Functional ovarian neoplasms have unique clinical manifestations related to hormone

overproduction and may give rise to a broad spectrum of clinical syndromes. Sex cord–stromal
tumors, the most common functional ovarian neoplasms, are associated with either
hyperestrogenism (as in granulosa cell tumor and thecoma) or hyperandrogenism (as in Sertoli-
Leydig cell tumor and Leydig cell tumor). Other, less common ovarian neoplasms that may have
Endocrine or nonendocrine syndromic manifestations include germ cell tumors associated with the
excessive production of human chorionic gonadotropin (eg, choriocarcinoma, dysgerminoma),
monodermal teratomas (eg, carcinoid tumor, struma ovarii) associated with carcinoid syndrome
and hyperthyroidism, and primary epithelial ovarian cancers associated with paraneoplastic
syndromes. The application of diagnostic algorithms based on patient demographic information,
clinical manifestations, laboratory findings, and cross-sectional Imaging features may help identify
ovarian neoplasms in complex clinical settings.

Introduction
The ovary is an important source of estrogens, progesterone, and androgens, which play a
critical role in cyclic changes in the female reproductive tract. A broad spectrum of endocrine and
nonendocrine syndromes are associated with ovarian neoplasms. An algorithmic approach helps
identify the most likely underlying ovarian tumor in a specific clinical scenario (Figs 1, 2).
Functional ovarian neoplasms commonly cause ovarian steroid hormone–related complications,
whereas tumors such as struma ovarii and carcinoid cause excess production of hormones that are
not indigenous to the ovary. A subset of ovarian epithelial cancers is characterized by
paraneoplastic syndromes such as nervous system or hematologic disorders. The Radiologist
should Be familiar with the imaging features of ovarian neoplasms that cause a broad spectrum of
clinical syndromes.
Although some ovarian tumors have clinical and imaging features that overlap, the
predominance of certain clinical manifestations and imaging features among tumors of a specific
type may aid in their accurate identification. The article describes the clinical syndromes
associated with ovarian tumors, describes pertinent imaging findings, and offers an algorithmic
approach to diagnosis that is based on patient demographics, clinical manifestations, and imaging
findings.
Granulosa Cell Tumor
Granulosa cell tumor is the most common malignant sex cord–stromal tumor, and it
accounts for 70% of all sex cord–stromal tumors. It is also the ovarian tumor that most frequently
manifests with hyperestrogenism. However, granulosa cell tumors are rare, accounting for only
2%–3% of Ovarian malignancies. The adult Type of granulosa cell tumor is more common (95%
of granulosa cell tumors) than the juvenile type and usually causes symptoms that are related to
excessive estrogen production, such as vaginal bleeding, endometrial hyperplasia, and carcinoma.
Adult and juvenile tumors differ in their histologic appearance and in the patient’s age at
presentation. Juvenile tumors occur in the first 2 decades of life, and they are rarely seen in patients
older than 30 years. Adult tumors manifest in middle-aged and postmenopausal patients. An
estimated 50% of patients with granulosa cell tumors are postmenopausal. Approximately 80% of
children with a juvenile granulosa cell tumor present with hyperestrogenism. Ovarian granulosa
cell tumors account for approximately 10% of cases of isosexual precocity in girls. Virilization
due to ovarian granulosa cell tumors is rare.
At imaging, granulosa cell tumors most commonly manifest as complex cystic masses and
are overwhelmingly unilateral (>95% of cases) (Fig 3a, 3b). Solid granulosa cell tumors are
uncommon and have a heterogeneous appearance, with regions of hemorrhage, fibrosis, or both.
Unlike epithelial ovarian cancers, granulosa cell tumors rarely manifest with peritoneal disease.
An estimated 80% of granulosa cell tumors are associated with endometrial abnormalities, mainly
endometrial hyperplasia; endometrial cancer occurs in approximately 10% of cases (12). Other
features of coexistent hyperestrogenism also may be detected at imaging (Fig 3b, 3c). Granulosa
cell tumors generally have low malignant potential, and the prognosis is usually good. Juvenile
tumors are associated with a better prognosis than adult tumors, but juvenile tumors tend to recur
within a shorter interval after treatment than adult tumors do. Increased risks of endometrial cancer
and breast cancer have been reported in patients with granulosa cell tumors, especially juvenile
tumors. A tendency of late recurrence (as long as 25 years after the initial diagnosis) also has been
observed with granulosa cell tumors. Surgery remains the treatment of choice, and the prognosis
is largely dependent on the tumor stage at the time of diagnosis and treatment.
Leydig Cell Tumor
Leydig cell tumors, a subtype of steroid cell tumors, are rare ovarian neoplasms composed
of lutein cells, Leydig cells, and adrenocortical cells. Steroid cell tumors account for approximately
0.1% of ovarian neoplasms and are subcategorized as stromal luteomas, Leydig cell tumors, and
steroid cell tumors not otherwise specified (8). Most Leydig cell tumors are benign, small
(diameter, <3 cm), and solid (21). Both Leydig cell tumors and stromal luteomas are predominantly
seen in postmenopausal women (mean age, 58 years). Stromal luteoma is estrogenic in as many as
60% of cases and androgenic in 12% of cases. In contrast, approximately 75% of Leydig cell
tumors are virilizing. On US and CT images, Leydig cell tumors manifest as solid masses (Fig 7).
An abundant lipid content produces areas of low attenuation on CT images, high signal intensity
on T2- and T1-weighted MR images, and intense enhancement on MR images obtained after the
administration of gadolinium-based contrast material. However, the signal intensity on T2
weighted MR images varies in accordance with the extent of fibrous stroma within the tumors.

