saturn1
Member
HCG/HMG spermatogenesis/hypogandism restoration
Very good read for those who have been shut down hard and/or those looking to have a family.
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<BODY><B><A name=chp1>History </A></B>
<P>40-year-old patient with unfulfilled wish for a child since 6 years because
of primary sterility. Slight bilateral testicular contusion at the age of 10
(medical treatment was not required). Since the age of 23, engagement as
bodybuilder. The couple runs a fitness center. The patient states to have
abstained from anabolics for at least 4 years; in recent years he has only taken
high doses of vitamin preparations. Before that time he had injected anabolic
agents, mostly intramuscularly, at varying cycles for at least 10 years:
testosterone enanthate (250 mg/ week), human chorionic gonadotropin (5000 IU/
week) as well as the anabolics nandrolone decanoate (100 mg/ week), methenolone
acetate (100 mg/3 weeks) and stanozolol(50 mg/2 weeks).
<P>Normal pubertal development (e.g., first shave at the age of 15, vocal
change). Unimpaired olfactory sense. It could not be taken from the history
whether testicular size was normal after puberty. The 33-year-old wife is known
to have bilateral tubal occlusion.
<HR>
<B><A name=chp2>Preliminary findings </A></B>
<P>At physical examination at another place in April of 1997, "small plum-sized
testicles" were noted on both sides. As shown on Tables 1 and 2 and by the
laboratory parameters presented with the first consultation, the patient had
hypogonadotropic hypogonadism at that time, already.
<P><A name=tbl1></A><I>Table 1 </I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD>Date
<TD>FSH (follicle stimulating hormone)
<TD>LH (luteinizing hormone)
<TD>Basal testosterone </TD>
<TR>
<TD>5/1995
<TD>1.0 mU/ml (1.1-10.5)
<TD>0,4 mU/ml (0.9-10)
<TD>1.2 ng/ml (4.0-9.0) </TD>
<TR>
<TD>3/1997
<TD>0.3 mU/ml (1.1-10.5)
<TD><0,1 mU/ml (0.9-10)
<TD>3.6 ng/ml (4.0-9.0) </TD></TR></TBODY></TABLE>
<P>
<P><A name=tbl2></A><I>Table 2 </I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD>Time of examination
<TD>Sperm findings </TD>
<TR>
<TD>4/1993
<TD>Cryptozoospermia (1 living and 1 dead spermatozoon each in all viewing
fields) </TD>
<TR>
<TD>9/1993
<TD>Azoospermia </TD>
<TR>
<TD>2/1997
<TD>Azoospermia </TD></TR></TBODY></TABLE>
<P>
<HR>
<B><A name=chp3>Clinical examination </A></B>
<P>Height 1.78 m, weight 95 kg, extremely athletic build. The patient's relative
overweight is explained by the overproportionate mass of muscles (Pictures 1 and
2).
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img1></A><A
</A>
<TD><I>Picture 1</I> </TD></TR></TBODY></TABLE>
<P>
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img2></A><A
</A>
<TD><I>Picture 2</I> </TD></TR></TBODY></TABLE>
<P>
<P>Testicular size 3.6 ml on the left, 5 ml on the right (Pictures 3 and 4).
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img3></A><A
</A>
<TD><I>Picture 3</I> </TD></TR></TBODY></TABLE>
<P>
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img4></A><A
</A>
<TD><I>Picture 4</I> </TD></TR></TBODY></TABLE>
<P>
<P>Normal findings on further clinical examination including inspection or
palpation of penis, epididymes, deferent ducts, pampiniform plexus, prostate and
hair as well as Doppler sonography.
