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Microsoft word - tue supporting information and validities - november 2012 _3_.docx

TENNIS ANTI-DOPING PROGRAMME
THERAPEUTIC USE EXEMPTIONS
The International Standard for Therapeutic Use Exemptions (TUEs) requires applications to be submitted no less than thirty (30) days before approval to use the prohibited substance(s) is required (Article 8.3). TUE applications must include a comprehensive medical history and the results of all examinations, laboratory investigations and imaging studies relevant to the application (Article 8.9). This document provides a summary of the minimum medical information that is required to accompany applications for TUEs for various medical conditions. It is recommended that players and medical practitioners review this document prior to submitting an application to help ensure that the application is complete and accurate, and so help to avoid unnecessary delays. This document should, in particular, be read in conjunction with the principles set out in the International Standard for TUE regarding the granting criteria for TUE (Article 4.2 to 4.5). It was drafted in order to guide and assist TUECs in decision making for TUE applications. This Medical Information must be considered as the most widely accepted medical best practice at present. This Medical Information is not mandatory and has no legal value. Failure to provide the required supporting information shown in table 1, or providing information that is illegible, may result in the application being denied, or returned unprocessed. Information that is inconclusive may result in a request to supply additional information, which will thereby delay the processing of that application. The full WADA documents, on which the summaries in table 1 are based, can be found in the TUE section of the WADA website: http://www.wada-ama.org/en/Science-Medicine/TUE. Table 2 provides an indication of the duration of a TUE granted for common conditions. These validities have been agreed by the Tennis Anti-Doping Programme independent TUE Committee, and are subject to change. TABLE 1. MEDICAL EVIDENCE TO BE SUPPLIED WITH A TUE APPLICATION.
CONDITION
MEDICAL EVIDENCE REQUIRED
A record of the onset of symptoms and the DSM-IV or ICD-10 criteria. The Connor scale has also shown utility in correlating the psychopathology in children with ADHD. The SNAP or other DSM-IV based tool can also be used as rating scales. Note: Some recent research indicates that objective diagnosis by PET (Positron Emission Tomography) or SPECT (Single-photon Emission Computed Tomography) may be of possible diagnostic assistance in the near future, but are not currently being used to diagnose ADHD. When ADHD first appears at a young adult age, diagnostic confirmation demands a second expert opinion. Medical history (which must confirm the time of onset, acute onset/crisis or chronic disease), physical examination, laboratory measurements and tests (see note). The tests should be undertaken by an endocrinologist in an established laboratory. In chronic disease, symptoms of the patient in the course of treatment over time should be documented and reported by the treating physician, e.g. any exacerbation (acute crisis), required adaptation of doses of glucocorticosteroids and mineralocorticosteroids. Genetic analyses in congenital disease may confirm diagnosis. Note: Laboratory measurements are as follows:  Complete blood count: Relative lymphocytosis and neutropenia, eosinophilia  Blood urea nitrogen, creatinine  Electrolytes: hyponatremia with or without hyperkalemia is commonly found in primary adrenal insufficiency, occasionally in secondary  Fasting blood glucose: hypoglycemia particularly in children or in athletes during/after exercise  Serum cortisol (Diagnosis is confirmed if serum cortisol level measured between 8.00 am and 9.30 am after an overnight fast (basal cortisol) is less than 3 μg/dL. Values below 18 μg /dL in the presence of a markedly elevated ACTH and plasma renin concentrations are very suggestive of adrenal insufficiency and require further investigation by provocative testing (cosyntropin, CRH, insulin). Values above 18 μg /dL rule out adrenal insufficiency.)  Plasma adrenocorticotropic hormone concentration (ACTH): ACTH can be decreased or normal (central adrenal insufficiency) or increased (peripheral adrenal insufficiency)  Plasma renin and aldosterone concentration  17-hydroxyprogesterone level: marked elevation (>242.4 nmol/L; normal value <8.9 nmol/L) is a diagnostic indicator of classic 21-OH- or 11β-OHdeficiency. Elevated early morning values can be used for screening of the non-classic form, but are not diagnostic. Testing may be as follows: Cosyntropin testing; Corticotropin-releasing hormone (CRH) stimulation test; Insulin-tolerance testing or metyrapone stimulation; Antibody tests; Imaging studies. Medical history (a detailed history of the episode and on recognition of sudden onset of characteristic