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PubMed2004

Differences in serum bisphenol a concentrations in premenopausal normal women and women with endometrial hyperplasia.

Exposure to endocrine disrupting chemicals (EDCs) has been raised in relation to its potential for adverse health outcomes. Bisphenol A (BPA) is an estrogenic EDC widely found in plastic products. We determined BPA concentrations in premenopausal women by an enzyme-linked immunosorbent assay and evaluated possible linkage between its contamination levels and endometrial hyperplasia, an estrogen-related disorder of the uterus. It has been implied that higher levels of BPA, which binds to estrogen receptor and plays estrogenic roles may, enhance endometrial hyperplasia. Serum BPA was detectable in all subjects and its concentrations in healthy controls with normal endometrium were 2.5 +/- 1.5 ng/ml (mean +/- SD). BPA levels in patients with simple endometrial hyperplasia with benign nature were 2.9 +/- 2.0 ng/ml and were not significantly different from the controls. Unexpectedly, BPA levels in patients with complex endometrial hyperplasia with malignant potential were 1.4 +/- 0.4 ng/ml and significantly lower compared to both control and simple endometrial hyperplasia groups. In addition, we measured the serum BPA levels in postmenopausal endometrial cancer patient (1.4 +/- 0.5 ng/ml), which were also significantly lower than control and simple endometrial hyperplasia groups. These findings suggest the presence of associations between BPA exposure and complex endometrial hyperplasia and endometrial cancer. The mode of action of BPA may be more complex than expected and the contradictory results may serve as a clue to addressing the mechanisms of linkage between occurrence of estrogen-dependent diseases and endocrine disruption.

Benzhydryl Compounds↗
PubMed1995

Prevalence of nifedipine-induced gingival hyperplasia.

This study investigated the prevalence of gingival hyperplasia in subjects who were undergoing treatment with a calcium channel blocker, nifedipine, in dentate and edentulous subjects. In addition, the relationship between gingival hyperplasia and 5 other variables (duration of nifedipine intake, dose, age, oral hygiene index, and number of teeth) was investigated. Results of statistical analyses showed overwhelming evidence that the percent of nifedipine subjects with gingival hyperplasia was greater than that of the control subjects (P < 0.05) and that, across treatment group, the percent of dentate subjects with hyperplasia was significantly higher than that for edentulous subjects (P < 0.05). The chi2 test showed a strong univariate relationship between gingival hyperplasia and, separately, oral hygiene and number of teeth. For 24% of the subjects with gingival hyperplasia index (GHI) values of 2 or 3, gingivectomy was performed, and the tissues were prepared for histological examination. Microscopic examination of the biopsy material showed findings similar to those from previously reported cases of nifedipine- or phenytoin-induced hyperplasia.

Age Factors↗
PubMed2000

Mast cells are not involved in the development of cyclosporin A-induced gingival hyperplasia: a study with mast cell-deficient mice.

BACKGROUND: A previous study suggested that mast cells (MC) are involved in the development of cyclosporin A-induced gingival hyperplasia, since an increased number of MC were observed in the tissue sections of enlarged gingiva. To determine the role of MC in gingival hyperplasia, an MC-deficient mouse model was used in the current study. METHODS: MC-deficient mice (WBB6F1xW/Wv) and their littermates (+/+) were fed sucrose-containing diets supplemented with or without varying concentrations (300, 400, 500, 600 mg) of cyclosporin A/kg of diet. After 30 days, the mice were sacrificed and the degree of gingival hyperplasia was evaluated by the appearance of the gingiva. Tissue MC were stained with toluidine blue to confirm the presence or absence of MC in the enlarged gingiva. RESULTS: Both W/Wv and +/+ mice, when fed with 600 mg cyclosporin A/kg diet for 30 days, exhibited a similar degree of gingival hyperplasia, while other test mice or control mice did not. Toluidine blue staining of the tissue sections confirmed the presence of MC in the enlarged gingiva of the +/+ mice, but not the W/Wv mice. CONCLUSIONS: These results indicate that mast cells are not necessary in the development of cyclosporin A-induced gingival hyperplasia, and that the increased number of MC observed in the enlarged gingiva may be a secondary effect of gingival hyperplasia. We also conclude that a study of mice lacking certain molecules or cells would be quite useful in determining the molecules or cell types responsible for the pathogenesis of drug-induced gingival hyperplasia.

