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Proviron, HCG & Clomid | tokyo-sinderera.info
By G-man99 , October 7, in Steroid and Testosterone information. Seminal analysis were assayed 3 times and serum follicle stimulating hormone FSH luteinizing hormone LH and plasma testosterone were assayed once before treatment and repeated at 3, 6, 9 and 12 months after the initiation of treatment. There was no significant adverse effect on testosterone levels or on liver function. Those with severe oligospermia count less than 5 million do not seem to benefit from this therapy. I can't remember if I used Clomid.
Certainly Proviron and HCG. I read numerous studies about it at the time. My sperm test came back normal, but I didn't want normal. My load amount was low, but had a decent amount in the load.
Mobility came in 3 categories. Mine were mostly 2's, so I started Proviron etc to improve it. You also have to be aware that so many things can slow pregnancy down. Your partners diet, stress levels. You only have 2 days a month apparently to get the job done. Seems very high and expensive but I guess if a child means that much then can't really put a figure on it.
Want to boost my chances first whilst on cycle and then if nothing has happened in a few months, then will do power PCT etc and do everything properly. I came off for 18 months, nothing happened. We decided to stop trying and let it happen. I went back on orals and did the Proviron etc and 2 months later we were pregnant. Could have been the meds or the fact that our stress levels had dropped. September This topic last updated: On the other hand, sperm production can usually be stimulated to a level sufficient to restore fertility in men who are infertile as a result of secondary hypogonadism, ie, due to damage to the pituitary or hypothalamus.
Men who have pituitary disease can be treated with gonadotropins, while those with hypothalamic disease can be treated with gonadotropins or gonadotropin-releasing hormone GnRH. See "Causes of secondary hypogonadism in males". In practice, testosterone secretion virtually always increases to normal after replacement of LH, and sperm production more often than not increases after replacement of LH alone or LH plus FSH.
Testosterone replacement alone will not restore spermatogenesis. Which patients are likely to respond? See "Clinical features and diagnosis of male hypogonadism". Gonadotropin treatment will not increase the sperm count in men who have idiopathic oligospermia, in which a subnormal sperm count is associated with a normal serum testosterone concentration .
Several factors enhance the likelihood that the sperm count will be increased, and increased sooner after gonadotropin administration: Development of hypogonadism after puberty rather than before.
Partial hypogonadism, rather than complete, as judged by less severe abnormalities of testicular size  and reductions in the serum concentrations of FSH, inhibin, and testosterone. Descent of both testes into the scrotum at birth or by one year of age, rather than unilateral or bilateral cryptorchidism which may damage the seminiferous tubules requiring surgical correction [2,6]. In one report, as an example, only one of the seven men with prepubertal hypogonadism and cryptorchidism had an increase in sperm count to within the normal range in response to hCG and hMG .
Use of gonadotropin with assisted reproductive technologies — Gonadotropin treatment of men with hypogonadotropic hypogonadism results in the appearance of sperm in the ejaculate in up to 90 percent of these men, but often not to normal . Even if pregnancy does not occur spontaneously, the number of sperm is often sufficient that pregnancy can be achieved with the help of an assisted reproductive technique, which may be as simple as insemination with the patient's semen intrauterine insemination, IUI or as elaborate as intracytoplasmic sperm injection ICSI .
See "Intracytoplasmic sperm injection". Use of human chorionic gonadotropin — Human chorionic gonadotropin hCG has the biologic activity of LH but a longer half life in the circulation; it stimulates the Leydig cells of the testes to synthesize and secrete testosterone.
It is approved by the Food and Drug Administration for this purpose. Both urinary and recombinant hCG preparations are available. There is no theoretical reason to use recombinant human LH, since it has a shorter half life 10 hours than hCG and therefore would probably not be effective given three times a week. LH stimulates the Leydig cells to secrete testosterone, which results in an intratesticular testosterone concentration times that in the peripheral circulation, a concentration essential to stimulate spermatogenesis.
See "Male reproductive physiology". After stopping testosterone therapy, hCG is administered according to the following regimen: Patients are taught to self-administer the medication intramuscularly in the thigh at an initial dose of units three times a week the recombinant preparation, which is dosed differently, is administered subcutaneously. See "In vitro fertilization". Some patients require as little as units per dose and others as much as 10, units.
On rare occasions the serum testosterone concentration fails to respond to hCG, a problem thought to be due to antibodies to hCG [9,10]. The sperm count is measured every two to four weeks, but the value is not used to adjust the hCG dose. The addition of hMG should be considered if the sperm count does not reach one-half normal by 12 to 24 months. The sperm produced by this regimen are qualitatively normal; thus, less than a normal number of sperm is usually sufficient to restore fertility figure 1 .
