Ovarian dysgerminoma


Ovarian dysgerminoma

Description, Causes and Risk Factors:

Ovarian dysgermination is most common maligant germ cell tumor (GCT) of ovary. One percent of all ovarian cancers are dysgerminoma cases. Eighty percent of these maligant tumor cases occur during 2nd and 3rd age decades and their mean and median occur in late teens and early twenties.

It mostly occurs in virgin girls and their early adult life. In pre pubertal girls its occurrence is around 5%. It also occurs in married women in the age group of 20-30 years. After menopausal periods its occurrence is almost rare. Its male or testicular counterpart is seminoma. Dysgerminoma exactly corresponds to its male counterpart seminoma, histologically and pathologically. Of all the gem cell tumors of ovaries, dysgerminoma is the most common malignant ovarian germ cell tumor Chromosome 12p abnormalities are genetic hallmarks of testicular seminoma. The genetic changes or mutations in dysgerminoma.are yet to be discovered. All dysgerminoma are considered malignant, but only one third of dysgerminoma behave aggressively. Besides dysgerminoma the other germ cell tumors found in ovaries are

The exact etiology of dysgerminomas has not been determined. Typically, germ cells are encapsulated at birth within the primordial follicle. Should they somehow escape encapsulation, cell death usually occurs. Should the germ cells survive, rapid growth ensues because no cellular contexts exist that can provide normal contact inhibition, hence GCT formation. All dysgerminomas are considered malignant, but only one third of dysgerminomas behave aggressively.

Abnormal gonads (due to gonadal dysgenesis and androgen insensitivity syndrome) have a high risk of developing a dysgerminoma. Most dysgerminomas are associated with elevated serum lactic dehydrogenase (LDH), which is sometimes used as a tumor marker.

Other Risk Factors:

    Usually teenage girls or young women.

  • 2% ovarian neoplasms.

  • 1/2 of malignant germ cell neoplasms.

  • Gonadal dysgenesis may be setting for some.

Symptoms:

The symptoms can be summarized as:

    Asymptomatic in early stages of growth and development.

  • Pelvic pain.

  • Excessive and abnormal bleeding during menstruation.

  • Dysuria.

  • Increased frequency of urination.

  • Mild abdominal symptoms.

  • Pelvic mass or pelvic fullness.

Diagnosis:

Regardless of the clinical environment, obtain a urine pregnancy test. This test should be mandatory in any woman of reproductive age who presents with abdominopelvic symptoms.

Because dysgerminoma tumors affect women of a reproductive and sexually active age, cultures for gonorrhea and Chlamydia and a wet mount are indicated at the time of speculum examination, especially if patients experience abdominopelvic pain. In this way, sexually transmissible diseases may be detected and treated before surgery.

The standard workup for suspected GCTs requires lactic dehydrogenase (LDH), alpha-fetoprotein (AFP), and beta-human chorionic gonadotropin (bHCG) levels because these agents have endocrine activity and will help to diagnose and follow patients who have germ cell tumors. Dysgerminomas are an exception to this rule. The absence of an elevated AFP or bHCG does not exclude the diagnosis of dysgerminomas because they rarely produce hormones. In extremely rare cases, dysgerminomas can become infiltrated with syncytiotrophoblastic giant cells, which produce human chorionic gonadotropin.

Useful tumor markers for dysgerminomas include the following:

    bHCG (beta-human chorionic gonadotropin).

  • AFP (alpha-fetoprotein)

  • Lactate dehydrogenase (LDH)

  • Cancer antigen 125 (CA-125).

These markers can also be used for postoperative follow-up care or for tracking the success of adjuvant therapy.

Imaging: Secondary imaging studies, such as CT, are used to rule out metastasis.Chest radiographs are performed to rule out pulmonary spread.Body imaging with CT scanning and MRI can be of value in patients with GI or genitourinary signs of obstruction

Treatment:

Treatment of dysgerminoma may include the following:

    Unilateral salpingo-oophorectomy with or without lymphangiography (an x-ray study of the lymph system, the tissues and organs that filter and destroy harmful substances and help fight infection and disease) or CT scan (a series of detailed pictures of areas inside the body, created by a computer linked to an x-ray machine).

  • Unilateral salpingo-oophorectomy followed by observation (closely monitoring a patient's condition without giving any treatment until symptoms appear or change).

  • Unilateral salpingo-oophorectomy followed by radiation therapy.

  • Unilateral salpingo-oophorectomy followed by chemotherapy.

It is important that therapy of ovarian dysgerminoma be optimized because of the young age of women affected and the threat that therapy may pose to fertility. Our understanding of dysgerminoma has improved, so that treatment schemes with better therapeutic ratio may now be used. Approximately 65% of patients present with stage IA disease. For those wishing to preserve fertility, conservative surgery with close clinical, radiologic, and serologic follow-up is the treatment of choice, with chemotherapy for relapse. Cure rates should approach 100%, and fertility is usually preserved. Intra-abdominal relapse in those not wishing to preserve fertility should be treated with modest-dose pelvic and abdominal irradiation. For those patients with disease presenting in stages IB, II, and III who wish to maintain fertility, unilateral oophorectomy followed by combination chemotherapy may be curative and spare ovarian function. Otherwise, complete surgery, followed by abdominopelvic radiation therapy, is recommended. This treatment produces less morbidity than chemotherapy and will cure approximately two-thirds of patients. Chemotherapy should be used for salvage of subsequent relapse. Both radiation and chemotherapy are highly effective treatment modalities for dysgerminoma. This information, coupled with better understanding of the patterns of disease spread and improved ability to identify nondysgerminomatous elements using serum tumor markers, means that a more conservative approach can be taken to management without compromising the chance of cure. Cure rates for dysgerminoma should now approach the role of 97% achieved in the comparable tumor, testicular seminoma.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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