<HR>
<B><A name=chp4>Laboratory parameters </A></B>
<P><A name=tbl3></A><I>Table 3: Hormonal parameters before and after therapy
</I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD colSpan=4>
<TD>HCG/HMG
<TD>HCG/HMG </TD>
<TR>
<TD>Date
<TD>17.10.1997
<TD>14.11.1997
<TD>30.01.1998
<TD>27.03.1998
<TD>29.05.1998 </TD>
<TR>
<TD>FSH (1.2-10.1 mU/ml)
<TD><0.5
<TD>0.6
<TD>0.9
<TD>
<TD>1.5 </TD>
<TR>
<TD>FSH 30 min after GnRH
<TD>
<TD>
<TD>3.1
<TD>
<TD> </TD>
<TR>
<TD>LH (0.8-8.3 mU/ml)
<TD>< 0.5
<TD><0.5
<TD><0.5
<TD>
<TD><0.5 </TD>
<TR>
<TD>LH 30 min nach GnRH
<TD>
<TD>
<TD>13.2
<TD>
<TD> </TD>
<TR>
<TD>Basal testosterone (2.2-9.2 ng/ml)
<TD>1.8
<TD>0.3
<TD>1.72
<TD>3.86
<TD>3.28 </TD>
<TR>
<TD>Free testosterone (9-47 pg/ml)
<TD>
<TD>2.5
<TD>
<TD>18.6
<TD>25.7 </TD>
<TR>
<TD>Prolactin (1-15 ng/ml)
<TD>
<TD>5.1
<TD>
<TD>
<TD> </TD>
<TR>
<TD>Androstenedione (116-392 ng/dl)
<TD>
<TD>
<TD>155
<TD>
<TD> </TD>
<TR>
<TD>DHEA (130-1400 ng/dl)
<TD>
<TD>
<TD>691
<TD>
<TD> </TD>
<TR>
<TD>DHEA sulfate (0.2-4.2 µg/ml)
<TD>
<TD>1.52
<TD>1.86
<TD>
<TD> </TD>
<TR>
<TD>Estradiol (<5-48 pg/ml)
<TD>
<TD><5
<TD>22.8
<TD>
<TD> </TD>
<TR>
<TD>Progesterone (<240 ng/dl)
<TD>
<TD>
<TD>185
<TD>
<TD> </TD>
<TR>
<TD>SHBG (11-71 nmol/l)
<TD>
<TD>11.1
<TD>21.8
<TD>32.8
<TD>93.5 </TD>
<TR>
<TD>HCG (0-5 mU/ml)
<TD><1.0
<TD>
<TD><1.0
<TD>
<TD> </TD>
<TR>
<TD>AFP (<10 IU/ml)
<TD>2.6
<TD>
<TD>2.6
<TD>
<TD> </TD></TR></TBODY></TABLE>
<P>
<P><A name=tbl4></A><I>Table 4: Spermiogram parameters before and after therapy
</I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD colSpan=2>
<TD>HCG/HMG
<TD>HCG/HMG </TD>
<TR>
<TD>Date
<TD>17.10.1997
<TD>29.05.1998
<TD>26.06.1998 </TD>
<TR>
<TD>Days of abstinence
<TD>10
<TD>10
<TD>14 </TD>
<TR>
<TD>Volume (ml)
<TD>2.5
<TD>1.5
<TD>4.8 </TD>
<TR>
<TD>Consistency
<TD>Liquid-schollig
<TD>Liquid
<TD>Liquid-schollig </TD>
<TR>
<TD>Sperm concentration (1 000 000/ml)
<TD>No spermatozoa in native preparation and centrifuged sample
<TD>2.0
<TD>4.0 </TD>
<TR>
<TD>Total sperm count (1 000 000)
<TD>
<TD>3.0
<TD>19.2 </TD>
<TR>
<TD>Eosin
<TD>
<TD>36
<TD> </TD>
<TR>
<TD>Global motility (%)
<TD>
<TD>24
<TD>50 </TD>
<TR>
<TD>Rapidly progressive motile WHO A (%)
<TD>
<TD>3
<TD>37 </TD>
<TR>
<TD>Slowly progressive motile WHO B (%)
<TD>
<TD>14
<TD>8 </TD>
<TR>
<TD>Locally motile WHO C (%)
<TD>
<TD>7
<TD>5 </TD>
<TR>
<TD>Immotile WHO D (%)
<TD>
<TD>76
<TD>50 </TD>
<TR>
<TD>Normal forms (%)
<TD>
<TD>0
<TD>3 </TD>
<TR>
<TD>Head defects (%)
<TD>
<TD>90
<TD>90 </TD>
<TR>
<TD>Acrosomal disorders (%)
<TD>
<TD>27
<TD>26 </TD>
<TR>
<TD>Elongation (%)
<TD>
<TD>87
<TD>72 </TD>
<TR>
<TD>Mid-piece defects (%)
<TD>
<TD>1
<TD>3 </TD>
<TR>
<TD>Flagellar defects (%)
<TD>
<TD>93
<TD>80 </TD></TR></TBODY></TABLE>
<P>
<HR>
<B><A name=chp5>Human genetics </A></B>
<P>The patient was found to have a numerically and structurally normal male
genome with 46, XY. Search for microdeletions on Yq11 was negative. No
pathological findings on examination for mutations in the CFTR gene (cystic
fibrosis transmembrane conductance regulator gene).
