Research results on reversal HPTA
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.
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
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).
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 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
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 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
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 � years to return to normal (Jarow
& Lipshultz, 1990). This case of a 39-year old male who previously used AAS
was found to have low serum testosterone levels (6nmol/L, range 14 to 28 nmol/L)
2 � 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 � 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
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 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 gonada
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.
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.
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.
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
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.
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 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.
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.
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
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 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 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
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
Alen M, Rahkila P, Reinila M, Vihko R. Androgenic-Anabolic Steroid Effects on
Serum Thyroid, Pituitary and Steroid Hormones in Athletes. American Journal of
Sports Medicine. 1987; 15: 357-361.
Alexander GM, Swerdloff RS, Wang C, Davidson T, McDonald V, Steiner B, Hines M.
April Androgen-behavior Correlations in Hypogonadal Men and Eugonadal Men. II.
Cognitive Abilities. Hormones and Behavior. 1998; 33(2): 85-94.
Anderson FH, Francis RM, Faulkner K. Androgen Supplementation in Eugonadal Men
with Osteoporosis: Effects of Six Months of Treatment on Bone Mineral Density
and Cardiovascular Risk Factors. Bone. 1996 Feb; 18(2): 171-177.
Anderson FH, Francis RM, Peaston RT, Wastell HJ. Androgen Supplementation in
Eugonadal Men With Osteoporosis: Effects of Six Months� Treatment on Markers
of Bone Formation and Resorption. Journal of Bone and Mineral Research. 1997
Bagatell CJ, Heiman JR, Matsumoto AM, Rivier JE, Bremner WJ. Metabolic and
Behavioral Effects of High-Dose, Exogenous Testosterone in Healthy Men. Journal
of Clinical Endocrinology and Metabolism. 1994 Aug; 79(2): 561-567.
Bagatell CJ, Matsumoto AM, Christensen RB, Rivier JE, Bremner WJ. Comparison of
a gonadotropin releasing �hormone antagonist plus testosterone (T) versus T
alone as potential male contraceptive regimens. Journal of Clinical
Endocrinology and Metabolism. 1993 Aug; 77(2): 427-32.
Balagopal P, Rooyackers OE, Adey DB, Ades PA, Nair KS. Effects of Aging on In
Vivo Synthesis of Skeletal Muscle Myosin Heavy-Chain and Sarcoplasmic Protein in
Humans. American Journal of Physiology. 1997; 273 (4 pt 1): E790-800.
Baran DT, Bergfeld MA, Teitelbaum SL, Avioli LV. Effect of Testosterone Therapy
on Bone Formation in an Osteoporotic Hypogonadal Male. Calcified Tissue
Research. 1978 Dec; 26(2): 103-106.
Barrio R, de Luis D, Alonso M, Lamas A, Moreno JC. Induction of Puberty with
Human Chorionic Gonadotropin and Follicle-Stimulating Hormone in Adolescent
Males With Hypogonadotrophic Hypogonadism. Fertility and Sterility. 1999 Feb;
Bartsch G, Scheiber K. Tamoxifen Treatment in Oligozoospermia. European Urology.
1981; 7(5): 283-287.
Behre HM, Kliesch S, Leifke E, Link TM, Nieschlag E. Long-Term Effect of
Testosterone Therapy on Bone Mineral Density in Hypogonadal Men. Journal of
Clinical Endocrinology and Metabolism. 1997 Aug; 82(8): 2386- 2390.
Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ,
Tricker R, Shirazi A, Casaburi R. The Effects of Supraphysiologic Doses of
Testosterone on Muscle Size and Strength in Normal Men. New England Journal of
Medicine. 1996 July 4; 335: 1-7.
Bhasin S, Storer TW, Berman N, Yarasheski KE, Clevenger B, Phillips J, Lee WP,
Bunnell TJ, Casaburi R. Testosterone Replacement Increases Fat-Free Mass and
Muscle Size in Hypogonadal Men. Journal of Clinical Endocrinology and
Metabolism. 1997; 82(2): 407-413.
Bhasin S, Storer TW, Javanbakht M, Berman N, Yarasheski KE, Phillips J, Dike M,
Sinha-Hikim I, Shen R, Hays RD, Beall G. Testosterone Replacement and Resistance
Exercise in HIV-Infected Men With Weight Loss and Low Testosterone Levels. JAMA.
