Ovarian Neoplasms

Ovarian enlargement may be found incidentally on physical exam or may present with symptoms.

Simple Cyst: Physiologic cyst (Luteal or Follicular Cysts): This is the most common cyst that occurs during the reproductive years. It is asymptomatic, unless torsion has occurred (as in large cysts). The β-hCG is negative; ultrasound shows fluid-filled simple cystic mass.

Management: Follow-up exam in 6-8 weeks (resolves spontaneously). Steroid contraception prevents new cysts. Laparoscopic removal if cyst >5 cm diameter; or has been previous steroid contraception without resolution of the cyst.

Complex Cyst: Benign Cystic Teratoma (Dermoid cysts): These are benign tumors. They can contain cellular tissue from all 3 germ layers. Rarely, squamous cell carcinoma can develop. The β-hCG is negative; ultrasound shows a complex mass.

Management: laparoscopic/laprotomy removal, either cystectomy (to retain ovarian function); oopherectomy (if fertility is no longer desired).

Bilateral Ovarian Enlargement: Polycystic Ovarian Syndrome (PCOS).

Ovarian Hyperthecosis: this refers to nests of luteinized theca cells in the ovarian stroma that produce higher levels of androgens. Most common seen in postmenopausal woman, or premenopausal with severe hirsutism and virilization.

Management: oral contraceptive pills (estrogen and progestin) to suppress and that and production (by reducing LH stimulation of the theca cells) into decrease free androgens (by stimulating sex hormone binding globulin).

During pregnancy

Luteoma of Pregnancy. This is a rare, non-neoplastic, tumor like mass of the ovary that emerges during pregnancy and regresses spontaneously after delivery. Found incidentally during caesarean section or postpartum tubal ligation. It can be hormonally active and produce androgens resulting in maternal and fetal hirsutism and virilization. No treatment is needed.

Theca Lutein Cysts. These benign neoplasms are caused by highr levels of FSH and β-hCG. The are associated with twins and molar pregnancies. The spontaneous regress after pregnancy.

Prepubertal or Postmenopausal Ovarian Mass. Any ovarian enlargement in prepubertal or postmenopausal women is always suspicious for an ovarian neoplasm.

Risk factors: BRCA1 gene, positive FH, high number of lifetime ovulation, infertility, use of perineal talc powder.

Protective factors: Conditions that decrease the number of ovulations – OCPs, chronic ovulation, breast-feeding, short reproductive life.

Initial workup of an ovarian mass involves the following: β-hCG, U/S, and laproscopy/laprotomy if complex is >5 cm.

Germ Cell Tumor: most common and young women in present in early stage disease. The most common malignant epithelium cell type is dysgerminoma.

Tumor markers: LDH, β-hCG, α-FB.

Epithelial Tumor: this is the most common ovarian cancer posmenopausal women. The most common malignant subtype is serous.

Tumor markers: CA-125, CEA

Granulosa-theca (stromal tumor): this ovarian tumor secretes estrogen and can cause endometrial hyperplasia.

Tumor marker: Estrogen

Sertoli-Leydig cell (stromal cell): this ovarian tumor secretes testosterone. Patients present with masculinization syndromes.

Tumor markers: Testosterone

Krukenberg tumor: Metastatic gastric cancer

Tumor marker: Mucin-producing tumor from the stomach.

Management:

    • Sonogram (CT scan for postmenopausal women)

    • Biopsy via laproscopy for simple cysts (no septations or solid components) or postmenopausal without ascites.

    • Tumor markers

    • Cystectomy for benign tissue

    • Premenstrual women: Salpingoopherectomy

    • Postmenopausal women: TAH; BSO and postoperative chemotherapy for malignant tissue.

Ovarian cancer can develop from three distinctive cell types (germ cells, stromal cells, and epithelial cells). Epithelial ovarian cancer is the most common (5%) and the leading cause of from gynecologic cancer in the United States. More than cervical and endometrial cancer combined.

Epithelial tumors, unlike germ cell and stromal tumors, are uncommon before the age of 40 years. High incidence in women with a family history; those who have been exposed to asbestos or talc; in industrialized nations; and in women with disordered ovarian function, including infertility, nulliparity, and frequent miscarriages. Ovulation-inducing drugs such as clomiphene has been implicated. Reduction in ovarian cancer risk is associated pregnancy, breastfeeding, in tubal ligation. Oral contraceptives reduce the risk of ovarian cancer in patients with the family history of cancer in the general population.

Familial cases account for about 10% of all ovarian cancer. Two types of autosomal dominant familial cancers have been identified:

Breast/ovarian cancer syndrome

The cumulative risk of ovarian cancer with critical mutations of BRCA1 or BRCA2 is 25%.

Lynch type II cancer family syndrome with nonpolyposis CRC, endometrial cancer, and ovarian cancer.

Ovarian Cancer

    • Look for a woman >50 with increasing abdominal girth at the same time as weight-loss.

    • Diagnostic testing: there is no routine screening test for ovarian cancer. CA125 is a marker of progression and response to therapy for ovarian cancer, not a diagnostic test.

    • Treatment: surgical debulking followed by chemotherapy, even in cases of extensive local metastatic disease. Ovarian cancer is unique in that surgical resection is beneficial even when there is a large volume of tumor spread through the pelvis and abdomen. Removing all visible tumor still helps.