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Estrogen oligospermia
1. Hypothetic Scheme for Therapy of
Oligospermia
Purushottam Sah
Nightingale Hospital Kolkata
P Sah. A Therapeutic Scheme For Oligospermia Based On Serum Levels
Of FSH And Estradiol. The Internet J Gyn Obs 2006 Vol 8 No 1
2. Oligospermia is treated Empirically:
Emphasis is on Stimulatory role of
Testosterone & Inhibitory role of Estrogens
๏ฎ In the last decade
Positive role of
Estrogens in Male
Reproduction has been
reported.
๏ฎ A Therapeutic Scheme
for Oligospermia based
on serum levels of FSH
and Estradiol, is
presented.
3. Aim is to develop a Scheme to Identify a
Suitable Therapy before starting the
Treatment of Oligospermia
๏ฎ It is extremely uncommon to find clinically
significant abnormalities in LH and testosterone
levels in the presence of normal FSH levels [1]
and FSH is also the most suitable hormone for
diagnostic classification of Oligospermia [7].
Hence, LH and testosterone are not included in
the proposed scheme and only FSH and estradiol
are included.
4. Theoretically the maximum number of possible
combinations of FSH and Estradiol is Nine. But in
practice all the possible combinations may not
exist, Six groups are identified
๏ฎ Idiopathic: serum levels of FSH and Estradiol are normal as may be
found in most of the oligospermic men.
๏ฎ Spermatogenic Deficiency or Seminiferous tubular failure: these men
have elevated (may be normal) serum levels of FSH [7] and normal
serum levels of estradiol.
๏ฎ Estrogen Resistance: elevated serum levels of FSH and of Estradiol are
found in these men [8].
๏ฎ Estrogen Excess: these men have elevated serum levels of Estradiol
and normal (or depressed) serum levels of FSH [1].
๏ฎ Hypogonadotropism: these men have depressed serum levels of FSH
and of Testosterone, and consequently they may have depressed (or
normal) levels of Estradiol, because FSH causes aromatisation of
testosterone to estrogen [9].
๏ฎ Aromatase Deficiency: these men may have undetectable (depressed)
serum levels of Estradiol and elevated serum levels of FSH
[10, 11, 12].
7. References
๏ฎ 1. Sigman M and Howards SS (1992) Male
infertility. Philadelphia, USA, pp. pp.
664,665,675,680,689.
๏ฎ
2. Rochira V et al.(2001) Mol Cell Endocrinol
178,107-115.
๏ฎ
3. Pentikainen V et al (2000) J Clin Endocrinol
Metab 85(5), 2057- 2067.
๏ฎ
4. Sah P (1998) Fertil Steril 70, 780-781.
๏ฎ
5. Sah P (2002) Asian J Androl 4 (4), 307-308
๏ฎ
6. Sah P (2005) The Internet Journal of
Endocrinology 2(1).
๏ฎ
7. Rowe PJ et al (2000) Who Manualโฆ
Cambridge University Press, Cambridge p.28
๏ฎ 8. Smith EP, et al(1994) N Engl J Med
331,1056- 1061.
๏ฎ
9. Kula K and Chilarski A (1987) Pediatr Pol
62(9), 623-627.
๏ฎ
10. Carani C et al (1997) N Engl J Med 337,
91- 95.
๏ฎ
11. Herrman BL et al (2002) J Clin
Endocrinol Metab 87, 5476 -5484.
๏ฎ
12. Morishima A et al (1995) J Clin
Endocrinol Metab 80, 3689- 3699.
๏ฎ
13. Adamopoulos DA et al(2003) Fertil Steril
80(4), 914-920.
๏ฎ
14. Attia AM et al (2006) Cochrane
Database of Systematic Reviews, Issue 1.
Art. No.: CD005071.