pct en 45 jours

[Strong-GearXXL]

45 Day PCT Cycle. Never seen dosing like this?

--------------------------------------------------------------------------------

Please translate these. I found this on differnet site. This guy saying things ive never heard before????? Especially the part under METHODS

HPGA Normalization Protocol After Androgen Treatment
N Vergel, AL Hodge, MC Scally
Program for Wellness Restoration, PoWeR

Objective Results Discussion
To develop an approach to cycle androgens that would
result in significant changes in body composition and
accelerate the normalization of the hypothalamic
pituitary gonadal axis (HPGA) after cessation of
androgens.

Methods
An uncontrolled study of 19 HIV-negative eugonadal
men, ages 23 – 57 years, administered testosterone
cypionate and nandrolone decanoate for 12 weeks,
and then were treated simultaneously with a combined
regimen of human chorionic gonadotropin (hCG) (2500
IU/QODx16d), clomiphene citrate (50 mg PO BID x 30d)
and tamoxifen (20 mg PO QD x 45d), to restore the
HPGA.

Mean FFM by DEXA increased from 64.1 to 69.8 kg
(p<.001); percent body fat decreased from 23.6 to 20.9
(p<.01); strength increased significantly from 357.4 lb
to 406.4 lb (p=.02). No significant changes in serum
chemistries and liver function tests were found. HDL-C
decreased from a mean value of 44.3 to 38.0 (p=.02).
Mean values for luteinizing hormone (LH) and total
testosterone (T) were 4.5 and 460, respectively prior
to androgen treatment. At the conclusion of the 12-
week treatment with androgens the mean LH <0.7
(p<.001) and total testosterone was 1568 (p<.001). The
mean values after treatment with the combined
regimen were LH=6.2 and testosterone=458.

The use of androgens has been reported to improve
lean body mass, strength, sexual function, and mood
accompanied by side effects caused by continuous
uninterrupted use of these compounds (polycythemia,
testicular atrophy, hypertension, liver dysfunction
[oral androgens] and alopecia.) Androgen-induced
HPGA suppression causes a severe hypogonadal state in
most patients that often require an extensive period of
considerable duration for normalization. This prevents
most if not all individuals from cycling off these
medications due to the adverse impact of this state on
their previously gained LBM and quality of life. The
protocol of hCG-clomiphene-tamoxifen was successful
in restoring the HPGA within 45 days after androgen
cessation. Further controlled studies are needed to
determine if these results can be duplicated in HIV-
positive subjects.
Patient General Characteristics
Mean SD Range
Age (yrs) 36.4 9.6 23-57
Height (cm) 179.3 10.3 152.4-198.1
Weight (kg) 87.7 9.8 71.7-106.6
BMI (kg/m2) 27.5 4.7 22.3-42.8

Mean Hormone Levels During Program
Initial Day 30 Day 90 Final Change P
Mean SD Mean SD Mean SD Mean SD Mean SD
T 459.5 224.4 1568.0* 551.6 1262.9* 551.6 457.9 206.7 -1.6 17.7 NS
LH 4.5 1.9 <0.7* - <0.7* - 6.2 5.5 1.7 3.6 NS
* P<.001 to initial value.

Serum Chemistry
Initial Final Change P
Mean SD Mean SD Mean SD
BUN 20.1 5.5 20.7 6.2 0.6 0.7 NS
ALKP 75.8 15.4 65.6 20.1 10.2 4.8 .005
ALT 37.1 23.9 42.3 35.9 5.2 12.0 NS
AST 32.8 14.4 38.9 25.7 6.1 11.4 NS
Chol,Total 191.2 45.5 185.3 39.5 5.9 6.0 NS

Mean Body Composition & Strength
Initial Final Change P
Mean SD Mean SD Mean SD
Fat (%) 23.6 7.2 20.9 4.8 2.8 2.4 .02
Weight (kg) 87.7 9.8 91.5 9.2 3.8 0.6 .001
Fat Free Mass (kg) 64.1 7.3 69.8 7.7 5.7 0.3 .001
Fat (kg) 23.4 7.0 21.6 5.0 1.9 1.9 NS


article tirer sur anabolex

 

[Strong-GearXXL]

traduc please :hein:

en gros une etude a ete faite sur des patiens agés de 23 à 57 ANS on leur a administrer de la testo cypionate et du deca durabolin sur 12 semaines
leur % de gras a diminuer , la musculature et force a augmenter
mais les effets sur l hypotalamus ont ete là aussi cad la LH etait inferieur a 0.7 et leur testo total etait de 1568 donc l hypophyse casiment a l arret comme chez moi:weights:

apres le traitement de 45 j leur LH 6.2 et testo à 458

hcg 2500ui sur 16 jours
clomid 50x2 sur 30 jours
nova 20 sur 45 jours

 

[doc]

en gros une etude a ete faite sur des patiens agés de 23 à 57 ANS on leur a administrer de la testo cypionate et du deca durabolin sur 12 semaines
leur % de gras a diminuer , la musculature et force a augmenter
mais les effets sur l hypotalamus ont ete là aussi cad la LH etait inferieur a 0.7 et leur testo total etait de 1568 donc l hypophyse casiment a l arret comme chez moi:weights:

apres le traitement de 45 j leur LH 6.2 et testo à 458

hcg 2500ui sur 16 jours
clomid 50x2 sur 30 jours
nova 20 sur 45 jours

j'ai le meme probleme que toi mon ami et comme je copmte bien faire un break un jour ,si j'ai bien compris ,il faut faire
hcg 2500ui par jour pendant 16 jours
suivi du clomid sur 30 jours
puis nolva sur 45 jours
ou alors tout ca en meme temps?
ou seulement clomid + nolva en meme temps ?

 

[Strong-GearXXL]

j'ai le meme probleme que toi mon ami et comme je copmte bien faire un break un jour ,si j'ai bien compris ,il faut faire
hcg 2500ui par jour pendant 16 jours
suivi du clomid sur 30 jours
puis nolva sur 45 jours
ou alors tout ca en meme temps?
ou seulement clomid + nolva en meme temps ?

si je comprends bien le hcg c est tt les 4jours ; le clomid x2 par jours mais le nova je vois pas bien les dosage?

 

[invité]

Hm, c'est assez difficile d'être sûr exactement ce qu'ils ont fait. Il faut porter attention aux détails des doses. Par exemple si je dis hCG 2500ui QOD/16 jours, ben je vais administrer 2500ui TOTAL de hCG sur 16 jours à raison d'à chaque 2 jours, donc environ 300ui par injection.

Si je dis 2500ui QOD x 16 jours, ça veut dire des injections de 2500ui à tous les 2 jours pendant 16 jours, soit 8 ou 9 injections total.

Dans ce cas-ci, 2500ui/QOD x 16jours ça devrait signifier le deuxième scénario ci-haut donc des injections de 2500ui. Mais je ne suis pas absolument certain de ça. Par ailleurs, pour savoir si cette relance est vraiment efficace il faudrait mesurer à nouveau les taux 30 et 60 jours après la relance.

 

[invité]

si je comprends bien le hcg c est tt les 4jours ; le clomid x2 par jours mais le nova je vois pas bien les dosage?

hCG tous les 2 jours pendant 16 jours, Clomid 50mg 2x par jour, total 100mg pendant 30 jours et nolva 20mg par jour une fois par jour, 45 jours.

 

[Strong-GearXXL]

Hm, c'est assez difficile d'être sûr exactement ce qu'ils ont fait. Il faut porter attention aux détails des doses. Par exemple si je dis hCG 2500ui QOD/16 jours, ben je vais administrer 2500ui TOTAL de hCG sur 16 jours à raison d'à chaque 2 jours, donc environ 300ui par injection.

Si je dis 2500ui QOD x 16 jours, ça veut dire des injections de 2500ui à tous les 2 jours pendant 16 jours, soit 8 ou 9 injections total.

Dans ce cas-ci, 2500ui/QOD x 16jours ça devrait signifier le deuxième scénario ci-haut donc des injections de 2500ui. Mais je ne suis pas absolument certain de ça. Par ailleurs, pour savoir si cette relance est vraiment efficace il faudrait mesurer à nouveau les taux 30 et 60 jours après la relance.

d accord mais je pense qu ici le principale est que l hypophyse est denouveau operationnel non? ou y a t il risque d arret apres relance ? car on sais que les stero l arrete mais ici avec cette ptc elle est redenouveau operationel non???

donc pour toi Qdo serais tout les deux jours? n est pas edo ?

