Background: Luteinizing hormone (LH) is a useful parameter in diagnosing precocious puberty. The pubertal response of serum LH to a GnRH stimulation test is varied and clinical symptoms of precocious puberty are sometimes disproportionate with serum LH levels. Many patients present in a state of precocious puberty that advances rapidly but the post-GnRH peak LH is still prepubertal. LH receptor mutations are suspected of involvement in the unusual progression of precocious puberty. Objective: To examine the association between LHCGR polymorphism and central precocious puberty (CPP) subjects exhibiting a peak LH 5 IU/L on a GnRH stimulation test. Methods: In total, 102 girls with CPP and 100 normal adult women were enrolled. GnRH agonist treatment outcomes were analyzed. All subjects underwent LHCGR gene analysis by the Sanger method and patients and controls were compared. Auxological data and gonadotropin levels were analyzed in the 102 patients. Of these patients, 75 completed GnRH agonist treatment, and treatment outcomes were analyzed. Results: In total, seven polymorphisms were identified. Two missense mutations were found in the patient group: g.48698754 G/A was found in one patient and g.48688613 G/A was found in another patient. One missense mutation, g.48694236 A/G, and one synonymous mutation, g.48688732 T/C, were found in both groups. Two missense mutations and one insertion were found in controls: g.48687721 C/A was a novel mutation. GnRH agonist treatment decreased bone age advancement and increased predicted adult height in 75 patients with CPP. Conclusions: LHCGR gene polymorphism was not associated with lower stimulated LH in patients with CPP. GnRH agonist treatment improved clinical parameters in these patients.