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PubMed1991

[Nodular regenerative hyperplasia of the liver associated with azathioprine therapy].

Three cases of nodular regenerative hyperplasia of the liver associated with azathioprine therapy are reported. The indication of azathioprine differed in each of the 3 cases including kidney transplantation, graft-versus-host disease following bone marrow transplantation, and suspicion of bowel inflammatory disease, respectively. In all three patients, nodular regenerative hyperplasia was discovered after a prolonged administration of azathioprine (24 to 40 months), with a cumulative dose of 52 to 120 g. Under light microscopy, vascular lesions were associated with nodular regenerative hyperplasia in the 3 cases and consisted of sinusoidal dilatation (2 cases), perisinusoidal fibrosis (2 cases), and peliosis (1 case). In two patients, nodular regenerative hyperplasia was responsible for severe portal hypertension which was treated by portacaval shunt. These findings are strongly suggestive of a role of azathioprine in the occurrence of nodular regenerative hyperplasia. The mechanism of azathioprine-induced nodular regenerative hyperplasia could be related to sinusoidal lesions caused by azathioprine and responsible for liver hypoperfusion, with regenerative hyperplasia in the areas remaining normally perfused. Patients receiving long-term therapy with azathioprine should be followed-up regularly and liver biopsy should be performed when clinical or biochemical liver abnormalities are observed.

Adult↗

PubMed1989

[The effect of danazol and tamoxifen on endometrial hyperplasia].

Endometrial hyperplasia has been considered as a hormone dependent lesion. Besides atypical genital bleeding, the possibility of endometrial carcinoma is also of significance. In this study, we administered 400mg daily of Danazol in 29 cases or 20mg daily of tamoxifen in 20 cases, respectively, for climacteric or postmenopausal women with different types of endometrial hyperplasia, and discussed their effect. Genital bleeding due to hyperplasia disappeared within 10-28 days in the danazol group and within 7-30 days in the tamoxifen group. In the latter group also, 2 climacteric women experienced menopause. The tortuous gland of hyperplasia became smaller and rounder. At the end of the treatment the glandular epithelium was low and showed a very poor secretory phase. The nuclei mitosis both in the glandular and stromal cells disappeared. The regression of hyperplasia was obtained after 1, 3, 6 months of danazol therapy in 37.9%, 72.4%, 93.1% and with tamoxifen therapy in 65%, 80%, 90% respectively, without undesirable side effects. In conclusion, the control of the endometrial hyperplasia with danazol and tamoxifen was suggested, and the results of the use of the suggested method were no further occurrence and/or progression of the disease. Both of the drugs were effective and safe alternative therapy for endometrial hyperplasia to progesterone.

Danazol↗

PubMed1989

Correlation of phorbol ester promotion in the resistant C57BL/6J mouse with sustained hyperplasia but not ornithine decarboxylase or protein kinase C.

The activation of protein kinase C, induction of ornithine decarboxylase (ODC), and hyperplasia have been suggested to be linked, sequential processes resulting from phorbol ester application to mouse skin. However, evidence is presented indicating that these events are not necessarily linked or dependent on one another and that significant differences exist in these responses between phorbol ester promotion sensitive (SSIN) and resistant (C57BL/6J) mice. The epidermis from SSIN mice treated with a single application of 12-O-tetradecanoylphorbol-13-acetate (TPA) displayed a large induction of ODC and a subsequent extensive hyperplasia. A second TPA treatment at 24 or 48 h after the first did not result in ODC induction (refractory state), and protein kinase C was shown to be down-regulated at these times. By 72 h, however, a responsive state had returned even through protein kinase C remained down-regulated. The epidermis of C57BL/6J responds to a single application of TPA with a level of ODC induction similar to that of the SSIN mice. Protein kinase C was down-regulated by approximately 75% after 24 h and was virtually completely down-regulated at 48 and 72 h (95-97%). In contrast to the above findings for the sensitive mice, however, little, if any, hyperplasia was produced. In addition, while a second TPA treatment at 24 h did not result in ODC induction (refractory state), hyperplasia did occur within 24 to 48 h. When the second TPA application was given 48 h after the first, at a time when protein kinase C was down-regulated, an overinduction of ODC occurred, as well as subsequent hyperplasia. Furthermore, a significant number of papillomas resulted when these increased treatment frequencies, i.e., once a day or every other day, were used to promote dimethylbenz(a)anthracene-initiated C57BL/6J mice. It is concluded that, while hyperplasia remains an apparent requirement for tumor promotion, the ODC induction following an initial TPA treatment is insufficient for or not causally related to this hyperplasia. In addition, subsequent ODC induction, at least in the C57BL/6J mouse, is probably not mediated by protein kinase C.