 

[invité]

[/COLOR]


d accord mais je pense qu ici le principale est que l hypophyse est denouveau operationnel non? ou y a t il risque d arret apres relance ? car on sais que les stero l arrete mais ici avec cette ptc elle est redenouveau operationel non???

donc pour toi Qdo serais tout les deux jours? n est pas edo ?

QOD est en latin. C'est du jargon scientifique et non du jargon culturiste... :lumiere:

Effectivement l'Hypophyse est opérationnelle dans ce cas-ci mais il faut savoir si les testicules continueront eux de l'être. La hCG peut provoquer une sur-stimulation qui à court terme génère des taux de testo élevés mais qui à plus long terme justement les rend paresseux. Il faut à mon avis être prudent avec le hCG.

 

[Strong-GearXXL]

An Uncontrolled Clinical Trial for Treatment of
Androgen Induced Hypogonadism
2
An Uncontrolled Clinical Trial for Treatment of
Androgen Induced Hypogonadism
By
Michael C. Scally, M.D.
And
Andrew L. Hodge, M.S.
Michael C. Scally, M.D., P.A. Clinic
8707 Katy Freeway, Suite C
Houston, TX 77024



Total Words- 3023
4
Abstract- 237 words
Objective: Although shown to be effective for their intended medical treatment,
AAS have been shown to induce hypogonadotropic hypogonadism in adult
males. The medical literature is conflicting in the reports of spontaneous return
and long-term suppression of gonadal suppression post AAS usage. This
observational study documents the treatment protocol of HCG, clomiphene
citrate, and tamoxifen in returning hormonal function to normal post AAS usage.
Design: Five HIV-negative males age 27-49, weighing 77-100 kg, with
serum total testosterone levels below 240 ng/dL and luteinizing hormone (LH)
levels below 1.5 mIU/mL were considered for this observational study. All five
patients were administered the treatment protocol.
Methods: Treatment consisted of combination therapy which included
concurrent administration of (a) Human Chorionic Gonadotropin, (b) Clomiphene
Citrate and (c) Tamoxifen Citrate for a standard duration of 45 days. This
protocol was repeated with every patient until serum LH and total testosterone
values reached normal ranges.
Results: All five patients were considered eugonadal by normal laboratory
reference ranges by the conclusion of treatment. Average serum total
testosterone rose from 98.2 to 692.8 ng/dL (p<.001) while the average serum LH
rose from an average undetectable value of less than 1.0 to 7.92 mIU/mL
(p<.0008).
5
Conclusions: Although the treatment protocol of HCG, clomiphene citrate, and
tamoxifen proved beneficial in reversing AAS induced hypogonadotropic
hypogonadism, future controlled studies need to be performed to confirm the
beneficial effects of this combined pharmacotherapy in returning HPGA
functioning to normal.
Key Words- anabolic-androgenic steroids, clomiphene, HCG, tamoxifen,
testosterone, HIV
6
INTRODUCTION
Testosterone and testosterone analogues, anabolic-androgenic steroids
(AAS), have long been used in the athletic community for improving lean muscle
tissue and strength. A positive correlation has been shown with testosterone to
include: increased protein synthesis resulting in lean muscle tissue development
(Bhasin et al, 1996; 1997; Hervey et al, 1981; Tenover, 1992), enhanced sexual
desire (libido) (Schiavi et al, 1991), increased muscular strength (Bhasin et al,
1996; 1997; Hervey et al, 1981; Sih et al, 1997), increased erythropoiesis
(Bhasin et al, 1997; Evans & Amerson, 1974; Sih et al, 1997; Tenover, 1992), a
possible positive effect on bone development (Anderson et al, 1996; 1997; Baran
et al, 1978; Tenover, 1992), improved mental cognition and verbal fluency
(Alexander et al, 1998), and male masculinizing characteristics (Starr & Taggart,
1992). Recently, however, clinicians have recognized the potential benefits of
their use in the treatment of various disorders and ailments. Numerous studies
have discussed the use of AAS in the treatment of HIV-associated conditions
(Bhasin et al, 2000; Grinspoon et al, 1998; 1999; 2000; Rabkin et al, 1999; 2000;
Sattler et al, 1999; Strawford et al, 1999; Van Loan et al, 1999), hypogonadism
(Bhasin et al, 1997; Davidson et al, 1979; Rabkin et al, 1999; Sih et al, 1997;
Snyder et al, 2000; Tenover, 1992; Wagner & Rabkin, 1998; Wang et al, 2000),
impotence (Carani et al, 1990; Carey et al, 1988; Klepsch et al, 1982; Lawrence
et al, 1998; McClure et al, 1991; Morales et al, 1994; 1997; Nankin et al, 1986
Rakic et al, 1997; Schiavi et al, 1997), burn victims (Demling et al, 1997), various
7
anemia’s (Doney et al, 1992; Gascon et al, 1999; Hurtado et al, 1993; Stricker et
al, 1984), deteriorated myocardium (Tomoda, 1999), glucose uptake (Hobbs et
al, 1996), continuous ambulatory peritoneal dialysis (CAPD) (Dombros et al,
1994), alcoholic hepatitis (Bonkovskyet al 1991; Mendenhall et al, 1993),
hemochromatosis (Kley et al, 1992) and prevention of osteoporosis (Anderson et
al, 1996; 1997; Baran et al, 1978; Behre et al 1997; Hamdy et al, 1998;
Prakasam et al, 1999).
While AAS have proven effective in cases of lean muscle wasting
conditions (HIV/AIDS), this class of medicines is not without their inherent
problems. AAS have been shown to induce hypogonadotropic hypogonadism
(Alen et al, 1987; Bhasin et al, 1996; Bijlsma et al, 1982; Clerico et al, 1981;
Jarow & Lipshultz, 1990; Strawford et al, 1999; Stromme et al, 1974). This
condition typically results from an abnormality in the normal functioning of the
hypothalamic-pituitary-gonadal axis (HPGA), usually from a negative feedback
inhibition of one of the hormone secreting glands, causing a cascading
unbalance in the rest of the axis. Possibly resulting from a physiological
abnormality (i.e. mumps orchitis, Klinefelters syndrome, pituitary tumor) or as an
acquired result of exogenous factors (i.e. androgen therapy, AAS administration).
Clerico et al (1981) found a dramatic suppression of serum gonadotropin levels
in athletes given methandrostenelone, suggesting a direct action of AAS on the
hypothalamus. Similar results of suppressed gonadotropins have been found in
patients supplementing solely testosterone (Bhasin et al, 1996; Marynick et al,
1979; Strawford et al, 1999; Tenover, 1992). Case report studies discussed a
8
36-year old male competitive bodybuilder and a 39-year old father, each using
various AAS regimens over extended periods of time, who showed a blunted
response to GnRH stimulation tests (Jarow & Lipshultz, 1990). One particular
study administered 600 mg of nandrolone decanoate to 30 HIV-positive males
over twelve weeks (Sattler et al, 1999). The results made no reference to LH or
testosterone levels. The lack of gonadotropin measurement is puzzling as the
data showed 12 of 30 subjects experienced testicular shrinkage, implying Leydig
cell dysfunction and suppressed testosterone levels. Other studies using AAS
have also shown no reference to LH or FSH levels but suppressed values are
expected in each case (Bagatell et al, 1994; Behre et al, 1997; Sheffield-Moore
et al, 1999; Tricker et al, 1996).
Declining, or suppressed, circulating testosterone levels as a result of
either pathophysiological or induced hypogonadal conditions can have many
negative consequences in males. Declining levels of testosterone have been
directly linked to a progressive decrease in muscle mass (Mauras et al, 1998),
loss of libido (Schiavi et al, 1991), decrease in muscular strength (Balagopal et
al, 1997; Mauras et al, 1998) impotence (Rakic et al, 1997), oligospermia or
azoospermia (Vermeulen & Kaufman, 1995), increase in adiposity (Mauras et al,
1998) and an increased risk of osteoporosis (Wishart et al, 1995).
While some research suggests that the hormonal axis will spontaneously
return to normal shortly after cessation of testosterone administration (Knuth et
al, 1989), documented cases have taken up to 2 ½ years to return to normal
(Jarow & Lipshultz, 1990). This case of a 39-year old male who previously used
9
AAS was found to have low serum testosterone levels (6nmol/L, range 14 to 28
nmol/L) 2 ½ years after his last administration of the drugs (Jarow & Lipshultz,
1990). For most men, suffering with diminished libido, impotence, depression,
fatigue, muscle atrophy, and infertility for 2 ½ years is not a pleasant option.
Other androgen or anabolic steroid induced cases of hypogonadotropic
hypogonadism have taken 6 months (Gazvani et al, 1997; Wu et al, 1996), 8
months (Gazvani et al, 1997), 10 months (Boyadjiev et al, 2000), 12 months
(Schurmeyer et al, 1984), and 18 months (Gazvani et al, 1997) to finally return to
eugonadal status.
The individual use of human chorionic gonadotropin (HCG), clomiphene
citrate, and tamoxifen citrate in the treatment of testicular sub-function and
gonadotropin suppression, respectively, is well documented. HCG has been
shown to significantly improve gonadal function in hypogonadotropic
hypogonadal adult males (Barrio et al, 1999; Burgess & Calderon, 1997;
Cisternino et al, 1998; D’Agata et al, 1982; 1984; Dunkel et al, 1985; Kelly et al,
1982; Ley & Leonard, 1985; Liu et al, 1988; Martikainen et al, 1986; Okuyama et
al, 1986; Ulloa-Aguirre et al, 1985; Vicari et al, 1992). Studies using clomiphene
citrate to induce endogenous gonadotropin production in males found significant
improvements in LH and FSH values after treatment (Bjork et al, 1977; Burge et
al, 1997; Guay et al, 1995; Landefeld et al, 1983; Lim & Fang, 1976; Ross et al,
1980; Spijkstra et al, 1988). Tamoxifen citrate has also been found to produce a
profound increase in serum LH levels as well as improved semen and sperm
10
quality (Gazvani et al, 1997; Krause et al, 1985; Lewis-Jones et al, 1987; Wu et
al, 1996).
As HCG’s effect is centralized at the Leydig cells of the testicles,
clomiphene citrate and tamoxifen citrate act upon the hypothalamic-pituitary
region in stimulating gonadotropin production. Tamoxifen, a nonsteroidal
antiestrogen, and clomiphene citrate, a nonsteroidal ovulatory stimulant, compete
with estrogen for estrogen receptor binding sites, thus eliminating excess
estrogen circulation at the level of the hypothalamus and pituitary and allowing
gonadotropin production to resume normally. The normal operation of both the
testicular and hypothalamic-pituitary regions is crucial in returning HPGA function
to normal. Returning one component of the axis to normal without concurrently
returning the other would sabotage and inhibit the operation of the entire HPGaxis.
It was with this understanding that HCG was eventually combined with
clomiphene citrate and tamoxifen as attempted therapy to reverse gonadal
function in hypogonadotropic hypogonadal males.
In accordance with previous studies, each medication was used
individually, and along with HCG, in initial trials. The simultaneous use of
clomiphene citrate and tamoxifen was determined through preliminary use of
clomiphene citrate and tamoxifen individually. It was discovered that although
both clomiphene citrate and tamoxifen met with some success, when combined
together they achieved a more significant increase in gonadotropin production.
This clinical outcome resulted in the combination therapy of HCG, clomiphene
citrate and tamoxifen.
11
Following is a clinical evaluation of the combined, simultaneous use of
HCG, clomiphene citrate, and tamoxifen citrate as a treatment option in
suppressed testosterone and gonadotropin levels in hypogonadotropic
hypogonadal adult males. This observational analysis of the aforementioned
treatment protocol assessed the efficacy of these medicines under non-controlled
conditions.
12
METHODS