Animals↗
PubMed2003

Pathologic review of atypical hyperplasia identified by image-guided breast needle core biopsy. Correlation with excision specimen.

CONTEXT: Management of breast needle core biopsies diagnosed as atypical ductal hyperplasia, atypical lobular hyperplasia, and lobular carcinoma in situ is controversial. Current recommendations involve excisional biopsy to rule out ductal carcinoma in situ and/or invasive carcinoma, which have been reported in more than 50% of cases in some series. OBJECTIVE: To determine how frequently these diagnoses made on needle core biopsy are ultimately found to represent in situ or invasive carcinoma based on excisional biopsy specimens, in order to identify predictive factors. DESIGN: One thousand eight hundred thirty-six image-guided needle core biopsies were performed between January 1, 1995 and May 1, 2001. Fifty-four (2.9%) patients diagnosed with atypical ductal hyperplasia (n = 36), atypical lobular hyperplasia (n = 12), atypical ductal hyperplasia + atypical lobular hyperplasia (n = 3), or lobular carcinoma in situ (n = 3) subsequently underwent breast excisions. Pathologic features were reviewed in each of the needle core biopsies using Page's criteria and were then correlated with excision specimens. SETTING: University medical center. RESULTS: Review of the needle core biopsy cases with either ductal carcinoma in situ or invasive carcinoma + ductal carcinoma in situ on final excision showed that nucleoli were evident in most of the needle core cases, with foci of nuclear pleomorphism and individual cell necrosis or apoptosis. CONCLUSION: A more precise diagnosis can be made by using strict criteria for atypical ductal hyperplasia versus ductal carcinoma in situ on needle core biopsy. Cytologic atypia, even if in a small area, particularly when there is apoptosis/individual cell necrosis, correlates with the finding of a more serious lesion on excision.

Biopsy, Needle↗
PubMed1999

Echo-enhanced Doppler sonography of focal nodular hyperplasia of the liver.

Lesions of focal nodular hyperplasia are hypervascular, benign focal liver lesions whose differentiation from other focal liver lesions is of significant clinical relevance. The purpose of this study was to investigate the echo-enhancing agent SHU 508A (Levovist) in the evaluation of focal nodular hyperplasia with Doppler sonography. We examined 49 patients with 71 lesions of focal nodular hyperplasia in the liver with gray scale and power Doppler sonography. In all patients Levovist was administered intravenously in a concentration of 300 to 400 mg galactose per milliliter. Visualization of the feeding vessels and the vascularity of the lesions were evaluated, and the resistive indices in the feeders and the hepatic arteries were assessed. In comparison with unenhanced power Doppler sonography, echo-enhanced power Doppler sonography yields a higher sensitivity in the detection of the feeding artery (97% versus 82%) in focal nodular hyperplasia and in the depiction of the radial vascular architecture in such lesions, especially those located in the left lobe of the liver. Lesions less than 3 cm in diameter do not consistently show a characteristic vascular architecture with echo-enhanced Doppler sonography. The resistive index of the tumor-feeding artery (mean, 0.51 +/- 0.09) is significantly (P < 0.0001) lower than that of the hepatic artery (mean, 0.65 +/- 0.06) and decreases as the size of the focal nodular hyperplasia increases. The administration of Levovist may improve the signal-to-noise ratio and thus visualization of the vascular architecture in focal nodular hyperplasia. Lesions located in the left lobe of the liver, which commonly are subject to disturbing motion artifacts in color Doppler sonography, will significantly benefit from the administration of Levovist. Echo-enhanced power Doppler sonography, however, is not capable of depicting a characteristic vascular pattern in small (< or = 3 cm) lesions of focal nodular hyperplasia that would guarantee a specific diagnosis.