Animals↗

PubMed1984

[Cushing's disease caused by adrenocortical nodular hyperplasia--diagnosis and surgical treatment].

Six cases of Cushing's disease, in which perplex diagnostic problem was encountered, were reported. In the endocrinological examination two cases were not suppressed by a high dose of dexamethasone (8 mg), and the other four cases showed complicated clinical findings due to adrenocortical nodular hyperplasia. Among those four cases with adrenocortical nodular hyperplasia two of them were of functionally autonomic and showed different attitude in responding endocrine assay. When the serum cortisol is not suppressed by a high dose of dexamethasone, differential diagnosis from other causes, such as Cushing's syndrome due to adrenocortical macronodular hyperplasia, becomes quite important for surgical treatment. Usually plasma ACTH in the case of Cushing's disease is slightly increased over the normal range and, on the other hand, it is lower than normal value in the case of Cushing's syndrome due to autonomic adrenocortical nodular hyperplasia because of negative feed back phenomenon. However, in some cases of Cushing's disease plasma ACTH is within normal range or even lower than normal level, and, furthermore, it is not extremely unusual to find a case of adrenocortical macronodular hyperplasia with slightly increased plasma ACTH level over normal range. Those cases offer particularly complex problem in making diagnosis and therapeutic indication. According to our clinical experiences with those six cases, selective venous sampling is found quite useful in differentiating Cushing's disease from other causes and ACTH value in selective venous sampling from inferior petrosal vein is remarkably increased in the cases due to pituitary ACTH secreting adenoma. Cushing's disease with adrenocortical nodular hyperplasia reduces the ACTH value in the sampling to the lower normal range as the adrenocortical nodular hyperplasia progresses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMed1983

The cytodynamics of endometrial hyperplasia and carcinoma. A review.

Current evidence suggests that endometrial hyperplasia represents a spectrum of increasingly atypical proliferation of glands and their lining epithelium that is correlated with increasing persistence, recurrence and progression rates, to carcinoma following curettage and/or progestagen therapy. Hyperplasia can be divided into two phases of pathogenetic development. An initial proliferative phase leading to hypertrophy and a second or remodelling phase, characterized by increasing morphokinetic and biochemical alterations of gland cells. Histologically, the proliferative phase is classified into anovulatory, persistent proliferative endometrium and cystic glandular hyperplasia and the remodelling phase, into adenomatous hyperplasia without and with significant cytologic atypia. The histologic subsets can further be classified as mild, moderate and severe hyperplasia according to their respective clinical behaviour. The data suggest, furthermore, that endometrial C.I.S. represents a transitional state between severe hyperplasia and early, invasive adenocarcinoma. From a pathogenetic standpoint, hyperplasia is induced by longstanding, unopposed estrogenic stimulation and its early phase is made of estradiol-sensitive cells. Paralleling the gradual increase in architectural and cytologic atypia, clones of cells are produced that are relatively insensitive to estradiol and have impaired response to growth-control mechanisms. These estradiol-independent cells are presumably susceptible to malignant transformation.

Adenocarcinoma↗

PubMedDate not supplied

Spontaneous endometrial hyperplasia. A prospective, 5 year follow-up of 246 patients after abrasio only, including 380 patients followed-up for 2 years.

