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At least 811 records · Page 45Linked to original sources
PubMed2002

Increased intimal hyperplasia in experimental vein graft stenting compared to arterial stenting: comparisons in a new rabbit model of stent injury.

BACKGROUND: In-stent restenosis due to intimal hyperplasia is an important clinical problem. Animal models of stent injury are limited by inconsistent arterial responses to stenting, and less intimal hyperplasia than diseased human vessels. To address these issues, we aimed to compare the degree of intimal hyperplasia in stented rabbit jugular-carotid interposition grafts (vein grafts) versus stented carotid arteries. METHODS: Jugular-carotid vein grafts were constructed in rabbits, then stented or left unstented. Carotid arteries were treated with similar stents or left instrumented only. After 3 or 28 days, vessels were perfusion fixed, embedded in resin, and sections were cut with a diamond saw. Intimal and medial thicknesses were measured in stained sections. RESULTS: After 3 days, inflammatory changes were observed in the intima of all stented vessels. After 28 days, intimal thickness in stented vein grafts was 2-fold greater than in control vein grafts and approximately 4-fold greater than in stented carotid arteries. In addition, the intimal hyperplasia response was markedly more consistent in stented vein grafts compared with stented carotid arteries. CONCLUSIONS: Stent deployment in experimental vein grafts results in increased and more reproducible smooth muscle cell intimal hyperplasia than carotid arterial stenting. This is a promising small-animal model for investigating the intimal response to stenting.

Anastomosis, Surgical↗
PubMed1976

Aldosterone regulation in primary aldosteronism: differences between adenoma and bilateral hyperplasia.

1. The diurnal patterns of plasma aldosterone, plasma renin activity (PRA), cortisol and adrenocorticotrophic hormone (ACTH) in the supine and in the upright position have been studied in fourteen patients with primary aldosteronism, five with adenoma and nine with bilateral hyperplasia. Blood samples were drawn at intervals from 6 h to 30 min. 2. Supine patients with an adenoma showed marked diurnal variations of aldosterone, with maximal values at 08.00 hours and minimal values of 18.00 hours and secretory spurts beginning after 02.00 hours. Plasma cortisol paralleled aldosterone, and ACTH seemed to anticipate aldosterone and cortisol variations; PRA remained unchanged. In patients with hyperplasia, aldosterone was significantly lower than in the adenoma group at 08.00 hours, and its decline during the day was less marked; fluctuations rather than secretory episodes were seen. 3. After patients assumed the upright posture, aldosterone remained unchanged or decreased in patients with adenoma, whereas it significantly increased in hyperplasia; PRA remained low, although a slight increment was seen in the latter group. The different response of aldosterone in the two groups was not modified by the administration of propranolol, apparently excluding a renin-dependent mechanism. On the other hand, dexamethasone seemed to affect the response of aldosterone to the upright posture in both groups; in adenoma there was a slight but significant increase, and in hyperplasia the usual rise was partially suppressed. 4. It is concluded that ACTH has a predominant role in regulating aldosterone secretion in primary aldosteronism due to adenoma, whereas its action in bilateral hyperplasia is only permissive.

Adenoma↗
PubMed1995

Endometrial hyperplasia and the risk of carcinoma.

Recent reports suggest that atypical endometrial hyperplasia diagnosed by biopsy or curettage is accompanied by a higher than expected risk of coexistent invasive cancer. In order to test this hypothesis we reviewed the pathology and clinical history of all patients at our institution who underwent hysterectomy for endometrial hyperplasia with or without cytologic atypia. We found 24 patients of 45 with a preoperative diagnosis of hyperplasia with cytologic atypia, and 21 with simple or complex hyperplasia without atypia. No cancers were found at surgery in the latter group nor were any significant historical differences found between the two groups. Of the patients with atypia, 12/24 (50%) had an endometrial carcinoma and nine patients (37.5%) were stage IB or greater. This is a significantly greater risk than previously reported in the literature. Endometrial hyperplasia with cytologic atypia may carry a higher risk of coexistent invasive endometrial carcinoma than previously believed. Methods to identify those patients at highest risk should be determined.

Journal Article↗
PubMed2003

[Micronodular pneumocyte hyperplasia in pulmonary lymphangioleiomyomatosis and tuberous sclerosis].