Adult↗
PubMed1999

Congenital adrenal hyperplasia: not really a zebra.

Congenital adrenal hyperplasia was once considered a rare inherited disorder with severe manifestations. Mild congenital adrenal hyperplasia, however, is common, affecting one in 100 to 1,000 persons in the United States and frequently eluding diagnosis. Both classic and nonclassic forms of the disease are caused by deficiencies in the adrenal enzymes that are used to synthesize glucocorticoids. The net result is increased production from the adrenal gland of cortisol precursors and androgens. Even mild congenital adrenal hyperplasia can result in life-threatening sinus or pulmonary infections, orthostatic syncope, shortened stature and severe acne. Women with mild congenital adrenal hyperplasia often present with hirsutism, oligomenorrhea or infertility. Congenital adrenal hyperplasia is diagnosed by demonstration of excess cortisol precursors in the serum during an adrenal corticotropic hormone challenge. Diagnosis of congenital adrenal hyerplasia in fetuses that are at risk for congenital adrenal hyperplasia can be determined using human leukocyte antigen haplotype or by demonstration of excess cortisol precursors in amniotic fluid. Treatment includes carefully monitored hormone replacement therapy. Recognition of the problem and timely replacement therapy can reduce morbidity and enhance quality of life in patients that are affected by congenital adrenal hyperplasia.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

[Phonosurgery and conservative therapy of contact hyperplasia of the vocal cords].

INTRODUCTION: Functional-traumatic lesions of the vocal folds include mucous stranding, "nodular" lesions, polyps, cysts; contact hyperplasia and haematoma [1]. Unlike the other lesions, contact hyperplasia is localized at the medial surface of the vocal processes. These are bilateral lesions, often asymmetric, with a central depression resembling an ulcer (Fig. 1). The epithelium is thickened, and evidences of a slight inflammatory process are present. The lesion is the result of the prolonged voice misuse, and is particularly frequent within entertainment professionals [6]. In addition, many patients have some apparent signs of gastric reflux. Contact hyperplasia interferes with glottic closure, but has almost no relation with the vibration pattern. The treatment is phonosurgical, followed by voice therapy. This paper is aimed to check the results of our therapeutic strategy. MATERIAL AND METHOD: We studied 51 patients with contact hyperplasia, who were classified into two groups: a group with massive hyperplasia and a group with minor lesions. The former group of patients underwent surgery as a primary mode of treatment, while the latter group was first treated by voice therapy, and the operative treatment was carried out only in patients who did not show significant voice improvement. Massive lesions were operated on by the use of direct microlaryngoscopy (DML), while some patients were treated by indirect surgery (microstroboscopy--IMS and videostroboscopy--IVS). RESULTS: Over the last 10 years we operated 1550 patients with benign vocal fold lesions. There were only 51 cases with contact hyperplasia (3%). Surgery was the first choice of treatment in 7 subjects (14%), who were operated by the use of DML. The other 14 patients were first treated by voice therapy followed by indirect surgery (IMS and IVS). Surgery was performed in 21 patients (41%). DISCUSSION: Treatment of contact hyperplasia is somewhat prolonged in relation to other benign vocal fold lesions. Small growths are better treated by indirect procedures, to avoid additional trauma to the local tissue of this "sensitive" area.

Humans↗
PubMedDate not supplied

[An immunohistochemical study of the steroid hormone receptors in endometrial hyperplasia].

