ABSTRACT
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.
Subject(s)
Female , Humans , Drug Therapy , Estrogen Replacement Therapy , Gestational Trophoblastic Disease , Hysterectomy , Molecular Structure , Ovariectomy , Radioimmunoassay , Sterilization , Trophoblasts , Uterine DiseasesABSTRACT
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.
Subject(s)
Female , Humans , Drug Therapy , Estrogen Replacement Therapy , Gestational Trophoblastic Disease , Hysterectomy , Molecular Structure , Ovariectomy , Radioimmunoassay , Sterilization , Trophoblasts , Uterine DiseasesABSTRACT
The safety of ICSl as a novel procedure of assisted fertilization may be assessed by the health of the baby born. In order to evaluate the safety of ICSI, perinatal outcome and congenital anomaly of the babies born after ICSI were compared with those of babies born after IVF (control group). We analysed the clinical data from the obstetric and pediatric records, including the information obtained through telephone. The results are as follows; Mean gestaional age (+/-SEM) and birth weight in singleton pregnancy were 38.8+/-1.9 weeks and 3209.7+/-501.9gm in IVF group, 39.0+/-2.2 weeks and 3289.9+/-479.5gm in ICSI group, respectively. Mean gestational age and birth weight in twins were 36.8+/-2.1 weeks and 2512.8+/-468.0gm in IVF group, 36.5+/-2.8 weeks and 2492.7+/-537.1gm in ICSI group. In IVF group, perinatal mortality rates were 8.5 in singletons and 56.6 in twinst for the ICSI singletons and ICSI twins, the perinatal mortality rates were 11.6 and 49.0, respectively. The incidence of congenital malformations was 3.6% (8/224) in IVF group and 2.1% (4/188) in ICSI group, there was no statistical difference (p>0.05, Fisher's exact test). The incidence of major congenital anomalies was 0.9% (2/224; pulmonary artery hypoplasia, renal cystic dysplasia) in IVF group and 1.1% (2/188; holoprosencephaly, Cri du chat syndrome) in ICSI groups (p>0.05, Fisher's exact test). Similarly, there was no significant difference in incidence of minor congenital anormalies 2.7% (6/224) in IVF group and 1.1% (2/188) in ICSI group respectively (p>0.05, Fisher's exact test). In conclusion, there was no difference in the perinatal outcome and the incidence of congenital anomalies between the babies born after ICSI and those after conventional IVF.