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Alan Gibstein, M.D.
Alan Gibstein, M.D., OB/GYN (Doctor)
Category: OB GYN
Satisfied Customers: 1833
Experience:  Assistant Professor of OB/GYN with 40 years of experience treating patients. Fellow of The American Congress of Obstetricians and Gynecologists.
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complex hyperplasia without atypia what is the likelyhood

Customer Question

complex hyperplasia without atypia what is the likelyhood of getting cancer? I have found several different answers and been told by my doctor only 5-8% but she is pushing for a uterus removal I'm 38 and not having kids also overweight. several websites support the 5-8% but others say it is higher. Just looking for a straight answer and someplace I can go and read info on it tried webmd, mayo clinic, and johnshopkins sites, but are hard to get around and not giving me what I'm looking for
Submitted: 3 years ago.
Category: OB GYN
Expert:  khagihara replied 3 years ago.

Endometrial hyperplasia is believed to produce a continuum of lesions that may be precursor to endometrial carcinoma of endometrioid histology. The classification of endometrial hyperplasia has had numerous terminology. The classification below is currently the most commonly accepted system and is accepted by the World Health Organization (WHO) and the International Society of Gynecologic Pathologists. This system characterizes the glandular architectural pattern as simple or complex and describes the presence or absence of nuclear atypia.

  • Simple hyperplasia - Increased number of glands but regular glandular architecture
  • Complex hyperplasia - Crowded irregular glands
  • Simple hyperplasia with atypia - Simple hyperplasia with presence of cytologic atypia (prominent nucleoli and nuclear pleomorphism)
  • Complex hyperplasia with atypia - Complex hyperplasia with cytologic atypia
The original study by Kurman et al found that lesions with varying degrees of complexity and presence of atypia, when left untreated, progressed to adenocarcinoma at different rates. Simple hyperplasia was associated with a 1% rate of progression to cancer, 3% rate of progression to complex hyperplasia, and 8% rate of progression to simple atypical hyperplasia, whereas complex atypical hyperplasia had a 29% rate of progression to cancer.

Once a tissue diagnosis of endometrial hyperplasia is made, treatment depends on the patient's symptoms such as degree of bleeding, presence of cytologic atypia, patient's surgical risks, and wish for future childbearing. Progestins can effectively treat endometrial hyperplasia, and they can serve as prevention of recurrence in those with continued risk factors. Hyperplasia without atypia responds well to progestins. More than 98% of women with hyperplasia treated with cyclic progestins experienced regression of the disease in 3-6 months. The PEPI trial showed a 94% normalization of complex or atypical hyperplasia in 45 women treated with progestins. Multiple regimens of progestin therapy have been found effective in reversing hyperplasia.

  • Medroxyprogesterone acetate (Provera), 10-20 mg qd, or cyclic 12-14 days per month
  • Micronized vaginal progesterone (Prometrium), 100-200 mg qd or cyclic 12-14 days per month
  • Levonorgestrel-containing IUD (Mirena), 1-5 years
  • Megestrol acetate (Megace), 40-200 mg per day, usually reserved for women with atypical hyperplasia
If hyperplasia with atypia is found on dilation and curettage (D&C) or endometrial biopsy, definitive treatment with hysterectomy is recommended due to the high rate of concurrent endometrial cancer. However, if the patient has not completed childbearing or is not a surgical candidate, then concurrent cancer must first be ruled out by D&C with hysteroscopy prior to medical management. Because D&C and Pipelle biopsy only sample 50-60% of the endometrial lining, focal lesions containing adenocarcinoma may be missed. Biopsy is recommended after 3 months to check for response to medical therapy, and continued surveillance after regression of the lesion is recommended every 6-12 months if risk factors persist.

The need for hysterectomy to exclude concurrent myoinvasive endometrioid adenocarcinoma presents a barrier to nonsurgical management of endometrial hyperplasia. A recent Gynecologic Oncology Group study examined the histomorphometric 4-class rule ("4C", which measures epithelial abundance, thickness, and nuclear variation) as applied to diagnostic biopsies to predict myoinvasive cancer outcomes at hysterectomy. Women with endometrial biopsies or curettages with a community diagnosis of atypical endometrial hyperplasia were enrolled in a clinical trial in which subsequent hysterectomy was scored for endometrial adenocarcinoma, and 4C rule ability to predict cancer outcomes was measured.

Qualifying biopsies were stratified into high- and low-risk histomorphometric subgroups. Assignment to a high-risk category by 4C rule was highly sensitive in predicting any (71%) or deeply (92%) myoinvasive adenocarcinoma at hysterectomy, and assignment to a low-risk group had a high negative predictive value for absence of any (90%) or deeply (99%) myoinvasive disease.