An open lung biopsy was performed in a 28-year-old woman with tuberous sclerosis and with spontaneous pneumothorax and interstitial changes in the chest X-ray. Microscopically a micronodular pneumocyte hyperplasia in addition to a lymphangioleiomyomatosis was found. The micronodular pneumocyte hyperplasia is considered to be a very rare lesion. Only 27 well documented such cases have been recorded so far, 24 in women and 3 in men. The age of the patients ranged between 20 and 57 years, with an average of 36 years. The micronodular pneumocyte hyperplasia occurs mainly in patients with tuberous sclerosis (20 of 27 cases) and it is often combined with a lymphangioleiomyomatosis (19 cases). In the differential diagnosis the atypical adenomatous hyperplasia is to be considered in the first place. In contrast to it, the proliferating cells of the micronodular pneumocyte hyperplasia show no atypia. The differentiation from a papillary adenoma can be difficult in small biopsies.

Adult↗
PubMed2001

Mechanisms in the inhibition of neointimal hyperplasia with triflavin in a rat model of balloon angioplasty.

RGD-containing peptides are able to inhibit the binding of ligands to certain beta3 integrins, such as alpha(IIb)beta3 and alpha(v)beta3, both of which are involved in neointimal hyperplasia. The present study was designed to elucidate the detailed mechanisms involved in the inhibition of neointimal hyperplasia with triflavin in a rat model of balloon angioplasty. Triflavin (0.25 mg x kg(-1) x d(-1)), an RGD-containing disintegrin, time dependently inhibited both neointimal hyperplasia and lumen occlusion after angioplasty in carotid arteries of rats. Furthermore, electron micrographs highlighted that SMCs were phenotypically different from the typical contractile, spindle-shaped SMCs normally seen in uninjured vessel walls. PDGF-BB was strongly produced in thrombus formation and neointimal SMCs after angioplasty, and triflavin significantly reduced PDGF-BB expression in vessel lumens and neointimal SMCs after angioplasty. Balloon angioplasty caused a significant increase of nitrate and cyclic guanosine monophosphate levels compared with levels found in sham-operated rats, and these were not significantly changed with infusion of triflavin (0.25 mg x kg(-1) x d(-1)). Furthermore, the plasma level of TXB2 obviously increased after angioplasty, and triflavin markedly suppressed the elevation of plasma TXB2 concentration. The results indicate that triflavin effectively prevents neointimal hyperplasia, possibly through the following 2 mechanisms. First, triflavin binds to alpha(IIb)beta3 integrin on platelet membranes, resulting in inhibition of platelet adhesion, secretion, and aggregation in injured arteries, followed by inhibition of TXA2 formation and PDGF-BB release from platelets. Second, triflavin may also bind to alpha(v)beta3 integrin on SMCs, thus subsequently inhibiting cell migration and proliferation. These results provide new insights into the mechanisms of neointimal hyperplasia and have significant implications for disintegrin therapy for the treatment of restenosis and atherosclerosis.

Angioplasty, Balloon↗
PubMed1978

Ectopic ACTH-MSH producing carcinoid tumor with multiple endocrine hyperplasia in a child.

An autopsy case of a 9-year-old Japanese girl revealed a carcinoid tumor originating in the duodenum and hyperplasia of the multiple endocrine organs as manifested by ectopic ACTH syndrome, carcinoid syndrome and giantism. The tumor cells were positive for histochemical argyrophile reaction and two types of secretory granules were identified by electron microscopy. Biochemical assay revealed the production of ACTH and beta-MSH by the tumor cells. Other changes of multiple endocrine organs included acidophil dominant hyperplasia of the pituitary, diffuse hyperplasia of the thyroid, chief cell hyperplasia of the parathyroid, hyperplasia of the islets of Langerhans and the adrenal cortex. This case was considered to be a type of multiple endocrine adenomatosis including carcinoid tumor. The relationship between the carcinoid tumor and multiple endocrine adenomatosis was discussed.

Adenoma↗
PubMed1990

Multicentric angiofollicular lymph node hyperplasia with peripheral neuropathy, pseudotumor cerebri, IgA dysproteinemia, and thrombocytosis in women. A distinct syndrome.

