In >1,300 GnRH-antagonist IVF cycles, adding hMG (urinary LH activity) to recombinant FSH did not improve outcomes: rec FSH alone retrieved ~2.1 more oocytes, ~2.2 more mature oocytes, ~1.9 more fertilized oocytes, and ~1.5 more cleaved embryos; clinical pregnancy rates were similar (rec FSH favored by ~6%, only approaching significance) .
A separate 476-cycle comparison found recombinant FSH needed fewer ampules and lower total dose than highly purified urinary FSH to reach follicular maturity, with similar pregnancy rates .
The story is not simply 'more LH is worse.' In 207 women on rFSH with GnRH-agonist down-regulation, mid-follicular LH showed an inverted-U relationship: both low (<0.5 IU/L; fertilization 45.9%) and high (>1.51 IU/L; fertilization 38.9%) LH were inferior to the 1.01β1.5 IU/L band (fertilization 63.7%), and FSH consumption fell inversely with LH (P < 0.002) .
A randomized HP-hMG vs rFSH trial (n=731, Ferring-funded) reported higher serum leptin with HP-hMG but no link between leptin and ovarian response or outcomes .
What would change this conclusion: adequately powered randomized trials showing equal or superior oocyte yield with hMG-containing regimens, or subgroup evidence that LH supplementation benefits poor responders/low-LH patients specifically β the window data above make such subgroups biologically plausible.
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