An observational study was done on the medical records of 5 adult male
patients presenting to a clinic with induced hypogonadotropic hypogonadism.
Patients were monitored and treatment recorded for the purposes of this
observational study.
SUBJECTS
The medical records of five males age 27-49, mean 35.2, weighing 77-100
kg, mean 89.8 kg, with serum total testosterone levels below 240 ng/dL and
serum luteinizing hormone (LH) levels below 1.5 mIU/mL were examined.
Average presenting testosterone level was 98.2 ng/dL (normal= 240-827 ng/dL)
while average LH level was undetectable at <1.0 mIU/mL (normal= 1.5-9.3
mIU/mL). The 5 patients had a history of AAS usage ranging from 9-60 months
prior to presentation. All patients had ceased any testosterone therapy or AAS
usage prior to initiation of treatment. Initial laboratory values confirmed that all
patients had discontinued AAS long enough for endogenous lab values to fall
below normal reference ranges. All patients were muscular in nature with an
average BMI less than 27 at presentation. Table 1 presents the patient
characteristics, anabolic history, and side effects upon presentation of the 5
patients.
13
LABORATORY STUDIES
Initial blood screening consisted of:
AST, ALT, GGT, TOTAL CHOLESTEROL, LH, FSH, TESTOSTERONE,
GLUCOSE, PROLACTIN, PSA TOTAL, TSH, T3 UPTAKE, T4 TOTAL, T4
FREE, HEMOGLOBIN, HEMATOCRIT
Table 2 shows all baseline serum blood levels at presentation. Baseline blood
screening excluded any form of hyperprolactinemia or hypothyroidism as causes
of hypogonadism in most patients. After physician examination and history and
physical evaluation, it was determined that a history of AAS usage was present
and most likely the cause of the patients’ hypogonadotropic hypogonadal lab
values; not hyperprolactinemia or hypothyroidism.
Laboratory testing was performed by Quest Diagnostics Inc., (Houston,
TX) and SmithKline Beecham Clinical Laboratories, (Houston, TX). Repeat
serum LH & testosterone samples were measured by immunoassay using chiron
reagant kits on an ACS-180 instrument.
METHODS
A review of patients’ medical records showed a treatment intervention of
(a) human chorionic gonadotropin (HCG) (Ferring Pharmaceuticals), (b)
clomiphene citrate (Teva Pharmaceuticals), and (c) tamoxifen (AstraZeneca).
Typical dosage of HCG consisted of 2500 units every other day for 16 days. All
14
HCG injections were self-administered intramuscularly. Starting dosages of
clomiphene citrate and tamoxifen were 50mg and 20 mg daily, respectively.
Patients started all three medications simultaneously and reported for the first
follow-up blood work after completion of HCG, 16 days later. The post HCG
blood analysis assessed testosterone-total response only. If testicular
stimulation, i.e. testosterone production, was inadequate, additional HCG was
administered at this stage of therapy rather than waiting an additional 30-45 days
before the protocol completion. If the testicular response to the HCG
demonstrated sufficient testicular stimulation (typically a blood serum level of
>300 ng/dL), clomiphene citrate and tamoxifen were continued for 15 and 30
days, respectively. The arbitrary cut-off level of 300 ng/dL was used as a general
assessment where sufficient Leydig cell stimulation was taking place even in light
of artificial stimulation from HCG. A repeat blood sample was then taken at day
45 to assess hypothalamic-pituitary-gonadal axis status via luteinizing hormone
and total testosterone levels. Because of the varying cessation times of the
medications, the concluding blood sample was taken after a 30 and 15-day
washout period of HCG and clomiphene citrate, respectively. For HPGA function
to be considered normal, both LH and testosterone values had to fall within the
normal reference ranges. For the purposes of patient treatment, if LH and
testosterone values were still below normal limits at the conclusion of 45 days of
treatment, a repeat protocol administration of HCG, clomiphene citrate, and
tamoxifen was given. This protocol was repeated with every patient until LH and
testosterone values reached normal ranges.
15
RESULTS
All five patients were considered eugonadal by normal laboratory
reference ranges by the conclusion of treatment. Average serum total
testosterone rose from 98.2 to 692.8 ng/dL. Average serum LH rose from <1.0 to
7.92 mIU/mL. An average of 48,974 U of HCG (five 10,000 Unit boxes),
3412.5 mg of clomiphene citrate (68.25 50mg tablets), and 968.71 mg of
tamoxifen (48.44 20mg tablets) were used to treat all patients to eugonadal.
Total treatment time ranged from 43-120 days. Mean elapsed time from
initiation of treatment to eugonadal was 68.6 days. Statistical analysis was
performed using repeated measures ANOVA. Pre and post treatment
testosterone values were significantly (p<.001) different as were the LH values
(p<.0008). Table 3 demonstrates the hormone changes during the treatment
period and the duration to eugonadal.
ADVERSE EVENTS
None of the study subjects had any serious or treatment-terminating
effects as a result of the multi-drug protocol. No problems were noted with
regards to parameters of normal urologic function or treatment causing
gynecomastia. Any side effects documented at presentation were reversed by
the conclusion of treatment.
16
DISCUSSION
This observational study demonstrates the possible efficacy of HCG,
clomiphene citrate, and tamoxifen citrate in returning the HPGA to normal
physiological function in adult males suffering from androgen induced
hypogonadotropic hypogonadism. In the case of decreased testicular function
manifested by low testosterone levels, it is of primary importance to first return
the normal function of the testicular cells. The initial lack of response to HCG
should not immediately be a cause for the initiation of testosterone replacement
therapy, as with the current accepted therapy modality by many physicians.
Blood analysis confirmed that no exogenous testosterone was administered
during the treatment period, as exogenous androgens would have had a
suppressive effect on endogenous gonadotropin production. Therefore, because
of the corresponding normal gonadotropin and testosterone values, it is accepted
that gonadotropin and testicular function were normal by the conclusion of
treatment.
The standard treatment of HIV-related muscle wasting, AAS therapy, may
involve decades of treatment and the attendant problems with any therapy of a
prolonged nature. Polycythemia vera, elevated hepatic enzymes, and prolonged
negative alterations in lipid profile are a few of the dangers experienced by HIV
patients administered AAS for extended periods. Of greatest concern is the
increasing numbers of individuals who are currently being treated with AAS to
increase muscle mass either for medicinal or recreational means without
17
attention being given to periodically returning the HPGA to normal. With roughly
4 million men in the U.S. being considered hypogonadal (Lacayo R., 2000;
Sheffield-Moore et al, 1999; Shelton DL, 2000), an estimated 200,000 men are
currently receiving testosterone treatment for the condition (Shelton DL, 2000).
As stated earlier, AAS are being prescribed to HIV & AIDS sufferers to combat
progressive muscle loss. The Centers for Disease Control and Prevention (CDC)
reported an estimated 635,000+ men diagnosed with AIDS through December
2000 while an estimated 97,700 have been reported with HIV (Centers for
Disease Control, vol.12, No. 2, table 5; Centers for Disease Control, vol. 12, No.
2, table 6). In 2000 alone over 31,000 men were diagnosed with the AIDS virus
(Centers for Disease Control, vol. 12, No. 2, figure 3). Between hypogonadal,
AIDS, & HIV males, potentially over 900,000 men are being administered AAS
therapy.
Studies recently published on patients suffering from various tissuedepleting
conditions and HIV affliction (Bhasin et al, 2000; Grinspoon et al, 1998;
1999; 2000; Rabkin et al, 1999; 2000; Sattler et al, 1999; Strawford et al,
1999;1999; Van Loan et al, 1999) have not identified what should be done to
restore normal endocrine status post-treatment. Considering the dosages and
compounds administered in many studies, there is no question that subjects
were left hypogonadal after therapy. In the cases where the periodic use of
testosterone or AAS are necessary, intervention to return the HPGA to normal
should be initiated as soon as possible after the cessation of the AAS. As
18
described herein, a possible treatment modality may be the combined regimen of
HCG, clomiphene citrate, and tamoxifen.
Medical history has demonstrated examples of physician-induced
complications resulting from treatment. Iatrogenic hyperthyroidism (Bartsch &
Scheiber, 1981) and iatrogenic Cushing’s syndrome (Cihak & Beary, 1977;
Kimmerle & Rolla, 1985; Smidt & Johnston, 1975; Tuel et al, 1990) are cases
were administered medications or treatments provoked abnormalities in patients’
normal physiology. The administration of testosterone as a treatment for
hypogonadotropic hypogonadism falls into this same category of causing
endocrine related abnormalities (Bhasin et al, 1996; Marynick et al, 1979;
Strawford et al, 1999; Tenover, 1992). Testosterone replacement therapy has
proven to be very effective in reversing the symptoms of suppressed
testosterone production, but does not treat the underlying cause of the
deficiency. Positive effects of testosterone treatment; i.e. improved sex drive,
improved sense of well-being, lean body mass; are all transient in light of
plummeting gonadotropin levels. Upon cessation of testosterone treatment
patients can expect a complete reversal of positive benefits as exogenously
influenced testosterone levels metabolize and decline rapidly.
Further controlled studies need to be performed showing the combined
effects of HCG, clomiphene citrate, and tamoxifen in returning HPGA functioning
to normal. Long-term follow-up on these patients returning to normal will be
necessary to ensure permanent reversal of hypogonadotropic hypogonadal
conditions. In addition, studies documenting dose-response curves for pituitary
19
inhibition and reversal due to AAS administration are critical in determining the
correct dose, duration, and form of treatment that is optimal without causing
permanent damage. When the need for long-term androgen use presents, using
moderately supraphysiologic doses of androgens as suggested by Strawford and
colleagues (1999) coupled with post-treatment HPGA restoration as
demonstrated here, may be a more effective means over high-dose protocols
used to offset negative alterations in lean body mass. Unfortunately current
studies have yet to adequately address a standard of patient care post-androgen
therapy. Because of the negative impact of the hypogonadal state on physical
and mental well- being, pharmacotherapy that restores HPGA function more
rapidly than current modalities would greatly benefit men with hypogonadotropic
hypogonadism.
While we believe that the treatment protocol was effective in returning
normal hormonal function to these men, the lack of randomization or a control
group leaves room for speculation. Although cases of spontaneous return to
eugonadism with no medicinal intervention have been published, these reports
documented durations anywhere from 6-18 months before normal hormone
status was achieved (Gazvani et al, 1997; Wu et al, 1996). If the alternative
treatment modality described herein can reverse suppressed gonadotropin
production and AAS associated side effects much sooner than non-treatment,
further evaluation of this therapy should continue.