AIM: Evaluation of the estrogen and progesterone receptors (ER and PR) in different degrees of endometrial hyperplasias. METHODS: 10 cases of each degree of endometrial hyperplasia (simple, complex and atypical) were analyzed using the avidin-biotin-peroxidase technique and monoclonal antibodies applied to formalin-fixed, paraffin-embedded tissue. RESULTS: We found similar, high level of both ER and PR in simple and complex hyperplasias and a significant decrease of these in atypical hyperplasia. CONCLUSIONS: Endometrial hyperplasias develop in a setting of estrogen excess. This explains the high level of endometrial receptors and the response to progesterone in typical hyperplasia. In atypical hyperplasia, the decrease of steroid receptors results in a low sensibility of this lesion to progestative therapy, but there are cases with high receptor levels which could have a chance for hormonal therapy.

Biomarkers↗
PubMed2000

Direct effect of danazol on endometrial hyperplasia in adenomyotic women: treatment with danazol containing intrauterine device.

It is well known that danazol has a direct effect on endometriosis tissue and cell. We have been treating adenomyotic women with danazol containing intrauterine device (D-IUD) from June 1993 to August 2000 and significant decrease of dysmenorrhea and serum CA-125 levels were observed. Of fifty-nine adenomyotic women, eight women were also diagnosed by endometrial biopsy as endometrial hyperplasia and one woman was diagnosed as atypical endometrial hyperplasia. In these endometrial hyperplastic patients, endometrial tissues were obtained before insertion and at the time of removal or exchange of D-IUD and examined pathologically. In all of the 9 women, histopathological findings of endometrial hyperplasia disappeared after D-IUD treatment. In particular, in one patient, findings of atypical endometrial hyperplasia also disappeared after D-IUD treatment. She is now closely observed at our clinic using D-IUD. By these evidences, we postulate that D-IUD is one of the treatment choices of endometrial hyperplasia given exposure of the endometrium to such an extraordinary high concentration of danazol released by D-IUD and avoidance of adverse effects of oral danazol or general administration of GnRH and progesterone. In particular, in atypical endometrial hyperplasia case, its mechanisms might give great benefit to patient. However, mechanisms of direct effect of danazol on endometrial hyperplasia remain to be elucidated in the future study.

Adult↗
PubMed1998

[A study on diagnosis of ocular adnexal lymphoid hyperplasia by polymerase chain reaction amplified IgH CDR-III sequence].

OBJECTIVE: To study the diagnosis and classification of ocular adnexal lymphoid hyperplasia and investigate its cell origin by using some molecular biological techniques. METHODS: 29 cases (31 eyes) of ocular adnexal lymphoid hyperplasia were examined for immunoglobulin heavy-chain (IgH) gene rearrangements by means of polymerase chain reaction (PCR) to amplify the complementarity determining region III (CDR-III) with formalin-fixed and paraffin-embedded tissue combining with histopathologic examination and immunophenotypic analysis. RESULTS: 17 eyes of malignant lymphoma and 5 eyes of reactive lymphoid hyperplasia demonstrated clear single band of the rearranged gene for the IgH chain between 100 bp. to 120 bp. The bilateral ocular adnexal lymphoma occurring simultaneously in 4 eyes (two individuals) exhibited identical band. 1 eye of malignant lymphoma, 8 eyes of atypical lymphoid hyperplasias and 6 eyes of reactive lymphoid hyperplasia showed no band or a smear band. CONCLUSIONS: The results show that this method can determine the clonality of the lymphoid hyperplasias. It may be as well in the examination of small monoclonal B cell populations for which immunophenotypical analysis is difficult. The method is an objective, accurate and useful approach for the diagnosis of ocular adnexal lymphoid hyperplasias.

Complementarity Determining Regions↗
PubMed2001

[Expression of glucose transporter-1 in endometrial hyperplasia and well-differentiated endometrioid adenocarcinoma].

