|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 378-379
Immature ovarian teratoma with peritoneal gliomatosis
R Agarwal, S Sehgal, S Verma, S Singh
Specialist Pathologist, Department of Pathology, Swami Dayanand Hospital, Shahdara, New Delhi, India
|Date of Web Publication||10-Dec-2014|
Dr. S Singh
Specialist Pathologist, Department of Pathology, Swami Dayanand Hospital, Shahdara, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Agarwal R, Sehgal S, Verma S, Singh S. Immature ovarian teratoma with peritoneal gliomatosis. Indian J Cancer 2014;51:378-9
We present an interesting case of immature ovarian teratoma (OT) with gliomatosis peritonei (GP). An 18-year-old girl presented to gynecology department with abdominal swelling. During laparotomy, left ovary was completely replaced by a cystic tumor and omentum was finely granular. Left salpingo-oophorectomy and biopsy of omental implants were performed and sent to pathology department.
On gross inspection, left ovarian mass measured 22 × 19 × 15 cm. Cut section was variegated with solid and cystic areas. Bony hard areas and tuft of hair were also identified. Omentum, received as fibrofatty tissue, showed fine nodular deposits. Microscopically, most areas of tumor were composed of abundant mature glial tissue along with choroid plexus, skin, gut mucosa, respiratory epithelium, smooth muscle, adipose tissue, bony trabeculae, mature and immature cartilage [Figure 1]. Focal areas showed primitive neuroepithelium with rare mitosis [Figure 1]c. The omental implants were composed of nodular mature astroglial tissue [Figure 2] and were positive for glial fibrillary acidic protein (GFAP) and S-100 [Figure 3] and negative for smooth muscle actin (SMA). Final diagnosis of GP in immature OT (grade 1) was made.
|Figure 1: (a) Section showing skin with adnexae and mature cartilage (H and E, ×10); (b) section showing tooth-like structure (×40, H and E); (c) section showing neuroepithelium (H and E, ×40); (d) section showing mature brain tissue along with intestinal epithelium (H and E, ×10)|
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|Figure 2: Section from omentum showing nodules of mature glial tissue (H and E, ×10) and inset showing higher magnification (H and E, ×40)|
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|Figure 3: (a) Section from omentum showing GFAP positivity in glial implants (GFAP, DAB, ×10); (b) section from omentum showing S-100 positivity in glial implants (S-100, DAB, ×40)|
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GP is a rare condition almost exclusively associated with immature OT and is characterized by nodules of mature glial tissue in the peritoneum.  Based on numerous studies performed to evaluate the origin of GP, two theories have been proposed regarding pathogenesis of GP. , The first theory suggests that glial foci arise from primary teratoma through rupture of capsule with subsequent implantation in peritoneum. The second theory is more widely accepted and suggests that glial foci arise independently from pluripotent Mullerian stem cells. Intraoperatively, gross appearance of GP can be confused with other multicentric intraabdominal diseases like peritoneal leiomyomatosis, peritoneal carcinomatosis, tuberculosis, endometriosis, melanosis, and ectopic decidua.  Hence, the role of microscopy and panel of immunostains to arrive at a definite diagnosis.
According to two defining criteria of GP proposed by Thulrbeck and Scully,  GP should be composed of entirely mature glial tissue. , Other cases where immature glial implants (grade 1, 2, 3) were found should be diagnosed as metastatic teratoma and require further aggressive therapy. This suggests that GP does not adversely affect the prognosis of OT. 
To conclude, GP is a rare benign condition associated almost exclusively with immature teratoma of ovary. Despite widespread involvement of peritoneal surfaces, GP does not adversely affect the prognosis and the method of treatment should be judged only by the stage and grade of primary OT. However, long-term follow-up even in the face of mature peritoneal glial implants is highly recommended because few case reports have documented malignant transformation of glial implants long after initial surgery.
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[Figure 1], [Figure 2], [Figure 3]