Luteinizing Hormone (LH)

LH is a heterodimeric glycoprotein sharing the common alpha subunit with FSH, TSH and hCG, with an LH-specific beta subunit conferring receptor specificity. It acts on LHCGR, a G protein-coupled receptor on Leydig cells in the testis and theca cells in the ovary, where cyclic AMP signalling raises steroidogenic acute regulatory protein and pushes cholesterol into the steroid pathway; after ovulation the same receptor supports luteinisation of granulosa cells and progesterone production by the corpus luteum. Its carbohydrate chains are less sialylated than those of hCG, so it is cleared in tens of minutes.

That short half-life, combined with pulsatile GnRH input, means LH in blood is a series of spikes rather than a level. In men, pulses arrive roughly every one and a half to two hours; in women the mid-cycle surge precedes ovulation by about a day and a half, which is what urinary ovulation predictor kits detect. Recombinant lutropin alfa exists, but hCG is used far more often when LH activity is needed, because it hits the same receptor for much longer.

Clinically LH does the work of localisation. Paired with a sex steroid it separates gonadal failure, where LH is high because feedback is gone, from central failure, where LH is low or inappropriately normal. It is also the readout for a pituitary-level intervention, since drugs acting on feedback or the GnRH receptor show their effect here before testosterone moves.

The mistake is treating a single LH as a stable analyte. Because of pulsatility, two samples twenty minutes apart in the same man can differ substantially, and one low value is weak evidence in isolation. The second error assumes that pushing LH higher pushes testosterone up in proportion. In primary testicular failure LH is already at or near maximal and the limit is Leydig cell capacity, so more stimulation buys nothing.