SOURCE ANABOLEX FORUM

 

[roadrunner]

:hein:wow,,,erdu:

 

[invité]

Re : pct en 45 jours

Puisque nous re-discutons de cette étude, je voudrais commenter en particulier le paragraphe des résultats obtenus de cette thérapie hCG/clomid/nolva.

Essentiellement, leur protocole de traitement consiste en des administrations combinées de 2500ui de hCG à chaque 2 jours pour 16 jours, clomid 50mg/j continué 15 jours après cessation du hCG et nolva à 20mg/j continué 15 jours après cessation du clomid. La testo totale (fourchette normale 240ng/dL-827ng/dL) est mesurée à la fin du hCG et si le niveau est en-dessous de 300ng/dL, une ronde additionnelle de hCG (16jours à 2500iu chaque 2è jour) est donnée, en combinaison avec le clomid et nolva tel que décrit ci-dessus.

Les résultats :

All five patients were considered eugonadal by normal laboratory
reference ranges by the conclusion of treatment. Average serum total
testosterone rose from 98.2 to 692.8 ng/dL. Average serum LH rose from <1.0 to
7.92 mIU/mL. An average of 48,974 U of HCG (five 10,000 Unit boxes),
3412.5 mg of clomiphene citrate (68.25 50mg tablets), and 968.71 mg of
tamoxifen (48.44 20mg tablets) were used to treat all patients to eugonadal.
Total treatment time ranged from 43-120 days. Mean elapsed time from
initiation of treatment to eugonadal was 68.6 days. Statistical analysis was
performed using repeated measures ANOVA. Pre and post treatment
testosterone values were significantly (p<.001) different as were the LH values
(p<.0008). Table 3 demonstrates the hormone changes during the treatment
period and the duration to eugonadal.

La testo totale a monté en moyenne de 98.2 à 692.8 ng/dL et la LH de "indétectable" à 7.92mIU/mL (normal = 1.5-9.3 mIU/mL). En moyenne les gars on utilisé 48.974ui de hCG, soit 5 boîtes de 10.000ui. À 2500ui aux 2 jours ça donne 40 jours de hCG en moyenne. Comptons 15 j de plus en clomid et encore 15j de plus en nolva, donc la durée totale MOYENNE du traitement a été de 70 jours (68.6 jours en fait et de 43 à 120 jours selon l'individu).