<HR>
<B><A name=chp6>Magnet resonance imaging </A></B>
<P>MRI of the skull did not indicate an intracranial space-occupying process or
other pathological findings.
<HR>
<B><A name=chp7>Determination of anabolics </A></B>
<P>On August 18, 1998, the patient's urine was examined for anabolics to secure
the credibility of his anamnestic data. No anabolics were demonstrated,
endogenous steroids were normal, only HCG was increased, as expected, during
therapy with 30 mU/ml.
<HR>
<B><A name=chp8>Diagnosis </A></B>
<P>Hypogonadotropic hypogonadism after abuse of anabolics.
<HR>
<B><A name=chp9>Therapy </A></B>
<P>Since March of 1998, hormonal stimulation of spermatogenesis with HCG/HMC
(Pregnesin = 2500 IU HCG, twice a week subcutaneously, and Pergonal = 75 IU FSH
and 75 IU LH, three times a week subcutaneously). This therapy induced
spermatogenesis (see Table 5) and also increased the testicular volume, from 3.6
ml to 7.6 ml on the left and from 5.2 ml to 9.0 ml on the right (Picture 3 and 5
and 4 and 6, respectively).
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img5></A><A
</A>
<TD><I>Picture 5</I> </TD></TR></TBODY></TABLE>
<P>
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img6></A><A
</A>
<TD><I>Picture 6</I> </TD></TR></TBODY></TABLE>
<P>
<P>Oligoasthenoteratozoospermia was found on May 29, 1998, and
oligoteratozoospermia on June 26, 1998. The ejaculate of June 26 was
cryopreserved in order to have spermatozoa available for possible assisted
reproductive techniques. Because of the wife's tubal factor, in vitro
fertilization (IVF) has to be considered. Based on the current semen parameters,
the only realistic possibility would be intracytoplasmic sperm injection (ICSI)
because the quality of the ejaculate is too poor for conventional IVF. Human
genetic examination, which is required for ICSI, had been without pathological
findings in both partners.
<HR>
<B><A name=chp10>Comment </A></B>
<P>Suppression of spermatogenesis resulting from the intake of anabolic steroids
is generally known and was examined by Knuth et al. (1989) in relation to the
time past since the last intake. Bodybuilders who had not taken anabolics for
more than 4 months were mostly found to have normal spermatogenesis; however, 3
men had oligozoospermia. It is generally assumed that spermatogenesis is
spontaneously restored after months following withdrawal of anabolics (Holma et
al., 1977; Lukas et al., 1993). Persistent reduction in testosterone as late as
16 weeks after the last administration of anabolics was shown by Alen et al.
