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PubMed1989

Association of focal nodular hyperplasia and hepatic hemangioma.

The association between hepatic hemangioma and focal nodular hyperplasia has been occasionally reported. To evaluate the reality of this association, the prevalence of hemangioma was studied in 26 patients with focal nodular hyperplasia by comparison with 27 patients with hepatocellular adenoma. All of these patients underwent surgery, which provided the histologic confirmation of the type of tumor. The presence of hemangioma was assessed by preoperative ultrasonography, dynamic computed tomography, and pathological examination of resected liver specimens. No hemangioma was found in patients with hepatocellular adenoma, but 6 of the 26 patients with focal nodular hyperplasia (23%) had one or two associated hemangiomas that varied in size from 1.5 to 4 cm. All 6 patients having focal nodular hyperplasia and hemangioma were women who had previously used oral contraceptives. None of the patients who had not used oral contraceptives had this association. Moreover, oral contraceptives were taken for a significantly longer period by the women with focal nodular hyperplasia and hemangioma than by those without this association. It is concluded that (a) the association of hemangioma with focal nodular hyperplasia is frequent (23%) and not fortuitous, and (b) prolonged administration of oral contraceptives may facilitate the recognition of this association, possibly by affecting the growth of these tumors.

Adult↗
PubMed1996

Effects of inflation pressure of balloon catheter on vascular injuries and subsequent development of intimal hyperplasia in rabbit aorta.

Balloon catheter de-endothelialization is the most popular means of arterial injury in experimental animals and has been used as the model system to investigate atherogenesis and restenosis after percutaneous transluminal coronary angioplasty (PTCA). The aim of this study was to examine the relationship between balloon inflation pressure and vascular damage and also subsequent intimal hyperplasia. Retrograde pullback balloon injury of rabbit aortas was made at three different balloon pressures (1.5, 1.75, and 2.0 atm). The medial injuries, such as necrosis of smooth muscle cells and disruption of elastic lamina, were occasionally found in the injured segment of the aorta by balloon catheter at 1.75 atm and more frequently at 2.0 atm. No prominent medial injury was observed in the aortic segment to balloon catheter injury at 1.5 atm; Intimal hyperplasia developed in each animal and increased with time, 2, 4, and 8 weeks after injury. The intimal hyperplasia followed by balloon injury at 1.75 and 2.0 atm was more prominent than that at 1.5 atm, however, the development of the intimal hyperplasia was not parallel to the degree of inflation pressure. On the other hand, decrease of DNA content of the media and reduction of norepinephrine-induced vasoconstriction were observed in a pressure-dependent manner after balloon injury. These findings indicate that intimal hyperplasia is not proportionally correlated to the severity of the vascular injury. The control of inflation pressure is very important in order to examine vascular injuries, subsequent intimal hyperplasia and vasomotor responses in animal models of balloon catheter injury.

Animals↗
PubMed1992

Pathologic observations of intrahepatic peribiliary glands in 1,000 consecutive autopsy livers: IV. Hyperplasia of intramural and extramural glands.

Hyperplastic changes of intrahepatic peribiliary glands have rarely been reported, with the exception of hepatolithiasis. To determine whether there are any hyperplastic changes in the glands in livers without hepatolithiasis, we examined 1,000 consecutive autopsy liver specimens that had no hepatolithiasis. The glands were divided into intramural mucous glands and extramural seromucous glands. The hyperplastic changes were found in "normal" livers and in livers with various hepatobiliary diseases, and they were classified into three categories: hyperplasia of intramural glands (49 cases; 4.9%), hyperplasia of extramural serous acini (35 cases; 3.5%), and hyperplasia of extramural mucous acini (92 cases; 9.2%). Two or more of these three hyperplastic changes occasionally coexisted in the same liver. Hyperplasia of intramural glands was seen rather evenly in normal livers and in livers with various hepatobiliary diseases. Prevalence of hyperplasia of extramural serous acini was high in intrahepatic cholangitis and submassive hepatic necrosis. Prevalence of hyperplasia of extramural mucous acini was high in cirrhosis, submassive hepatic necrosis, cholangitis, systemic infection, and extrahepatic biliary obstruction. The hyperplastic intramural glands and mucous acini of extramural glands contained more neutral, carboxylated, and sulfated mucin than normal glands. Although their pathogenesis is unclear, these hyperplastic changes may enhance seromucous secretion into biliary lumens and may lead to biliary dysfunctions such as retardation of bile flow and increased bile viscosity. These hyperplastic changes may be preexisting conditions predisposing to hepatolithiasis.