2000 Feb 9; 283(6): 763-770.
Bijlsma JWJ, Duursma SA, Thijssen JHH, Huber O. Influence of Nandrolondecanoate
on the Pituitary-Gonadal Axis in Males. Acta Endocrinologica. 1982 Sep; 101:
Bjork JT, Varma RR, Borkowf HI. Clomiphene Citrate Therapy in a Patient with
Laennec�s Cirrhosis. Gastroenterology. 1977 Jun; 72(6): 1308-1311.
Bonkovsky HL, Singh RH, Jafri IH, Fiellin DA, Smith GS, Simon D, Cotsonis GA,
Slaker DP. A Randomized, Controlled Trial of Treatment of Alcoholic Hepatitis
with Parental Nutrition and Oxandrolone. II. Short-term Effects on Nitrogen
Metabolism, Metabolic Balance, and Nutrition. American Journal of
Gastroenterology. 1991 Sep; 86(9): 1209-1218.
Boyadjiev NP, Georgieva KN, Massaldjieva RI, Gueorguiev SI. Reversible
Hypogonadism and Azoospermia as a Result of Anabolic-Androgenic Steroid Use in a
Body Builder With Personality Disorder. A Case Report. Journal of Sports
Medicine and Physical Fitness. 2000 Sep; 40(3): 271-274.
Burge MR, Lanzi RA, Skarda ST, Eaton RP. Idiopathic Hypogonadotropic
Hypogonadism in a Male Runner is Reversed by Clomiphene Citrate. Fertility and
Sterility. 1997 April; 67(4): 783-785.
Burgess S, Calderon MD. Subcutaneous Self-Administration of Highly
Purified Follicle Stimulating Hormone and Human Chorionic Gonadotrophin for the
Treatment of Male Hypogonadotrophic Hypogonadism. Spanish Collaborative Group on
Male Hypogonadotropic Hypogonadism. Human Reproduction. 1997 May; 12(5):
Carani C, Zini D, Baldini A, Della Casa L, Ghizzani A, Marrama P. Effects of
Androgen Treatment in Impotent Men with Normal and Low Levels of Free
Testosterone. Archives of Sexual Behavior. 1990 Jun; 19(3): 223-234.
Carey PO, Howards SS, Vance ML. Transdermal Testosterone Treatment of
Hypogonadal Men. Journal of Urology. 1988 Jul; 140(1): 76-79.
Centers for Disease Control. Division of HIV/AIDS Prevention. Survey Report vol.
12, No. 2. Table 6. www.cdc.gov
Centers for Disease Control. Division of HIV/AIDS Prevention. Survey Report vol.
12, No. 2. Figure 3. www.cdc.gov
Centers for Disease Control. Division of HIV/AIDS Prevention. Survey Report vol.
12, No. 2. Table 5. www.cdc.gov
Cihak RW, Beary FD. Elevated Triiodothyronine and Dextrothyroxine Levels: A
Potential Cause of Iatrogenic Hyperthyroidism. Southern Medical Journal. 1977
Feb; 70(2): 256-257.
Cisternino M, Manzoni SM, Coslovich E, Autelli M. Hormonal Replacement Therapy
with HCG and HU-FSH in Thalassaemic Patients Affected by Hypogonadotropic
Hypogonadism. Journal of Pediatric Endocrinology and Metabolism. 1998; 11 Suppl
Clerico A, Ferdeghini M, Palombo C, Leoncini R, Del Chicca MG, Sardano G,
Mariani G. Effect of Anabolic Treatment on the Serum Levels of Gonadotropins,
Testosterone, Prolactin, Thyroid Hormones and Myoglobin of Male Athletes Under
Physical Training. Journal of Nuclear Medicine and Allied Science. 1981
July-Sep; 25(3): 79-88.
Cook LH, Freinkel RK, Zugerman C, Levin DL, Radtke R. Iatrogenic
Hyperadrenocorticism During Topical Steroid Therapy: Assessment of Systemic
Effects by Metabolic Criteria. Journal of American Academy of Dermatology. 1982
Jun; 6(6): 1054-1060.
D�Agata R, Heindel JJ, Vicari E, Aliffi A, Gulizia S, Polosa P. HCG-Induced
Maturation of the Seminiferous Epithelium in Hypogonadotropic Men. Hormone
Research. 1984; 19(1): 23-32.
