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Deflazacort : Can it substitute Prednisolone?


Glucocorticoids represent the most important and frequently used class of anti-inflammatory drugs However, unfortunately, the currently available ones act nonselectively; therefore, in the long run, they may impair many healthy anabolic processes. Various complications associated with this drug class warrant caution. Monitoring each of the drugs with separate formulation and considerable research have been focused recently on elaboration of selectively acting novel glucocorticoid drugs that possess the same efficacy in conditions for which they are used today but with reduction in one or more of the dose-limiting side effects.
Pharmacological properties

A new glucocorticoid deflazacort was introduced in 1969; it is a D-ring substituted steroid, otherwise similar to cortisol.

Deflazacort is a glucocorticoid. Its anti-inflammatory and immunosuppressive effects are used in treating various diseases and are comparable to other antiinflammatory steroids. Clinical studies have indicated that the average potency ratio of deflazacort to prednisolone is 0.69-0.89 and 6 mg of deflazacort is equivalent to 5 mg of prednisolone. However, the therapeutic dosage ratio has been reported to range from 1:1.2 to 1:1.5.


Orally administered deflazacort appears to be well absorbed and is immediately converted by plasma esterases to the pharmacologically active metabolite (D 21-OH), which achieves peak plasma concentrations in 1.5 to 2 h. It is 40% protein bound and has no affinity for corticosteroid binding globulin (transcortin) and binds to plasma protein and blood cells instead, crossing the blood-brain barrier in very low concentrations.These pharmacokinetic and biochemical properties of deflazacort may prevent it from reaching the hypothalamic or pituitary circulation during the first years; however, we can speculate that after a long-term treatment, deflazacort levels could increase in the central nervous system and finally produce effects similar to other glucocorticosteroids.Its plasma elimination half-life is 1.1 to 1.9 h. Elimination takes place primarily through the kidneys; 70% of the administered dose is excreted in the urine, and the remaining 30% is eliminated through the feces.

Indications and Uses

It is indicated for various different conditions as indicated in other glucocorticoids and has demonstrated equivalent efficacy to prednisolone and other oral steroids in rheumatoid arthritis, nephritic syndrome, SLE, transplantation, polymyalgia rheumatica, sarcoidosis and juvenile chronic arthritis. Although very few clinical trials have been performed under various dermatological conditions, it is shown to be effective in various steroid responsive cases.

Being a derivative of prednisolone, same precaution should be exercised as for other glucocorticoids. As it is metabolized in liver, it is recommended to increase the maintenance dose of deflazacort if drugs, which are liver enzyme inducers, are co-administered.

Pregnancy and Lactation:

The ability of corticosteroids to cross the placenta varies between individual drugs; however, deflazacort does cross the placenta. As with all drugs, corticosteroids should only be prescribed when the benefits to the mother and child outweigh the risks. When corticosteroids are essential, however, patients with normal pregnancies may be treated as if they were in the nongravid state. Corticosteroids are excreted in breast milk, although no data are available for deflazacort. Doses of up to 50 mg daily of deflazacort are unlikely to cause systemic effects in the infant. Infants of mothers taking higher doses than this may have a degree of adrenal suppression, but the benefits of breast-feeding are likely to outweigh any theoretical risk.


Deflazacort is a glucocorticoid derived from prednisolone and 6 mg of deflazacort it has approximately the same anti-inflammatory potency as 5 mg prednisolone or prednisone. Doses vary widely in different diseases and different patients. In more serious and life-threatening conditions, high doses of deflazacort may need to be given. When deflazacort is used for long term in relatively benign chronic diseases, the maintenance dose should be kept as low as possible. Dosage may need to be increased during periods of stress or during exacerbation of illness. The dosage should be individually titrated according to diagnosis, severity of disease and patient response and tolerance. The lowest dose that will produce an acceptable response should be used .In patients with hepatic impairment; blood levels of deflazacort may be increased. Therefore, the dose of deflazacort should be carefully monitored and adjusted to the minimum effective dose. In renal impairment, no special precautions other than those usually adopted in patients receiving glucocorticoid therapy are necessary. In elderly patients, no special precautions other than those usually adopted in patients receiving glucocorticoid therapy are necessary. There has been limited exposure of children to deflazacort in clinical trials. In children, the indications for glucocorticoids are the same as for adults, but it is important that the lowest effective dosage is used. Alternate day administration may be appropriate. Doses of deflazacort usually lie in the range 0.25-1.5 mg/kg/day.