Autopsy↗
PubMed2006

[Thymic hyperplasia following treatment for nephroblastoma].

UNLABELLED: Thymic hyperplasia in response to stress is a well known phenomenon. Thymic hyperplasia has also been described after chemotherapeutic treatment for malignancies in children. CASE REPORT: A three-year-old girl was followed up from the age of 18 months for a left kidney nephroblastoma treated by combination of chemotherapy (vincristin, actinomycin and adriamycin) and surgery. Assessment at the end of treatment was normal. Four months after the end of treatment, pulmonary radiography showed mediastinal enlargement, which was shown to originate in the thymus at thoracic CT scan. A recurrence of the disease was suspected. Biopsy showed thymic hyperplasia without evidence of tumor cells. Mediastinal enlargement then disappeared spontaneously 2 months later. CONCLUSION: Thymic hyperplasia occurring during remission of a cancer treated by chemotherapy is a diagnostic dilemma as it suggests mediastinal reccurence of the disease. Needle aspiration cytology is an appropriate investigation in thymic hyperplasia. No steroid therapy should be used before histologic diagnosis of thymic hyperplasia.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2005

Accumulated endogenous nitric oxide synthase inhibitors, enhanced arginase activity, attenuated dimethylarginine dimethylaminohydrolase activity and intimal hyperplasia in premenopausal human uterine arteries.

The present study was designed to investigate the involvement of nitric oxide synthase (NOS), endogenous NOS inhibitors, arginase, which shares L-arginine as a common substrate with NOS, and dimethylarginine dimethylaminohydrolase (DDAH) as a metabolizing enzyme of NOS inhibitors in the occurrence of intimal hyperplasia in premenopausal human uterine arteries. Fifty-two uterine arteries were obtained from 52 patients undergoing total hysterectomy with an informed consent for the present study. All specimens were assessed histologically and the intima:media ratio (%) was evaluated as an index of intimal hyperplasia. Nineteen specimens were found to be histologically normal (intima:media ratio=16.1+/-0.8%), whereas remaining 33 specimens were categorized as intimal hyperplasia (intima:media ratio=34.4+/-1.5%). The intimal hyperplasia was associated with the impaired cyclic GMP production without change in endothelial NOS activity per se, accumulation of endogenous NOS inhibitors in endothelial cells, attenuated DDAH activity in endothelial cells and enhanced arginase activity in endothelial cells and smooth muscle layer. These findings suggest that the impaired cyclic GMP production as a marker of NO production is possibly due to the accumulated endogenous NOS inhibitors and enhanced arginase activity, which, in turn, closely relates to the occurrence of intimal hyperplasia, and that the impaired DDAH activity would result in the accumulation of endogenous NOS inhibitors in endothelial cells. Because of the enhanced arginase activity in endothelial cells and smooth muscle layer, the accelerated polyamine biosynthetic pathway may be implicated in the occurrence of intimal hyperplasia in premenopausal human uterine arteries.

Adult↗
PubMed2005

Tenascin-C is an essential factor for neointimal hyperplasia after aortotomy in mice.

