Is there any benefit to using more than
1 single 100mcg injection of GnRH (Triptorelin)? I was curious due to the prices of it coming down alot lately if it was ok to use it more than once at 100mcg for restoring Male HPTA?
Basically for males what is the max usage dose for what period of time? can i use more than 100mcg?
Sorry for thread revival, found one post from another forum and then research studying GnRH .. Looks like most try 100mcg and if that doesnt work go up to 600mcg dosing 200mcg every 2 days but bloods should be done and only if your under someones care and completely shut down.
A more conservative approach would be 100mcg and then another 100mcg a week later another 100mcg.
Study
Androgenic Anabolic Steroid Use and Severe Hypothalamic-Pituitary Dysfunction: a Case Study, E. van Breda Int J Sports Med 2003; 24(3): 195-196
...We describe a patient who developed persistent hypogonadism due to the use of mixtures of AAS, which did not recover spontaneously after AAS cessation, and the successful recovery of pituitary-testicular axis after priming with LH-releasing hormone (LHRH).
Case description
A previously fit 37-year-old caucasian male semi-professional bodybuilder was seen by us at the exercise endocrinology unit with a chief complaint of gynaecomasty and severe acne associated with headaches and weight gain. He had no other history of severe medical problems. He smoked no tobacco and drank no alcoholic beverages. Sexual function and desire were greatly diminished. There was no family history of endocrine abnormalities. Anabolic regimens consisted of two periods of 18 weeks a year with mixtures of methylandrostenediol, stanozolol, mesterolone, metenolone enanthate, trenbolone acetate nandrolone laurate and drostanolone propionate as the main anabolic components.
On physical examination the patient appeared very muscular and trained. Blood pressure and pulse rate were normal. Examination of heart, lungs and abdomen were otherwise unremarkable. There were acne-like lesions on the torso. Genital examination revealed testicular atrophy (testes were very small, volume 2 ml, and weak).
Blood count and chemistry were normal. Endocrinological investigations showed luteinizing hormone (LH) (< 0.5 IU/L) and follicle stimulating hormone (FSH) (< 0.5 IU/L) levels to be below the detection limit. Plasma testosterone (T) was critically low (4.5 nmol/L). Serum Thyrotropin (TSH) (2.9 nmol/L), Thyroxine (T4) (19.9 nmol/L) and cortisol (547 nmol/L) were all within the normal range. In view of the probable diagnosis of severe hypogonadotropic hypogonadism a hypothalamic test was performed with 50 µg LHRH. This test resulted in an inadequate stimulation of LH release from the hypothalamus (0.5 IU/L and 14.8 IU/L, for baseline and 2 hour value respectively).
Despite testicular atrophy, semen analysis revealed a normal count (77 × 10 6 spermatozoa/ml) and mild morphology derangements (between 45 and 56 %).
Since this situation had persisted for months after AAS withdrawal, it was decided to treat the patient with a high dose of LHRH injections on 3 consecutive days in order to restore the normal pituitary-testicular axis interplay. The patient received 3 injections on consecutive days with 200 µg LHRH. Two hour values on 3 consecutive days were: LH (7.9; 4.1 and 6.2 IU/L) FSH (2.4, 1.8 and 2.3 nmol/L) and T (9.0, 13.3 and 11.1 nmol/L ) and were within the normal range. The patient reported to the out patient clinic three times in the next 12 months. On all three occasions plasma T levels remained within the normal range (11.2, 17.7 and 12.9 nmol/L) indicating a normal hypothalamic-gonadotropic function.
Discussion
This case clearly shows that AAS not only produces the obvious peripheral side effects such as gynaecomasty, acne, headaches, aggressiveness, and anxiety but also the more imperative central side effect of hypothalamic-pituitary dysfunction. The case described above with a non-responsive pituitary LH release to clinical doses of LHRH [8] should alert physicians to a more thorough regimen of LH-RH therapy.
We suggest that a thorough medical check-up of patients using AAS should focus more on a central endocrine dysfunction rather than to the obvious peripheral side effects. We therefore suggest that hypothalamic-pituitary dysfunction should always be considered during the differential diagnosis in athletes seen with typical presentation of anabolic steroid abuse. In order to regain normal hypothalamic-pituitary function, supraphysiological doses of 200 µg LH-RH should be considered when the physiological challenge test with LH-RH (50 µg) fails to show an acceptable response.
In conclusion, we would like to suggest that supraphysiological doses of LH-RH should be considered when a) there are clear symptoms of gynaecomasty and acne, b) there are critically low T and LH values and c) when there are no signs of improvement during a standard physiological LH-RH challenge test (50 µg).