The treatment of patients with endometrial hyperplasia differs widely, ranging from immediate hysterectomy to no treatment or follow-up at all. This is due to the fact that a vital question has not been answered, namely: is endometrial hyperplasia a predecessor to carcinoma or not? In order to investigate whether endometrial hyperplasia is a premalignant state we have followed up 246 patients with abrasio only for 5 years. We found that there was no higher risk of CGH and adenomatous hyperplasia developing into a carcinomatous state than in normal cases. We found it possible to follow up these patients with abrasio only as scheduled. The very few patients developing carcinoma did so already at the first control after 3 months. Among atypical endometrial hyperplasias there was an increased risk of developing endometrial carcinoma. We could divide these patients into two groups: one with very severe atypia so close to carcinoma that an immediate hysterectomy was recommended. Nine out of 12 had already developed carcinoma at the time of the operation. In another group of 21 patients followed with abrasio only, 2 had developed carcinoma at the first control. This means that among 368 patients with endometrial hyperplasia followed-up with abrasio for 2 years, 13 were found to have carcinoma. Twelve patients with very severe atypia were recommended to have an operation and 9 were found to have cancer. Among the other 356 patients, 4 were found to have cancer at the first control (2 with an initial diagnosis of CGH and 2 with atypical hyperplasia).

Adenoma↗

PubMedDate not supplied

[Mastopathy and endometrial hyperplasia--coexistence, relationships].

Samples of endometrium were examined histologically in 161 female patients with endometrial hyperplasia or mastopathy. Moreover, LH, FSH, prolactin, testosterone, and dehydroepiandrosterone sulphate levels were assayed in 51 patients. Mastopathy was found in 36.8% of patients with endometrial hyperplasia. An estimate risk of mastopathy within 13 years following a diagnosis of endometrial hyperplasia is 33%. Endometrial hyperplasia accompanied mastopathy in 24.8% of cases, and an estimated risk of endometrial hyperplasia within 21 years following a diagnosis of mastopathy is 37%. Hormonal status of patients with endometrial hyperplasia-mastopathy is similar to that in patients with endometrial and breast cancer. The authors suggest that both endometrial hyperplasia and mastopathy should be considered markers of the risk of uterine and breast cancer.

Adolescent↗

PubMed1998

[Reversible hypophyseal disfunction and hyperplasia in two cases of primary hypothyroidism].

BACKGROUND: Some patients with primary hypothyroidism (HP) develop massive thyrotrope cell hyperplasia determining pituitary hyperplasia with suprasellar enlargement and pituitary dysfunction. Although TRH secretion undoubtedly has some influence, the intervention of other possible factors determining this hyperplasia and dysfunction has been little assessed. PATIENTS AND METHODS: Two patients with primary hypothyroidism with a serum TSH > 1,000 mU/I were studied. By means of CT and MR a pituitary hyperplasia was ascertained in the two patients. The pituitary functional reserve was investigated by the serum response of TSH and prolactin to the administration of TRH (400 micrograms, i.v.), bromocriptine (BRC, 5 mg, oral route), somatostatine (ST, 50 micrograms/kg/min, i.v. perfusion), and gonadotropin releasing hormone (GnRH, 100 micrograms, i.v.). RESULTS: The TRH induced increment of TSH was 145% and 193%, respectively, compared with basal values. After the administration of BRC, TSH decreased to 57% and 84% of basal values, and PRL to 46% and 43%, respectively. TSH and PRL concentrations did not change after the administration of ST or GnRH. In both cases, hyperplasia and pituitary dysfunction returned to normality after substitutive therapy with levothyroxine. CONCLUSIONS: Basal hyperprolactinemia and TSH and PRL responses to BRC administration suggest that central dopaminergic activity is decreased or abolished in patients with HP and pituitary hyperplasia. The massive thryrotrope cell hyperplasia and hypothyroidism itself determine pituitary dysfunction, which reverts after therapy with levothyroxine, a fact which is scarcely documented in literature.

Adolescent↗

PubMed1998

Relationship between ovarian production of estrone, estradiol, testosterone, and androstenedione and the ovarian degree of stromal hyperplasia in postmenopausal women.