At present, this use of histomorphometry is most suited to a centralized reference laboratory performing histomorphometry for a variety of diagnostic applications. However, in the future, formal histomorphometry of endometrial biopsies using the 4C rule may become a more common method to identify a subset of women with premalignant disease who are unlikely to have concurrent myoinvasive adenocarcinoma and therefore may qualify for nonsurgical therapy.
Customer: replied 3 years ago.
why is this so hard to find out every website I visit gives a difernt answer? It looks like you're telling me I have about a 29-30% chance of getting cancer. where as every site that has numbers tells me less than 10%. is there no uniformity or has new research come out that these websites haven't updated. and Why would my doctor tell me 5-8% if it's closer to 30%?
Expert:  khagihara replied 3 years ago.
Read it carefully. 29% of complex hyperplasia with atypia progresses to cancer. In your case, you don't have atypia.

Simple hyperplasia was associated with a 1% rate of progression to cancer, 3% rate of progression to complex hyperplasia, and 8% rate of progression to simple atypical hyperplasia, whereas complex atypical hyperplasia had a 29% rate of progression to cancer.

Sorry this article doesn't mention how much % of complex hyperplasia without atypia progresses to cancer. Here is the original reference. The article makes a mistake. Your risk is 3%.

Endometrial curettings from 170 patients with all grades of endometrial hyperplasia, who did not undergo a hysterectomy for at least 1 year were evaluated in order to correlate the histopathologic features with behavior. Follow-up ranged from 1 to 26.7 years (mean, 13.4 years). Cytologic and architectural alterations were analyzed separately in order to assess their respective roles in predicting the likelihood of progression to carcinoma. Classification of proliferative lesions based solely on the presence of cytologic atypia revealed that atypia was a discriminant factor. Proliferations lacking cytologic atypia were designated hyperplasia and those displaying atypia were designated atypical hyperplasia. Only 2 (1.6%) of 122 patients with hyperplasia progressed to carcinoma compared with 11 (23%) of women with atypical hyperplasia (P = 0.001). Subclassification of the two forms of hyperplasia (those with cytologic atypia and those without) was performed using the degree of architectural abnormalities. Hyperplasia and atypical hyperplasia displaying marked glandular complexity and crowding producing a back-to-back appearance were designated complex hyperplasia (CH) and complex atypical hyperplasia (CAH), respectively. Hyperplasia and atypical hyperplasia with lesser degrees of glandular complexity and crowding were designated simple hyperplasia (SH) and simple atypical hyperplasia (SAH), respectively. Progression to carcinoma occurred in 1 (1%) of 93 patients with SH, in 1 (3%) of 29 patients with CH, in 1 (8%) of the patients with SAH, and in 10 (29%) of the patients with CAH. The differences between the four subgroups suggest a trend but are not statistically significant. The findings in this study provide a rationale for classifying noninvasive endometrial proliferations primarily on the basis of cytologic atypia since this is the most useful criterion in predicting the likelihood of progression to carcinoma. In addition, the presence of concommitant architectural alterations appears to identify a particularly high-risk subgroup.

Kurman RJ; Kaminski PF; Norris HJ, Cancer. 1985; 56(2):403-12. The behavior of endometrial hyperplasia. A long-term study of "untreated" hyperplasia in 170 patients.
Customer: replied 3 years ago.
ok Any idea as to why the need to remove uterus? is it because I am having reactions to the meds and this is the only alternative to ensure I don't get cancer. I'm still not clear as to why with a less than 105 chance we need to rush into a uterus removal. when I told her I want to wait and see, she told me I don't have that option. she wants me to go se a gyno oncologist. Should I go or just have the removal? I will take you advice as part of my research and just opinion sice you have not ssen my records and I have a 2nd opinion scheduled for a ob/gyn in my area
Expert:  Alan Gibstein, M.D. replied 3 years ago.
Dear JACUSTOMER-rnlbwla1; Dr.Khagihara has actually spelled it out for you very well. I would quote your risk as about 3% but have to add an additional risk for obesity. If you could lose enough weight, that could actually reverse the hyperplasia without surgery. Obesity is a very powerful stimulus for hyperplasia. The fact that you reacted poorly to Megace does not mean you would do the same with norethisterone or Delalutin or Prometrium.I used a regimen of daily small dose for thirty days, then allow a bleed, then do a D&C. I would consult with an oncologist since being overweight does add a significant risk of complications with surgery. Good luck
Alan Gibstein, M.D., OB/GYN (Doctor)
Category: OB GYN
Satisfied Customers: 1833
Experience: Assistant Professor of OB/GYN with 40 years of experience treating patients. Fellow of The American Congress of Obstetricians and Gynecologists.
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