MASSIVE OVARIAN EDEMA

Eighteen cases of massive ovarian oedema are presented, The age of pat ients averaged 26 years and 16 presented with an acute abdomen, Hormon al symptoms included virilism in three cases and one with precocious p seudopuberty. Ultrasonographic findings were variable and not diagnost ically accurate. When performed, CA 125 levels were not raised, Sevent y-two percent of cases occurred in the right ovary and none were bilat eral, Torsion occurred in 14 cases. Salpingo-oophorectomy was performe d in all cases. To elucidate its pathogenesis, be this either due to i ntermittent chronic torsion or to a proliferative phenomenon. immunohi stochemistry for Ki-67 and PCNA proliferation antigens, alpha-actin an d oestrogen and progesterone receptors was performed, The Ki-67 prolif eration index ranged between 0% and 3%, demonstrating the low prolifer ative status of stromal cells. The PCNA indices, however, were unusual ly high (60% and above), The divergence between these findings is expl ained by the fact that PCNA positivity may be related to nuclear repar ation subsequent to ischaemia, Alpha-actin was consistently positive i n stromal cells, reflecting a myofibroblastic transformation of these cells. These findings together with the clinical evidence of torsion i n 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 and progesterone receptors and may undergo sti mulatory changes responsible for the hormonally related symptoms often found associated with massive ovarian oedema.