symptoms and signs, usually within minutes to hours of exposure to the trigger). Appropriate family and clinical history, documented elevated recordings of systolic and/or diastolic blood pressure and a report of the physical examination. Other investigations such as ECG, echocardiography, and vascular ultrasonographic examinations may be considered in special cases. Laboratory investigations may be necessary to search for other medical conditions and risk factors particularly in the search for causes of secondary hypertension. Evidence of a sustained trial of non-prohibited agents must be included in the medical information or there must be a clear reason from a specialist physician why a prohibited agent is chosen over a permitted one. Medical history, physical examination, laboratory testing (spirometry, bronchial provocation tests). In accordance with the International TUE Standard and consistent with current best medical practice, the medical file required to support an application for a TUE in the case of an athlete with asthma or any of its clinical variants must include the following details: a) a complete medical history as described; b) a comprehensive report of the clinical examination with specific focus on the respiratory system; d) if airway obstruction is present, the spirometry will be repeated after inhalation of a short acting beta-2 agonist to demonstrate the reversibility of bronchoconstriction; e) in the absence of reversible airway obstruction, a bronchial provocation test is required to establish the presence of airway hyperresponsiveness. Test results should not be older than four years at the time of application; f) exact name, speciality and contact details of examining physician. Note that since salbutamol/salmeterol and formoterol are permitted, an explanation must be included as to why an alternate Beta-2 agonist is being prescribed. The intent is not to deny the use of these alternate beta-2 agonists particularly where a treatment regimen has already been established. - The diagnosis of GH deficiency is established by provocative testing of GH secretion. The insulin tolerance
test is the diagnostic test of choice. It should be performed in an endocrine unit where the test is
performed frequently. After insulin-induced hypoglycemia most normal subjects respond with a peak of
GH in serum above 5 mcg/L. A peak of GH to less than 3 mcg/L constitutes a severe GH deficiency. In
patients with contraindications to the insulin tolerance test, the arginine test combined with GHR can be
used as an alternative.
One provocative test is sufficient for the diagnosis of GH deficiency in adults with hypothalamic-pituitary
disease. To diagnose isolated GH deficiency it is recommended that a second biochemical test of GH status
be abnormal. The cut-off point of 5 mcg/L is used for provocative tests as the current reference, regardless
the stimulation test or the GH assay used. It does not vary with age.
- A serum IGF-1 concentration below the normal range is suggestive but not conclusive proof of GH deficiency. It is recommended that the diagnosis be confirmed by a provocative test of GH release. - GH and IGF-1 results should be expressed in mass units. - Currently, the benefits of the treatment of partial GH deficiency remain debatable. Consequently, only patients with documented, severe GH deficiency should be eligible for an exemption to use growth hormone therapeutically. Medical history, a comprehensive clinical assessment combined with biochemical tests of the GH-IGF axis In a child with a history and clinical suggestions of GHD, testing for IGF-1/IGFBP-3 levels and GH provocation tests are required. In suspected isolated GH deficiency, two GH provocation tests are required. If there is defined central nervous system pathology, irradiation, MPHD, or a genetic defect, one GH test is sufficient. The evaluation of spontaneous GH secretion over 12 or 24 hours can be applied in accordance with a standardized protocol when GH and IGF-1 data are in conflict (normal GH and low IGF-1).It is not necessary when IGF-1 is normal and GH is low. However there are some patients who have IGF-1/ IGFBP-3 levels below the normal range on repeated tests but GH responses in provocation tests above the cut-off level. These children have an abnormality of the GH axis and could be considered for GH treatment, despite not being classically GH deficient. In this case the response to GH treatment must be carefully reviewed by a specialist in pediatric endocrinology. - Biological markers other than the GH-IGF axis (bone density, body composition, and bone markers) are presently not considered specific enough to diagnose GHD. - Bone age estimated from an X ray of the left wrist and hand should be undertaken as part of the routine evaluation in children. It should be read by an experienced person. - An MRI (or CT scan) of the brain with particular attention to the hypothalamic-pituitary region may be carried out in any child diagnosed