HMG to HCG IU equivalency?

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WayneP

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Does anyone know roughly how much IU of HMG would equal 500IU of HCG?

The HMG comes in 75IU or 150IU amps, and apparently 75IU is enough for our needs. Just would like to know the equivalency between HMG and HCG, if even possible to calculate.
 
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In fact it is pretty complicated, and a direct comparison may not even be possible. You must start by defining what you mean by "equal". The most quantifiable approach is to say that you want the equivalent LH content in the hMG. But the ratio of FSH to LH in hMG varies by product. A 1:1 ratio is fairly common, so use that as an example. The next problem is that hCG and LH are not interchangeable on an IU basis. They have different relative activity levels in different tissues. For simplicity let's accept one author's statement that 1 IU of hCG is roughly equivalent to 6-8 units of LH. It's not clear if this comparison accounts for the very short half-life of LH versus hCG. In any case, this means your 500 IU of hCG is going to be matched by 3,000-4,000 IU of hMG. I hope you're rich!

Seriously though, hMG is probably better considered as a complement to hCG. The FSH is the important part because it can stimulate Sertoli cells, unlike hCG or LH. In sum, the short half-life and high cost of hMG make it an unrealistic replacement for endogenous LH.
 
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Does anyone know roughly how much IU of HMG would equal 500IU of HCG?

The HMG comes in 75IU or 150IU amps, and apparently 75IU is enough for our needs. Just would like to know the equivalency between HMG and HCG, if even possible to calculate.

Most would never use hMG as a sole replacement to substitute LH.

hCG is used as it mimics LH which stimulates the Leydig cells in the testes to produce ITT (intra-testicular testosterone) and hMG or rhFSH would be added (@75-150 IU 3 X weekly) as the main reason would be to stimulate Sertoli/germ cells.

Could you imagine the dose/cost needed to use hMG as a sole replacement not to mention other issues it may cause!

*Human menopausal gonadotropin contains both LH- and FSH-activity. However, a dose that provides adequate FSH activity does not maintain Leydig cell function because the LH-activity is low. Thus a combination with hCG is required to achieve fertility.





 Gonadotropin Therapy

In order to achieve fertility in cases of pituitary lesions or GnRH receptor gene defects, the regimens using gonadotropins must be applied, but they are also a useful option in hypothalamic disorders. Historical therapy used hCG and hMG, both purified extractions from urine. In recent years, however, purified urinary FSH and recombinant human FSH have replaced hMG in most countries for various reasons [1].


Treatment with hCG/hMG

As the subunits of hCG and LH are structurally very similar, they act on the same receptor located on Leydig cells
. This effect is used to substitute LH with purified urinary hCG or recombinant hCG. Human menopausal gonadotropin contains both LH- and FSH-activity. However, a dose that provides adequate FSH activity does not maintain Leydig cell function because the LH activity is low. Thus a combination with hCG is required to achieve fertility.

95% of hMG consists of co-purified proteins that lack LH or FSH activity and is believed to cause the hypersensitivity reactions occasionally observed under hMG therapy, but not under highly purified FSH or recombinant FSH [22–24].

HCG may also induce antibody formation [25], which may neutralize hCG bioactivity [26–28].

Therapy in men is initiated by the administration of hCG alone, which is given intramuscularly or subcutaneously. The usual dose is 1500–3000 IU applied twice per week (Monday and Friday) for a period of 8–12 weeks; adjustments have to be made to achieve testosterone levels within the normal range. In some cases, sperm can be found in the ejaculate by then, due to residual FSH secretion [11, 31, 32].

Following the induction phase, hMG or rhFSH is administered intramuscularly at a dose of 75–150 IU thrice weekly (Monday, Wednesday, Friday). Sometimes it may be necessary to reduce the hCG dose due to increased testosterone levels or the development of gynecomastia caused by increased levels of testosterone which are aromatized to estradiol. A review of 9 patients with IHH, 9 patients with Kallmann syndrome (group A), and 21 patients with hypopituitarism (group B) treated with this regimen showed the appearance of first sperm in the ejaculate after an average period of 6 months (1–18 months) in group A, and 4 months (2–16 months) in group B. Sperm concentrations were 1.2 mill/ml (0.1–9.0 mill/ml) in group A and 8.1 mill/ml (0.1–180 mill/ml) in group B [10].

As mentioned above, the duration of therapy depends on the initial testicular size and the patients’ history of uni- or bilateral maldescensus. Pregnancies were induced in 5 of 10 patients belonging to group A (time to pregnancy on average 8 months) and in 17 of 21 patients of group B (time to pregnancy on average 10 months). Testicular size increased from 4.4 ± 2.86 to 15.3 ± 7.4 ml (group A), and from 14.0 ± 8.7 to 28.3 ± 10.9 ml (group B; [10]).
 
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