Dysgerminoma
Dysgerminoma, the ovarian counterpart of testicular seminoma, is the second most
common ovarian germ cell tumor and the most common malignant germ cell tumor. However, it
accounts for less than 2% of ovarian malignancies. Pure dysgerminomas do not secrete hormones;
however, 5% of the tumors may contain syncytiotrophoblasts, which produce β−hCG.
Dysgerminoma is commonly seen in young women in the 2nd–3rd decade of life. At imaging, a
dysgerminoma manifests as a multilobulated, usually unilateral, solid mass with calcification (Fig
10).

Epithelial Ovarian Cancers

Epithelial ovarian tumors account for more than 60% of all ovarian tumors and 85% of
malignant ovarian neoplasms (51). At US and CT, epithelial ovarian cancers manifest as unilocular
or multilocular cystic masses with varying amounts of solid tissue (Figs 14, 15). A large maximal
diameter (>4 cm), thick septa (>3 mm), solid mural nodules, and vascular solid components, with
or without ascites, peritoneal metastases, and lymphadenopathy, are features suggestive of an
epithelial ovarian malignancy. The characteristic MR imaging features include solid components
with intermediate signal intensity on T2-weighted images, thick enhancing irregular walls, septa,
and mural nodules (52). Ascites, peritoneal implants, local invasion, lymphadenopathy, and
metastases are corroborative findings of malignancy.

Case Report
An urban, smoker, nulliparous, 56 years old female patient, with known family history of
cancer (mother had an ovarian cancer) was diagnosed with right breast adenocarcinoma 10 years
ago, for which she had undergone radical mastectomy, followed by chemotherapy (according to
the scheme cyclophosphamide 1 g, methotrexate 80 mg, 5-fluorouracil 1 g - 6 cycles) and
radiotherapy (at a dose of 50 Gy during 6 weeks). Two years later she was diagnosed with a
relapsed disease in the contralateral mammary gland, for which she had also undergone radical
mastectomy.