(1985). A number of case reports have stated that abuse of anabolic steroids may
result in long-lasting disturbed spermatogenesis which persists after withdrawal
(Jarow et al., 1990; Turek et al., 1995). In these cases, too, hypogonadotropic
hypogonadism continued to be found several years after the last intake of
anabolics, as was the case in our patient. The patient described by Turek had
also taken nandrolone decanoate and stanozolol. As in other cases of
hypogonadotropic hypogonadism (e.g., Kallmann's syndrome), spermatogenesis can
be well stimulated by administration of gonadotropins, which was also successful
in our patient. It remains unclear why hypogonadotropic hypogonadism persists
after withdrawal of anabolics in some cases. Previous damage to the hormonal
regulation of spermatogenesis must certainly be considered but cannot be
determined retrospectively. In view of the athletic build of our patient, his
statement to have abstained from anabolics for at least 4 years must be viewed
critically. A kind of doping control on August 18, 1998, for possible detection
of anabolic steroids in the morning urine, was negative.
<HR>
<B><A name=chp11>References </A></B>
<P>Alen M, Reinila M, Vihko R (1985) Response of serum hormones to androgen
administration in power athlets. Med Sci Sports Exerc 17:354-359.
<P>Holma PK (1977) Effects of an anabolic steroid (metandienone) on
spermatogenesis. Contraception 15:151-162.
<P>Jarow J P, Lipshultz LI (1990) Anabolic steroid-induced hypgonadotropic
hypogonadism. Amer J Sports Med 18:429-434.
<P>Knuth UA, Maniera H, Nieschlag E (1989) Anabolic steroids and semen
parameters in bodybuilders. Fertil Steril 52:1041-1047.
<P>Lukas SE (1993) Current perspectives on anabolic-androgenic steroid abuse.
Trends Pharmacol Sci 14:61-67.
<P>Turek PJ, Williams RH, Gilbaugh JH, Lipshultz LI (1995) The reversibility of
anabolic steroid-induced azoospermia. J Urol 153:1628-1630. </P></BODY></HTML>
Very good read for those who have been shut down hard and/or those looking to have a family.
<!DOCTYPE HTML PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN">
<HTML><HEAD>
<META http-equiv=Content-Type content="text/html; charset=iso-8859-1">
<META content="MSHTML 6.00.2800.1476" name=GENERATOR></HEAD>
<BODY><B><A name=chp1>History </A></B>
<P>40-year-old patient with unfulfilled wish for a child since 6 years because
of primary sterility. Slight bilateral testicular contusion at the age of 10
(medical treatment was not required). Since the age of 23, engagement as
bodybuilder. The couple runs a fitness center. The patient states to have
abstained from anabolics for at least 4 years; in recent years he has only taken
high doses of vitamin preparations. Before that time he had injected anabolic
agents, mostly intramuscularly, at varying cycles for at least 10 years:
testosterone enanthate (250 mg/ week), human chorionic gonadotropin (5000 IU/
week) as well as the anabolics nandrolone decanoate (100 mg/ week), methenolone
acetate (100 mg/3 weeks) and stanozolol(50 mg/2 weeks).
<P>Normal pubertal development (e.g., first shave at the age of 15, vocal
change). Unimpaired olfactory sense. It could not be taken from the history
whether testicular size was normal after puberty. The 33-year-old wife is known
to have bilateral tubal occlusion.
<HR>
<B><A name=chp2>Preliminary findings </A></B>
<P>At physical examination at another place in April of 1997, "small plum-sized
testicles" were noted on both sides. As shown on Tables 1 and 2 and by the
laboratory parameters presented with the first consultation, the patient had
hypogonadotropic hypogonadism at that time, already.
