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Re: canaries&herring; no mercuryFrom: Terrence Jones (Terrence.Jones@KP.ORG)Mon Jan 15 18:37:10 2001
El, can You clarify this pedunculated myoma further? I'm guessing the "8 cm" measurement desribes its length (as it would be unlikely to remove an 8 cm diameter wide pedunculated myoma thru a vag incision, (with the uterus in situ and containing an additional 7 cm intramural myoma), without first bisecting or morcellating it). It sounds as tho it was removed intact, and the neoplastic change was encapsulated, and that the endometrium itself demonstrated no neoplasia. So it would represent malignant transfromation of the glandular element of an adenomyoma/adenomyosis/atypical polypoid adenomyo(fibro)ma. As the capsule was intact, the only means of residual disease would be preop lymphatic dissemination. Is there suspicion for lymphovascular space involvement? Any features suspicious for invasion with desmoplastic response? What tumor markers were studied? The folks in Vancouver described a series of 30 classic adenomyomas (ie: not atypical adenomyofibroma or endocervical), of ! which 3 were subserous. Some evidence of suspicious mitotic activity was described in the glandular or mesenchymal component in one third. Five of 14 cases submitted for consultation had been initially read out as adenocarcinoma or adenosarcoma (Gilks, Int J Gynecol Path, 7/00, 19:195-205). A study from Detroit also describes the atypical polypoid adenomyo(fibro)ma as an entity that can mimic endometrial carcinoma (Jaques, Int J Gynecol Path 1/98, 17:42-5). While the Japanese (with prolific reporting of APA [atypical polypoid adenomyoma] have reported on the apparent progression of adenomyoma to adenocarcinoma (Sugiyama, Gynecol Oncol 10/98, 71:141-4). The folks at Stanford evaluated certain immunohistochemical tumor markers in APA and found them to be indistinguishable from adenocarcinoma (Soslow, Int J Gynecol Path 7/96), 15:209-16). These same authors presented an extensive clinicopathologic review (55 cases) on APA (Am J Surg Path 1/96, 20:1-20). If consultation confirms ! adenocarcinoma, then recent studies regarding prognosis might suggest some value in proliferative kinetic markers, tho ploidy (cytometrics) was not of much use. SPF (S-phase fraction) and TLI (thymidine labeling index) helped identify a subset of Pts with 'unexpected poor outcome' who were otherwise low risk (Mariani, Anticancer Res 9-10/00, 20:3569-74). Perhaps the FLT-4 receptor for VEGF will prove to be a useful prognostic indicator (in the absence of data re: myometrial invasion or nodal mets) in the future (Yokoyama, Gynecol Oncol 6/00, 77:413-8). A 55-60 yo multiparous postmenopausal Pt is coming to surgery for dysplastic (left sided) colonic polyp. She had mild focal simple hyperplasia of the endometrium on EMB 1992 (perimenopausal), which reversed to normal with progestin. Her FHx is sig for maternal uncle with Colon Ca Dx'd i! n His 60's. His (the Uncle's) Dau was Dx'd with colon Ca in Her early 50's. The Pt's Mom had endometrial Ca (Dx'd in Her 70's). No specific markers for HNPCC have been studied on any family member. Not an easy Pt. to counsel WRT the subtleties of risk/benefit, as much of the time spent in consultation is directed to why Her request for a Sal-Est test is probably of little benefit in assessing the efficacy of the hormonal lotions prescribed by Her 'outside' provider. (These would be the lotions She began after stopping Her HRT 8 months ago due to worsening 'hot flushes'.) She has had no bleeding in the recent past. Her EEC by EVS is somewhat indistinct, due to atrophy and distortion by fibroids, but measures < 3mm. I know what the CANCERLIT recommendations (including the Jan '01 update) would suggest (Burke et al, JAMA 1997, 277:915-9). Still, something about this history makes me worry. Besides Zach (& Garry), would anyone push strongly for anything more than Hyscopy+ D&C at! time of Her colon surgery? Kathi, You're correct, the hypophosphatasia from deficiency of tissue non-specific isoenzymes of alkaline phosphatase (TNSALP) corrects during the third trimester thanks to PALP (placental alk phos). But maternal problems are not the main concern. Instead, would worry re: fetal transmission. Particularly: is FOB a carrier? Your Genetics Dept should be of help. They'd be familiar with the local mutations, penetrance, and related incidence of fetal & neonatal sequelae. As Ilderton is in the southwest, would wonder if their kindred is Manitoba Mennonites? Approx 1/25 are HOPS (hypophosphatasia) carriers. Lactation question would be best directed to Your local endocrine resource - would like to hear their recommendation, WRT ability to restore losses after weaning.
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