Il est important de remarquer qu'ici on n'utilise pas le hCG en mini-injections de 250ui 2 fois semaine comme NOUS le faisons en cure, afin de "garder éveillés" les testicules. Ces gars-là ont laissé leurs noix devenir des raisins secs, ils doivent donc les réveiller à grands coups de gong. Ajourd'hui il est considéré plus efficace d'utiliser moins de hCG pour les garder éveillés plutôt que de les stimuler énormément afin de les réveiller d'une torpeur profonde. L'une des raisons est que la relance peut durer beaucoup moins longtemps.

Dans cette étude on passe en moyenne 40 jours à réveiller les testicules pour ensuite passer un tout petit 30 jours à rétablir un profil hormonal plus ou moins normal. J'insiste sur le "plus ou moins" car ici la dernière mesure des taux hormonaux est faite lors de la cessation du nolva, c'est à dire alors que la suppression des estrogènes est encore bien établie. Ceci peut expliquer le taux moyen de testo moyen relativement élevé rencontré en mesure de clôture. L'étude ne fait pas de re-mesure, disons 30 jours après la fin du traitement, ce qui nous donnerait en quelque sorte une "note finale" pour cette relance.

En somme, bonne relance mais hCG en cure à 500ui par semaine et torémifène en relance, nous donnerait sûrement de bien meilleurs résultats, surtout du point de vue culturisme car 70 jours sans testostérone, c'est du grand catabolisme sauvage, ça.

 

[Strong-GearXXL]

Re : pct en 45 jours

c est pas 2500ui au deux jours mais bien au 4jours sur 16 jours soit 10000ui ( 4 injection de 2500 )
4 X 10 000UI SOIT 1JOUR SUR DEUX c est ceux qui n ont pas repondu a la premiere methode

bref a essayer

 

[invité]

Re : pct en 45 jours

c est pas 2500ui au deux jours mais bien au 4jours sur 16 jours soit 10000ui ( 4 injection de 2500 )
4 X 10 000UI SOIT 1JOUR SUR DEUX c est ceux qui n ont pas repondu a la premiere methode

bref a essayer

An Uncontrolled Clinical Trial for Treatment of
Androgen Induced Hypogonadism
2
An Uncontrolled Clinical Trial for Treatment of
Androgen Induced Hypogonadism
By
Michael C. Scally, M.D.
And
Andrew L. Hodge, M.S.
Michael C. Scally, M.D., P.A. Clinic
8707 Katy Freeway, Suite C
Houston, TX 77024