as having GHD. - To report assay data, a clear statement of methodology is required. An assay that measures 22-kDa hGH, using monoclonal antibodies, is recommended. - For GH provocation tests a limited number of provocative agents should be used in a well standardized protocol (arginine, clonidine, glucagons, insulin and L-Dopa, Betablockers, coupled tests) and monitored carefully by an experienced team. As an indication in a child with clinical criteria of GHD, a peak GH concentration below 10 microg/L is traditionally used to support the diagnosis. The criteria values should be based on the updated consensus guidelines for the diagnosis of GHD in a child (see references at the end of the document). Male factor infertility: Abnormal semen analysis showing hypomobility, a high incidence of abnormal forms PCOS: Medical history, including absence or irregular menstrual cycles and clinical evidence of androgen excess (hirsutism, acne). One of: Ultrasound evidence of ovarian volume 10 cm3, >12 follicles between 2-9 mm per ovary; Altered hormonal profile is not necessary for diagnosis as serum as androgen levels (testosterone, androstenedione, DHEAS) may be in the normal or high range. Bilateral blockage of Fallopian tubes: Medical history, evidence of proximal or distal blockage of tubes by hysterosalpingogram, sonohysterogram or surgery. Medical history, routine laboratory screening, GI tract imaging studies. Ulcerative colitis on the other hand requires stool examination, sigmoidoscopy to demonstrate typical mucosal changes and biopsy evidence of chronic inflammation and altered mucosal vascularity. A precise description of the clinical situation and specific medical indication for the IV infusion must accompany the TUE application. This should include a clear description of the substance to be infused, the rate of infusion and any other relevant clinical information from the treating physician. The application must establish a clear, well-justified diagnosis; that no permitted alternative treatment exists; that the treatment will not enhance performance other than to return the athlete to a normal state of health. The TUE application must include dates of evaluation, copies of laboratory and testing results. If androgen deficiency is iatrogenic in origin (orchiectomy, pituitary surgery or irradiation, radiotherapy or chemotherapy), details of the diagnosis and treatment including surgery reports should be submitted. The evaluation for androgen deficiency, unless otherwise stated, must include: a. Pubertal progression - incomplete or delayed sexual development c. Decreased spontaneous erections and/or ejaculations e. Non specific symptoms – decreased energy, depressed mood, dysthmia, poor concentration, sleep disturbance, hypersomnolence, mild anemia, reduced muscle bulk & strength, increased body fat and BMI, diminished work performance f. Low or zero sperm count (may not be associated with low testosterone) g. Low bone density (loss of height or low trauma fractures) h. History of cryptorchidism, torsion or significant testicular injuries b. Changes in hair pattern (axillary & pubic), reduced shaving, absence of temporal recession c. Decreased testicular volume (small testes) <15cc by orchidometry or ultrasound 3. Testing/Laboratory evaluation (blood drawn in the morning) to demonstrate consistent androgen deficiency should be provided with the TUE application including: a. Total testosterone – assay using an accurate and reliable method b. Free testosterone – using an accurate and reliable method (e.g. calculated free testosterone from total testosterone and SHBG measurements or free testosterone by equilibrium dialysis), if available e. Semen analysis including sperm count if fertility an issue g. Urine drug screens may be requested and organized by the Anti-Doping Organization a, b (if available) & c must be drawn on at least two occasions at least a week apart in a 4-week period.
4. If hypogonadotropic hypogonadism or hypopituitarism is diagnosis: a. MRI of brain with pituitary (sella) cuts with and without contrast b. Pituitary function tests if appropriate c. Other appropriate diagnostics to identify an organic etiology for secondary hypogonadism (e.g. prolactin, iron studies and genetic testing for hereditary hemochromatosis). d. Documentation of appropriate evaluation of the etiology of hypogonadism should be provided A thorough history and physical examination. Imaging studies (x-ray, MRI, CT-scan, nuclear studies, ultrasound) may be necessary to determine the exact nature of the injury and to establish necessity for the use of prohibited substances. Medical history. Fulfilment of the diagnostic criteria adapted from the AASM (American Academy of Sleep Medicine) criteria: 1. Complaint of excessive daytime sleepiness occurring daily for at least 3 months; typically, patients sleep for a short time and feel refreshed afterwards. 