Four women with multicentric angiofollicular lymph node hyperplasia had a distinct clinical syndrome characterized by peripheral neuropathy, pseudotumor cerebri, IgA dysproteinemia, and thrombocytosis. The nodes displayed typical morphologic changes of the plasma cell variant of multicentric angiofollicular lymph node hyperplasia. The pathologic changes are morphologically distinct from angioimmunoblastic lymphadenopathy with dysproteinemia although clinical similarities do exist. In these four cases, the lymphadenopathy was usually bulky and multicentric. There was frequent splenic involvement. The neuropathies were severe and disabling. Clinical courses have been variable with some responses to therapy with steroids and alkylating agents. No neoplastic transformations have occurred. Multicentric angiofollicular lymph node hyperplasia may represent a reactive lesion in which the antigenic stimulus is unknown but results in follicular hyperplasia, angiogenesis, and the systemic manifestations of hyperimmune stimulation. We believe this clinical syndrome may represent a distinct variant of multicentric angiofollicular lymph node hyperplasia, and it requires close observation for neoplastic transformation and other complications of its multisystem nature.

Biopsy↗
PubMed2004

[Study on differential diagnosis between MALT-type lymphoma and reactive lymphoid hyperplasia of the ocular adnexa].

OBJECTIVE: To study the methods of differential diagnosis between mucosa-associated lymphoid tissue (MALT) type lymphoma and reactive lymphoid hyperplasia in ocular adnexa. METHODS: The clinical, morphologic, immunohistochemical, and molecular biologic (polymerase chain reaction [PCR]) studies were performed on 29 patients with MALT-type lymphoma and 8 patients with reactive lymphoid hyperplasia of the ocular adnexa. RESULTS: 29 cases with MALT-type lymphoma expressed B-cell markers and but T-cell makers, whereas 8 cases of reactive lymphoid hyperplasia all expressed B and T cell markers and the positive rate of T-cell marker was up to 30%. immunohistochemistry staining showed 11 cases were positive for immunoglobin light chain (kappa or lambda), however it was positive in one chain of the immunoglobin in 15 cases of MALT type lymphoma by PCR. No significant difference in the clinical characteristics was observed between the MALT type lymphoma and reactive lymphoid hyperplasia in ocular adnexa. CONCLUSION: Immunohistochemical analysis and PCR are helpful in confirming the diagnosis between the MALT-lymphoma and the reactive lymphoid hyperplasia.

Adolescent↗
PubMed1997

Relationship between Helicobacter pylori infection and gastric follicular hyperplasia. A retrospective study.

BACKGROUND: The occurrence of lymphoid follicles in the gastric mucosa was recently considered to be acquired in respose to infection by Helicobacter pylori. METHODS: In order to investigate whether there is any correlation between follicular hyperplasia and Helicobacter pylori colonization, a morphological study was performed in antral biopsy specimens from 267 patients with H. pylori-associated gastritis, and from 312 subjects with histological evidence of chronic gastritis, but without H. pylori colonization. RESULTS: Follicular hyperplasia was observed in 33 (12.3%) specimens with H. pylori-associated gastritis, and in 56 (9%) samples from non-infected group (p=ns). In both H. pylori-positive and H. pylori-negative specimens lymphoid follicular hyperplasia showed a significant correlation with the degree of the gastritis. In these two groups the prevalence of follicular hyperplasia was also significantly higher in the elderly. CONCLUSIONS: On the basis of these results, we were unable to find any significant correlation between H. pylori infection and occurrence of lymphoid follicular hyperplasia. The appearance of organized follicular structures in the gastric mucosa seems to be acquired in response to multiple events, and not exclusively in consequence of the colonization by Helicobacter pylori.

Journal Article↗
PubMedDate not supplied

Pigmented adrenal hyperplasia with myelolipomatous changes and bilateral testicular enlargement in an untreated man with 21-hydroxylase deficiency.

OBJECTIVE: To report the occurrence of a giant left adrenal tumor and bilateral testicular masses (adenomatous hyperplasia of Leydig cells) in a young man with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. METHODS: The clinical, radiologic, endocrinologic, and pathologic features of this case are correlated with the findings in the literature. RESULTS: The interesting elements in this case are the rare pathologic features of the left adrenal lesion (pigmented adrenal hyperplasia with myelolipomatous changes) and the association with the infrequent testicular adrenal rest tumors. The absence of enlargement of the right adrenal gland was unexplained. CONCLUSION: The presence of these two rare complications seemed to be associated with poor adherence to medical treatment recommendations for congenital adrenal hyperplasia.

Adenoma↗
PubMed1976

Primary diffuse microscopical hyperplasia of the parathyroid glands: surgical importance.