OBJECTIVE: To study the relationship between ovarian production of estrone (E ), estradiol (E2), testosterone (T), and androstenedione (A) and the ovarian degree of stromal hyperplasia in postmenopausal women. DESIGN: In 18 postmenopausal women, the ovarian vein hormone levels of E1, E2, T, and A were compared with the degree of ovarian stromal hyperplasia. The degree of stromal hyperplasia was assessed by histological analysis (group 1: atrophic ovaries, n = 8; group 2: slight stromal hyperplasia, n = 8; group 3: moderate or severe stromal hyperplasia, n = 2). RESULTS: The ovarian levels of E1 and E2 did not correlate with the ovarian degree of stromal hyperplasia. The ovarian levels of A in group 3 were significantly higher than those in groups 1 and 2 (p < 0.02 and p < 0.01, respectively). The ovarian levels of T in group 3 were significantly higher than those in group 1 (p < 0.01) but did not differ significantly from those in group 2. CONCLUSIONS: The amount of stromal hyperplasia in postmenopausal ovaries is correlated with the ovarian vein levels of A and T. Morphological characteristics of the postmenopausal ovary determine the local (pelvic) endocrine status and may play a role in the etiology of hormone-dependent diseases of the internal genitals.

Aged↗

PubMed1989

[Adenomatous hyperplasia--hysterectomy or drug therapy?].

Adenomatous hyperplasia of the endometrium requires either gestagen treatment or hysterectomy, depending on the patient's age and grade of hyperplasia. 51 patients, in whom adenomatous hyperplasia of grade I-III had been ascertained by curettage, were hysterectomized not more than 4 weeks following diagnosis at the Kiel University Clinic of Obstetrics and Gynecology during the years 1985-1989. Only few of the patients received hormone treatment. For all grades of hyperplasia, histological findings from curettage and hysterectomy were identical in only 40% of the cases. In patients older than 40 years, 54% of 13 patients with adenomatous hyperplasia grade III in the curettage specimen had already developed a well differentiated adenocarcinoma, which was detected in the extirpated uterus. In our opinion, when adenomatous hyperplasia of grade II or III is present in a curettage specimen in the age group over 40 years women, hysterectomy should be recommended. For younger women and for adenomatous hyperplasia grade I, we recommend individual therapy.

Adenoma↗

PubMed2006

Sclerosing lobular hyperplasia of breast: cytomorphologic and histomorphologic features: a case report.

BACKGROUND: Mammary sclerosing lobular hyperplasia is an uncommon benign lesion of adolescent and young women. Fine-needle aspiration cytology of mammary sclerosing lobular hyperplasia is said to show characteristic features that include an absence of stromal fragments. CASE PRESENTATION: In this article, we describe a case of sclerosing lobular hyperplasia that occurred in the right breast of a 12-year-old girl. Fine-needle aspiration cytology showed some fibroadenoma-like features including the presence of stromal fragments, while branched tubular fragments were not seen. The diagnosis of sclerosing lobular hyperplasia was made on histologic examination that showed preserved acinar architecture with lobular hyperplasia and sclerosis of intralobular and interlobular stroma. CONCLUSION: Fine-needle aspiration cytology features of mammary sclerosing lobular hyperplasia are not diagnostic and overlap with those of fibroadenoma; however, a distinction between the two benign entities is of no clinical significance. The definitive diagnosis of sclerosing lobular hyperplasia requires histopathologic evaluation.

Journal Article↗

PubMed2002

[Relationship between expressions of telomerase genes and apoptosis related genes in mammary ductal atypical hyperplasia].