D�Agata R, Vicari E, Aliffi A, Maugeri G, Mongioi A, Gulizia S. Testicular
Responsiveness to Chronic Human Chorionic Gonadotropin Administration in
Hypogonadotropic Hypogonadism. Journal of Clinical Endocrinology and Metabolism.
1982 Jul; 55(1): 76-80.
Davidson JM, Camargo CA, Smith ER. Effects of Androgen on Sexual Behavior in
Hypogonadal Men. Journal of Clinical Endocrinology and Metabolism. 1979 Jun;
Demling RH, DeSanti L. Oxandrolone, an Anabolic Steroid, Significantly Increases
the Rate of Weight Gain in the Recovery Phase After Major Burns. The Journal of
Trauma. 1997 Jul; 43(1): 47-51.
Dombros NV, Digenis GE, Soliman G, Oreopoulos DG. Anabolic Steroids in the
Treatment of Malnourished CAPD Patients: a Retrospective Study. Peritoneal
Dialysis International. 1994; 14(4): 344-347.
Donega P, Gallerani M, Vigna GB, Fellin R. Reversible Hyperthyroidism and
Cardiomyopathy Caused by Consumption of Iodocasein. American Journal of Medical
Science. 2000 Aug; 320(2): 148-150.
Doney K, Pepe M, Storb R, Bryant E, Anasetti C, Appelbaum FR, Buckner CD,
Sanders J, Singer J, Sullivan K, et al. Immunosuppressive Therapy of Aplastic
Anemia: Results of a Prospective, Randomized Trial of Antithymocyte Globulin (ATG),
Methylprednisolone, and Oxymetholone to ATG, Very High-Dose Methylprednisolone,
and Oxymetholone. Blood. 1992 May 15; 79(10): 2566-2571.
Dunkel L, Perheentupa J, Sorva R. Single versus Repeated Dose Human Chorionic
Gonadotropin Stimulation in the Differential Diagnosis of Hypogonadotropic
Hypogonadism. Journal of Clinical Endocrinology and Metabolism. 1985 Feb; 60(2):
Evans RP and Amerson AB. 1974 Androgens and Erythropoiesis. Journal of Clinical
Pharmacology. 1974; 14: 94-101.
Gascon A, Belvis JJ, Berisa F, Iglesias E, Estopinan V, Terul JL. Nandrolone
Decanoate is a Good Alternative for the Treatment of Anemia in Elderly Male
Patients on Hemodialysis. Geriatric Nephrol Urol. 1999; 9(2): 67-72.
Gazvani MR, Buckett W, Luckas MJM, Aird IA, Hipkin LJ, Lewis-Jones DI.
Conservative management of azoospermia following steroid abuse. Human
Reproduction. 1997; 12(8): 1706-1708.
Grinspoon C, Corcoran C, Askari H, Schoenfeld D, Wolf L, Burrows B, Walsh M,
Hayden D, Parlman K, Anderson E, Basgoz N, Klibanski A. Effects of Androgen
Administration in Men With the AIDS Wasting Syndrome. A Randomized,
Double-Blind, Placebo-Controled Trial. Annals of Internal Medicine. 1998 July 1;
Grinspoon S, Corcoran C, Anderson E, Hubbard J, Stanley T, Basgoz N, Klibanski
A. Sustained Anabolic Effects of Long-Term Androgen Administration in Men With
AIDS Wasting. Clinical Infectious Diseases. 1999 Mar; 28(3): 634-636.
Grinspoon S, Corcoran C, Parlman K, Costello M, Rosenthal D, Anderson E, Stanley
T, Schoenfeld D, Burrows B, Hayden D, Basgoz N, Klibanski A. Effects of
Testosterone and Progressive Resistance Training in Eugonadal Men With AIDS
Wasting. A Randomized, Controlled Trial. Annals of Internal Medicine. 2000 Sep
5; 133(5): 348-355.
Grinspoon S, Corcoran C, Stanley T, Baaj A, Basgoz N, Klibanski A. Effects of
Hypogonadism and Testosterone Administration on Depression Indices in
HIV-Infected Men. Journal of Clinical Endocrinology and Metabolism. 2000 Jan;
Grubb SR, Cantley LK, Jones DL, Carter WH. Iatrogenic Cushing�s Syndrome After
Intrapericardial Corticosteroid Therapy. Annals of Internal Medicine. 1981 Dec;
Guay AT, Bansal S, Heatley GJ. Effect of Raising Endogenous Testosterone Levels
in Impotent Men With Secondary Hypogonadism: Double Blind Placebo-Controlled
Trial with Clomiphene Citrate. Journal of Clinical Endocrinology and Metabolism.