In two of 182 patients with verified primary hyperparathyroidism, microscopical hyperplasia was present in all parathyroid glands that were normal in size or only slightly enlarged. All parathyroid glands in another two patients showed microscopical hyperplasia and varied from a normal size of 190 mg. In seven additional patients, microscopical hyperplasia was present in one, several, or all parathyroid glands, which varied in weight from normal to 350 mg. Familial hyperparathyroidism or multiple endocrine neoplasia was evident in five of 11 patients. Contributing to difficulties was the experience in five patients in whom removal of mildly enlarged parathyroid glands corrected hypercalcemia, but definite microscopical abnormalities were not evident by routine histologic study of the glands. Thus, there appears to be a spectrum of abnormalities relative to size and microscopical changes in parathyroid glands of patients with primary hyperparathyroidism. The surgeon should be aware of these patterns of parathyroid hyperplasia that require a search for a fifth parathyroid gland and a subtotal parathyroidectomy.

Adult↗
PubMed1995

Halofuginone, a specific collagen type I inhibitor, reduces anastomotic intimal hyperplasia.

OBJECTIVE: To determine if halofuginone hydrobromide, a specific type I collagen inhibitor, could prevent intimal hyperplasia at a vascular anastomosis. DESIGN: Intimal hyperplasia is characterized by smooth muscle cell proliferation and extracellular matrix accumulation. Halofuginone was used to block collagen production and smooth muscle cell proliferation in cell cultures and in a rabbit model of an end-to-end anastomosis of the right common carotid artery. Animals were fed a nontoxic dose of halofuginone. Eighteen rabbits were fed the inhibitor in a randomized blinded fashion and were examined after 4 weeks by harvesting the arteries after perfusion fixation at physiologic pressures. RESULTS: Halofuginone inhibited smooth muscle cell proliferation in vitro and had no effect on cell viability. Morphometric quantification verified that halofuginone treatment significantly attenuated anastomotic intimal thickness. CONCLUSION: Oral administration of halofuginone inhibits intimal hyperplasia at vascular anastomoses. Intimal hyperplasia inhibition by halofuginone may be a therapeutic option for preventing arterial stenosis in vascular surgery.

Anastomosis, Surgical↗
PubMed1998

Photodynamic therapy with local photosensitizer delivery inhibits experimental intimal hyperplasia.

BACKGROUND: Photodynamic therapy (PDT), the light activation of photosensitizer dyes for the production of free radicals, effectively inhibits experimental intimal hyperplasia with systemic administration of the photosensitizer. The local application of the photosensitizer directly into a vascular lesion to avoid systemic side effects and tightly control dose administration has theoretical appeal. The aim of this study was to quantify serum and arterial tissue uptake after site-specific photosensitizer delivery and, following PDT, determine its effectiveness at inhibiting intimal hyperplasia. STUDY DESIGN/MATERIALS AND METHODS: The rat common carotid artery was balloon-injured, pressurized at 400 mm Hg for 2 minutes with the photosensitizer dye benzoporphyrin-derivative (BPD), and irradiated with 690 nm laser light at a fluence of 100 J/cm2. Control animals were pressurized with saline only, or received no additional treatment than balloon-injury. RESULTS: Pressurization with BPD resulted in complete penetration of the intima and media and was associated with relatively high tissue, but almost no detectable serum BPD concentrations. No skin photosensitization or other systemic side effects were observed with photosensitizer administration. After 9 days, PDT-treated arteries displayed a significantly lower number of smooth muscle cells in the arterial wall than balloon-injured (P < 0.001) or saline-pressurized arteries (P < 0.0002), and no intimal hyperplasia. At 21 days, IH after PDT was significantly reduced as compared with balloon-injured (P < 0.0004), or saline-pressurized arteries (P < 0.003) with no arterial dilatation. CONCLUSIONS: Site-specific delivery of liposomal BPD followed by PDT represents a safe method to treat arteries, and may be effectively used in vivo to inhibit the development of intimal hyperplasia.

Animals↗
PubMed1998

Psoralen and long wavelength ultraviolet radiation as an adjuvant therapy for prevention of intimal hyperplasia and constrictive remodeling after balloon dilation: a study in the rabbit iliac artery.

