Vaginal adenosis
Vaginal adenosis is a
congenital. Postpubertal lesions have also been observed to grow de novo. It has a rather common incidence, of about 10% of adult women.[1][2][3]
Causes
Vaginal adenosis is characterised by the presence of
contraceptives were discontinued, incidence has dropped dramatically.[4] Risk is however still present in subsequent generations due to recent exposure.[5]
It is thought steroid hormones play a stimulatory growth in adenosis formation.[6] Vaginal adenosis is also often observed in adenocarcinoma patients.[7][8]
Diagnosis
embryonic. Its mucinous cells resemble the normal cervical lining, while its tuboendometrial cells resemble the lining of normal fallopian tubes or endometrium.[11]
It is sometimes considered a precancerous lesion, given clear-cell adenocarcinoma patients present these lesions in close proximity to atypical tuboendometrial glands,[12] and microglandular hyperplasia has been seen to arise from these lesions.[13]
References
Further reading
- O'Brien, P. C.; Noller, K. L.; Robboy, S. J.; Barnes, A. B.; Kaufman, R. H.; Tilley, B. C.; Townsend, D. E. (March 1979). "Vaginal epithelial changes in young women enrolled in the National Cooperative Diethylstilbestrol Adenosis (DESAD) project". PMID 424101.
- Laronda, Monica M.; Unno, Kenji; Butler, Lindsey M.; Kurita, Takeshi (2012). "The development of cervical and vaginal adenosis as a result of diethylstilbestrol exposure in utero". Differentiation. 84 (3): 252–260. .
- Ganesan, R.; Ferryman, S. R.; Waddell, C. A. (1999). "Vaginal adenosis in a patient on Tamoxifen therapy: a case report". Cytopathology. 10 (2): 127–130. S2CID 33999959.
- Laronda, M. M.; Unno, K.; Ishi, K.; Serna, V. A.; Butler, L. M; Mills, A. A.; Orvis, G. D.; Behringer, R. R.; Deng, C.; Sinha, S.; Kurita, T. (2013). "Diethylstilbestrol induces vaginal adenosis by disrupting SMAD/RUNX1-mediated cell fate decision in the Müllerian duct epithelium". Developmental Biology 381(1): 5-16. doi: 10.1016/j.ydbio.2013.06.024. PMID 23830984.