Total Words- 3023
4
Abstract- 237 words
Objective: Although shown to be effective for their intended medical treatment,
AAS have been shown to induce hypogonadotropic hypogonadism in adult
males. The medical literature is conflicting in the reports of spontaneous return
and long-term suppression of gonadal suppression post AAS usage. This
observational study documents the treatment protocol of HCG, clomiphene
citrate, and tamoxifen in returning hormonal function to normal post AAS usage.
Design: Five HIV-negative males age 27-49, weighing 77-100 kg, with
serum total testosterone levels below 240 ng/dL and luteinizing hormone (LH)
levels below 1.5 mIU/mL were considered for this observational study. All five
patients were administered the treatment protocol.
Methods: Treatment consisted of combination therapy which included
concurrent administration of (a) Human Chorionic Gonadotropin, (b) Clomiphene
Citrate and (c) Tamoxifen Citrate for a standard duration of 45 days. This
protocol was repeated with every patient until serum LH and total testosterone
values reached normal ranges.
Results: All five patients were considered eugonadal by normal laboratory
reference ranges by the conclusion of treatment. Average serum total
testosterone rose from 98.2 to 692.8 ng/dL (p<.001) while the average serum LH
rose from an average undetectable value of less than 1.0 to 7.92 mIU/mL
(p<.0008).
5
Conclusions: Although the treatment protocol of HCG, clomiphene citrate, and
tamoxifen proved beneficial in reversing AAS induced hypogonadotropic
hypogonadism, future controlled studies need to be performed to confirm the
beneficial effects of this combined pharmacotherapy in returning HPGA
functioning to normal.
Key Words- anabolic-androgenic steroids, clomiphene, HCG, tamoxifen,
testosterone, HIV
6
INTRODUCTION
Testosterone and testosterone analogues, anabolic-androgenic steroids
(AAS), have long been used in the athletic community for improving lean muscle
tissue and strength. A positive correlation has been shown with testosterone to
include: increased protein synthesis resulting in lean muscle tissue development
(Bhasin et al, 1996; 1997; Hervey et al, 1981; Tenover, 1992), enhanced sexual
desire (libido) (Schiavi et al, 1991), increased muscular strength (Bhasin et al,
1996; 1997; Hervey et al, 1981; Sih et al, 1997), increased erythropoiesis
(Bhasin et al, 1997; Evans & Amerson, 1974; Sih et al, 1997; Tenover, 1992), a
possible positive effect on bone development (Anderson et al, 1996; 1997; Baran
et al, 1978; Tenover, 1992), improved mental cognition and verbal fluency
(Alexander et al, 1998), and male masculinizing characteristics (Starr & Taggart,
1992). Recently, however, clinicians have recognized the potential benefits of
their use in the treatment of various disorders and ailments. Numerous studies
have discussed the use of AAS in the treatment of HIV-associated conditions
(Bhasin et al, 2000; Grinspoon et al, 1998; 1999; 2000; Rabkin et al, 1999; 2000;
Sattler et al, 1999; Strawford et al, 1999; Van Loan et al, 1999), hypogonadism
(Bhasin et al, 1997; Davidson et al, 1979; Rabkin et al, 1999; Sih et al, 1997;
Snyder et al, 2000; Tenover, 1992; Wagner & Rabkin, 1998; Wang et al, 2000),
impotence (Carani et al, 1990; Carey et al, 1988; Klepsch et al, 1982; Lawrence
et al, 1998; McClure et al, 1991; Morales et al, 1994; 1997; Nankin et al, 1986
Rakic et al, 1997; Schiavi et al, 1997), burn victims (Demling et al, 1997), various
7
anemia’s (Doney et al, 1992; Gascon et al, 1999; Hurtado et al, 1993; Stricker et
al, 1984), deteriorated myocardium (Tomoda, 1999), glucose uptake (Hobbs et
al, 1996), continuous ambulatory peritoneal dialysis (CAPD) (Dombros et al,
1994), alcoholic hepatitis (Bonkovskyet al 1991; Mendenhall et al, 1993),
hemochromatosis (Kley et al, 1992) and prevention of osteoporosis (Anderson et
al, 1996; 1997; Baran et al, 1978; Behre et al 1997; Hamdy et al, 1998;
Prakasam et al, 1999).
While AAS have proven effective in cases of lean muscle wasting
conditions (HIV/AIDS), this class of medicines is not without their inherent
problems. AAS have been shown to induce hypogonadotropic hypogonadism
(Alen et al, 1987; Bhasin et al, 1996; Bijlsma et al, 1982; Clerico et al, 1981;
Jarow & Lipshultz, 1990; Strawford et al, 1999; Stromme et al, 1974). This
condition typically results from an abnormality in the normal functioning of the
hypothalamic-pituitary-gonadal axis (HPGA), usually from a negative feedback
inhibition of one of the hormone secreting glands, causing a cascading
unbalance in the rest of the axis. Possibly resulting from a physiological
abnormality (i.e. mumps orchitis, Klinefelters syndrome, pituitary tumor) or as an
acquired result of exogenous factors (i.e. androgen therapy, AAS administration).
Clerico et al (1981) found a dramatic suppression of serum gonadotropin levels
in athletes given methandrostenelone, suggesting a direct action of AAS on the
hypothalamus. Similar results of suppressed gonadotropins have been found in
patients supplementing solely testosterone (Bhasin et al, 1996; Marynick et al,
1979; Strawford et al, 1999; Tenover, 1992). Case report studies discussed a
8
36-year old male competitive bodybuilder and a 39-year old father, each using
various AAS regimens over extended periods of time, who showed a blunted
response to GnRH stimulation tests (Jarow & Lipshultz, 1990). One particular
study administered 600 mg of nandrolone decanoate to 30 HIV-positive males
over twelve weeks (Sattler et al, 1999). The results made no reference to LH or
testosterone levels. The lack of gonadotropin measurement is puzzling as the
data showed 12 of 30 subjects experienced testicular shrinkage, implying Leydig
cell dysfunction and suppressed testosterone levels. Other studies using AAS
have also shown no reference to LH or FSH levels but suppressed values are
expected in each case (Bagatell et al, 1994; Behre et al, 1997; Sheffield-Moore
et al, 1999; Tricker et al, 1996).
Declining, or suppressed, circulating testosterone levels as a result of
either pathophysiological or induced hypogonadal conditions can have many
negative consequences in males. Declining levels of testosterone have been
directly linked to a progressive decrease in muscle mass (Mauras et al, 1998),
loss of libido (Schiavi et al, 1991), decrease in muscular strength (Balagopal et
al, 1997; Mauras et al, 1998) impotence (Rakic et al, 1997), oligospermia or
azoospermia (Vermeulen & Kaufman, 1995), increase in adiposity (Mauras et al,
1998) and an increased risk of osteoporosis (Wishart et al, 1995).
While some research suggests that the hormonal axis will spontaneously
return to normal shortly after cessation of testosterone administration (Knuth et
al, 1989), documented cases have taken up to 2 ½ years to return to normal
(Jarow & Lipshultz, 1990). This case of a 39-year old male who previously used
9
AAS was found to have low serum testosterone levels (6nmol/L, range 14 to 28
nmol/L) 2 ½ years after his last administration of the drugs (Jarow & Lipshultz,
1990). For most men, suffering with diminished libido, impotence, depression,
fatigue, muscle atrophy, and infertility for 2 ½ years is not a pleasant option.
Other androgen or anabolic steroid induced cases of hypogonadotropic
hypogonadism have taken 6 months (Gazvani et al, 1997; Wu et al, 1996), 8
months (Gazvani et al, 1997), 10 months (Boyadjiev et al, 2000), 12 months
(Schurmeyer et al, 1984), and 18 months (Gazvani et al, 1997) to finally return to
eugonadal status.
The individual use of human chorionic gonadotropin (HCG), clomiphene
citrate, and tamoxifen citrate in the treatment of testicular sub-function and
gonadotropin suppression, respectively, is well documented. HCG has been
shown to significantly improve gonadal function in hypogonadotropic
hypogonadal adult males (Barrio et al, 1999; Burgess & Calderon, 1997;
Cisternino et al, 1998; D’Agata et al, 1982; 1984; Dunkel et al, 1985; Kelly et al,
1982; Ley & Leonard, 1985; Liu et al, 1988; Martikainen et al, 1986; Okuyama et
al, 1986; Ulloa-Aguirre et al, 1985; Vicari et al, 1992). Studies using clomiphene
citrate to induce endogenous gonadotropin production in males found significant
improvements in LH and FSH values after treatment (Bjork et al, 1977; Burge et
al, 1997; Guay et al, 1995; Landefeld et al, 1983; Lim & Fang, 1976; Ross et al,
1980; Spijkstra et al, 1988). Tamoxifen citrate has also been found to produce a
profound increase in serum LH levels as well as improved semen and sperm
10
quality (Gazvani et al, 1997; Krause et al, 1985; Lewis-Jones et al, 1987; Wu et
al, 1996).
As HCG’s effect is centralized at the Leydig cells of the testicles,
clomiphene citrate and tamoxifen citrate act upon the hypothalamic-pituitary
region in stimulating gonadotropin production. Tamoxifen, a nonsteroidal
antiestrogen, and clomiphene citrate, a nonsteroidal ovulatory stimulant, compete
with estrogen for estrogen receptor binding sites, thus eliminating excess
estrogen circulation at the level of the hypothalamus and pituitary and allowing
gonadotropin production to resume normally. The normal operation of both the
testicular and hypothalamic-pituitary regions is crucial in returning HPGA function
to normal. Returning one component of the axis to normal without concurrently
returning the other would sabotage and inhibit the operation of the entire HPGaxis.
It was with this understanding that HCG was eventually combined with
clomiphene citrate and tamoxifen as attempted therapy to reverse gonadal
function in hypogonadotropic hypogonadal males.
In accordance with previous studies, each medication was used
individually, and along with HCG, in initial trials. The simultaneous use of
clomiphene citrate and tamoxifen was determined through preliminary use of
clomiphene citrate and tamoxifen individually. It was discovered that although
both clomiphene citrate and tamoxifen met with some success, when combined
together they achieved a more significant increase in gonadotropin production.
This clinical outcome resulted in the combination therapy of HCG, clomiphene
citrate and tamoxifen.
11
Following is a clinical evaluation of the combined, simultaneous use of
HCG, clomiphene citrate, and tamoxifen citrate as a treatment option in
suppressed testosterone and gonadotropin levels in hypogonadotropic
hypogonadal adult males. This observational analysis of the aforementioned
treatment protocol assessed the efficacy of these medicines under non-controlled
conditions.
12
METHODS
An observational study was done on the medical records of 5 adult male
patients presenting to a clinic with induced hypogonadotropic hypogonadism.
Patients were monitored and treatment recorded for the purposes of this
observational study.
SUBJECTS
The medical records of five males age 27-49, mean 35.2, weighing 77-100
kg, mean 89.8 kg, with serum total testosterone levels below 240 ng/dL and
serum luteinizing hormone (LH) levels below 1.5 mIU/mL were examined.
Average presenting testosterone level was 98.2 ng/dL (normal= 240-827 ng/dL)