1995 Dec; 80(12): 3546-3552.
Hamdy RC, Moore SW, Whalen KE, Landy C. Nandrolone Decanoate for Men with
Osteoporosis. American Journal of Therapeutics. 1998 Mar; 5(2): 89-95.
Hankins JH, Heise CM, Cowan RJ. Iatrogenic Hyperthyroidism Secondary to
Dextrothyroxine Administration. Clinical Nuclear Medicine. 1984 Jan; 9(1):
Hervey GR, Knibbs AV, Burkinshaw L, Morgan DB, Jones PRM, Chettle DR, Vartsky D.
Effects of Methandienone on the Performance and Body
Composition of Men Undergoing Athletic Training. Clinical Science. 1981; 60(4):
Hobbs CJ, Jones RE, Plymate SR. Nandrolone, a 19-Nortestosterone, Enhances
Insulin-Independent Glucose Uptake in Normal Men. Journal of Clinical
Endocrinology and Metabolism. 1996 Apr; 81(4): 1582-1585.
Hurtado R, Sosa R, Majluf A, Labardini JR. Refractory Anaemia (RA) Type I FAB
Treated With Oxymetholone (OXY): Long-Term Results. British Journal of
Haematology. 1993 Sep; 85(1): 235-236.
Jarow JP and Lipshultz LI. Anabolic Steroid-Induced Hypogonadotropic
Hypogonadism. American Journal of Sports Medicine. 1990 Jul-Aug; 18(4): 429-431.
Kelly WF, Kjeld JM, Mashiter K, Joplin GF. Reassessment of the Human Chorionic
Gonadotropin Stimulation Test in Hypogonadal Males. Archives of Andrology. 1982
Feb; 8(1): 53-59.
Kimmerle R, Rolla AR. Iatrogenic Cushing�s Syndrome Due to Dexamethasone Nasal
Drops. American Journal of Medicine. 1985 Oct;
Klepsch I, Maicanescu-Georgescu M, Marinescu L. Clinical and Hormonal Effects of
Testosterone Undecanoate (TU) in Male Sexual Impotence. Endocrinologie. 1982
Oct-Dec; 20(4): 289-293.
Kley HK, Stremmel W, Kley JB, Schaghecke R. Testosterone Treatment of Men With
Idiopathic Hemochromatosis. Clinical Investigation. 1992 Jul; 70(7): 566-572.
Krause W, Hubner HM, Wichmann U. Treatment of Oligozoospermia by Tamoxifen: No
Evidence for Direct Testicular Action. Andrologia. 1985 May- June; 17(3):
Lacayo R. Are You Man Enough? Time Magazine. 2000 April 24; 155: 58-64.
Landefeld CS, Schambelan M, Kaplan SL, Embury SH. Clomiphene- Responsive
Hypogonadism in Sickle Cell Anemia. Annals of Internal Medicine. 1983 Oct;
Lawrence IG, Price DE, Howlett TA, Harris KP, Feehally J, Walls J. Correcting
Impotence in the Male Dialysis Patient: Experience With Testosterone Replacement
and Vacuum Tumescence Therapy. American Journal of Kidney Disorders. 1998 Feb;
Lewis-Jones DI, Lynch RV, Machin DC, Desmond AD. Improvement in Semen Quality in
Infertile Males After Treatment with Tamoxifen. Andrologia. 1987 Jan-Feb; 19(1):
Ley SB, Leonard JM. Male Hypogonadotropic Hypogonadism: Factors Influencing
Response to Human Chorionic Gonadotropin and Human Menopausal Gonadotropin,
Including Prior Exogenous Androgens. Journal of Clinical Endocrinology and
Metabolism. 1985 Oct; 61(4): 746-752.
Lim VS, Fang VS. Restoration of Plasma Testosterone Levels in Uremic Men With
Clomiphene Citrate. Journal of Clinical Endocrinology and Metabolism. 1976 Dec;
Liu L, Banks SM, Barnes KM, Sherins RJ. Two-year Comparison of Testicular
Responses to Pulsatile Gonadotropin-Releasing Hormone and Exogenous
Gonadotropins from the Inception of Therapy in Men with Isolated
Hypogonadotropic Hypogonadism. Journal of Clinical Endocrinology and Metabolism.