BACKGROUND AND OBJECTIVE: Restenosis after balloon angioplasty is the summated effect of intimal hyperplasia and arterial shrinkage, both caused by hyperproliferation. In the present study, the potential of a photochemotherapeutic modality (Psoralen + UVA: PUVA) for the prevention of angioplasty induced proliferation was explored. STUDY DESIGN/MATERIALS AND METHODS: In rabbit iliac arteries, balloon dilation followed by PUVA-therapy (H = 1 J/cm2) was performed (n = 15). Contralateral arteries served as control. After 2 and 28 days of survival, the contribution of intimal hyperplasia and remodeling to lumen loss was determined by means of angiography and histological analysis. RESULTS: After 2 days, large parts of the media had become acellular, while proliferation was occurring predominantly in the adventitia in both groups. After 28 days, late loss, arterial shrinkage, but not intimal hyperplasia were larger in the PUVA group (P < 0.05). CONCLUSION: PUVA-therapy did not prevent intimal hyperplasia following balloon dilation but enhanced luminal narrowing by augmented constrictive remodeling.

Analysis of Variance↗
PubMed1999

The use of histological and immunohistochemical markers to distinguish pleural malignant mesothelioma and in situ mesothelioma from reactive mesothelial hyperplasia and reactive pleural fibrosis.

Distinguishing malignant mesothelioma from reactive mesothelial hyperplasia and reactive fibrosis can be a diagnostic problem in small pleural biopsies, made more difficult by the recent recognition of mesothelioma-in-situ. Antibodies to epithelial membrane antigen (EMA), p53, and bcl-2 have all been advocated for differentiating reactive from neoplastic conditions, but reports are inconsistent. These antibodies have therefore been applied to 31 cases of malignant mesothelioma, 34 cases of reactive pleural disease (20 reactive mesothelial hyperplasia and 14 reactive pleural fibrosis) and four small biopsies that were initially coded as suspicious, from patients who later developed frank mesothelioma. Thirty out of 31 (97 per cent) cases of mesothelioma showed positive nuclear staining for p53, with a higher incidence of positivity in epithelioid than in sarcomatoid elements and 30/31 (97 per cent) showed diffuse linear membrane staining for EMA, again more intense in the epithelioid elements. No mesothelioma was positive for bcl-2. In seven cases that contained both in situ and invasive mesothelioma, the in situ elements showed similar staining patterns to the invasive epithelioid elements. Thirteen out of 20 (65 per cent) cases of reactive mesothelial hyperplasia showed occasional nuclear positivity for p53 and 5/20 (25 per cent) cases showed focal weak membrane staining for EMA. Three out of 14 (21 per cent) cases of reactive pleural fibrosis showed positive nuclear staining for p53 and 6/14 (43 per cent) cases showed focal membrane staining with EMA. No reactive cases stained for bcl-2. All four suspicious cases showed diffuse linear staining with EMA and three showed focal staining for p53. It is concluded that strong diffuse linear staining for EMA is a good marker of malignancy when differentiating epithelioid malignant mesothelioma and mesothelioma-in-situ from reactive mesothelial hyperplasia, although weak focal staining may occur in reactive conditions. Nuclear staining for p53 is also suggestive of epithelioid mesothelioma, but should be regarded as no more than suspicious. The antibodies used in this investigation are less helpful in differentiating sarcomatoid mesothelioma from reactive pleural fibrosis.

Biomarkers, Tumor↗
PubMed1999

Aberrant expression of MUC1 mucin in ductal hyperplasia and ductal carcinoma In situ of the breast.

MUC1 mucin is a high molecular weight transmembrane glycoprotein expressed on the apical cell surface of normal glandular epithelia. In many human adenocarcinomas, this protein is up-regulated and/or underglycosylated, and its expression changes from apical to the entire cell membrane. It is thought that entire cell membrane expression of MUC1 reduces cell-cell and cell-extracellular matrix interactions and therefore may facilitate invasive growth and development of metastases. In this study, we determined immunohistochemically the expression of normal and underglycosylated MUC1 in normal breast tissue (n = 8) and in a spectrum of breast lesions, including usual ductal hyperplasia (n = 23), atypical ductal hyperplasia (n = 7), and ductal carcinoma in situ (DCIS) (n = 22). We used 4 monoclonal antibodies; 115D8 is directed to a glycopeptide, the other 3 to the peptide core of the molecule, of which 139H2 is not affected by the degree of glycosylation of MUC1, whereas SM3 and VU-4-H5 stain only underglycosylated forms. All cases showed apical positivity for 115D8 and 139H2. Entire cell membrane expression of fully (normal) glycosylated MUC1 was mainly found in DCIS lesions. Apical staining of SM3 was found in 38% of normal cases and 60% of the ductal lesions with no difference between the different subgroups. Apical staining of VU-4-H5 was found more often in DCIS (27%) than in normal tissue or ductal hyperplasia (3%). Membrane expression of underglycosylated MUC1 was found only in poorly differentiated DCIS. In conclusion, aberrant expression of MUC1, i.e., on the entire cell membrane and/or underglycosylated forms, can be found in ductal hyperplasia with atypia and especially in DCIS of the breast. This finding implies that these lesions with aberrant expression are at higher risk for developing subsequent invasive breast carcinoma.

