hello
how many people here tried triptorelin?
what was your T level before and after?
thank you
I would like to know how safe this drug is.
Some bodybuilders have experimented with it as a PCT. Results are mixed. There are 2 case studies. Most people are not aware of the portion in red below.
Pirola I, Cappelli C, Delbarba A, Scalvini T, Agosti B, Assanelli D, Bonetti A, Castellano M. Anabolic steroids purchased on the Internet as a cause of prolonged hypogonadotropic hypogonadism. Fertil Steril. 2010 Apr 21. [Epub ahead of print]
OBJECTIVE: To report a case of hypogonadotropic hypogonadism due to the chronic abuse of anabolic steroids purchased over the Internet. DESIGN: Case report. SETTING: Endocrinology unit of the University of Brescia. PATIENT(S): A 34-year-old man. INTERVENTION(S): A single dose (100 mug) of triptorelin (triptorelin test). MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen normalization, levels of serum testosterone, follicle-stimulating hormone, and luteinizing hormone. RESULT(S): Within 1 month, the patient’s serum testosterone was in the normal range, and he reported a return to normal energy and libido. CONCLUSION(S): The World Anti-Doping Code has proved to be a very powerful and effective tool in the harmonization of antidoping efforts worldwide, but it is insufficient to combat this illegal phenomenon. To tackle the serious side effects caused by doping we believe that it is necessary to increase monitoring and adopt severe sanctions, particularly with regard to Internet sites.
Androgenic Anabolic Steroid Use and Severe Hypothalamic-Pituitary Dysfunction: a Case Study
E. van Breda1, H. A. Keizer1, H. Kuipers1, B. H. R. Wolffenbuttel2
1 Department of Movement Sciences , Nutrition and Toxicology Research Institute Maastricht (NUTRIM), University, Maastricht, the Netherlands
2 Department of Endocrinology, University Hospital Maastricht, Maastricht, the Netherlands
The data of the present case demonstrate that the abuse of androgenic anabolic steroids (AAS) may lead to serious health effects. Although most clinical attention is usually directed towards peripheral side effects, the most serious central side effect, hypothalamic-pituitary-dysfunction, is often overlooked in severe cases. Although this latter central side-effect usually recovers spontaneously when AAS intake is discontinued, the present case shows that spontaneous recovery does not always take place. We suggest that hypothalamic-pituitary dysfunction should always be considered in the differential diagnosis in athletes seen with typical presentation of anabolic steroid use. In order to regain normal hypothalamic-pituitary function, supraphysiological doses of 200 ÎĽg LH-RH should be considered when the physiological challenge test with LH-RH (50 ÎĽg) fails to show an acceptable response.
Key words
Hypogonadism - high dose LHRH-treatment - body building - drug abuse
Introduction
The use of androgenic anabolic steroids (AAS) has been linked to the occurrence of premature cardiovascular events in healthy strength athletes [5]. Furthermore, its use not only among strength athletes but among adolescents in general appears to be related with the use of other psychotropic drugs, alcohol and tabacco and is often secondarily related with strength-sport involvement [4][9]. Finally, it has been suggested that anabolic-androgenic steroids act as a gateway to opioid dependence [1].
A growing number of users take AAS for periods ranging from 8 to 16 weeks several times a year and often take the more serious health threats for granted. Self-administration of AAS may result in much higher doses than therapeutically recommended, with possibly more severe side effects, and more profound effects on endocrine function. For instance, in men, AAS administration disturbs, through the negative feedback loop of the hypothalamic-pituitary gonadal axis, the production of luteinising hormone and follicle stimulating hormone [3][7]. Although full spontaneous recovery of these disturbances has been reported, there are indications that complete recovery may take years in long-term users [2][6]. 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 Ă— 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).
Anyone tried Triptorelin lately?Im thinikng of trying it…Just 0,1 to try and restore my HPTA Axis…Not saying that it would cure me, but its still nice to have normal sized ball instead of my 2 squishy grapes…
Isn’t this used for prostate cancer???
Its not only used to castrate men with hormone sensitive Prostate cancer, which for this indication the dosis is 36 higher (3,6mg) than the dosis i would take…Triptorelin is a GNRH analogon… GNRH is a peptide that tells our pituitary to release LH/FSH…Triptorelin at doses of 0,1 is also used for women to stimulate their egg production…
I find it really strange, that many here havent tried it yet…Again im not saying it would be a cure, but to hell, before i start injecting T, i would really make sure to have used everything else to jumpstart my pituitary.
GnRH the more effective way to restore HPG axis is using a pulsating administration of GnRH.
I didn’t know what type of doctors or clinic will do the procedure.
So…anybody tried this?
Just found this interesting
I did 3 shots of triptorelin over the span of one year…each 0.1mg…it did nothing for me…while I didn’t test my T, I’m sure that it didn’t even raise it a bit…I know this becuz my severe dry eye symptoms are totally T dependent…And they didn’t change a bit after the shot.Even one sachet if T Gel clear my dry eyes for several days…
As for the source of my triptorelin… I bought it from a local pharmacy, so it’s 100% legit
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