BACKGROUND & OBJECTIVE: Recent studies showed that the activating of telomerase and excessive expression of apoptosis suppressor genes were related to the development of many tumors. This study was designed to investigate the expression of telomerase genes (hTR, hTRT) and apoptosis related genes (p53, bcl-2) in mammary atypical ductal hyperplasia for exploring the change of telomerase activity and apoptosis related genes in the process of mammary ductal dysplasia to malignant transformation. METHOD: Expressions of telomerase genes (hTR, hTRT) and apoptosis related genes (p53, bcl-2) were detected by in situ hybridization and expression of the mutant p53 protein was detected by immunohistochemistry were detected in 44 patients with mammary atypical ductal hyperplasia, those expression were compared with those of the 6 benign hyperplasia and 26 breast carcinoma. RESULT: High expressions of telomerase genes (hTR, hTRT mRNA) in severe atypical ductal hyperplasia (60.9%, 52.1%) is of significantly difference from that in mild-medium atypical ductal hyperplasia (22.2%, 11.1%; 33.3%, 25.0%) and breast cancer (88.5%, 80.8%). The upgrading of atypia link with decreased expression of wild p53 mRNA (mild: 55.6%; medium: 41.7%; severe: 26.1%) and increased expression of the mutant p53 protein (mild: 11.1%; medium: 25.0%; severe: 34.8%). As for bcl-2 mRNA, it shows moderate expression, especially in severe atypical ductal hyperplasia. CONCLUSION: Our study revealed significant correlation between expressions of telomerase genes (hTR, hTRT) and the state of malignant transformation in mammary atypical ductal hyperplasia. Decreased expression of wild p53 gene, increased expression of mutant p53 protein, and overexpression of bcl-2 gene were associated with telomerase.

Apoptosis↗

PubMed1996

Clinical observation on efficacy of electro-acupuncture therapy in hyperplasia of mammary glands and its effect on immunological function.

Based on our work on electro-acupuncture therapy of hyperplasia of mammary glands and in order to observe further the relationship between immunological function and E2 in hyperplasia of mammary glands, we determined the change not only in immunological function before and after electro-acupuncture in 44 in-patients with hyperplasia of mammary glands and having the same menstruation date, but also in electro-acupuncture treated rat hyperplasia of mammary glands model. We found that there was decrease of immunological function in hyperplasia of mammary glands and this function could be remarkably enhanced by electro-acupuncture both in hyperplasia of mammary glands patients and in rat hyperplasia of mammary glands model. The mechanism implies it might be that the inhibitory effect on immunological function exerted by high concentration of E2 was lowered by electro-acupuncture, hence the immunological function was reinforced. The results of this study are important in exploration of both the pathogenesis of this disease and the mechanism of electro-acupuncture, and in reducing the incidence of breast carcinoma.

Adult↗

PubMed1997

Cutaneous vascular proliferation. Part II. Hyperplasias and benign neoplasms.

This second part of our review about vascular proliferations summarizes the clinicopathologic features of the cutaneous vascular hyperplasias and benign neoplasms. Hyperplasias comprise a heterogeneous group of vascular proliferations that eventually show a tendency to regression. Angiolymphoid hyperplasia with eosinophilia is included within the group of hyperplasias because of its historical denomination and its reactive nature, probably as a consequence of an arteriovenous shunt, although usually the lesions do not regress. Pyogenic granuloma, bacillary angiomatosis, intravascular papillary endothelial hyperplasia, and pseudo-Kaposi's sarcoma qualify as vascular hyperplasias because they regress when the stimulus that initiated them is removed. Benign neoplasms form a large group of hemangiomas with distinctive clinicopathologic characteristics, although some of them are of recent description and may produce diagnostic difficulties. We classified cutaneous benign vascular neoplasms according to their cell lineage of differentiation, for example, endothelial, glomus cell, and pericytic differentiation. Subsequent categories are established according to the size of the involved vessels (capillaries, venules and arterioles, or veins and arteries) or the nature of the proliferating vessels (blood or lymphatic vessels). Capillary and cavernous hemangiomas have been the terms classically used to name the most common variants of benign vascular neoplasms (i.e., infantile hemangiomas), but they are not the most appropriate denominations for these lesions. First, these names are not contrasting terms. Furthermore, most of the socalled "cavernous" hemangiomas are not hemangiomas (neoplasms) at all, but venous malformations. The most important conceptual issue is that, at any point in time, a particular hemangioma has its own histopathologic pattern throughout the depth of the lesion. For these reasons, we classified hemangiomas into superficial and deep categories. Some of the lesions reviewed have been recently described in the literature, and they may histopathologically mimic lesions of Kaposi's sarcoma; these include targetoid hemosiderotic hemangioma, microvenular hemangioma, tufted hemangioma, glomeruloid hemangioma, kaposiform hemangioendothelioma, spindle-cell hemangioendothelioma, and benign lymphangioendothelioma. In each of these lesions, we update and emphasize those clinical and histopathologic features that are helpful for differential diagnosis with lesions of authentic Kaposi's sarcoma in any of its three stages of development (patch, plaque, or nodule).

