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Knowledge Area 14: Gynaecological Oncology
Published in Rekha Wuntakal, Ziena Abdullah, Tony Hollingworth, Get Through MRCOG Part 1, 2020
Rekha Wuntakal, Ziena Abdullah, Tony Hollingworth
Meigs syndrome is mainly caused due to ovarian fibromas. When a benign pelvis mass (such as ovarian fibroma or fibroids) is associated with ascites and right-sided pleural effusion, it is named Meigs syndrome.Further readingSarris I, Sangeeta A, Susan B. Training in Obstetrics and Gynecology: The Essential Curriculum. Oxford, UK: Oxford University Press, 2009, pp. 391–416.
Answers
Published in Thomas Hester, Iain MacGarrow, Surgical SBAs for Finals with Explanatory Answers, 2018
On examination the patient may have a palpable mass, ascites (as in this case) or a pleural effusion. The triad of ascites, pleural effusion (usually on the right side) and a benign ovarian tumour is known as Meigs’ syndrome. If an ovarian cancer is suspected a Ca 125 should be requested. Imaging should be arranged, ideally CT staging involving the chest, abdomen and pelvis.
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Ovarian Tumor [Latin: ovarium, ovary] The Krukenberg tumor, a bilateral fibrosarcoma of the ovary, was described by Friedrich Ernst Krukenberg (1871–1946) of Germany in 1896. The Brenner tumor, a peculiar benign neoplasm of the ovary, was described as ‘oophoroma folliculare’ by another German, Fritz Brenner (b 1877), in 1907. A similar neoplasm of the ovary was described by Ernst Gottlieb Orthmann (1858–1922) in 1899. Arrhenoblastoma, a tumor of the ovary made of convoluted tubules resembling the seminiferous tubules of the testis, was described by E. P. Pick of Berlin in 1905, and G. Schikele described a second case with similar histology in 1906. The term ‘arrhenoblastoma’ was proposed by Robert Meyer of Berlin to denote the group of similar masculinizing tumors in 1930. The presence of an ovarian tumor associated with ascites and pleural effusion (Meigs syndrome) was described by Joe Vincent Meigs (1892–1963) of America in 1937.
Is there any relationship between massive ascites and elevated CA-125 in systemic lupus erythematosus? Case report and review of the literature
Published in Modern Rheumatology Case Reports, 2021
Elias Quintero-Muñoz, María Alejandra Gómez Pineda, Carolina Araque Parra, Camilo Alfonso Vallejo Castillo, Víctor Ortega Marrugo, Juan Bonilla Jassir, José Fernando Polo Nieto, Rafael Parra-Medina, Adriana Rojas-Villarraga
There is a rare disease called Meigs syndrome which is the association of benign ovarian tumours (primary fibroid, thecoma, Brenner's tumour) with pleural effusion, ascites, and elevation of CA-125. When this syndrome is related to other types of tumours, it is called Pseudo Meigs Syndrome (PMS) [6,7]. The patient in Case 2 was diagnosed with PMS due to the fact that there was a mass in the left adnexal region that continued towards the peritoneum with a histopathological finding of Pseudo Peritoneal Myxoma coming from the ovary. Among the causes of lupus ascites, there is a rare syndrome first reported in 2005. Tjalma et al. described a case of ascites, pleural effusion and elevation of the CA-125 in a patient with SLE. They ruled out neoplastic and infectious aetiology and called it Tjalma Syndrome. Later Schmitt et al. named this pathology PPMS [8,9]. The patient in Case 1 was thought to have PPMS since she had all the characteristics of this syndrome.
Hyperthyroidism associated with struma ovarii – a case report and review of literature
Published in Gynecological Endocrinology, 2021
Agnieszka Podfigurna, Anna Szeliga, Paulina Horwat, Marzena Maciejewska-Jeske, Blazej Meczekalski
Kempers et al. [1] sustain that ascites is found mainly in cases of SO associated with malignancy. In contrast, Sitasuwan et al. [14] presented a case in which ascites was present, but with no signs of malignancy found. When a triad of benign ovarian fibroma, ascites, and pleural effusion is present, Meigs syndrome can be considered. This is confirmed with the resolution of symptoms once the tumor is resected. Pseudo-Meigs syndrome differs from its original counterpart in that the benign mass is not exclusively limited to an ovarian fibroma, but can be, for example a SO, or a mature teratoma. A malignant tumor would exclude Meigs syndrome [1].
The predictive role of thrombocytosis in benign, borderline and malignant ovarian tumors
Published in Platelets, 2020
Ganiy Opeyemi Abdulrahman, Nagindra Das, K Lutchman Singh
The finding of a potential association between ovarian fibroma/fibrothecoma is also noteworthy. It appears that this is the first time that a potential link has been reported in the literature and this may contribute to our understanding of the pathophysiology of thrombocytosis in ovarian tumorigenesis, especially because of the association with ascites and pleural effusion. Ovarian fibromas/fibrothecomas are uncommon benign tumors that account for only 3.3% of ovarian tumors with potential malignant transformation [30–32]. These cases can be quite challenging to diagnose as they commonly present with pleural effusions or ascites (Meigs’ syndrome), thus mimicking advanced ovarian cancer [33]. Despite being rare, that they account for 50% of the few benign ovarian tumors with thrombocytosis in our study could further aid their diagnosis when combined with imaging findings. Although there has been suggestion that SUShi Domain containing two (SUSD2), a type I transmembrane protein, might play a role in platelet activation and binding to cancer cells in an inverse correlation with the presence of SUSD2, this has not been validated in human primary cultures [34]. It has also been reported that the production of thrombopoietic cytokines such as interleukin-6 and thrombopoietin in tumor and host tissue results in paraneoplastic thrombocytosis but this study only included high-grade serous ovarian malignancies and did not include other histological subtypes of ovarian cancer, borderline, or benign tumors [35], particularly ovarian fibromas/fibrothecomas which our study has identified could also potentially be associated with thrombocytosis. Furthermore, as thrombopoietin is usually produced in the liver and kidneys, it would be expected that patients with reduced liver and renal functions should have less risk of developing ovarian cancer or slower progression. This has not been demonstrated in the literature. It would be interesting to see whether or not these findings at cellular level are also observed in ovarian fibromas/fibrothecomas as well as establish why some women with ovarian cancer do not exhibit thrombocytosis. Understanding the definitive biology of thrombocytosis in ovarian cancer could have significant clinical implication beyond cancer diagnosis and could in fact be exploited in the treatment of ovarian malignancy with target therapies. It is likely that platelet plays a role in the metastasis of ovarian cancer.