She came in Pulmonology Hospital Sibiu for intense abdominal pain, increased
abdominal volume and dry cough in September 2014. On physical examination she was without
fever, with decreased vesicular breath sounds basal bilateral, rhythmic heart sounds; her abdomen
was increased in volume and sensitive. Laboratory tests were normal, and the chest X-ray
showed bilateral basal pleural effusions, predominantly on the right side, and also increased
interstitial markings. The thoracoabdominal CT scan showed bilateral pleural effusions, a
retractable area in the right posterior-basal side, and a punctate size pulmonary micro-nodule with
a difficult to be established etiology; no pathologic axillary, mediastinal or retrocrural lymph
nodes were present; the liver had some hypodense areas with an aspect of hepatic cysts; epigastric
and left flank peritoneum appeared to be thickened - aspect suggestive for peritoneal
carcinomatosis; a fine perihepatic liquid collection was found. A right thoracentesis was
performed and the pleural fluid was serocitrin, Rivalta- positive, with pleural glucose of 65
mg/dL, pleural protein content of 36 mg/dL, lactate dehydrogenase (LDH) of 206 mg/ dL,
pleural LDH/serum LDH ratio of 206 mg/dL, negative for Koch bacillus, with tumor cells
cytology. She received treatment with antibiotics, diuretics, and hepatoprotective drugs, and the
recommendation to be hospitalized in the oncology service for further investigations.

This hospitalization on the Oncology service of the Emergency County Clinical Hospital
Sibiu occurred in October 2014, when she had an ECOG performance status of 2, preserved
consciousness, anorexia, mat sound in the lung bases with abolished breath sounds, increased
abdominal volume due to ascites fluid (shifting dullness), anxiety, oliguria, bilateral post-
mastectomy supple scars without signs of recurrence. Laboratory analyzes were in normal limits.
The value of tumor markers was: CA 125-9629 U/ mL and CA 15-3-255 U/mL. Repeated
thoracoabdominopelvic CT scan showed an increased amount of bilateral pleural effusion
(compared to the last examination), with a right posterior-basal retractable area, a stationary
punctate size pulmonary micro- nodule, without pathological axillary, mediastinal or retrocrural
lymph nodes; the liver had a stationary CT scan aspect, peritoneum in the epigastric region and left
flank was ticked, signifying possible peritoneal metastases; the uterus was inhomogen and the
ovaries - slightly increased in size and native homogeneous. The presence of pleural effusions,
ascites with tumor cells and the increased value for CA125 were arguments for an ovarian cancer.
The first series of polychemotherapy was started with carboplatin (450 mg) and paclitaxel (260
mg), with appropriate premedication and antiemetic protection, tolerated without any incident,
followed by further 5 cycles of polychemotherapy, with the same dosage regimen. A partial
response was obtained at the end of the treatment. The determination of CA 125 and the control
CT scan showed a bilateral very fine residual pleural fluid trace; liver cysts were stationary; the
peritoneal thickening was reduced; the uterus and the ovaries were reduced in size compared to
the previous examination. Therefore it was decided to go for surgery, given the decrease in the
amounts CA 125 and the favorable development of CT scan control. The patient was admitted
to the Gynecology service in April 2015, where a total hysterectomy with bilateral oophorectomy
was made; in addition - omentectomy with biopsies of diaphragmatic domes and flanks
collection. The diagnosis of left ovarian papillary adenocarcinoma with peritoneal dissemination
was established at the histopathological examination. After surgery, the evolution was favorable
with subsequent normalization of CA 125 values and 3 more courses of chemotherapy were given.
On physical examination the patient had an ECOG performance status of 2, anxiety, an
abdomen diffusely sensitive on palpation, with increased volume due to the fat storage, and a
supple postoperative scarring, with no signs of relapse.