OBJECTIVE: To investigate the expression of glucose transporter-1 (GLUT1) in endometrial hyperplasia and well-differentiated endometrioid adenocarcinomas. METHODS: Sixty formalin fixed, paraffin-embedded sections of various endometrial hyperplasia and well-differentiated endometrioid adenocarcinomas were immunostained with rabbit anti-GLUT1 antibody using streptavidin-biotin method. RESULTS: Two of 12 simple hyperplasia and one of seven complex hyperplasia without atypia were focally positive in metaplastic epithelia. All complex atypical hyperplasia showed positive in varied degree, and 26 among 28 cases of adenocarcinoma were stained positively. CONCLUSIONS: Overexpression of GLUT1 is a consistent feature of atypical hyperplasia and adenocarcinoma. GLUT1 immunostaining is found to be helpful in distinguishing hyperplasia with atypia from those without atypia.

Adenocarcinoma↗
PubMed1992

Distinctive patterns of hyperplasia in transgenic mice with mouse mammary tumor virus transforming growth factor-alpha. Characterization of mammary gland and skin proliferations.

Eight lines of transgenic mice expressing a mouse mammary tumor virus (MMTV) human transforming growth factor-alpha (TGF alpha) fusion gene were established. Three lines with distinctive phenotypes are presented. All have proliferative changes of the mammary gland. One line has sebaceous gland hyperplasia of the skin. Five histologic patterns of mammary gland hyperplasia based on two of these lines were identified: cystic hyperplasia, solid hyperplasia, dysplasia, adenoma, and adenocarcinoma. Human TGF alpha mRNA and protein were produced in all patterns but appeared reduced in solid hyperplasia, dysplasia, and adenocarcinoma. TGF alpha immunoreactivity in the mammary tissue, cystic fluid, and serum did not show significant differences; hyperplasia developed in 65% of multiparous mice and 45% of virgin mice by 12 months of age. Adenocarcinoma developed in 40% of multiparous mice and 30% of virgin mice by 16 months of age. These transgenic lines may provide useful models of mammary and sebaceous gland hyperplasia analogous to human disease.

Animals↗
PubMed1992

Relationships of parathyroid hormone, parathyroid secretory protein, parathyroid hormone messenger RNA, parathyroid secretory protein mRNA, and replication in human parathyroid adenoma and secondary hyperplasia tissues and cultures.

BACKGROUND: The purpose of this study was to clarify the relationships of extractable and secreted parathyroid hormone (PTH) and parathyroid secretory protein (PSP) in human parathyroid tumors to PTH messenger RNA (mRNA), PSP mRNA, and cell replication. METHODS AND RESULTS: In tissue cultures of seven adenomas and five secondary hyperplasias, we found a direct correlation for secreted PTH versus PSP for both adenomas and secondary hyperplasias. Secreted PTH:PSP was elevated for adenomas (11:1) compared to that of secondary hyperplasias (2:1), and adenomas secreted significantly more PTH and PSP than did secondary hyperplasias. In extracts of eight adenomas and six secondary hyperplasias, the ratio of PTH:PSP was unexpectedly low (2:1) and similar for both adenomas and secondary hyperplasias. The ratio of extractable PTH mRNA:PSP mRNA was extremely low for both adenomas (1:7) and for secondary hyperplasias (1:5). Flow cytometry indicated that percent replication was inversely correlated with PTH mRNA and PSP mRNA. CONCLUSIONS: Increased PTH secretion by adenomas cannot be attributed to increased biosynthetic capacity because it is less than expected. Hypersecretion of PTH by adenomas and coincident marked reductions in PTH mRNA suggest either a defect in cytoplasmic storage of PTH or impairment of normal posttranslational degradation of PTH. As parathyroid tumor cells increase replication, PTH mRNA is reduced. Possible explanations for this include decreased PTH gene transcription or decreased mRNA half-life.

Adenoma↗
PubMedDate not supplied

[Endometrial hyperplasia predicts a better prognosis in endometrial carcinoma].