while average LH level was undetectable at <1.0 mIU/mL (normal= 1.5-9.3
mIU/mL). The 5 patients had a history of AAS usage ranging from 9-60 months
prior to presentation. All patients had ceased any testosterone therapy or AAS
usage prior to initiation of treatment. Initial laboratory values confirmed that all
patients had discontinued AAS long enough for endogenous lab values to fall
below normal reference ranges. All patients were muscular in nature with an
average BMI less than 27 at presentation. Table 1 presents the patient
characteristics, anabolic history, and side effects upon presentation of the 5
patients.
13
LABORATORY STUDIES
Initial blood screening consisted of:
AST, ALT, GGT, TOTAL CHOLESTEROL, LH, FSH, TESTOSTERONE,
GLUCOSE, PROLACTIN, PSA TOTAL, TSH, T3 UPTAKE, T4 TOTAL, T4
FREE, HEMOGLOBIN, HEMATOCRIT
Table 2 shows all baseline serum blood levels at presentation. Baseline blood
screening excluded any form of hyperprolactinemia or hypothyroidism as causes
of hypogonadism in most patients. After physician examination and history and
physical evaluation, it was determined that a history of AAS usage was present
and most likely the cause of the patients’ hypogonadotropic hypogonadal lab
values; not hyperprolactinemia or hypothyroidism.
Laboratory testing was performed by Quest Diagnostics Inc., (Houston,
TX) and SmithKline Beecham Clinical Laboratories, (Houston, TX). Repeat
serum LH & testosterone samples were measured by immunoassay using chiron
reagant kits on an ACS-180 instrument.
METHODS
A review of patients’ medical records showed a treatment intervention of
(a) human chorionic gonadotropin (HCG) (Ferring Pharmaceuticals), (b)
clomiphene citrate (Teva Pharmaceuticals), and (c) tamoxifen (AstraZeneca).
Typical dosage of HCG consisted of 2500 units every other day for 16 days. All
14
HCG injections were self-administered intramuscularly. Starting dosages of
clomiphene citrate and tamoxifen were 50mg and 20 mg daily, respectively.
Patients started all three medications simultaneously and reported for the first
follow-up blood work after completion of HCG, 16 days later. The post HCG
blood analysis assessed testosterone-total response only. If testicular
stimulation, i.e. testosterone production, was inadequate, additional HCG was
administered at this stage of therapy rather than waiting an additional 30-45 days
before the protocol completion. If the testicular response to the HCG
demonstrated sufficient testicular stimulation (typically a blood serum level of
>300 ng/dL), clomiphene citrate and tamoxifen were continued for 15 and 30
days, respectively. The arbitrary cut-off level of 300 ng/dL was used as a general
assessment where sufficient Leydig cell stimulation was taking place even in light
of artificial stimulation from HCG. A repeat blood sample was then taken at day
45 to assess hypothalamic-pituitary-gonadal axis status via luteinizing hormone
and total testosterone levels. Because of the varying cessation times of the
medications, the concluding blood sample was taken after a 30 and 15-day
washout period of HCG and clomiphene citrate, respectively. For HPGA function
to be considered normal, both LH and testosterone values had to fall within the
normal reference ranges. For the purposes of patient treatment, if LH and
testosterone values were still below normal limits at the conclusion of 45 days of
treatment, a repeat protocol administration of HCG, clomiphene citrate, and
tamoxifen was given. This protocol was repeated with every patient until LH and
testosterone values reached normal ranges.
15
RESULTS
All five patients were considered eugonadal by normal laboratory
reference ranges by the conclusion of treatment. Average serum total
testosterone rose from 98.2 to 692.8 ng/dL. Average serum LH rose from <1.0 to
7.92 mIU/mL. An average of 48,974 U of HCG (five 10,000 Unit boxes),
3412.5 mg of clomiphene citrate (68.25 50mg tablets), and 968.71 mg of
tamoxifen (48.44 20mg tablets) were used to treat all patients to eugonadal.
Total treatment time ranged from 43-120 days. Mean elapsed time from
initiation of treatment to eugonadal was 68.6 days. Statistical analysis was
performed using repeated measures ANOVA. Pre and post treatment
testosterone values were significantly (p<.001) different as were the LH values
(p<.0008). Table 3 demonstrates the hormone changes during the treatment
period and the duration to eugonadal.
ADVERSE EVENTS
None of the study subjects had any serious or treatment-terminating
effects as a result of the multi-drug protocol. No problems were noted with
regards to parameters of normal urologic function or treatment causing
gynecomastia. Any side effects documented at presentation were reversed by
the conclusion of treatment.
16
DISCUSSION
This observational study demonstrates the possible efficacy of HCG,
clomiphene citrate, and tamoxifen citrate in returning the HPGA to normal
physiological function in adult males suffering from androgen induced
hypogonadotropic hypogonadism. In the case of decreased testicular function
manifested by low testosterone levels, it is of primary importance to first return
the normal function of the testicular cells. The initial lack of response to HCG
should not immediately be a cause for the initiation of testosterone replacement
therapy, as with the current accepted therapy modality by many physicians.
Blood analysis confirmed that no exogenous testosterone was administered
during the treatment period, as exogenous androgens would have had a
suppressive effect on endogenous gonadotropin production. Therefore, because
of the corresponding normal gonadotropin and testosterone values, it is accepted
that gonadotropin and testicular function were normal by the conclusion of
treatment.
The standard treatment of HIV-related muscle wasting, AAS therapy, may
involve decades of treatment and the attendant problems with any therapy of a
prolonged nature. Polycythemia vera, elevated hepatic enzymes, and prolonged
negative alterations in lipid profile are a few of the dangers experienced by HIV
patients administered AAS for extended periods. Of greatest concern is the
increasing numbers of individuals who are currently being treated with AAS to
increase muscle mass either for medicinal or recreational means without
17
attention being given to periodically returning the HPGA to normal. With roughly
4 million men in the U.S. being considered hypogonadal (Lacayo R., 2000;
Sheffield-Moore et al, 1999; Shelton DL, 2000), an estimated 200,000 men are
currently receiving testosterone treatment for the condition (Shelton DL, 2000).
As stated earlier, AAS are being prescribed to HIV & AIDS sufferers to combat
progressive muscle loss. The Centers for Disease Control and Prevention (CDC)
reported an estimated 635,000+ men diagnosed with AIDS through December
2000 while an estimated 97,700 have been reported with HIV (Centers for
Disease Control, vol.12, No. 2, table 5; Centers for Disease Control, vol. 12, No.
2, table 6). In 2000 alone over 31,000 men were diagnosed with the AIDS virus
(Centers for Disease Control, vol. 12, No. 2, figure 3). Between hypogonadal,
AIDS, & HIV males, potentially over 900,000 men are being administered AAS
therapy.
Studies recently published on patients suffering from various tissuedepleting
conditions and HIV affliction (Bhasin et al, 2000; Grinspoon et al, 1998;
1999; 2000; Rabkin et al, 1999; 2000; Sattler et al, 1999; Strawford et al,
1999;1999; Van Loan et al, 1999) have not identified what should be done to
restore normal endocrine status post-treatment. Considering the dosages and
compounds administered in many studies, there is no question that subjects
were left hypogonadal after therapy. In the cases where the periodic use of
testosterone or AAS are necessary, intervention to return the HPGA to normal
should be initiated as soon as possible after the cessation of the AAS. As
18
described herein, a possible treatment modality may be the combined regimen of
HCG, clomiphene citrate, and tamoxifen.
Medical history has demonstrated examples of physician-induced
complications resulting from treatment. Iatrogenic hyperthyroidism (Bartsch &
Scheiber, 1981) and iatrogenic Cushing’s syndrome (Cihak & Beary, 1977;
Kimmerle & Rolla, 1985; Smidt & Johnston, 1975; Tuel et al, 1990) are cases
were administered medications or treatments provoked abnormalities in patients’
normal physiology. The administration of testosterone as a treatment for
hypogonadotropic hypogonadism falls into this same category of causing
endocrine related abnormalities (Bhasin et al, 1996; Marynick et al, 1979;
Strawford et al, 1999; Tenover, 1992). Testosterone replacement therapy has
proven to be very effective in reversing the symptoms of suppressed
testosterone production, but does not treat the underlying cause of the
deficiency. Positive effects of testosterone treatment; i.e. improved sex drive,
improved sense of well-being, lean body mass; are all transient in light of
plummeting gonadotropin levels. Upon cessation of testosterone treatment
patients can expect a complete reversal of positive benefits as exogenously
influenced testosterone levels metabolize and decline rapidly.
Further controlled studies need to be performed showing the combined
effects of HCG, clomiphene citrate, and tamoxifen in returning HPGA functioning
to normal. Long-term follow-up on these patients returning to normal will be
necessary to ensure permanent reversal of hypogonadotropic hypogonadal
conditions. In addition, studies documenting dose-response curves for pituitary
19
inhibition and reversal due to AAS administration are critical in determining the
correct dose, duration, and form of treatment that is optimal without causing
permanent damage. When the need for long-term androgen use presents, using
moderately supraphysiologic doses of androgens as suggested by Strawford and
colleagues (1999) coupled with post-treatment HPGA restoration as
demonstrated here, may be a more effective means over high-dose protocols
used to offset negative alterations in lean body mass. Unfortunately current
studies have yet to adequately address a standard of patient care post-androgen
therapy. Because of the negative impact of the hypogonadal state on physical
and mental well- being, pharmacotherapy that restores HPGA function more
rapidly than current modalities would greatly benefit men with hypogonadotropic
hypogonadism.
While we believe that the treatment protocol was effective in returning
normal hormonal function to these men, the lack of randomization or a control
group leaves room for speculation. Although cases of spontaneous return to
eugonadism with no medicinal intervention have been published, these reports
documented durations anywhere from 6-18 months before normal hormone
status was achieved (Gazvani et al, 1997; Wu et al, 1996). If the alternative
treatment modality described herein can reverse suppressed gonadotropin
production and AAS associated side effects much sooner than non-treatment,
further evaluation of this therapy should continue.