She was hospitalized again in the Oncology service in October 2015, anxiously and
depressive, with chest pain, an ECOG performance status of 1, increased abdominal volume
due to the fat storage, diffuse and spontaneously sensitive on palpation, sensitive in hypogastric
region, postoperative supple scars. The biological tests highlighted an increased value of CA
125 (132.2 U/mL). The CT scan showed: small bilateral pleural effusions, without any
condensation in adjacent lungs, and a stationary punctate size pulmonary micro-nodule; no
pathological axillary, mediastinal or retrocrural lymph nodes were present; the liver
CT scan aspect was stationary; no peritoneal thickening or peritoneal nodules were
shown; there was present a pelvic tissue nodule located on the right side of the rectum
measuring 7 cm (considered to be a post-hysterectomy tumor recurrence); it was without
ascites or retroperitoneal lymphadenopathy (Figure 1).
Abdominal ultrasound examination also found a homogeneous tumor with mixed
content, without proper wall at about 3 cm, located near the bladder. The diagnosis of relapsed
tumor was established; this was the reason to resume the chemotherapy, with a changed
therapeutical scheme. At the moment, the patient is under the second course of treatment
with liposomal doxorubicin, with good gastric tolerance, under antiemetic protection,
associated with pain relievers. Her ECOG performance status at discharge was 1

Discussion
The initial diagnosis was established with some difficulties, as the patient presented pleural
effusions and ascites but the ovaries were only slightly enlarged and homogenous at CT scan. The
CT scan aspect suggestive for peritoneal carcinoma and the presence of malignant cells in the
abdominal fluid were arguments for the presence of a neoplasm. The increased value of CA125
suggested an ovarian neoplasm. The ovarian cancer is characterized by a rapid volume increase and
an intra and extra-peritoneal spreading with presence of ascites and pleural effusion. The presence
of ascites plays an important role in the progression of the disease and inhibition of chemotherapy
response; thus, once appeared, the management of a large quantity of ascites can be a big issue.
The patients undergo paracentesis frequently in order to reduce the symptoms [2].

The ovarian adenocarcinoma associated with serous pleural and peritoneal effusions causes
problems regarding the positive and differential diagnosis. Most times it is confused with Demons
Meigs Syndrome. This syndrome associates a benign tumor with ascites and pleural effusion. The
tumor removal leads to serous effusions remission. The marked increase of CA125 associated with
Demons Meigs Syndrome is a very rare condition, with few cases reported in the literature. In
these situations, the precise diagnosis is made by a histopathological examination [6].

The patient’s mother had an ovarian neoplasm. The existence of an increased risk of
ovarian adenocarcinoma was reported in females with a familial history of cancer. The heredity of
the ovarian cancer is attributed to mutations in genes BRCA1 and BRCA2; these can be transmitted
in an autosomal dominant way to the next generation. BRCA1 and BRCA2 are considered tumor
suppressors - they encode proteins with the role of repairing DNA. The mutations of these genes
may lead to the loss of their function and produce a genomic instability with a high risk of
malignant transformation [7-9].

The coexistence of multiple primary neoplasms is due to a mutation in the glutathione S-

transferase gene M1, T1, P1. These encode an important group of enzymes that participate in the
xenobiotics metabolism. The members of this subfamily of genes would be involved in the
development of multiple cancers [10].

The fact that our patient was treated previously by chemo- and radiotherapy is important. Chemo-
and radiotherapy (especially the use of alkylating agents, as to our patient) are considered to be
risk factors concerning the appearance of multiple neoplasms. The chemo- and radiotherapy doses,
the dimension of irradiated area, and the age of the patient would be involved in the
appearance of new cancers – even 10 years after initiation of first treatment; the bigger the doses,
the higher the risk [11].

Which are the prognostic factors of patients with ovarian cancer which evolves with serous
effusions? This is an important issue as the survival rate at 5 years of patients with such advanced
stage ovarian cancer is only 20% [12]. An immuno-histochemical analysis of serous effusions
obtained from 143 patients with ovarian cancer found in an advanced stage, treated with
chemotherapy based on platinum was made. The effusions were analyzed pre- and post-
chemotherapy. In pre-chemotherapy samples, it was shown that survivin (which is an apoptosis
inhibitor) was associated with a longer progression free survival, and survivin, signal transducer
and activator of transcription 5B, and p21-activated kinase-1 were associated with a longer overall
survival. Instead, peroxisome proliferator-activated receptor gamma and human leukocyte antigen-
G were associated with a poor progression free survival in patients with post chemotherapy disease
recurrence with effusions [13].