AIM: To evaluate the significance of the associated Endometrial Hyperplasia in Endometrial Carcinoma. STUDY DESIGN: 93 hysterectomy specimens for endometrial carcinoma were histologically reviewed on paraffin sections stained H&E and tricromic VG. RESULTS: 45 cases were associated with endometrial hyperplasia; 48 cases without endometrial hyperplasia were: 35 cases with the entire endometrial cavity occupied by carcinoma, 11 associated with endometrial atrophy and 2 with normal proliferative endometrium. In this second group, 37 cases (77%) were in advanced stages. A correlation was found between the presence of Endometrial Hyperplasia and the degree of differentiation, the FIGO stage of the carcinoma, and the age of the patient. CONCLUSIONS: Endometrial Carcinomas associated with Endometrial Hyperplasia involve younger women and have lower aggressivity than those without hyperplasia. Endometrial Hyperplasia may demonstrate a favorable prognosis in Endometrial Carcinomas.

Carcinoma, Endometrioid↗
PubMed2004

[Toxoplasmosis in patients with lymphoid hyperplasia of the head and neck].

OBJECTIVES: To investigate the incidence of toxoplasmosis in patients with lymphoid hyperplasia of the head and neck. PATIENTS AND METHODS: In this study, 53 patients (32 males, 21 females; mean age 11.2+/-4.3 years, range 5 to 22) were investigated. There were hypertrophic tonsillitis in 13 patients, hypertrophic tonsillitis and adenoid hyperplasia in 22 patients, adenoid hyperplasia in 10 patients, and lymphadenopathy of the neck in eight patients. In venous blood samples, IgM and IgG antibodies for Toxoplasma gondii were investigated with the enzyme-linked immunoabsorbent assay (Axsym, Abbott). RESULTS: Positive IgG was determined in 23 patients (48%) with hypertrophic tonsillitis (n=6), hypertrophic tonsillitis and adenoid hyperplasia (n=10), adenoid hyperplasia (n=3), and lymphadenopathy of the neck (n=4). Positive IgM was determined in 5 patients (9.4%) with hypertrophic tonsillitis (n=1), hypertrophic tonsillitis and adenoid hyperplasia (n=1), and lymphadenopathy of the neck (n=3). CONCLUSION: Toxoplasmosis, which is known to cause lymphadenopathy, may be a reason for lymphadenopathy of the neck. Toxoplasmosis should be considered in the differential diagnosis of untreated patients with tonsillitis, adenoid hyperplasia, and chronic neck lymphadenopathy.

Adenoids↗
PubMed2005

Proliferation and apoptosis in ovarian stromal hyperplasia and hyperthecosis.

The aim of our study was to investigate proliferation and apoptosis in ovarian stromal hyperplasia and hyperthecosis in reproductive women with and without polycystic ovarian disease. We have studied 104 patients with a histological diagnosis of ovarian stromal hyperthecosis and stromal hyperplasia. Paraffin sections were stained by hematoxylin-eosin, von Gieson and immunohistochemistry for Bcl-2 (anti-apoptotic protein) and Ki-67 antigen (proliferation marker). We assessed the number of Bcl-2-positive and Ki-67-positive cells. The patients were divided into 4 groups: group 1 -- 33 patients with polycystic ovarian disease and coexistent stromal hyperthecosis, group 2 -- 28 patients with polycystic ovarian disease and coexistent stromal hyperplasia, group 3 -- 24 patients with ovarian stromal hyperthecosis, group 4-19 patients with ovarian stromal hyperplasia. The results suggest that in ovarian stromal hyperthecosis coexistent with polycystic ovarian disease luteinized stromal cells show high proliferation activity and resistance to apoptosis, and internal and external theca cells show resistance to apoptosis. In ovarian stromal hyperplasia coexistent with polycystic ovarian disease, hyperplastic stromal cells show high proliferation activity and resistance to apoptosis. Proliferation activity is also increased in vascular endothelial and smooth muscle cells. Internal and external theca cells show resistance to apoptosis. In ovarian stromal hyperthecosis without polycystic ovarian disease, luteinized stromal cells show high proliferation activity and resistance to apoptosis. In ovarian stromal hyperplasia without polycystic ovarian disease, hyperplastic stromal cells show high proliferation activity and potential susceptibility to apoptosis. Proliferation activity is also increased in vascular endothelial and smooth muscle cells. These characteristics of proliferation and apoptosis have meaning in pathogenesis of ovarian stromal hyperthecosis and stromal hyperplasia with and without polycystic ovarian disease.