OBJECTIVE: Neointimal hyperplasia at the arterial anastomotic site is a critical problem during cardiovascular surgery. It has been suggested that tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, might play an important role in neointimal hyperplasia. In this study, the direct contribution of tenascin-C to neointimal hyperplasia after aortotomy was examined using tenascin-C-deficient (TNKO) mice. METHODS AND RESULTS: A simple aortotomy model was constructed in mice. In wild-type (WT) mice, neointimal hyperplasia was observed at the suture sites at days 14 and 28. Immunohistochemical staining showed strong expression of tenascin-C in both neointima and media around the suture line at day 14. At day 28, tenascin-C staining was detected in neointima, but not in media. In tenascin-C-deficient mice, much less neointimal hyperplasia was seen compared to that in wild-type mice, and the mean neointima/media area ratio decreased to 52.8% and 34.3% at days 14 and 28, respectively. The proliferating cell nuclear antigen indices in wild-type mice were twice those in tenascin-C-deficient mice at day 14. There were fewer Alcian blue-positive proteoglycans deposited in the neointima of tenascin-C-deficient mice than in wild-type mice. These results suggest that tenascin-C promotes neointimal cell migration and proliferation, and the deposition of proteoglycans. CONCLUSIONS: We have presented direct evidence that tenascin-C is a crucial molecule in neointimal hyperplasia at anastomotic sites.

Actins↗
PubMed2005

Genetic imbalances in endometrial hyperplasia and endometrioid carcinoma detected by comparative genomic hybridization.

OBJECTIVE: To evaluate the sequential genomic copy alterations related to the development of precursor lesions and endometrioid-type endometrial carcinomas, and its association with cellular atypia. STUDY DESIGN: Paraffin-embedded tissue specimens from 32 cases of endometrial hyperplasia, 15 of endometrial carcinoma, and 20 of normal endometrial tissue were retrospectively evaluated by the comparative genomic hybridization (CGH) technique. The average number of copy alterations (ANCA) index was used to define the incidence of genomic imbalances in each tissue group. Identified sequential genetic abnormalities were compared with the final histopathological diagnosis and the cellular atypia. RESULTS: Detectable and consistent chromosomal imbalances were found in 13 hyperplasia and 9 carcinoma specimens. There was a significant correlation between ANCA value and degree of cellular atypia and tumor grade. While 1p36-pter, 20q deletions, and 4q overrepresentation were the most prevalent imbalances detected in both complex hyperplasia and complex atypical hyperplasia, 17q22-qter deletion and amplification of 2p34 were only seen in hyperplasia with atypical cells. Overrepresentations of chromosomes 8q, 1q, and 3q are the most frequent aberrations in endometrial carcinomas, but were absent from all the precursor lesions except one. Underrepresentations of chromosomes 1p36-pter and 10q are the other commonly seen aberrations in carcinomas, the latter being more frequent in moderately differentiated than in poorly differentiated lesions. CONCLUSIONS: Different patterns of chromosomal aberrations are seen in precursor lesions than in endometrial carcinomas, except for the loss of 1p36-pter. The presence of 1p deletion in both endometrial hyperplasia and cancer specimens suggests that this is an early event in the development of carcinoma. These results support a stepwise mode of tumorigenesis with accumulation of a series of genomic copy alterations in endometrial carcinogenesis.

Chromosome Aberrations↗
PubMed2004

Expression of vascular endothelial growth factor (VEGF) and its receptors (VEGF-R1 [Flt-1] and VEGF-R2 [KDR/Flk-1]) in tumorlets and in neuroendocrine cell hyperplasia of the lung.