SOURCE ANABOLEX FORUM

Ils disent bien 2500ui 1 jour sur 2. D'ailleurs si tu reprends avec moi le calcul:

Moyenne de 48,974ui de hCG
À raison de 2500 par 2 jours donne 39.9 jours de hCG en moyenne, ce qui nous amène à calculer une durée totale moyenne du traitement de 69.9 jours. L'étude cite 68.6 jours, ce qui est probablement une erreur d'arrondissement.
Certainement en calculant le 48,974ui de hCG en 2500 aux 4 jours, cela donne 78.5 jours de hCG + 30 jours de clomid/nolva = 108.5 jours ce qui est loin d'être la durée moyenne du traitement citée.

Je me trompe rarement, puisque je revérifie toujours mes données à moins d'être parfaitement certain.

 

[porto78]

Re : pct en 45 jours

Ils disent bien 2500ui 1 jour sur 2. D'ailleurs si tu reprends avec moi le calcul:

Moyenne de 48,974ui de hCG
À raison de 2500 par 2 jours donne 39.9 jours de hCG en moyenne, ce qui nous amène à calculer une durée totale moyenne du traitement de 69.9 jours. L'étude cite 68.6 jours, ce qui est probablement une erreur d'arrondissement.
Certainement en calculant le 48,974ui de hCG en 2500 aux 4 jours, cela donne 78.5 jours de hCG + 30 jours de clomid/nolva = 108.5 jours ce qui est loin d'être la durée moyenne du traitement citée.

Je me trompe rarement, puisque je revérifie toujours mes données à moins d'être parfaitement certain.

ouff enfin, merci maitre grunt:cool1:

 

[Strong-GearXXL]

Re : pct en 45 jours

oui d accord avec toi grunt mais l etude a ete fait sur 5 patient :

15
RESULTS
All five patients were considered eugonadal by normal laboratory
reference ranges by the conclusion of treatment. Average serum total
testosterone rose from 98.2 to 692.8 ng/dL. Average serum LH rose from <1.0 to
7.92 mIU/mL. An average of 48,974 U of HCG (five 10,000 Unit boxes),
3412.5 mg of clomiphene citrate (68.25 50mg tablets), and 968.71 mg of
tamoxifen (48.44 20mg tablets) were used to treat all patients to eugonadal.
Total treatment time ranged from 43-120 days. Mean elapsed time from
initiation of treatment to eugonadal was 68.6 days. Statistical analysis was
performed using repeated measures ANOVA. Pre and post treatment
testosterone values were significantly (p<.001) different as were the LH values
(p<.0008). Table 3 demonstrates the hormone changes during the treatment
period and the duration to eugonadal

et le premier protocole est bien 4 injection de 2500ui etalé sur 16 jours , a ca certain au repondu positivement le traitement a durée 43 jours !
pour les autres il on bien recu 2500 ui tt les deux jours donc 40000ui avec le protocole qui a duree 120 jours

enfin bref ici je montre l etude pour moi ce n est que ca

et puis 40000ui qu est ce que c est ? j ai ete traiter avec au moins ca pour mon hypogodamisne et meme sur la notice il fait bien marquer peut etre pris 5000 UI plusieur fois par semaines pendant des mois donc pour moi la desensibilisation avec le hgc c est de la connerie LORS D UN HYPOGODAMISNE seulement aussinon ca peut stopper le retablisement ok mais lorsque c est stopper avec les produits comme moi ca ne peut que faire du bien :ange1:

 

[invité]

Re : pct en 45 jours

Je veux pas faire tourner cet excellent topic, mais tu prends où l'idée d'à chaque 4 jours? J'ai rien vu qui laisse supposer ça!

 

[invité]

Re : pct en 45 jours

salut tout le monde
je lance se post une autre fois car je suis en plein pct de 45j et franchement ça va pas du tout
je m'explique
je suis a 2500ui de hcg tout les 3j
100mg de clomid
50mg de nolvadex
le problème c'est quand je prend 100mg de clomid j'ai des envie de vomir et sa me tourne sévère la tête au point ou je suis obligé de me remettre au lit le temps que sa passe
mais si je prend que 50mg de clomid par jour tout se passe bien et aucun symptôme
quelqu'un a déjà eu ces problème la ou je suis le seul et si quelqu'un peut me conseiller je suis preneur
merci d'avance

 

[Burattino]

Re : pct en 45 jours

Tu split bien la prise en deux comme c'est indiqué?

 

[Befa]

Re : pct en 45 jours

C'est 50mg 2 fois dans la journée le clomid

 

[invité]

Re : pct en 45 jours

Tu split bien la prise en deux comme c'est indiqué?

j'ai splité en 2 mais la impossible de dormir pourtant je prend la deuxième partie le midi mais le soir je me couche pas avant 5h du matin et les vertige sont présent mais pas si fort que quand je prend le clomid en 100mg direct

 

[Befa]

Re : pct en 45 jours

j'ai splité en 2 mais la impossible de dormir pourtant je prend la deuxième partie le midi mais le soir je me couche pas avant 5h du matin et les vertige sont présent mais pas si fort que quand je prend le clomid en 100mg direct

Essaye matin et au coucher peut etre

 

[invité]

Re : pct en 45 jours

Essaye matin et au coucher peut etre

je vais tester ça ce soir vu que j'ai pris que 50mg se matin au petit dej je vais en prendre le reste avant de me coucher et je vous tien au courant

 

[Befa]

Re : pct en 45 jours

je vais tester ça ce soir vu que j'ai pris que 50mg se matin au petit dej je vais en prendre le reste avant de me coucher et je vous tien au courant

:nice:

 

[invité]

Re : pct en 45 jours

Essaye matin et au coucher peut etre

merci poto pour ton conseil
j'ai tester 50mg au petit dej et 50mg le diner tout se passe bien
je les prend au milieu des repas comme ça j'ai 0 vertige ou envie de vomir

 

[Befa]

Re : pct en 45 jours

merci poto pour ton conseil
j'ai tester 50mg au petit dej et 50mg le diner tout se passe bien
je les prend au milieu des repas comme ça j'ai 0 vertige ou envie de vomir

Niquel alors :nice:

 

[banner]

Re : pct en 45 jours

Salut à tous .
Je fais partager mon experience d'hier .
Je viens de lire plus haut et apparement je ne suis pas le seul .

Avant de connaitre le fofo je faisais 25mg de clomid et 20 mg de tamoxifene par jour pendant 1 mois .

hier j ai voulu commencer la pct en degressive . A savoir 100mg le 1er jour .
Je ne connaissais pas les effets secondaires du clomid à haute dose .
J'ai pris 50 au lever avec mon shaker et 50 à nouveau 2h apres avec mon ptit dej .

resultat .
A 11h du mat vue troublée . Vertiges . Nausées . Je rentre chez moi . 1h de bagnole (atroce) .
Une fois arrivé . Envie de rien , je me fou au lit . Je me retourne 30 fois impossible de dormir . Je me leve . Jambes lourdes , toujours les memes nausées .
Ma femme se leve du coup et on detaille mon debut de journée . On ecarte tout le reste et on fini donc sur le clomid . Elle cherche pour moi et me dit qu'il faut spliter au maximun .
Les effets sont partis petit à petit et j'etais OP seulement a 19h le soir .

Journée pourri ,passé à faire des allers retour lit/canap sans pourvoir dormir comme un pauvre type .

J'epluche le fofo tout les jours mais pas assez apparement .
Aujourd 'hui je devrais faire 50 de clomid mais j'avou que j'hesite vraiment .

Bonne relance à tous ceux qui sont sur cette page . et le mot du jour "fractionne le clomid " que je vais me faire tatouer sur le bras cet aprem .

 

[jarod]

Re : pct en 45 jours

"twice a day" comme le préconise le livre "anabolics 10th" , est ce que ça ne signifierais pas plutôt qu'il faut prendre les 50 mg de Clomid en 2 fois ?

C'est ce que je fais et je n'ai jamais eu tout les problèmes cités ci dessus et la PCT se passe très bien.

 

[body-youns]

Re : pct en 45 jours

salut les gars !
une petite question à vous poser :
vous parlez de taux de testo en "ng/dL" mais personellement je viens de pratiquer des analyses concernant ma testo et mes résultats sont en ng/mL et nmol/L pour la testo biodisponible ou en pg/mL pour la testo libre ?!!
vous pouvez m'en dire plus la dessus ? merci beaucoup

 

[yoda55]

Re : pct en 45 jours

Regarde un petit peu ce truc là, tu devrais déjà avoir quelques réponses.

http://musclesenmetal.is/forum/show...r-en-biochimie-m%E9dicale?p=340297#post340297

 

[body-youns]

Re : pct en 45 jours

merci yoda mais je ne comprends pas vraiment ce que donne ce lien , des convertions évidement mais consernant la testo ça me donnent des résultats étranges que je ne comprends pas trop ! ... tu peux m'expliquer un peu plus yoda merci ?
je peux te donner mes taux exact si tu veux ?!