Eighteen cases of massive ovarian oedema are presented. The age of patients averaged 26 years and 16 presented with an acute abdomen. Hormonal symptoms included virilism in three cases and one with precocious pseudopuberty. Ultrasonographic findings were variable and not diagnostically accurate. When performed, CA 125 levels were not raised. Seventy-two percent of cases occurred in the right ovary and none were bilateral. Torsion occurred in 14 cases. Salpingo-oophorectomy was performed in all cases. To elucidate its pathogenesis, be this either due to intermittent chronic torsion or to a proliferative phenomenon, immunohistochemistry for Ki-67 and PCNA proliferation antigens, alpha-actin and oestrogen and progesterone receptors was performed. The Ki-67 proliferation index ranged between 0% and 3%, demonstrating the low proliferative status of stromal cells. The PCNA indices, however, were unusually high (60% and above). The divergence between these findings is explained by the fact that PCNA positivity may be related to nuclear reparation subsequent to ischaemia. Alpha-actin was consistently positive in stromal cells, reflecting a myofibroblastic transformation of these cells. These findings together with the clinical evidence of torsion in the majority of cases, lead us to consider that ovarian oedema is a reactive, non-proliferative state of specific stromal cells, occurring as a response to torsion and subsequent ischaemia. The stromal cells have positive oestrogen progesterone receptors and may undergo stimulatory changes responsible for the hormonally related symptoms often found associated with massive ovarian oedema.
A number of data suggest that angiotensin II-dependent activation of the protooncogene c-myc participates in the proliferative response of smooth muscle cells (SMC) of rats with spontaneous hypertension (SHR). We therefore investigated the effects of chronic treatment with the angiotensin converting enzyme (ACE) inhibitor quinapril on the oncoprotein c-Myc and the proliferating cell nuclear antigen cyclin A in SMC of small intramyocardial arteries from the left ventricle of SHR. The expression of c-Myc and cyclin A was assessed by immunocytochemical analysis. The number of smooth muscle cells was assessed by morphometrical analysis. As compared to normotensive Wistar-Kyoto (WKY) rats, untreated SHR exhibited an increased percentages of cells expressing c-Myc (33% +/- 4% v 19% +/- 2%, mean +/- SEM, P < .005) and cyclin A (25 +/- 2 v 11% +/- 1%, P < .001). In quinapril-treated SHR compared with untreated SHR, we found decreased expression of c-Myc (22% +/- 2%, P < .005) and cyclin A (13% +/- 1%, P < .001). No significant differences were found between WKY rats and quinapril-treated SHR in the above parameters. Cyclin A was directly correlated with the number of SMCs in each group of rats. These results suggest that an enhanced expression of c-Myc may be involved in the increased proliferation seen in SMCs from small arteries of SHR. Quinapril administration normalizes proliferation in the SMCs of SHR, possibly by inhibiting the expression of the oncoprotein c-Myc and its effects on the cell cycle.
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