Pulmonary tumorlets and neuroendocrine (NE) cell hyperplasia are part of a continuous spectrum of NE-cell hyperplasia, going from NE hyperplasia to carcinoid. Vascular endothelial growth factor (VEGF) is a potent endothelial cell mitogen that has been shown to be increased in hypoxic lung. We hypothesized that tumorlets and NE-cell hyperplasia, which occur frequently in this context, were partly responsible for VEGF secretion. Immunohistochemical analysis of VEGF and both VEGF-R1 and VEGF-R2 was performed on paraffin sections of 12 lung tissues containing tumorlets and NE-cell hyperplasia in parallel with a control group of 11 lung specimens. VEGF and its receptor expressions were compared in bronchial epithelial cells and endothelial cells in both groups. VEGF and its receptors were consistently expressed in tumorlets and in NE-cell hyperplasia. When compared with control group lungs, the staining score for VEGF in lung bearing tumorlets was significantly higher in endothelial cells, but was not different in bronchial epithelial cells. VEGF-R1 expression was significantly increased both on bronchial epithelial cells (P = 0.001) and endothelial cells (P = 0.006), and VEGF-R2 expression was significantly increased on endothelial cell (P = 0.044). There was a significant positive correlation between the level of expression of VEGF and VEGF-R1 (P = 0.04) in both control groups and lung bearing tumorlets, but there was no significant correlation between VEGF and VEGF-R2 expression (P = 0.1). We concluded that VEGF is highly expressed in localized NE cell proliferations without potential of malignancy and might participate in local development of fibrosis.

Adult↗
PubMed2004

Evaluation of platelet deposition and neointimal hyperplasia of heparin-coated small-caliber ePTFE grafts in a canine femoral artery bypass model.

INTRODUCTION: Bypass graft failure due to acute thrombosis and intimal hyperplasia remains a major challenge in small-diameter vascular prosthetic graft reconstruction. Heparin has been shown to prevent thrombus formation and inhibit intimal antithrombotic in animal studies. In this study, we evaluated the effect of small-caliber heparin-coated expanded polytetrafluoroethylene (ePTFE) grafts on platelet deposition and intimal hyperplasia in a canine model of femoral artery bypass grafting. METHODS: Nine adult greyhound dogs underwent placement of bilateral femorofemoral artery bypass grafts with ePTFE grafts (4 mm diameter and 7 cm long). In each animal, a heparin-coated ePTFE graft was placed on one side while a noncoated graft was placed on the contralateral side which served as the control. Platelet deposition was measured by autologous (111)indium-labeling and scintillation camera imaging analysis in 24 h. The graft patency was assessed at 4 weeks following the bypass. The effect of intimal hyperplasia was assessed with histological and morphometric analysis. RESULTS: Platelet deposition on the heparin-coated grafts at 24 h was significantly reduced by 72% as compared to controls (P = 0.001). The patency rate was 44% in control grafts and 89% in heparin-coated grafts. There was a significant reduction of graft intimal hyperplasia at both proximal (0.38 +/- 0.21 mm(2)) and distal (0.19 +/- 0.06 mm(2)) anastomoses in the heparin-coated grafts as compared with proximal (1.01 +/- 0.28 mm(2)) and distal (0.42 +/- 0.01 mm(2)) anastomoses in the untreated control grafts, respectively (P < 0.05). Heparin coating significantly reduced graft neointimal hyperplasia at patent graft anastomoses by 55-72% as compared to controls. CONCLUSIONS: These data demonstrate that heparin coating of ePTFE significantly reduced early platelet deposition and inhibited anastomotic neointimal hyperplasia. Moreover, small-caliber heparin-coated ePTFE graft significantly increased graft patency in a canine femoral artery bypass model. This may represent a promising treatment strategy for improving the clinical performance of small-caliber prosthetic vascular grafts.

Anastomosis, Surgical↗
PubMed2004

Cigarette smoke increases intimal hyperplasia and homocysteine in a rat carotid endarterectomy.

