Endocrine Abstracts

False elevation of estradiol(E2) due to immunoassay interference is a rare but important phenomenon reported in the literature. It is most commonly related to cross-reactivity(CR) from drugs sharing structural similarity with E2, namely fulvestrant and exemestane. These laboratory interferences(LI) can lead to unnecessary investigation/inappropriate treatments. Therefore, in such instances, a more selective and sensitive method is required. We present the case of a young female with high E2 levels inconsistent with her clinical iatrogenic menopause. A 34 years-old female with a history of breast cancer(BC) was examined for estradiol(E2) concentration. Her past medical history was remarkable for BC diagnosed at age 31. She underwent a right simple mastectomy with sentinel node biopsy. Pathology revealed an invasive BC, that was estrogen and progesterone receptor positive-pT4N0M0. Oocyte cryopreservation was performed. The patient was treated with chemotherapy(doxorubicin, cyclophosphamide, paclitaxel), followed by locoregional radiotherapy. Given her high-risk lifetime BC occurrence as well as the fact that her BC was strongly estrogen receptor positive, she initiated ovarian suppression with goserelin plus exemestane. The determination of serum E2 concentration, being a part of the patient’s therapeutic monitoring, was requested. E2 levels were persistently elevated(90-100pg/ml) over a year, measured by the chemiluminescent immunoassay method, that rendered exemestante therapy ineffective. The patient had a complete clinical response to treatment, according to clinical symptoms, radiologic findings and normal levels of tumor biomarker. One year after starting hormone therapy(HT), since she maintained elevated levels of E2, a bilateral salpingo-oophorectomy was performed, no pathological changes were found. Three months after surgery she was referred to our Endocrinology Department for further investigation due to persisting elevated E2 levels (83-87). She was in amenorrhea since chemotherapy, reporting vasomotor symptoms since that time. Her clinical status was inconsistent with elevated E2 values. A suspicion of LI was raised. To rule out the suspected exemestane CR with 17β-estradiol levels were subsequently obtained and tested with a more sensitive and specific method(access sensitive estradiol-assay-competitive binding immunoenzymatic assay-Beckman Coulter), which showed the patient’s serum estradiol levels were undetectable. This confirmed that an exogenous compound, most likely exemestane, caused the CR with the immunoassay resulting in falsely increased serum E2. Clinicians should keep in mind that LI must be considered in the presence of increased estradiol levels that are contradictory to the clinical picture, in a patient under anti-HT, and therefore should be confirmed using alternative assays.