| Author | Message | ||
     Danz Advanced Member Username: Danz Post Number: 22 Registered: 08-2006 |
Hello everyone...I've checked out the WADA site and so far I can't find anything related to a drug an athlete is taking...the brand name is RHINOCORT AQUA and the active ingredient is budesonide...he's a little worried because he doesn't want to be "a cheater"...does anyone know anything about the drug and whether it's banned...his first day training after using it was great...I thought it was the training;)...t thanks dan | ||
| Andrew Senior Member Username: Andrew Post Number: 161 Registered: 04-2006 |
Budesonide is a steroid derivative, that is used in some oral, topical and nasal preparations to help reduce inflammation. The dose with the nasal spray prescribed to help reduve inflammation associated with post nasal drip and chronic sinusitis is extremely small, but could potentially show up in a blood test id used for extended periods of time. I do not know off-hand whether budesonide itself is a banned substance. It certainly does not have some of the same side effects of the more well-known steroid medications (cortisone, prednisone etc.). I do not have a list of banned substances, but would expect it would be on the list under the class of "steroids". http://en.wikipedia.org/wiki/Budesonide | ||
| Juerg Senior Member Username: Juerg Post Number: 1068 Registered: 04-2006 |
Budesonide. It is a WADA tested drug and will exceed the level in the urine for allowable amount. MONE LABORATORY - AKER UNIVERSITY HOSPITAL Cathrine Bakkene1, John Henninge2, Ingunn Hullstein2, Peter Hemmersbach1,2 1: School of Pharmacy, University of Oslo, Norway 2: Section for Doping Analysis, Aker University Hospital, Oslo, Norway Experimental Excretion study Betamethasone, prednisolone and budesonide, each in one local/topical and one systemic preparation, were administered to three groups of healthy volunteers (age 18 – 49, average 30.9). Each group consisted of eight persons, and each group received first the local/topical and later the systemic preparation of the same active compound, thereby acting as their own controls. All urine was collected for the first 36 hours, and spot urine samples were collected at 48 and 72 hours after administration. In one group receiving an intramuscular injection of betamethasone, weekly samples were collected for four weeks after administration. Background The WADA Prohibited List differentiates between various routes of administration of glucocorticoids. Since 2005, certain local/topical preparations are freely permitted; others require an approved Abbreviated Therapeutic Use Exemption (ATUE), whereas systemic routes of administration are prohibited. This may pose a challenge when it comes to interpretation of results, as relatively little is known about the urinary levels of glucocorticoids and their metabolites resulting from different routes of administration. Active compound Preparation Route of administration Amount of active compound Betnovat ”GlaxoSmithKline” Group 1 Cream 3 mg betamethasone1 Betamethasone Celeston Chronodose ”Schering-Plough” Intramuscular injection 5.7 mg betamethasone2 Ultracortenol ”Novartis” Eyedrops 0.9 mg prednisolone3 Group 2 Prednisolone Prednisolon ”Nycomed” Tablets 10 mg prednisolone Pulmicort ”AstraZeneca” Group 3 Inhalant powder 0.8 mg budesonide Budesonide Entocort ”AstraZeneca” Controlledrelease capsules 3 mg budesonide 1) As valerate 2) 3 mg as phosphate and 2.7 mg as acetate 3) As acetate Sample preparation and analysis A general sample preparation procedure and individual analytical methods were developed and validated. After addition of an internal standard (see table to the right), samples were extracted with t-butyl methyl ether at pH 9.5. After centrifugation, the organic phase was transferred to clean tubes and evaporated to dryness under nitrogen. The residue was reconstituted in 10 % aqueous acetonitrile, and the samples were analysed by LC-MS/MS on a Thermo Surveyor LC system coupled to a Thermo TSQ Quantum mass spectrometer. The column was a Thermo Betasil C18 (50x2.1 mm, 5 ìm particle size), and the mobile phase was an aqueous ammonium formiate / acetonitrile gradient. The mass spectrometer was operated in positive electrospray (ESI+) ionisation mode. Individual methods were optimised for each parent compound (and metabolite where applicable), with acquisition of three Selected Reaction Monitoring (SRM) transitions for each analyte and one for the internal standard. Compound Precursor ion m/z Product ion(s) m/z LOQ ng/mL CV % (30 ng/mL) Betamethasone 393 279, 237, 263 0.2 4 Desoximethasone (ISTD) 377 171 Prednisolone 361 171, 279, 289 0.5 3 Prednisone 359 171, 265, 237 1.0 4 D6-Prednisolone (ISTD) 367 270 Budesonide 431 226, 211, 277 0.1 11 16á-OH-prednisolone 377 323, 225, 277 0.2 6 Desonide (ISTD) 417 225 Results The concentration of the glucocorticoids was corrected for specific gravity (normalised to 1.020), and the average concentration within each group was plotted as a function of time. Only the concentration plots of betamethasone, prednisolone and 16á-hydroxyprednisolone are shown below. Prednisone, the metabolite of prednisolone, showed excretion curves similar to the parent compound, but the levels were somewhat lower and reached their maximum value three hours later on average (not shown). After administration of budesonide, the concentration of the parent compound did not exceed 2 ng/mL, regardless of the route of administration (not shown). Group 1 Group 2 Group 3 Average urinary concentration of betamethasone, corrected for specific gravity, after administration of Betnovat cream. Average urinary concentration of betamethasone, corrected for specific gravity, after administration of Celeston Chronodose, intramuscular injection. Average urinary concentration of prednisolone, corrected for specific gravity, after administration of Ultracortenol eye drops. Average urinary concentration of prednisolone, corrected for specific gravity, after administration of Prednisolon tablets. Average urinary concentration of 16á-OH-prednisolone, corrected for specific gravity, after administration of Pulmicort inhalant powder (budesonide). Average urinary concentration of 16á-OH-prednisolone, corrected for specific gravity, after administration of Entocort capsules (budesonide). Conclusion All three systemic preparations resulted in urinary levels exceeding the current WADA-specified reporting threshold of 30 ng/mL. With the exception of inhaled budesonide (detected in urine primarily as its 16á- hydroxyprednisolone metabolite), none of the local/topical preparations resulted in urinary levels exceeding the threshold. For the preparations and dosages included in this study, the current threshold does not fully exclude administration of local/topical preparations; however, it does facilitate reporting of glucocorticoid findings resulting from all systemic routes of administration. Furthermore, there appears to be a significant difference in the urinary concentration ratio between budesonide and its metabolite, 16á-hydroxyprednisolone, depending on whether budesonide was administered orally or by inhalation. This may be due to a greater degree of first-pass metabolism and/or degradation in the gastrointestinal tract in the case of the oral preparation, resulting in a lower ratio than was observed for the inhaled preparation. Ratio of budesonide to 16á-OH-prednisolone after administration of Pulmicort inhalation powder and |