BACKGROUND: Homocysteine and smoking are independent risks for CVD; however their importance in post-CEA intimal hyperplasia is unclear. We performed a CEA in rats exposed to cigarette smoke with the hypothesis that smoking would increase intimal hyperplasia that may be associated with an elevated serum homocysteine. Folic acid (FA) and the homocysteine metabolic enzymes MTHFR and CBS were used to test for the significance of homocysteine elevation. MATERIALS AND METHODS: Rats underwent an open CEA. N = 13 rats received smoke exposure 2 weeks prior, and 2 weeks post-CEA and N = 12 received no smoke. Each group was divided into either control or an FA-added diet resulting in four groups. Rats were sacrificed at 2 weeks post-CEA; liver, urine, blood, and carotid arteries samples were obtained. RESULTS: Smoked rats had increased urinary peak and trough cotinine levels versus non-smoke rats, which decreased with FA. Smoke exposure increased intimal hyperplasia versus non-smoke controls by nearly 120% (57.8 +/- 6.2 versus 26.8 +/- 5.4% luminal stenosis, P = 0.005). Smoke-exposed rats had an increased serum homocysteine versus non-smoke controls (8.3 +/- 0.8 versus 5.7 +/- 0.8 microm, P = 0.014). Smoked rats given FA had decreased serum homocysteine compared to the smoke group. Along with reductions in homocysteine, FA eliminated the increase in intimal hyperplasia seen with smoke exposure (33.5 +/- 6.1 versus 57.8 +/- 6.2% luminal stenosis, P = 0.03). CBS activity decreased in smoked rats by nearly 20% versus non-smoke rats. FA supplementation in smoked rats both (1) increased CBS activity and (2) decreased MTHFR compared to control non-smoke-exposure levels. CONCLUSION: Smoking increases plasma homocysteine and post-CEA intimal hyperplasia. This suggests homocysteine has an etiological role in the intimal hyperplasia increase observed with smoking, since both were negated with FA.

Animals↗
PubMed2004

Gene delivery to aortocoronary saphenous vein grafts in a large animal model of intimal hyperplasia.

OBJECTIVE: More than 50% of aortocoronary saphenous vein grafts are occluded 10 years after surgery. Intimal hyperplasia is an initial, critical step in the progression toward occlusion. To date, no clinically relevant large animal models of aortocoronary saphenous vein graft intimal hyperplasia have been fully characterized. Gene therapy holds promise as a novel treatment for aortocoronary saphenous vein graft intimal hyperplasia. The 2 objectives of this study are to characterize a canine model of aortocoronary saphenous vein graft intimal hyperplasia and to demonstrate that ex vivo gene delivery is possible in these grafts using adenoviral vectors. METHODS: Ten dogs underwent aortocoronary bypass grafting using saphenous veins. Six dogs underwent serial arteriograms to monitor graft patency. On postoperative day 90, the dogs were killed and their grafted and nongrafted saphenous veins were studied histologically. Four dogs underwent the same procedure, but their saphenous veins were treated with 1 x 10(12) total viral particles of a replication-deficient, recombinant adenovirus containing beta-galactosidase (n = 2) or the beta-adrenergic receptor kinase carboxyl terminus (n = 2). These animals were killed on postoperative day 7 for determination of transgene expression. RESULTS: All grafts were demonstrated patent by arteriogram before the animals were killed. The mean intimal area of the saphenous vein grafts was increased when compared with that of the nongrafted saphenous veins (2.83 mm(2) vs 0.09 mm(2), P <.0008). Adenoviral-treated saphenous vein grafts demonstrated positive transgene expression either by X-gal staining (beta-galactosidase) or Northern analysis (beta-adrenergic receptor kinase carboxyl terminus). CONCLUSION: This study characterizes a clinically relevant canine model of aortocoronary saphenous vein graft intimal hyperplasia. In addition, it demonstrates that adenoviral vectors can be delivered ex vivo to the saphenous vein graft vessel wall at subphysiologic distension pressures. This model may be used in future studies to manipulate molecular targets critical in aortocoronary saphenous vein graft intimal hyperplasia.

Animals↗
PubMed2006

Response to daily 10 mg alfuzosin predicts acute urinary retention and benign prostatic hyperplasia related surgery in men with lower urinary tract symptoms.