2. Definite history of cataplexy, i.e. sudden loss of muscle tone triggered by strong emotions (fear, surprise, or, most reliably, positive items, such as joking or laughing); this is transient (less than 2 minutes, usually much briefer); symptoms may involve the entire body, or only the knees, neck, or face. 3. Normal neurological and psychiatric examination. Negative drug screen. Brain imaging is not mandatory. 4. Exclusion of respiratory or other causes of sleep disturbance by night time polysomnography in an accredited Sleep-Wake Disorders Centre. 5. Demonstration of at least 2 sleep onsets in REM (SOREMs) during a Multiple Sleep Latency Test (MSLT), with a mean sleep latency of less than 8 minutes (typically less than 5 minutes) for the 5 sessions of the test. 6. HLA genotyping is almost constantly DQB1*0602 across all ethnic groups in sporadic cases. Its absence strongly argues against the diagnosis, unless cataplexy is ascertained, and SOREMs are repeatedly demonstrated. Conversely, DQB1*0602 presence in itself is clearly insufficient. 7. Hypocretin-1 level in CSF should be obtained in dubious cases (disputable cataplexy, unclear MSLT results). Levels below 110 pg/ml, or a third of reference value, confirm the hypocretinergic alteration, pathognomonic of the disease. Clinical variant: Narcolepsy without cataplexy
This diagnosis, in the context of a TUE application, may only be accepted with the greatest caution, if the following items are present: 1. Excessive daytime sleepiness with refreshing naps, and no clear cataplexy (which may however appear several years after the onset of sleepiness). 2. Absence of respiratory disturbance on night time polysomnography; in the case of repeated awakenings, upper airway resistance syndrome (i.e. multiple respiratory events related arousals) must be ruled out through esophageal pressure monitoring, and periodic limb movements through tibialis anterior EMG recording. 3. Demonstration of at least 2 SOREMs during the MSLT, with a mean sleep latency of less than 8 minutes. The preceding night time sleep duration should be more than 6 hours, in order to rule out “sleep rebound.” Recent use of antidepressants should be eliminated by drug screening, since there may be a rebound of REM-sleep in the days following cessation of these compounds. 4. CSF hypocretin-1 measurement is advisable: it is normal in 90% of cases, but if the level is significantly low, the diagnosis will be firmly established. Medical history. Clinical examination to ascertain the presence of other causes of chronic cough. A well-documented history of end-stage renal disease, a report from the renal physician and treating surgeon, including surgical procedures. ABRS Symptom Table
Facial Pain/pressure/fullness
Nasal Obstruction
Nasal purulence/discoloured postnasal Discharge
Smell: Hyposmia/anosmia
The diagnosis of ABRS requires the presence of ≥ 2 PODS symptoms, one of which must be O or D, and symptom duration of >7 days without improvement. The diagnosis is based on history and physical examination. Nasal culture and sinus aspirates are not necessary. Radiological imaging is not required for uncomplicated ABRS. Chronic Rhinosinusitis is diagnosed on clinical grounds but must be confirmed with at least 1 objective finding on endoscopy or computed tomography (CT) scan. CRS Symptom Control
Facial Congestion/fullness
Facial Pain/pressure/fullness
Nasal Obstruction
Nasal purulence/discolored postnasal Discharge
Smell: Hyposmia/anosmia
A diagnosis requires at least 2 CPODS present for 8-12 weeks, plus documented inflammation of the paranasal sinuses or nasal mucosa. CRS is a clinical diagnosis and must be confirmed with at least 1 objective finding such as nasal purulent nasal polyposis, on endoscopy or sinus opacification on CT scan. Objective testing is necessary to rule out the differential diagnosis of migraine, dental abscesses, allergic rhinitis and atypical facial pain syndromes. Medical history. Fasting plasma glucose levels and should be referenced. The traditional oral glucose tolerance test may assist in identifying previously undeclared diabetics (but this test may be influenced by aging and concurrent drug use). TABLE 2. TUE VALIDITIES UNDER THE TENNIS ANTI-DOPING PROGRAMME
CONDITION
VALIDITY1
8 years with annual review by an endocrinologist. 4 years (no annual review). Eligible for retroactive approval. 4 years with annual review; new pulmonary function tests every 4 years. (adults and children) Infertility/polycystic ovarian syndrome Clompiphene citrate: 1 year. Spironolactone: 2 years with annual review. IVF: 2 years. Male infertility and unexplained infertility: 2 years. Normally a single intervention of relatively short duration. Eligible for retroactive approval. 1 year, with review by a sleep specialist. Glucocorticosteroids: lifelong. EPO: 1 year. Diuretics: 4 years with annual review. Glucocorticosteroids: up to 10 days. Pseudoephedrine: 8 weeks 1 A new application is required for any change in treatment regime. November 2012

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