How can be managed more efficiently ascites and pleural effusions, outside the classical
therapy of ovarian adenocarcinoma? Monoclonal antibodies (as catumaxomab or bevacizumab)
and aflibercept (a recombinant fusion protein) were administered intraperitoneally in ascites of
patients with ovarian cancers. These medications have shown to reduce the signs and symptoms that
accompany ascites, leading to an improved quality of life, increased survival rate and interval
between paracentesis [14]. Intrapleural instillations (using a thoracoscope) of a slerotic agent
(talcum and doxycycline) were performed for the malignant pleural effusions. This procedure
helped to reduce the recurrence of pleural effusion to more than 6 months

Conclusions
Nearly all neoplasms have been reported to involve the pleura. In most studies, however,
lung carcinoma has been the most common neoplasm, accounting for approximately one-third of
all malignant effusions. Breast carcinoma is the second most common. Lymphomas, including
both Hodgkins disease and non-Hodgkins lymphoma, are also an important cause of malignant
pleural effusions. Tumours less commonly associated with malignant pleural effusions include
ovarian and gastrointestinal carcinomas. In 5–10% of malignant effusions, no primary tumour is
identified. The incidence of mesothelioma varies according to the geographical location. Post
mortem studies suggest that most pleural metastases arise from tumour emboli to the visceral
pleural surface, with secondary seeding to the parietal pleura. Other possible mechanisms include
direct tumour invasion (in lung cancers, chest wall neoplasms, and breast carcinoma),
haematogenous spread to parietal pleura, and lymphatic involvement. A malignant tumour can
cause a pleural effusion, both directly and indirectly. Interference with the integrity of the
lymphatic system anywhere between the parietal pleura and mediastinal lymph nodes can result in
pleural fluid formation. Direct tumour involvement with the pleura may also contribute to the
formation of pleural effusions. Local inflammatory changes in response to tumour invasion may
cause increased capillary permeability, with resultant effusions. The term "paramalignant
effusions" is reserved for those effusions that are not the direct result of neoplastic involvement of
the pleura but are still related to the primary tumour. Important examples include: postobstructive
pneumonia, with a subsequent parapneumonic effusion; obstruction of the thoracic duct, with the
development of a chylothorax; pulmonary embolism; and transudative effusions secondary to
postobstruction atelectasis and/or low plasma oncotic pressures secondary to cachexia. Treatment
of the primary tumour can also result in pleural effusions. Important causes in this category include
radiation therapy and such drugs as methotrexate, procarbazine, cyclophosphamide, and
bleomycin. Finally, concurrent nonmalignant disease, such as congestive heart failure, may
account for an effusion seen in a patient with cancer.
 A condition “pseudo-” Meigs’ syndrome when it is associated with any other type of
ovarian tumor, such as a mature teratoma, struma ovarii, metastatic ovarian tumor, or leiomyoma.
Several theories concerning the source of ascites in pseudo-Meigs’ syndromes have been proposed.
Some involve proposed production of ascitic fluid by the tumor; others suggest that lymphatic
obstruction, hormonal stimulation, release of inflammatory mediators, or tumor torsion is the
cause. One early suggestion was that a solid ovarian tumor could physically irritate the peritoneum
and stimulate the overproduction of peritoneal fluid. Another theory proposed that the solid tumor
compresses underlying lymph vessels and veins, slowing normal peritoneal fluid reabsorption and
lymph drainage. As reviewed by Rubinstein et al., yet other theories suggested that the syndrome
results from a discrepancy between the arterial supply to a large tumor mass tissue and the venous
and lymphatic drainage of the same mass, leading to stromal edema and transudation. Another
possibility is that pressure on the lymphatics in the tumor itself may cause the escape of fluid
through the superficial lymphatics of the tumor. Yet another scenario is that the ascites is caused
by cytokine-induced excessive production of fluid by the peritoneum.
Release of multiple inflammatory cytokines into the plasma, including IFNγ, IL-1β, IL-6,