PURPOSE: We analyzed the influence of treatment response on the risk of acute urinary retention and benign prostatic hyperplasia related surgery in 5,792 men complaining of lower urinary tract symptoms who were treated for 6 months with the selective alpha1-blocker alfuzosin at 10 mg once daily. MATERIALS AND METHODS: The influence of dynamic variables (International Prostate Symptom Score change and bother during treatment) and baseline variables (patient age, prior acute urinary retention managed conservatively, prostate specific antigen, International Prostate Symptom Score and bother severity) on the risk of acute urinary retention and benign prostatic hyperplasia related surgery was estimated using the Kaplan-Meier method and log rank test. The associated HR and 95% CI were calculated using Cox proportional hazard models. RESULTS: During alfuzosin treatment International Prostate Symptom Score improved by 3 or greater and greater than 6 points in 74.8% and 50.3% of men, respectively. In this unselected population, including 3.8% with prior unoperated acute urinary retention, the rate of acute urinary retention and benign prostatic hyperplasia related surgery events during treatment was low (0.5% and 1.1%, respectively). Men with stable or worsening International Prostate Symptom Score were at increased risk for acute urinary retention or surgery (HR 3.75, 95% CI 1.58 to 8.89, p = 0.003 and HR 4.71, 95% CI 2.69 to 8.24, p <0.001, respectively). Prior acute urinary retention was a strong predictor of acute urinary retention relapse and surgery (HR 10.35, 95% CI 4.29 to 26.08, p <0.001 and HR 3.57, 95% CI 1.59 to 7.98, p = 0.002, respectively). Bother score greater than 3 during treatment was the strongest predictor of surgery (HR 7.61, 95% CI 4.16 to 13.93, p <0.001). Prostate specific antigen had much less predictive value. CONCLUSIONS: This 6-month real life practice study shows that alfuzosin is associated with a low incidence of acute urinary retention and benign prostatic hyperplasia related surgery. It also suggests that responder status is the most important predictor of acute urinary retention and benign prostatic hyperplasia related surgery. Thus, first line treatment with alfuzosin may help select patients at risk for benign prostatic hyperplasia progression to optimize treatment.

Acute Disease↗
PubMed2006

The roles of progestagen and uterine irritant in the maintenance of cystic endometrial hyperplasia in the canine uterus.

Cystic endometrial hyperplasia (CEH) was induced in the left uterine horns of 14 mature ovariectomised greyhound bitches with an intra-luminal silk suture (uterine irritant) and treatment with estradiol benzoate and megestrol acetate (to simulate stages of a normal canine estrous cycle). Right uterine horns served as suture-free controls. From Day 30 of simulated diestrus, bitches received treatments of suture removal (n = 4), progestagen withdrawal (n = 5) or both (n = 5). Necropsies were performed 3 or 9 weeks later. At 3 weeks, severe cystic endometrial hyperplasia was present in all (6/6) left horns and in no (0/6) right horns. At 9 weeks, the left horns in 5/6 of bitches subjected to progestagen-withdrawal had recovered (in varying degrees) from cystic endometrial hyperplasia, whereas no recovery was evident in the left horns of bitches (n = 2) that continued to receive progestagen. This study demonstrated that: (i) cystic endometrial hyperplasia was reversible upon withdrawal of progestagen; (ii) progestagen maintained cystic endometrial hyperplasia in the presence or absence of irritant; and (iii) persistent endometrial irritation in the absence of progestagen may not maintain cystic endometrial hyperplasia.

Animals↗
PubMedDate not supplied

High rate of endometrial hyperplasia in renal transplanted women.