1988 Dec; 67(6): 1140-1145.
Martikainen H, Alen M, Rahkila P, Vihko R. Testicular Responsiveness to Human
Chorionic Gonadotrophin During Transient Hypogonadotrophic Hypogonadism Induced
by Androgenic/Anabolic Steroids in Power Athletes. Journal of Steroid
Biochemistry. 1986 July; 25(1): 109-112.
Marynick SP, Loriaux DL, Sherins RJ, Pita JC Jr, Lipsett MB. 1979 Sep Evidence
that Testosterone can Suppress Pituitary Gonadotropin Secretion Independently of
Peripheral Aromatization. Journal of Clinical Endocrinology and Metabolism.
Mauras N, Hayes V, Welch S, Rini A, Helgeson K, Dokler M, Veldhuis JD, Urban RJ.
Testosterone Deficiency in Young Men: Marked Alterations in Whole Body Protein
Kinetics, Strength, and Adiposity. Journal of Clinical Endocrinology and
Metabolism. 1998; 83: 1886-1892.
McClure RD, Oses R, Ernest ML. Mar Hypogonadal Impotence Treated by Transdermal
Testosterone. Urology. 1991; 37(3): 224-228.
Mendenhall CL, Moritz TE, Roselle GA, Morgan TR, Nemchausky BA, Tamburro CH,
Schiff ER, McClain CJ, Marsano LS, Allen JI. A Study of Oral Nutritional Support
with Oxandrolone in Malnourished Patients with Alcoholic Hepatitis: Results of a
Department of Veterans Affairs Cooperative Study. Hepatology. 1993 April; 17(4):
Morales A, Johnston B, Heaton JP, Lundie M. Testosterone Supplementation for
Hypogonadal Impotence: Assessment of Biochemical Measures and Therapeutic
Outcomes. Journal of Urology. 1997 Mar; 157(3): 849-854.
Morales A, Johnston B, Heaton JW, Clark A. Oral Androgens in the Treatment of
Hypogonadal Impotent Men. Journal of Urology. 1994 Oct; 152(4): 115-1118.
Nankin HR, Lin T, Osterman J. Chronic Testosterone Cypionate Therapy in Men with
Secondary Impotence. Fertility and Sterility. 1986 Aug; 46(2): 300- 307.
Noci I, Chelo E, Saltarelli O, Donati CG, Scarselli G. Tamoxifen and
Oligospermia. Archives of Andrology. 1985; 15(1): 83-88.
Okuyama A, Nakamura M, Namiki M, Aono T, Matsumoto K, Utsunomiya M, Yoshioka T,
Itoh H, Itatani H, Mizutani S, et al. Testicular Responsiveness to Long-Term
Administration of HCG and HMG in Patients with Hypogonadotrophic Hypogonadism.
Hormone Research. 1986; 23(1): 21-30.
Prakasam G, Yeh JK, Chen MM, Castro-Magana M, Liang CT, Aloia JF. Effects of
Growth Hormone and Testosterone on Cortical Bone Formation and Bone Density in
Aged Orchiectomized Rats. Bone. 1999 May; 24(5): 491-497.
Rabkin JG, Wagner GJ, Rabkin R. A Double-Blind, Placebo-Controlled Trial of
Testosterone Therapy for HIV-Positive Men With Hypogonadal Symptoms. Archives of
General Psychiatry. 2000 Feb; 57(2): 141-147.
Rabkin JG, Wagner GJ, Rabkin R. Testosterone Therapy for Human Immunodeficiency
Virus-Positive Men With and Without Hypogonadism. Journal of Clinical
Psychopharmacology. 1999 Feb; 19(1): 19-27.
Rakic Z, Starcevic V, Starcevic VP, Marinkovic J. Testosterone Treatment in Men
with Erectile Disorder and Low Levels of Total Testosterone in Serum. Archives
of Sexual Behavior. 1997 Oct; 26(5): 495-504.
Ross LS, Kandel GL, Prinz LM, Auletta F. Clomiphene Treatment of the Idiopathic
Hypofertile Male: High-Dose, Alternate-Day Therapy. Fertility and Sterility.
