Although chemotherapy remains to be the mainstay of treatment of trophoblastic disease, hysterectomy has been performed as the primary management of nonmetastatic trophoblastic disease who desire sterilization and for uterine disease resistant to chemotherapy. Clinically, the documentation of disease regression is provided by serial quantitative serum beta-hCG assays and the persistent disease may be indicated when the serum beta-hCG values rise for 2 weeks or plateau for 3 weeks or more. Because of similarity in molecular structure, the confounding effect of an elevated LH on beta-hCG assessment in castrated women after treatment for trophoblastic disease has been documented. This LH cross-reactivity may be suspected in women with bilateral oophorectomy demonstrating persistent low levels of beta-hCG. It is particularly true when the assay is perfo-rmed by conventional polyclonal radioimmunoassay. We have experienced two cases of nonmetastatic trophoblastic disease whose serum beta-hCG assay plateaued at a low level after total abdominal hysterectomy with bilateral salpingo-oophorectomy and chemotherapy. Clinical and radiologic work-ups were done for metastatic lesion in dose patients, but the results were negative. The quantitative LH assays (Serono LH MAIAclone kit, Roma, Italy) were performed with the sera obtained from the patients; the results were 37 and 31 mIU/ml (1st IRP) with beta-hCG of 14 and 13 mIU/ml (1st IRP), respec-tively. With the initiation of oral estrogen replacement thrapy to those patients, the quantitative beta-hCG values fell below 5 mIU/ml (1st IRP) and they remained in complete chemical remission without any additional chemotherapy for one year. The persistant low titers of beta-hCG in those patients were considered to be result of LH cross-reactivity on beta-hCG assessment. It is concluded that whenever the assay of beta-hCG shows persistent low titers in the oophorectomized patient for treatment of trophoblastic disease, LH cross-reactivity should be suspected.