UNLABELLED: A high rate of endometrial hyperplasia, an estrogen-dependent premalignant lesion of the endometrium, has been observed among female kidney allograft recipients. The aim of the study was to evaluate the incidence of endometrial abnormalities among renal transplanted women with abnormal uterine bleedings. MATERIAL AND METHODS: A retrospective analysis compared 45 renal transplanted women who underwent dilatation and curettage for abnormal uterine bleeding between January 1999 and September 2004 with 90 consecutive, nontransplanted, control patients who underwent dilatation and curettage for the same reason in 2004. RESULTS: Thirty-one cases (69%) of endometrial hyperplasia and one case (2%) of endometrial cancer were detected among the renal allograft recipients. The majority of transplant patients (28 cases, 62%) developed endometrial hyperplasia without atypia successfully treated with progestagens. There were 29 cases (32%) of hyperplasia without atypia, 2 cases (1%) of atypical hyperplasia, and 4 cases (4%) of endometrial cancer in the control group. CONCLUSIONS: Renal transplanted women seem to have an extremely high risk of endometrial hyperplasia. The majority of cases may be successfully treated with progestagens. Immunocompromised renal graft recipients, however, show other risk factors for carcinogenesis. Thus, frequent clinical surveillance should be recommended in this group of patients, also because there is conflicting evidence with regard to the risk of progression to carcinoma among untreated patients.

Adult↗
PubMed2003

Implementation of assisted reproductive technologies following conservative management of FIGO grade I endometrial adenocarcinoma and/or complex hyperplasia with atypia.

OBJECTIVE: The objective was to report a series of infertility therapy outcomes following conservative management of endometrial adenocarcinoma and/or complex hyperplasia with atypia. METHODS: A retrospective review of the University of Iowa assisted reproductive technology database was performed. All women presenting with International Federation of Obstetrics and Gynecology (FIGO) grade I uterine adenocarcinoma and/or complex hyperplasia with atypia were assessed for type and duration of medical management, initial, interim treatment, and preinfertility treatment endometrial biopsy (BX) findings. Assessment of infertility treatment outcomes and postinfertility endometrial biopsy findings were performed. All of the pathology samples were re-reviewed at the Gynecologic Oncology Tumor Board to confirm the diagnosis by a pathologist with a particular expertise in gynecologic pathology. RESULTS: Four infertile women, three nulligravid and one primigravid, were evaluated with the diagnosis of FIGO grade 1 endometrial adenocarcinoma and/or complex hyperplasia with atypia desiring to preserve fertility. Two women with FIGO grade 1 endometrial adenocarcinoma were successfully treated with high-dose progestational agents resulting in normal proliferative endometrium. In addition, both women with complex hyperplasia with atypia were successfully treated with progestins and/or ovulation induction. Successful pregnancy outcomes were achieved for three of the four women with assisted reproductive technology. A total of five successful pregnancies and eight healthy live-born infants were achieved among three women. One of the four women was unable to conceive despite three cycles of in vitro fertilization. Hysterectomy was performed for recurrent complex hyperplasia with atypia. In our series, we found it can take 3-10 months (mean, 6.25 months; median, 6 months) to obtain benign endometrium preceding infertility therapy. CONCLUSION: This report demonstrates that conservative management of well-differentiated endometrial adenocarcinoma and/or complex hyperplasia with atypia followed by aggressive assisted reproduction is an option to highly motivated and carefully selected women.

Adenocarcinoma↗
PubMed1996

Use of computerized morphometric analyses of endometrial hyperplasias in the prediction of coexistent cancer.

OBJECTIVE: Our purpose was to determine whether computerized morphometric analysis is predictive of coexistent cancer in uteri that show endometrial hyperplasia in curettings or biopsy specimens. STUDY DESIGN: Forty-five patients with endometrial hyperplasia and 10 patients with well-differentiated cancers diagnosed from curettings or biopsy specimens and treated by hysterectomy at Thomas Jefferson University Hospital between 1989 and 1993 were identified from the pathology department archives. Curettings were analyzed by computerized morphometric analysis at the Free University Hospital in Amsterdam. Pathologists performing the morphometric analyses were blinded to the pathologic diagnoses obtained by examining the hysterectomy specimens. The histopathologic classification of the hysterectomy specimens were used as the end point. RESULTS: Twelve of 45 patients with endometrial hyperplasia (26.7%) by preoperative histopathologic classification showed coexistent carcinoma at hysterectomy. All instances of carcinoma occurred in patients with atypical hyperplasia. Sensitivity of morphometric analysis to predict carcinoma was 100%, with a specificity of 88.5%. The positive predictive value was 83.3%, and the negative predictive value was 100%. A blinded reanalysis of the quantitative analysis in 16 patients showed good reproducibility of this technique (r = 0.93). CONCLUSIONS: Morphometric analysis is useful for predicting which patients with endometrial hyperplasia have coexistent carcinomas. Computerized morphometric analysis may be useful in therapeutic decision making for complex atypical hyperplasia.