For acute disorders up to 120 mg/day, deflazacort might be administered initially. The maintenance dose is usually within range 3-18 mg/day. The smallest effective dose should be used and increased if necessary.

Comparison with other Glucocorticoids:

An important issue to be addressed when comparing two glucocorticosteroids is their respective potency. Fewer side effects may be related to less primary activity. The bioequivalence of deflazacort and prednisolone has been investigated in various situations.

In normal subjects,15 mg deflazacort inhibits T cell reactivity to the same extent as 12.5 mg prednisolone, but for a longer period of time .The equivalence ratio of deflazacort/prednisolone may depend on the disease [i.e., 1.2:1 in rheumatoid arthritis,juvenile chronic arthritisand nephrotic syndrome,and 1.4:1 in asthmaand polymyalgia rheumatica. In a study comparing deflazacort vs. methylprednisolone using a 1.5:1 ratio (which is equivalent to a 1.2:1 deflazacort/prednisolone ratio), Elli et al.concluded that there was a more potent immunosuppressive activity of deflazacort with a lower ratio of CD4 + /CD8 + lymphocytes. It has been suggested that deflazacort depresses the osteoblast less than prednisolone, leading to a smaller decrease in serum osteocalcin levels with this drug.A bone-sparing effect of deflazacort at the level of lumbar spine has been described in various clinical situations. In a 1-year double blind prospective study of patients with the nephrotic syndrome, bone loss induced by prednisolone at the lumbar spine was 1.9-fold higher (12.5%/year) than that induced by deflazacort (6.8%).Other researchers have claimed that some of the bone-sparing effect of deflazacort compared to that of prednisolone could be explained by a less impaired intestinal calcium absorption by the former.In general, deflazacort appears to have less effect than prednisone on parameters that may be associated with the development of corticosteroid-induced osteoporosis. Further, the drug appears have less negative impact on growth rate in children with diseases requiring corticosteroid therapy. Thus, deflazacort may be associated with less serious metabolic sequelae than prednisone, but further well designed long-term trials are required to confirm this.

In children, however, even though the available efficacy data are minimal, deflazacort should be considered as an initial option in those requiring corticosteroid therapies since the adverse effects caused by this drug class are particularly debilitating in this patient group. Gastrointestinal symptoms are the most frequently reported adverse events in deflazacort recipients; other adverse events associated with the drug include metabolic and nutritional disorders, central and peripheral nervous system disturbances and psychiatric disorders.


Following clinical trials over more than 20 years, it has been approved in many countries (Italy, France, UK, Germany, and Spain) for use in inflammatory diseases. With regard to its effect, it has been claimed to have, at doses with equivalent anti-inflammatory efficacy to prednisolone, less severe adverse effects on bone, carbohydrate metabolism and linear growth and with less GI side effects. However, these claims have been questioned on the basis of some doubts as to the dose equivalence of deflazacort and the glucocorticoid of reference, prednisolone. Most of the data on the bone sparing effect of the drugs are obtained from trials that are relatively small or of short duration. Therefore, well-designed clinical trials are needed, especially to clarify the appropriate ratio of doses for bioequivalence with prednisone. However, we can state that it is worth considering those on long-term steroids, who are at higher risk of metabolic side effects, and in children as an initial option in those requiring corticosteroid therapies since the adverse effects caused by this drug class are particularly debilitating in this patient group. Such patients will be usually under specialist care, and this drug should be reserved for specialists only. Long-term study and trials in dermatological conditions are required before we can provide any concrete opinion regarding its utility for our domain.

Source: Internet.

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3 thoughts on “Deflazacort : Can it substitute Prednisolone?

  1. thank you very much!
    there are few reviews about deflazacort, this is a very good one.

    Posted by juan villarreal | October 23, 2010, 4:42 pm
    • in short course treatment deflazacort doesn’t have any advantage over prednisolone…more over it is far expensive…as a pediatrician since all the drug companies have stopped prednislone syrup we r forced to use deflazacort syrup…the studies on this drug is insufficient

      Posted by biju | September 3, 2012, 10:12 am
  2. its a good one

    Posted by dr susanta ku. Mohapatra | December 23, 2011, 7:45 pm

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