Angiolymphoid Hyperplasia with Eosinophilia↗

PubMed1995

Suppressors of oxygen metabolites fail to reduce vein graft intimal hyperplasia.

OBJECTIVE: To evaluate the role of reactive oxygen metabolites in the initiation of intimal hyperplasia of vein grafts inserted into the arterial circulation. SETTING: University pathologic research laboratory. ANIMALS: Sprague-Dawley rats. INTERVENTION: Animals were randomized to receive either the xanthine oxidase inhibitor allopurinol, the iron chelating agent starch-conjugated deferoxamine, or the free-radical scavenger 21-aminosteroid U74389G. Control animals were included for each group. The epigastric vein was inserted into the right common femoral artery. Vein grafts were harvested 30 days postoperatively. The degree of intimal hyperplasia at the two anastomoses as well as at the midgraft was calculated. MAIN OUTCOME MEASURES: The vein grafts were divided into three sections designated proximal anastomosis, midgraft, and distal anastomosis. Intimal and medial areas were determined in an observer-blind fashion and expressed as intimal area-medial area ratios. RESULTS: Pretreatment of the animals with any of these agents resulted in no significant reduction in the degree of intimal hyperplasia in any treated groups compared with the control animals 30 days postoperatively. CONCLUSIONS: Arterial reconstruction often involves interposition of vein segments into the arterial circulation. These veins are subject to ischemia and reperfusion, with the potential for generation of reactive oxygen metabolites and subsequent vein graft injury, resulting in intimal hyperplasia. We hypothesized that perioperative pharmacologic intervention either to scavenge or to reduce the production of reactive oxygen metabolites would attenuate the initial vein graft injury and thus limit the subsequent development of intimal hyperplasia. These data create doubt as to the influence of reactive oxygen metabolites in the initiation of intimal hyperplasia in the vein graft.

Allopurinol↗

PubMed1992

Morphological observations supporting muscle fiber hyperplasia following weight-lifting exercise in cats.

Although exercise-induced muscle fiber hyperplasia has been demonstrated through direct fiber counts following nitric-acid digestion of muscle, morphological studies to determine the mechanism of hyperplasia have not been performed previously. In this study, light and electron microscopy were used to evaluate evidence of muscle fiber splitting or de novo formation of new muscle fibers. Since both fiber hypertrophy and hyperplasia may result in alterations in the muscle nuclear populations, myonuclear number and satellite cell frequency were assessed quantitatively to determine their role in regulating muscle fiber size. Ten adult cats performed weight-lifting exercise, and the right (exercised) and left (control) forelimbs were fixed by vascular perfusion. Spaced serial sections were used to evaluate muscle fiber morphology along the length of fibers, and muscle fiber areas were measured. Myonuclei and satellite cells were counted using electron microscopy. Morphological evidence supporting muscle fiber hyperplasia was observed in exercised muscles. These observations included the presence of small fibers which may signify de novo fiber formation. Myonuclear counts indicate that myonuclear density is not a primary regulator of fiber size. Satellite cell frequency was unchanged following exercise. Autoradiographic studies revealed satellite cell activation by uptake of tritiated thymidine in exercised muscles. Satellite cell activation appears to result from increased activity in exercised muscles. These findings confirm previous studies demonstrating muscle fiber hyperplasia following weight-lifting exercise, and suggest that de novo fiber formation is the major mechanism contributing to muscle fiber hyperplasia in this model.

Animals↗

PubMed2002

Apoptosis and apoptosis-related factors Bcl-2, Bax, tumor necrosis factor-alpha, and NF-kappaB in human endometrial hyperplasia and carcinoma.