<P><A name=tbl1></A><I>Table 1 </I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD>Date
<TD>FSH (follicle stimulating hormone)
<TD>LH (luteinizing hormone)
<TD>Basal testosterone </TD>
<TR>
<TD>5/1995
<TD>1.0 mU/ml (1.1-10.5)
<TD>0,4 mU/ml (0.9-10)
<TD>1.2 ng/ml (4.0-9.0) </TD>
<TR>
<TD>3/1997
<TD>0.3 mU/ml (1.1-10.5)
<TD><0,1 mU/ml (0.9-10)
<TD>3.6 ng/ml (4.0-9.0) </TD></TR></TBODY></TABLE>
<P>
<P><A name=tbl2></A><I>Table 2 </I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD>Time of examination
<TD>Sperm findings </TD>
<TR>
<TD>4/1993
<TD>Cryptozoospermia (1 living and 1 dead spermatozoon each in all viewing
fields) </TD>
<TR>
<TD>9/1993
<TD>Azoospermia </TD>
<TR>
<TD>2/1997
<TD>Azoospermia </TD></TR></TBODY></TABLE>
<P>
<HR>
<B><A name=chp3>Clinical examination </A></B>
<P>Height 1.78 m, weight 95 kg, extremely athletic build. The patient's relative
overweight is explained by the overproportionate mass of muscles (Pictures 1 and
2).
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img1></A><A
</A>
<TD><I>Picture 1</I> </TD></TR></TBODY></TABLE>
<P>
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img2></A><A
</A>
<TD><I>Picture 2</I> </TD></TR></TBODY></TABLE>
<P>
<P>Testicular size 3.6 ml on the left, 5 ml on the right (Pictures 3 and 4).
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img3></A><A
</A>
<TD><I>Picture 3</I> </TD></TR></TBODY></TABLE>
<P>
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img4></A><A
</A>
<TD><I>Picture 4</I> </TD></TR></TBODY></TABLE>
<P>
<P>Normal findings on further clinical examination including inspection or
palpation of penis, epididymes, deferent ducts, pampiniform plexus, prostate and
hair as well as Doppler sonography.
<HR>
<B><A name=chp4>Laboratory parameters </A></B>
<P><A name=tbl3></A><I>Table 3: Hormonal parameters before and after therapy
</I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD colSpan=4>
<TD>HCG/HMG
<TD>HCG/HMG </TD>
<TR>
<TD>Date
<TD>17.10.1997
<TD>14.11.1997
<TD>30.01.1998
<TD>27.03.1998
<TD>29.05.1998 </TD>
<TR>
<TD>FSH (1.2-10.1 mU/ml)
<TD><0.5
<TD>0.6
<TD>0.9
<TD>
<TD>1.5 </TD>
<TR>
<TD>FSH 30 min after GnRH
<TD>
<TD>
<TD>3.1
<TD>
<TD> </TD>
<TR>
<TD>LH (0.8-8.3 mU/ml)
<TD>< 0.5
<TD><0.5
<TD><0.5
<TD>
<TD><0.5 </TD>
<TR>
<TD>LH 30 min nach GnRH
<TD>
<TD>
<TD>13.2
<TD>
<TD> </TD>
<TR>
<TD>Basal testosterone (2.2-9.2 ng/ml)
<TD>1.8
<TD>0.3
<TD>1.72
<TD>3.86
<TD>3.28 </TD>
<TR>
<TD>Free testosterone (9-47 pg/ml)
<TD>
<TD>2.5
<TD>
<TD>18.6
<TD>25.7 </TD>
<TR>
<TD>Prolactin (1-15 ng/ml)
<TD>
<TD>5.1
<TD>
<TD>
<TD> </TD>
<TR>
<TD>Androstenedione (116-392 ng/dl)
<TD>
<TD>
<TD>155
<TD>
<TD> </TD>
<TR>
<TD>DHEA (130-1400 ng/dl)
<TD>
<TD>