Antibodies, Monoclonal↗
PubMed1998

Clinical significance of histiocytes in the detection of endometrial adenocarcinoma and hyperplasia.

The purpose of this case-control study was to determine the clinical significance of histiocytes and normal endometrial cells as cytologic markers of adenocarcinoma or hyperplasia of the endometrium. Cervical-vaginal smears obtained in 102 patients with mean age 59.7 yr with abnormal uterine bleeding and endometrial pathology, and 101 controls with mean age 56.5 yr with postmenopausal bleeding and whose cytologic smear was negative, were evaluated. Histiocytes alone failed to predict either endometrial adenocarcinoma (odds ratio [OR], 1.02; 95% confidence interval [CI], 0.32-3.22) or hyperplasia (OR, 1.10; 95% CI, 0.37-3.30). The odds of endometrial carcinoma in symptomatic, postmenopausal women was three times greater in the presence of histiocytes with phagocytosis of acute inflammatory cells (PIC) (OR, 3.00; 95% CI, 1.16-7.70). Endometrial hyperplasia was more frequently observed when cervical smears contained normal endometrial cells (OR, 4.09; 95% CI, 1.14-14.67). Only histiocytes with PIC and normal endometrial cells carry a three- and fourfold greater likelihood of coexistent endometrial adenocarcinoma and hyperplasia, respectively. Such strong association may require endometrial biopsy or transvaginal ultrasonography to uncover lesional tissue in the endometrial cavity.

Adenocarcinoma↗
PubMed1998

Endometrial brush cytology of advanced postmenopausal endometrium: does endometrial intraepithelial neoplasia exist in the absence of hyperplasia?

Postmenopausal uterine bleeding is an indication to sample the endometrium for diagnostic purposes. The endometrial brush cytologies of 20 advanced postmenopausal women collected at the time of hysterectomy in order to benchmark the expected morphology of postmenopausal endometrial brushings were reviewed. No women had symptoms or gross findings of primary endomyometrial disease. Endometrium was collected at the surgical pathology laboratory using the Tao Brush and CytoRich Fixative System. After formalin fixation of the uterus, the entire endometrium was embedded for routine histology. Sixteen endometrial brushings and matched endometrial sections showed endometrial atrophy, one brushing showed many ciliated epithelial cells, and three brushings showed focal (less than 10%) epithelial-cell atypia. In two atypias, abnormal endometrial epithelial-cell sheets contained enlarged, clear nuclei with nuclear notches and grooves resembling papillary thyroid cancer. One case showed no histological counterpart to this finding. The other case showed thickening of the pericornual fundic endometrium with cystic glands. The third case with epithelial atypia showed abnormal endometrial-cell sheets with nuclei resembling atypical hyperplasia or type I endometrial adenocarcinoma; corresponding endometrial tissue sections showed rare, irregular glands and back-to-back gland clusters with equivalent nuclear features. Atypical epithelium may be found in atrophic uteri in the absence of gross endometrial thickening. This may be a common event related either to de novo intraepithelial dysplasia in a noncycling endometrium or to hyperplasia that has partly regressed with estradiol withdrawal. This study shows that, in addition to endometrial intraepithelial carcinoma (EIC), isolated atypical glands with morphological and immunohistochemical features of atypical hyperplasia or type I endometrial adenocarcinoma may be found in grossly normal advanced postmenopausal endometrium of asymptomatic patients. This atypical epithelium is readily apparent in endometrial brush preparations, but requires serial sectioning of the endometrium to be demonstrated histologically. We have not established the natural history of this lesion, and in the absence of EIC or gross endometrial thickening indicative of atypical hyperplasia, we do not know whether this degree of epithelial atypia should be an indication for hysterectomy.

Adenocarcinoma↗