1980 Jun; 33(6): 618-623.
Sattler FR, Jaque SV, Schroeder ET, Olson C, Dube MP, Martinez C, Briggs W,
Horton R, Azen S. Effects of Pharmacological Doses of Nandrolone Decanoate and
Progressive Resistance Training in Immunodeficient Patients Infected with Human
Immunodeficiency Virus. Journal of Clinical Endocrinology and Metabolism. 1999;
Schiavi RC, Schreiner-Engel P, White D, Mandeli J. The Relationship Between
Pituitary-Gonadal Function and Sexual Behavior in Healthy Aging Men.
Psychosomatic Medicine. 1991 Jul-Aug; 53 (4): 363-374.
Schiavi RC, White D, Mandeli J, Levine AC. Effect of Testosterone Administration
on Sexual Behavior and Mood in Men with Erectile Dysfunction. Archives of Sexual
Behavior. 1997 Jun; 26 (3): 231-241.
Schurmeyer T, Knuth UA, Belkien E, et al. Reversible Azoospermia Induced by the
Anabolic Steroid 19-Nortestosterone. Lancet. 1984; I: 417-420. Sheffield-Moore
M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN Wolfe RR, Ferrando AA.
Short-term Oxandrolone Administration Stimulates Net Muscle Protein Synthesis in
Young Men. Journal of Clinical Endocrinology and Metabolism. 1999; 84:
Shelton DL. 2000 Aug 7 Testosterone Therapy Hype May Be Creating False Hopes.
http://www.ama-assn.org/sci-pubs/am...oo/hll20807.htm Sih R, Morley JE, Kaiser
FE, Perry III HM, Patrick P, Ross C. Testosterone Replacement in Older
Hypogonadal Men: a 12-Month Randomized Controlled Trial. Journal of Clinical
Endocrinology and Metabolism. 1997; 82: 1661- 1667.
Smidt KP, Johnston E. Undetected Iatrogenic Hypothyroidism: A Late Complication
of Radio-Iodine Therapy. New Zealand Medical Journal. 1975 Apr 9; 81: 325-328.
Snyder PJ, Peachey H, Berlin JA, Hannoush P, Haddad G, Dlewati A, Santanna J,
Loh L, Lenrow DA, Holmes JH, Kapoor SC, Atkinson LE, Strom BL. Effects of
Testosterone Replacement in Hypogonadal Men. Journal of Clinical Endocrinology
and Metabolism. 2000 Aug; 85(8): 2670-2677. Spijkstra JJ, Spinder T, Gooren L,
van Kessel H. Divergent Effects of the Antiestrogen Tamoxifen and of Estrogens
on Luteinizing Hormone (LH) Pulse Frequency, but not on Basal LH Levels and LH
Pulse Amplitude in Men. Journal of Clinical Endocrinology and Metabolism. 1988
Feb; 66(2): 355-360.
Starr C, Taggart R. Integration and Contol: Endocrine Systems. In: Star C,
Taggart R, eds. Biology-The Unity and Diversity of Life. Belmont, California:
Wadsworth Publishing Company,1992: 587-590.
Strawford A, Barbieri T, Neese R, Van Loan M, Christiansen M, Hoh R, Sathyan G,
Skowronski R, King J, Hellerstein M. Effects of Nandrolone Decanoate Therapy in
Borderline Hypogonadal Men With HIV-Associated
Weight Loss. Journal of Acquired Immune Deficiency Syndromes and Human
Retrovirology. 1999 Feb 1; 20(2): 137-146.
Strawford A, Barbieri T, Van Loan M, Parks E, Catlin D, Barton N, Neese R,
Christiansen M, King J, Hellerstein MK. Resistance Exercise and Supraphysiologic
Androgen Therapy in Eugonadal Men With HIV-Related Weight Loss: a Randomized
Controlled Trial. JAMA. 1999 April 14; 281(14): 1282-1290.
Stricker RB and Shuman MA. Aplastic Anaemia Complicating Systemic Lupus
Erythematosus: Response to Androgens in Two Patients. American Journal of
Hematology. 1984 Aug; 17(2): 193-201.
Stromme SB, Meen HD, Aakvaag A. Effects of an Androgenic-Anabolic Steroid on
Strength Development and Plasma Testosterone Levels in Normal Males. Medicine
and Science in Sports and Exercise. 1974; 6: 203-208.
Tenover JS. Effects of Testosterone Supplementation in the Aging Male. Journal
of Clinical Endocrinology and Metabolism. 1992; 75: 1092-1098.