IL-8, IL-10, TNFα, PlGF, and HSP90B1, is frequently associated with epithelial ovarian cancers
(EOC). These cytokines can be released by tumor cells, supporting stromal cells or reactive
immune cells, and could play cumulative roles in the formation of ascites. The hypersecretion of
vascular endothelial growth factor (VEGF) from the oviducts has been singled out to play a role
in the pathogenesis of ascites.
It is known that pleural effusions can result from inflammation, such as in infection or
autoimmune disease, or from several other fairly common conditions. However, the pleural
effusion associated with the hydrothorax in pseudo-Meigs’ syndrome is thought to be caused by
migration of excessive ascites fluid into the pleural cavity via a unique class of lymphatic channels
in the diaphragm. The mechanism of pleural effusion development is even more obscure when in
the absence of ascites, as in some cases of pseudo-Meigs. The pleural effusion is classically, though
not exclusively, a transudate. It has been proposed that because the transdiaphragmatic lymphatic
channels are larger in diameter on the right, the pleural effusion in Meigs syndromes is classically
on the right side too. However, left-sided-only and bilateral pleural effusions have been reported.
In pseudo-Meigs’ syndrome, the amount of pleural effusion that accumulates usually has no direct
relationship with the amount of ascites present, nor is there a particular kind of ovarian tumor or
type of ascites predisposed towards producing and pseudo-Meigs’ syndrome’s characteristic
pleural effusion. There have been enumerable cases of each tumor type, accompanied by massive
serous ascites, where a pleural effusion was absent.
Presumably, whether hydrothorax occurs as a consequence of ascites depends on the
presence and nature of a pathway for ascites flow from the abdomen to the pleural cavity. It is thus
illustrative to note that a known complication of peritoneal dialysis for renal disease is the
movement of the dialysate into the pleural space, causing a serous hydrothorax. Peritoneal dialysis-
related hydrothorax is almost uniformly right-sided and represents one of many presentations of
the “porous diaphragm syndrome.”
In addition to diaphragm porosity, the inherent intestinal circulation, lower hydrostatic
pressure in the right upper quadrant, and liver capsule may contribute to this right-sided
predominance. In addition to Meigs syndrome, similar right-sided presentations have been
described in bilious effusions with gastric or duodenal perforations, hepatic hydrothorax, and
nephrotic syndrome-related chylothorax. Because peritoneal dialysis-induced hydrothorax is
relatively rare in this commonly done procedure, it suggests that there are individual differences
in susceptibility to the condition.
LeVeen et al. reported that hydrothorax occurred in only 5.3 percent of their ascitic
patients. Eighteen of the 21 spontaneous hydrothorax cases in their study occurred on the right
side. They proposed that the pleural effusion is derived from ascitic fluid that enters the chest
because of the negative pressure within the pleural space, and it does so via tiny defects in the
diaphragm. Studies have shown that these tiny defects are often covered by pleuroperitoneum, but
the high abdominal pressure accompanying ascites accumulation raises a bleb on the superior
surface of the diaphragm. Rupture of the blebs produces the hydrothorax. The broken bleb flap
acts as a one-way valve. The ascites is often initially relieved with the onset of the hydrothorax. A
direct thoracoabdominal communication was confirmed by a scan of the chest and abdomen after
intraperitoneal injection of contrast material. Peritoneal-to-pleural flow of fluid was demonstrated
by nuclear scanning, even when ascites was not clinically apparent.
We now know much more about the microscopic process of transdiaphragmatic fluid flow.
Lymphatics in the diaphragm form a specialized system for draining fluid from the peritoneal
cavity and returning it to the vascular system. Fluid from the abdomen enters subperitoneal
lymphatic lacunae located between muscle fibers of the diaphragm. The lacunae are separated from
the peritoneal cavity by a barrier comprising, successively, lymphatic endothelium, a layer of
collagenous fibers, a thin fenestrated layer of elastic tissue, and the peritoneal mesothelium. To
reach the lacunae, peritoneal fluid passes through specialized stomata located between cuboidal