Apoptosis↗
PubMed2006

[Outcome analysis of conservative treatment of well-differentiated endometrial adenocarcinoma and severe atypical hyperplasia in young women].

OBJECTIVE: To evaluate the effect of hormonal therapy on well-differentiated endometrial adenocarcinoma and severe atypical hyperplasia in young women aged 35 years and younger. METHODS: We retrospectively studied the clinical characteristics of 25 patients under 35 years of age (average: 28.6) diagnosed with well-differentiated endometrial adenocarcinoma or severe atypical hyperplasia, who were treated with progestin in Peking Union Medical College Hospital from 1991 to 2005. According to pathologic results, 25 patients were divided into two groups: 8 cases of endometrial carcinoma and 17 cases of severe atypical hyperplasia. In the endometrial carcinoma group, pelvic ultrasound, MRI, chest X-ray and serum CA(125) were used in pretreatment evaluation. Progesterone receptors were examined with immunohistochemical method. All patients received dilation and curettage of endometrium every 1-6 months as an assessment of treatment results. For chemotherapy, most of them were treated with medroxyprogesterone acetate. RESULTS: Six cases (6/7) in endometrial carcinoma group, and 17 cases (100%) in severe atypical hyperplasia group responded to treatment respectively; among them, 5 cases (5/7) and 14 cases (82%) had complete response, which was defined as the absence of any carcinoma or hyperplasia on endometrial samplings; one case (1/5) and 3 cases (21%) recurred within 6 to 30 months after their complete response. Follow-up on 14 patients with complete response, and the desire for childbearing showed that none of the 4 cases of endometrial carcinoma had conceived a pregnancy and 4 (40%) patients had pregnancy for totally 7 times of 10 cases of severe atypical hyperplasia. Three patients delivered full-term fetuses with induced ovulation, one of whom had artificial abortion 3 times after her delivery. One patient was lost to follow up after her spontaneous pregnancy. CONCLUSIONS: Progestin therapy is a good choice for young women having fertility desires diagnosed with well-differentiated endometrial adenocarcinoma or severe atypical hyperplasia. Endometrial carcinoma patients should be selected carefully before therapy. Pregnant rate is not satisfactory after conservative treatment. Assistant reproductive technology is potentially helpful to improve pregnant rate of patients responded to progestin therapy.

Adult↗
PubMedDate not supplied

Endometrial hyperplasia following estrogen treatment without the addition of gestagen. A follow-up study after withdrawal of estrogens.

From December 1980 to February 1991 24 patients with endometrial hyperplasia after estrogen treatment were followed-up at the Department of Obstetrics and Gynecology, University Hospital, Lund, Sweden. All were referred for post-menopausal bleeding. They were followed-up with abrasio three and nine months after the initial diagnosis. Seven patients demonstrated cystic glandular hyperplasia (CGH), six adenomatous hyperplasia (AD) and eleven atypical hyperplasia (AT). In the CGH-group five revealed atrophic endometria and one developed into endometrial carcinoma. In the AD-group two patients refused follow-up, four had atrophic endometria, in the AT-group five developed atrophia, one refused follow-up, one developed CGH, while three developed carcinoma. All four carcinomas in the series developed within the first three months of follow-up. The frequency of carcinomatous development was much higher for exogen estrogen induced hyperplasias compared to earlier findings for endogenously estrogen-induced endometrial hyperplasias. It is recommended that non-opposed estrogen treatment should be used in rare circumstances under close follow-up and that patients developing endometrial hyperplasias are followed-up until the hyperplastic changes have disappeared.

Endometrial Hyperplasia↗