Tomoda H. Effect of Oxymetholone on Left Ventricular Dimensions in Heart Failure
Secondary to Idiopathic Dilated Cardiomyopathy or to Mitral or Aortic
Regurgitation. American Journal of Cardiology. 1999 Jan 1; 83(1): 123-5.
Tricker R, Casaburi R, Storer TW, Clevenger B, Berman N, Shirazi A, Bhasin S.
The Effects of Supraphysiological Doses of Testosterone on Angry Behavior in
Healthy Eugonadal Men- A Clinical Research Center Study. Journal of Clinical
Endocrinology and Metabolism. 1996 Oct; 81(10): 3754- 3758.
Tuel SM, Meythaler JM, Cross LL. Cushing�s Syndrome from Epidural
Methylprednisolone. Pain. 1990 Jan; 40(1): 81-84.
Ulloa-Aguirre A, Mendez JP, Diaz-Sanchez V, Altamirano A, Perez-Palacios G.
Self-priming Effect of Luteinizing Hormone-Human Chorionic Gonadotropin (HCG)
Upon the Biphasic Testicular Response to Exogenous HCG. I. Serum Testosterone
Profile. Journal of Clinical Endocrinology and Metabolism. 1985 Nov; 61(5):
Valayer-Chaleat E, Calmels P, Giraux P, Fayolle-Minon I. Femoral Fracture and
Iatrogenic Hyperthyroidism in Spinal Cord Injury. Spinal Cord. 1998 Aug; 36(8):
Van Loan MD, Strawford A, Jacob M, Hellerstein M. Monitoring Changes in Fat-Free
Mass in HIV-Positive Men With Hypotestosteronemia and AIDS
Wasting Syndrome Treated With Gonadal Hormone Replacement Therapy. AIDS. 1999
Feb 4; 13(2): 241-248.
Vermeulen A, Kaufman JM. Ageing of the Hypothalamo-Pituitary-Testicular Axis in
Men. Hormonal Research. 1995; 43 (1-3): 25-28.
Vicari E, Mongioi A, Calogero AE, Moncada ML, Sidoti G, Polosa P, D�Agata R.
Therapy With Human Chorionic Gonadotrophin Alone Induces Spermatogenesis in Men
With Isolated Hypogonadotrophic Hypogonadism- Long-Term Follow-Up. International
Journal of Andrology. 1992 Aug; 15(4): 320-329.
Wagner GJ, Rabkin JG. Testosterone Therapy for Clinical Symptoms of Hypogonadism
in Eugonadal Men With AIDS. International Journal of STD and AIDS. 1998 Jan;
Wang C, Swedloff RS, Iranmanesh A, Dobs A, Snyder PJ, Cunningham G, Matsumoto
AM, Weber T, Berman N. Transdermal Testosterone Gel Improves Sexual Function,
Mood, Muscle Strength, and Body Composition Parameters in Hypogonadal Men.
Testosterone Gel Study Group. Journal of Clinical Endocrinology and Metabolism.
2000 Aug; 85(8): 2839-2853.
Watsky JG, Koeniger MA. Prevalence of Iatrogenic Hyperthyroidism in a Community
Hospital. Journal of the American Board of Family Practice. 1998 May-June;
Wishart JM, Need AG, Horowitz M, Morris HA, Nordin BE. Effect of Age on Bone
Density and Bone Turnover in Men. Clinical Endocrinology. 1995; 42: 141-146.
Wu FCW, Farley TMM, Peregoudov A, Waites GMH. Effects of testosterone enanthate
in normal men: experience from a multicenter contraceptive efficacy study.
Fertility and Sterility. 1996 Mar; 65(3): 626-636.
AAS Anabolic-Androgenic Steroids
AIDS Acquired Immunodeficiency Virus
ALT Alanine aminotransferase
AST Aspartate aminotransferase
BMI Body Mass Index
FSH Follicle Stimulating Hormone
GGT Gamma-glutamyl transferase
GnRH Gonadotropin Releasing Hormone
HCG Human Chorionic Gonadotropin
HIV Human Immunodeficiency Virus
HPGA Hypothalamic Pituitary Gonadal Axis
LH Luteinizing Hormone
mIU mili International Units
PSA Prostate Specific Antigen
TSH Thyroid Stimulating Hormone
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