Adverse effects of hCG therapy are few and generally similar to those of testosterone. See "Testosterone treatment of male hypogonadism". Recombinant human follicle stimulating hormone rhFSH is also available, but has been less well studied in men  and is more expensive.
This effect of FSH is probably exerted via the Sertoli cells of the seminiferous tubules. FSH appears to be necessary for the initiation of spermatogenesis, but not for its maintenance or reinitiation. As mentioned above, only one of eight men with a prepubertal onset of secondary hypogonadism responded to hCG alone; five of the seven nonresponders showed an increase in sperm count to above 40 million per ejaculate when hMG was added . The likelihood of a response was much less one of seven men when prepubertal hypogonadism was accompanied by cryptorchidism, presumably due to seminiferous tubular damage induced by the cryptorchidism figure 2.
After stopping testosterone therapy, the following regimen is used to administer hMG: The initial dose is 75 units the contents of one vial by intramuscular injection three times a week although an hMG preparation is now available that can be given subcutaneously ; it is most conveniently administered in the same syringe as hCG. Recombinant FSH preparations are also administered subcutaneously. The sperm count is measured once every two to four weeks. The reason for such frequent measurement of the sperm count is that individual values fluctuate considerably, so that many samples are needed to detect a trend.
The maximum count is usually achieved within three to 24 months. The hMG dose can be increased to units if the sperm count does not reach 20 million per ejaculate within six months. This will increase the serum FSH concentration from low-normal to high-normal, but it is less certain that it will increase the sperm count. As long as the sperm count is at least a few million, however, continuation of hCG and hMG administration is probably worthwhile, because even values this low can result in impregnation spontaneously  and is more than sufficient for assisted reproductive technologies.
The only undesirable feature of hMG administration is its cost: RhFSH is even more expensive. On the other hand, hCG which is much less expensive should be continued if the couple is considering another pregnancy. Monotherapy with hCG in this setting will usually keep the serum testosterone concentration in the normal range and maintain at least some degree of spermatogenesis.
When the couple does not wish to have more children, virilization can be maintained by continuing HCG alone or by using testosterone. The rationale for this treatment is that replacement of GnRH in a physiologic manner, in pulses every two hours, will stimulate the gonadotroph cells of the pituitary to secrete LH and FSH, which in turn will stimulate the testes to produce testosterone and sperm. See "Physiology of gonadotropin-releasing hormone" and "Male reproductive physiology".
The apparatus is worn continuously until pregnancy occurs. Sperm may appear in the ejaculate as soon as 12 months after the initiation of treatment but more often three years or more are required. See "Congenital gonadotropin-releasing hormone deficiency idiopathic hypogonadotropic hypogonadism ", section on 'Pulsatile GnRH'.
Virtually all patients treated with this regimen attain a normal serum testosterone concentration, and most develop some sperm in the ejaculate. Studies comparing gonadotropin to pulsatile GnRH treatment showed similar stimulation of spermatogenesis with both therapies [17,18].
GnRH is currently unavailable in the United States. Gonadotropin is more convenient to administer than GnRH and, if the onset of the hypogonadism was postpubertal, less expensive, because it is likely that only hCG will be necessary. We recommend treating initially with hCG alone and, if the sperm count is not normal within 6 to 12 months, adding hMG.
If pregnancy has not occurred spontaneously after a year or more of combined treatment, an assisted reproductive technique, using the patient's semen, should be strongly considered. J Clin Endocrinol Metab ; Stimulation of spermatogenesis by gonadotropins in men with hypogonadotropic hypogonadism. N Engl J Med ; Gonadotropin therapy in men with isolated hypogonadotropic hypogonadism: Eur J Endocrinol ; Outcome of gonadotropin therapy for male hypogonadotropic hypogonadism at university affiliated male infertility centers: J Urol ; Intracytoplasmic sperm injection as a complement to gonadotrophin treatment in infertile men with hypogonadotrophic hypogonadism.
Int J Androl ; J Clin Endocrinol Metab Development of anti-human chorionic gonadotropin antibodies in patients with hypogonadotropic hypogonadism. A study of four patients. Failure of gonadotropin therapy secondary to chorionic gonadotropin-induced antibodies. A low sperm concentration does not preclude fertility in men with isolated hypogonadotropic hypogonadism after gonadotropin therapy.
Fertil Steril ; Efficacy and safety of recombinant human follicle stimulating hormone Gonal-F with urinary human chorionic gonadotrophin for induction of spermatogenesis and fertility in gonadotrophin-deficient men.