BACKGROUND: Apoptosis controls cell homeostasis in the endometrium during normal menstrual cycles, and morphologic studies have suggested its association with the development of endometrial carcinoma. Apoptosis is regulated by several genes, especially those of the Bcl-2 gene family, but their significance in endometrial pathologies is not well understood. METHODS: To study the role and regulation of apoptosis in endometrial hyperplasia and carcinoma, human endometrial specimens were analyzed using in situ 3'-end labeling of apoptotic cells and in situ hybridization and immunohistochemistry of apoptosis-related factors. RESULTS: Apoptosis was scarce in normal proliferating endometrium as well as in simplex, complex, and atypical hyperplasia and was low in Grade I adenocarcinoma. In Grade II adenocarcinoma a significant increase in the rate of apoptosis was observed. Apoptosis decreased in Grade III adenocarcinoma, but it was still higher than in normal or hyperplastic endometrium. Bcl-2 and Bax were expressed in normal and hyperplastic endometrium, and the Bcl-2/Bax ratio was lower in endometrial carcinoma. Tumor necrosis factor-alpha was expressed in normal endometrium and simplex and complex hyperplasia, but it was down-regulated in atypical hyperplasia and endometrial carcinoma. The transcription factor NF-kappaB was present in proliferating endometrium and in endometrial hyperplasia, but its expression was lower in carcinoma. CONCLUSIONS: In endometrial proliferation and hyperplasia a low rate of apoptosis is present. In Grade I carcinoma the rate of apoptosis is decreased, but the rate is subsequently increased in advanced carcinoma. The decrease in the rate of apoptosis in Grade III adenocarcinoma may reflect loss of control of cell homeostasis, decreased differentiation, and increased malignancy.

Adult↗

PubMed2006

Cellular features of endometrial hyperplasia and well differentiated adenocarcinoma using the Endocyte sampler: Diagnostic criteria based on the cytoarchitecture of tissue fragments.

BACKGROUND: Because cellular atypia is often limited in endometrial hyperplasia and well-differentiated endometrial adenocarcinoma (WHO Grade 1 adenocarcinoma), diagnostic criteria for endometrial cytology have not been fully established. New diagnostic criteria based on the composition and architecture of tissue fragments (cytoarchitecture) in the smears were used in the present study. Cytologic features are of less importance because the distinction between endometrial hyperplasia and Grade 1 adenocarcinoma relies more on architectural features than cellular changes. Cell clumps of various size are usually collected abundantly with cytologic material using a disposable scraping device and it was noticed that those cell clumps reflected the histologic architecture. The purpose of the current study was to determine the form of the cytoarchitecture that reflects the histologic structure and to examine the cellular features in endometrial hyperplasia and Grade 1 adenocarcinoma. METHODS: The frequency of each type of cell clump (tube or sheet-shaped pattern, dilated or branched pattern, irregular protrusion, and papillotubular pattern) were obtained from 49 cases of normal proliferative endometrium (NPE) (patient age range, 28-51 yrs; average age, 39.9 yrs), 63 cases of endometrial hyperplasia without atypia (EH) (patient age range, 35-65 yrs; average age, 47.7 yrs), 13 cases of endometrial hyperplasia with atypia (AEH) (patient age range 47-65 yrs; average age, 53.8 yrs), and 49 cases of Grade 1 adenocarcinoma (patient age range, 42-73 yrs; average age, 58.9 yrs). RESULTS: Certain characteristics of the cytoarchitecture were observed. In the NPE, cell clumps with a tube or sheet-shaped pattern were found in 97.5% of cases. In the EH, cell clumps with a dilated or branched pattern were found in 34.9% of cases. In the Grade 1 adenocarcinoma, cell clumps with irregular protrusions were found in 61.8% cases, whereas a papillotubular pattern was present in 29.7% of cases. CONCLUSIONS: The results of the current study revealed that cytoarchitectural criteria appear to be more useful for the cytologic assessment of endometrial lesions, especially for the diagnosis of endometrial hyperplasia and Grade 1 adenocarcinoma.

Adenocarcinoma↗