mesothelial cells of the lacunar roof. Stoma patency is modifiable in response to stretch (as from
accumulating ascites) or active induction. Nitric oxide (NO), often associated with inflammatory
cells, enlarges the lymphatic stomata to increase the peritoneal lymph drainage.
While the distribution of mesothelial stomata across abdominal organ surfaces, and
subjacent lymphatic lacunae, varies in different species, these stomata appear to be predominantly
on the peritoneal surface of the diaphragm. From the lacunae, fluid traverses the diaphragm via
intrinsic lymphatic channels to reach collecting lymphatics beneath the diaphragmatic pleura. Both
intrinsic and collecting lymphatics contain valves. These one-way channels serve as the main
drainage route for absorption of ascites from the peritoneal cavity into the lymph system for return
to the blood vascular system. The collecting lymphatics of the diaphragm drain principally into
retrosternal (parasternal) lymphatic trunks that carry lymph to the great veins after it filters through
mediastinal lymph nodes.
Based on the most likely of these conjectures, and on scientific findings, we suggest
that hydrothorax is the result of the existence of either more numerous or more permissive
lymphatic channels in the diaphragm of predisposed individuals. It follows that there can
be bilateral differences in the distribution of these channels, and differences among
individuals for pleural effusion. The corollary is that there may be individuals who have
minimal numbers of lymphatic channels in the diaphragm and are thus more resistant to
hydrothorax and more predisposed to ascites accumulation. In such cases, pleural effusion
would be far less likely to occur, despite the existence of massive ascites.
In all our cases, no one wished to preserve their reproductive capacity. But one-third of
borderline ovarian tumors occur in women younger than 40 years, so they often wish that. Ludovisi
et al. reported the ultrasonographic findings that are helpful in diagnosis of serous ovarian tumors
and serous surface papillary borderline ovarian tumors. Given these findings, it is possible to
perform fertility-sparing surgery in those cases. In conclusion, in our normal practice we have
encountered three cases of borderline ovarian tumor accompanied with massive ascites. They were
atypical in that they were not advanced ovarian cancers, nor did they fit within the criteria of
Meigs’ or pseudo-Meigs’ syndrome, because they lacked pleural effusion. This is not unusual in
that various types of benign to highly malignant ovarian tumors may present as massive ascites of
unknown origin.
Physicians should be aware of the differential diagnostics needed to determine what type
of mass they are dealing with. Pathological confirmation of the tumor and its surgical removal are
primary goals in such cases, in order to avoid unnecessary neoadjuvant therapy and
radiation/chemotherapy. The most important risc factor of the ovarian cancer is represented by the
presence of an ovarian neoplasm in the patient’s family history. Other following risk factors are
mammary neoplasms and nulliparous women. The tumoral marker CA125, specific to ovarian
cancer, is useful for diagnosis and especially for monitoring patient outcomes; an increase of the
value of this marker suggests the appearance of local relapse. The surgical intervention, one of the
therapeutic tools, is important for the correct histopathological diagnosis establishment and also
in choosing appropriate treatment.
The most important risc factor of the ovarian cancer is represented by the presence of an
ovarian neoplasm in the patient’s family history. Other following risk factors are mammary
neoplasms and nulliparous women. The tumoral marker CA125, specific to ovarian cancer, is
useful for diagnosis and especially for monitoring patient outcomes; an increase of the value of
this marker suggests the appearance of local relapse. The surgical intervention, one of the
therapeutic tools, is important for the correct histopathological diagnosis establishment and also
in choosing appropriate treatment. The chemo and radiotherapy used for the treatment of
mammary neoplasm of our patient lead to a favorable health evolution in medium term, but in long
term they could be considered risk factors for the appearance of this ovarian neoplasm, and maybe
other cancers in the future.