<TD>691
<TD>
<TD> </TD>
<TR>
<TD>DHEA sulfate (0.2-4.2 µg/ml)
<TD>
<TD>1.52
<TD>1.86
<TD>
<TD> </TD>
<TR>
<TD>Estradiol (<5-48 pg/ml)
<TD>
<TD><5
<TD>22.8
<TD>
<TD> </TD>
<TR>
<TD>Progesterone (<240 ng/dl)
<TD>
<TD>
<TD>185
<TD>
<TD> </TD>
<TR>
<TD>SHBG (11-71 nmol/l)
<TD>
<TD>11.1
<TD>21.8
<TD>32.8
<TD>93.5 </TD>
<TR>
<TD>HCG (0-5 mU/ml)
<TD><1.0
<TD>
<TD><1.0
<TD>
<TD> </TD>
<TR>
<TD>AFP (<10 IU/ml)
<TD>2.6
<TD>
<TD>2.6
<TD>
<TD> </TD></TR></TBODY></TABLE>
<P>
<P><A name=tbl4></A><I>Table 4: Spermiogram parameters before and after therapy
</I>
<P>
<TABLE cellSpacing=0 cellPadding=1 border=1>
<TBODY>
<TR>
<TD colSpan=2>
<TD>HCG/HMG
<TD>HCG/HMG </TD>
<TR>
<TD>Date
<TD>17.10.1997
<TD>29.05.1998
<TD>26.06.1998 </TD>
<TR>
<TD>Days of abstinence
<TD>10
<TD>10
<TD>14 </TD>
<TR>
<TD>Volume (ml)
<TD>2.5
<TD>1.5
<TD>4.8 </TD>
<TR>
<TD>Consistency
<TD>Liquid-schollig
<TD>Liquid
<TD>Liquid-schollig </TD>
<TR>
<TD>Sperm concentration (1 000 000/ml)
<TD>No spermatozoa in native preparation and centrifuged sample
<TD>2.0
<TD>4.0 </TD>
<TR>
<TD>Total sperm count (1 000 000)
<TD>
<TD>3.0
<TD>19.2 </TD>
<TR>
<TD>Eosin
<TD>
<TD>36
<TD> </TD>
<TR>
<TD>Global motility (%)
<TD>
<TD>24
<TD>50 </TD>
<TR>
<TD>Rapidly progressive motile WHO A (%)
<TD>
<TD>3
<TD>37 </TD>
<TR>
<TD>Slowly progressive motile WHO B (%)
<TD>
<TD>14
<TD>8 </TD>
<TR>
<TD>Locally motile WHO C (%)
<TD>
<TD>7
<TD>5 </TD>
<TR>
<TD>Immotile WHO D (%)
<TD>
<TD>76
<TD>50 </TD>
<TR>
<TD>Normal forms (%)
<TD>
<TD>0
<TD>3 </TD>
<TR>
<TD>Head defects (%)
<TD>
<TD>90
<TD>90 </TD>
<TR>
<TD>Acrosomal disorders (%)
<TD>
<TD>27
<TD>26 </TD>
<TR>
<TD>Elongation (%)
<TD>
<TD>87
<TD>72 </TD>
<TR>
<TD>Mid-piece defects (%)
<TD>
<TD>1
<TD>3 </TD>
<TR>
<TD>Flagellar defects (%)
<TD>
<TD>93
<TD>80 </TD></TR></TBODY></TABLE>
<P>
<HR>
<B><A name=chp5>Human genetics </A></B>
<P>The patient was found to have a numerically and structurally normal male
genome with 46, XY. Search for microdeletions on Yq11 was negative. No
pathological findings on examination for mutations in the CFTR gene (cystic
fibrosis transmembrane conductance regulator gene).
<HR>
<B><A name=chp6>Magnet resonance imaging </A></B>
<P>MRI of the skull did not indicate an intracranial space-occupying process or
other pathological findings.
<HR>
<B><A name=chp7>Determination of anabolics </A></B>
<P>On August 18, 1998, the patient's urine was examined for anabolics to secure
the credibility of his anamnestic data. No anabolics were demonstrated,
endogenous steroids were normal, only HCG was increased, as expected, during
therapy with 30 mU/ml.
<HR>
<B><A name=chp8>Diagnosis </A></B>
<P>Hypogonadotropic hypogonadism after abuse of anabolics.