Aged↗
PubMed1997

Is bleeding a predictor of endometrial hyperplasia in postmenopausal women receiving hormone replacement therapy? Menopause Study Group (United States, Italy, Netherlands, Switzerland, Belgium, Germany, and Finland.

OBJECTIVE: We evaluated bleeding as a predictor of endometrial hyperplasia in postmenopausal women receiving conjugated estrogens (Premarin) alone or with medroxyprogesterone acetate. STUDY DESIGN: This study was a retrospective assessment of bleeding and endometrial histologic data gathered during the prospective Menopause Study Group trial. RESULTS: Approximately 20% of women (n = 57) who received unopposed conjugated estrogens for 1 year had endometrial hyperplasia. These women (n = 56) had more bleeding days than did women who did not have hyperplasia (p < 0.001). For users of unopposed conjugated estrogens, the predictive value of amenorrhea to indicate a nonhyperplasia diagnosis was 95%. Irregular bleeding did not appear to be indicative of hyperplasia when continuous or cyclic medroxyprogesterone acetate was added to conjugated estrogens. CONCLUSION: Unanticipated prolonged bleeding in postmenopausal women receiving unopposed estrogen is suggestive of endometrial hyperplasia. Some irregular bleeding is anticipated in women who receive conjugated estrogens plus medroxyprogesterone acetate as they acclimate to therapy, and this was not associated with hyperplasia.

Endometrial Hyperplasia↗
PubMed2002

Intraperitoneal infusion of homocysteine increases intimal hyperplasia in balloon-injured rat carotid arteries.

Hyperhomocysteinemia is a significant risk factor in atherosclerosis and thrombosis. However, its role in the development of intimal hyperplasia after arterial reconstructive procedures remains uncertain. We therefore studied the effect of homocysteine on intimal hyperplasia in a rat model of carotid artery balloon injury. Twenty-four Sprague-Dawley rats were divided into three groups: control (saline infusion), and low dose (0.14 mg/day) and high dose (0.71 mg/day) homocysteine delivered continuously via osmotic pumps implanted intraperitoneally. All animals underwent left common carotid artery balloon denudation with sacrifice after 14 days. Plasma homocysteine levels, intimal hyperplasia, and cell proliferation of rat carotid arteries were determined. In vitro rat smooth muscle cell (SMC) proliferation with homocysteine treatment was also performed. Plasma homocysteine levels at sacrifice were 1.80+/-0.35, 2.65+/-0.05 and 3.50+/-0.22 microM in three groups, respectively. Intimal hyperplasia developed in all balloon-injured arteries in both control and homocysteine-treated animals. The intimal area and intima/media area ratio were increased by 92% (P<0.05) and 105% (P<0.05), respectively, in the high dose-homocysteine-treated animals as compared to the control animals. Homocysteine (high dose) also significantly promoted the intimal cell proliferation (bromodeoxyuridine incorporation) by 2.2-fold as compared to controls. Furthermore, homocysteine treatment in the cell culture study showed a concentration-dependent increase of rat SMC proliferation. These data demonstrate that the continuous intraperitoneal administration of homocysteine significantly increases intimal hyperplasia and SMC proliferation after carotid artery balloon injury in the rat as well as in vitro SMC proliferation. This study suggests that, following arterial reconstructive procedures, elevated plasma homocysteine may increase the complications of clinical restenoses that are associated with intimal hyperplasia.

Animals↗