas, including dermatology, rheumatology, immunology and oncology.
Systemic corticosteroids, which are used to treat several pathological conditions, are similar to endogenous steroid hormones produced by the adrenal cortex, i. Although all corticosteroids share, to varying degrees, the properties of both adrenal hormones, some of them e. The precise knowledge of the characteristics and physiological effects of corticosteroids is essential to select the most appropriate drug and to avoid problems due to its inappropriate use; therefore, the equipotency ratios between steroids is an important aspect to be considered in long-term steroid therapy.
The anti-inflammatory potency of cortisol hydrocortisone is conventionally equal to 1; hence, based on the relative potencies of various corticosteroids, it is possible to identify the equivalent doses of every single steroid. Table 3 summarizes the relative potencies and the corresponding equivalent doses of systemic corticosteroids according to available literature data [ 20 ] see next paragraph for deflazacort, as it is not included in this Table.
Short-acting compounds, such as hydrocortisone cortisolshow lower potencies, while intermediate-acting drugs, like prednisone and methylprednisolone, are four to five times more potent than hydrocortisone; dexamethasone, a long-acting corticosteroid, shows a potency about 25 times higher than short-acting compounds. Corticosteroids therapeutic effects may often be associated with side effects, especially when higher doses and long-term treatment are required. To obtain the maximum benefit from therapy, it is important to prevent any potential adverse event by implementing appropriate preventive measures, as far as possible [ 19 ].
However, it should be emphasized that the risk of side effects is not only related to corticosteroid dose and duration of treatment; it also depends on the so-called Drug Therapeutic Index DTIi. In clinical studies, the therapeutic index can be determined by comparing the dose, or the drug concentration required to cause toxicity, with the concentration required to produce the therapeutic effects in the studied population. However, a wider therapeutic index usually indicates a lower number and severity of side effects associated with the use of the same drug [ 1 ].
Corticosteroid doses used in clinical practice may be highly variable, depending on the disease to be treated and its severity. Deflazacort is less potent than prednisone and is usually administered at proportionately higher doses. The potency ratio of prednisone to deflazacort is about The dose equivalence of orally administered deflazacort and prednisone has been evaluated in a large US trial.
On this basis, the minimum effective dose of deflazacort was With regard to the potential of drug-induced osteoporosis, an equipotency ratio of deflazacort versus prednisolone of 1. Consequently, at standard doses, the osteoporotic potential of deflazacort appears to be much lower than other steroids.
The patients enrolled in this study were randomized in two groups: 10 patients were treated for 6 months with deflazacort 7. The efficacy of treatment was evaluated in each group at day 0, 90, and Clinical efficacy parameters included: number of swollen joints; number of tender joints; pain measured by means of a Visual Analogue Scale VAS ; global self-assessment of efficacy expressed separately by the physician and the patient using a VAS; disability index calculated by means of the Health Assessment Questionnaire HAQ.
Similar trends of efficacy were observed in both groups, with significant improvements of clinical parameters already evident after 3 months of treatment; these improvements were maintained throughout the treatment period, regardless of the corticosteroid used. However, although several studies have determined the equipotency ratio of deflazacort versus other corticosteroids, to the best of our knowledge, no dose-conversion table that includes also deflazacort is so far available in the literature.
Therefore, to facilitate identification of the correct dosage of this drug in clinical practice, we propose here a novel conversion table of corticosteroids doses, elaborated from literature available data i. The anti-inflammatory effect of corticosteroids is one of the main reasons for the use of these therapeutic agents. Several studies on adrenal steroids with glucocorticoid activity have led to the synthesis of new molecules characterized by high anti-inflammatory potency and low incidence of side effects.
Safety issues are particularly relevant in some populations on long-term therapy with corticosteroids, such as children and adolescents, in whom steroid therapy may result in growth retardation and behavioral disorders, as well as in somewhat "fragile" individuals such as politreated elderly patients.
Deflazacort is a recent synthetic glucocorticoid characterized by high efficacy and good tolerability, as demonstrated by several clinical studies that have evaluated its therapeutic efficacy and safety of use.
We conclude that deflazacort in equipotent doses to prednisolone was effective in the treatment of children with idiopathic nephrotic syndrome. Remission rate. In conclusion, using DEFLA instead of PRED in kidney transplant patients is associated with decreased loss of total skeleton and lumbar spine BMD, but does not. safety for deflazacort and prednisone/prednisolone in the placebo arm. secondary endpoints evaluated the effect of treatment on proximal muscle function. While this study does demonstrate better efficacy and lower side effects of deflazacort vs prednisone, the data is 20 years old. In general, deflazacort appears to have less effect than prednisone on parameters that may be associated with the development of corticosteroid-induced. Receive exclusive offers and updates from Oxford Academic. Table 1 Relative potencies of main corticosteroids modified from [ 1 ] Full size table.Job Seekers Employers. Committee Opportunities. Learning Center. Self-Assessment Examinations. SAEs for Training Programs. Education for Technologists. Meeting Your MOC. Annual Meeting. Abstract Information and Submission. Future Annual Meetings. Spring Virtual Conference.
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State Liaison Program. Apply to Become a State Liaison. Position Statements. Action Center. Contact Your Legislators. Manage a Fellowship. Neuromuscular Medicine Fellowship Portal. Neurology 87, November 15, Submitted by Leigh Maria K. This was a phase III double blind placebo controlled study in 2 phases over the course of 52 weeks and included patients diagnosed with a dystrophinopathy either by genetic testing or muscle biopsy.
This multicenter trial initially had 4 groups to include a placebo group in the first phase of 12 weeks, then 3 treatment groups 1. Patients were between years old and could be either ambulatory or nonambulatory. The purpose of this study was to evaluate the safety and efficacy of deflazacort vs. The primary endpoint of this study was change from baseline of muscle strength based on the Medical Research Council scale.
The results demonstrated that in the first 12 weeks, compared to placebo, all three treatment arms demonstrated increased average muscle strength. The interval from weeks demonstrated a greater preservation of muscle strength of the high and low dose deflazacort arms compared to the prednisone arm. Overall, at week 52, there was greater preservation of muscle strength of the high and low dose deflazacort arms compared to the prednisone arm. The side effect profile was also more favorable with the deflazacort arms.
Behavioral changes were more common in the prednisone arm but Cushingoid appearance, short stature, and cataracts were more common in the deflazacort arms. Overall, this study does support deflazacort having better efficacy after 52 weeks compared to prednisone. There was no significant efficacy difference between the high and low doses of deflazacort. Thus, the authors concluded that steroids are better than placebo in preservation of motor function and that deflazacort had lower incidence of weight gain and psychiatric side effects.
Comment : Deflazacort, although already widely used in other countries, was recently approved by the FDA specifically for the treatment of boys with Duchene muscular dystrophy DMD. While this study does demonstrate better efficacy and lower side effects of deflazacort vs prednisone, the data is 20 years old. Endpoints that are used in current trials were not employed with this study such as the 6-minute walk distance which the authors did acknowledge.
Considering the cost of the drug, physicians need to give careful consideration of data in this article. It reviews articles in journals and websites, identifies newsworthy items in the field, and writes article summaries. View Related News Stories: Practice. Search for:. Careers Job Seekers Employers Fellowships.
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