A case of luteinizing thecoma with sclerosing peritonitis: revisiting a link with anti-epileptic drugs.

Luteinizing thecoma with sclerosing peritonitis (LTSP) is a rare ovarian tumor of unclear etiology and pathogenesis. The diagnostic entity was proposed in 1994, but a number of earlier reports described possible cases, and some suggested an association with anti-epileptic drugs (AEDs). In presenting a new case we review the literature of previous cases to evaluate the possibility of such a link. When cases in reproductively immature patients are considered, evidence for an association between LTSP and AEDs is strongly suggested despite the rarity of the condition.

Sclerosing peritonitis associated with bilateral luteinized thecoma, linked to anticonvulsant therapy.

OBJECTIVE: To present a new case of sclerosing peritonitis associated with bilateral luteinized thecoma of the ovaries, linked to anticonvulsant therapy. CASE: A 22-year-old patient, receiving carbamazepine for seizures and anxiety attacks presented with shortness of breath, abdominal pain, nausea and vomiting. Clinical and imaging examinations revealed bilateral ovarian masses with massive ascites. At emergency surgery, bilateral ovarian luteinized thecoma with sclerosing peritonitis was found. Due to recurrent, postoperative episodes of small bowel obstruction she was treated with nasogastric suction, intravenous fluids and electrolyte replacement. Total parenteral nutrition was introduced. Since only partial improvement was achieved tamoxifen was administered with resolution of the bowel obstruction. CONCLUSIONS: This is the 19th case of sclerosing peritonitis associated with luteinized thecoma of the ovaries and the 3rd to be associated with anticonvulsant therapy. Treatment should be aimed at relief of bowel obstruction symptoms, preferably with conservative methods. Tamoxifen for downregulation of TGF-beta production should be considered as a treatment modality, as it proved to be very helpful in the presented patient.

Influence of age on induction of mammary tumors by diethylstilbestrol in C3H/HeN mice with low murine mammary tumor virus titer.

C3H/HeN female mice with low murine mammary tumor virus titer (MTV-) were fed diets containing a targeted concentration of 640 ppb diethylstilbestrol [(DES) CAS: 56-53-1; 4,4'-(1,2-diethyl-1,2-ethenediyl)bis-phenol]. Mice were started on DES at 3, 5, 7, or 9 weeks of age. Some continued on the diet throughout the rest of their life-spans, whereas others were killed as soon as they had been fed DES for 2, 4, 6, 8, 10, or 12 weeks. Controls were also examined throughout the study. Among mice killed early, the only observation significantly influenced by age at the start of DES treatment was the presence or absence of corpora lutea (CL). DES did not prevent CL from appearing in mice started on DES at 7 or 9 weeks of age, but it did prevent their appearance in about 25% of the mice started at 5 weeks and in up to 75% of the mice started at 3 weeks of age. In the life-span-exposure groups, CL either disappeared or were never formed in 88% or more of the mice, regardless of age at the start of treatment. Neoplastic or presumptive preneoplastic lesions apparently influenced by DES in the life-span-treatment groups included ovarian tubular adenomas; granulosa cell tumors and luteomas; pituitary cystoid degeneration, hyperplasia, and adenomas; uterine adenocarcinomas and cervical adenosis; mesotheliomas; and mammary hyperplastic alveolar nodules (HANs) and adenocarcinomas. Luteoma and granulosa cell tumor incidences were reduced by DES, regardless of age at the start of treatment. Influence of age at the start of treatment was minimal or not apparent for mesotheliomas, uterine adenocarcinomas, or pituitary adenomas; however, pituitary cystoid degeneration and hyperplasia and cervical adenosis occurred in higher frequency and/or with shorter duration of DES exposure the earlier that treatment was started. A delay in the start of DES treatment was associated with a remarkable delay in HAN and mammary adenocarcinoma development. This was especially apparent in young mice (3-7 wk old) in which a 2-week delay in treatment resulted in a 20-week delay in HAN or tumor onset. Age at the start of treatment was a major factor in susceptibility of C3H/HeN-MTV- female mice to DES-induced mammary tumorigenesis.

High yields of granulosa cell tumors/luteomas in F344 rat ovaries after transplacental administration of N-nitrosobis(2-oxopropyl)amine.

Ovarian tumors were induced at very high incidence in the offspring of F344 rats receiving 3 subcutaneous injections of 10 mg/kg of N-nitrosobis(2-oxopropyl)amine on the 14th, 18th and 20 days of gestation. Histologically, all ovarian tumors were of the granulosa cell tumor and/or luteoma type. Many of them consisted of large, polygonal cells with abundant eosinophilic or vacuolated cytoplasm, arranged in sheets or in a pseudo-palisaded pattern separated by thin fibrovascular stroma, and they exhibited typical luteoma morphological character. The high yields, and the similarities in morphology as well as putative hormonal influence suggest that this experimental system may serve as a good animal model for granulosa cell tumor and/or luteoma development in women.

A new model for inducing malignant ovarian tumours in rats.

After the implantation of ovarian tissue into the spleen of gonadectomized female Sprague-Dawley rats (splenic ovary), luteomata and later benign granulosa or granulosa-theca cell tumours develop. Treatment of these rats with 7,12 dimethylbenz(a)anthracene (DMBA), given intravenously, 2 mg/kg body weight weekly, total dosage 40 mg/kg, immediately and especially 25 weeks after implantation of ovarian tissue into the spleen, led to malignant, partially metastasizing granulosa, and in one case theca cell tumours, 16-46 weeks after beginning the carcinogen treatment. No malignant neoplastic growth was seen when diethylnitrosamine (DEN), 20 mg/kg once weekly for life, was injected subcutaneously immediately or 25 weeks after implanting ovarian tissue.Since the normal, non-implanted rat ovary was not affected by DMBA treatment the malignant transformation of splenic ovaries in the respective experimental groups may be related to the increased stimulation by pituitary gonadotrophins and formation of luteomata or beginning granulosa and theca cell proliferations.