<HR>
<B><A name=chp9>Therapy </A></B>
<P>Since March of 1998, hormonal stimulation of spermatogenesis with HCG/HMC
(Pregnesin = 2500 IU HCG, twice a week subcutaneously, and Pergonal = 75 IU FSH
and 75 IU LH, three times a week subcutaneously). This therapy induced
spermatogenesis (see Table 5) and also increased the testicular volume, from 3.6
ml to 7.6 ml on the left and from 5.2 ml to 9.0 ml on the right (Picture 3 and 5
and 4 and 6, respectively).
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img5></A><A
</A>
<TD><I>Picture 5</I> </TD></TR></TBODY></TABLE>
<P>
<P>
<TABLE border=0>
<TBODY>
<TR>
<TD><A name=img6></A><A
</A>
<TD><I>Picture 6</I> </TD></TR></TBODY></TABLE>
<P>
<P>Oligoasthenoteratozoospermia was found on May 29, 1998, and
oligoteratozoospermia on June 26, 1998. The ejaculate of June 26 was
cryopreserved in order to have spermatozoa available for possible assisted
reproductive techniques. Because of the wife's tubal factor, in vitro
fertilization (IVF) has to be considered. Based on the current semen parameters,
the only realistic possibility would be intracytoplasmic sperm injection (ICSI)
because the quality of the ejaculate is too poor for conventional IVF. Human
genetic examination, which is required for ICSI, had been without pathological
findings in both partners.
<HR>
<B><A name=chp10>Comment </A></B>
<P>Suppression of spermatogenesis resulting from the intake of anabolic steroids
is generally known and was examined by Knuth et al. (1989) in relation to the
time past since the last intake. Bodybuilders who had not taken anabolics for
more than 4 months were mostly found to have normal spermatogenesis; however, 3
men had oligozoospermia. It is generally assumed that spermatogenesis is
spontaneously restored after months following withdrawal of anabolics (Holma et
al., 1977; Lukas et al., 1993). Persistent reduction in testosterone as late as
16 weeks after the last administration of anabolics was shown by Alen et al.
(1985). A number of case reports have stated that abuse of anabolic steroids may
result in long-lasting disturbed spermatogenesis which persists after withdrawal
(Jarow et al., 1990; Turek et al., 1995). In these cases, too, hypogonadotropic
hypogonadism continued to be found several years after the last intake of
anabolics, as was the case in our patient. The patient described by Turek had
also taken nandrolone decanoate and stanozolol. As in other cases of
hypogonadotropic hypogonadism (e.g., Kallmann's syndrome), spermatogenesis can
be well stimulated by administration of gonadotropins, which was also successful
in our patient. It remains unclear why hypogonadotropic hypogonadism persists
after withdrawal of anabolics in some cases. Previous damage to the hormonal
regulation of spermatogenesis must certainly be considered but cannot be
determined retrospectively. In view of the athletic build of our patient, his
statement to have abstained from anabolics for at least 4 years must be viewed
critically. A kind of doping control on August 18, 1998, for possible detection
of anabolic steroids in the morning urine, was negative.
<HR>
<B><A name=chp11>References </A></B>
<P>Alen M, Reinila M, Vihko R (1985) Response of serum hormones to androgen
administration in power athlets. Med Sci Sports Exerc 17:354-359.
<P>Holma PK (1977) Effects of an anabolic steroid (metandienone) on
spermatogenesis. Contraception 15:151-162.
<P>Jarow J P, Lipshultz LI (1990) Anabolic steroid-induced hypgonadotropic
hypogonadism. Amer J Sports Med 18:429-434.
<P>Knuth UA, Maniera H, Nieschlag E (1989) Anabolic steroids and semen
parameters in bodybuilders. Fertil Steril 52:1041-1047.
<P>Lukas SE (1993) Current perspectives on anabolic-androgenic steroid abuse.
Trends Pharmacol Sci 14:61-67.
<P>Turek PJ, Williams RH, Gilbaugh JH, Lipshultz LI (1995) The reversibility of
anabolic steroid-induced azoospermia. J Urol 153:1628-1630. </P></BODY></HTML>
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