Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPERPLASIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed2005

[Expression of cyclooxygenase-2 and inducible nitric oxide synthase in tongue hyperplasia and tongue squamous cell carcinoma].

BACKGROUND & OBJECTIVE: Recently, it has been recognized that both cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) produce important endogenous factors of human tumor progression. However, the biological significance of the adnormal expression of COX-2 and iNOS in tongue squamous cell carcinoma remains unclear. This study was to investigate the expression of COX-2 and iNOS in tongue squamous cell carcinoma and precancerous lesions, and analyze their interrelation. METHODS: The expression of COX-2 and iNOS in 59 specimens of tongue squamous cell carcinoma (SCC), 45 specimens of hyperplasia (22 cases of mild hyperplasia, 20 cases of moderate hyperplasia, and 3 cases of severe hyperplasia), and 36 specimens of pericancerous normal epithelium was detected by SP immunohistochemistry. RESULTS: The positive rates of COX-2 were 8.3% in normal epithelium, 4.5% in mild hyperplasia, 5.0% in moderate hyperplasia, 0 in severe hyperplasia, and 45.8% in SCC, respectively; those of iNOS were 44.4% in normal epithelium, 72.7% in mild hyperplasia, 80.0% in moderate hyperplasia, 100% in severe hyperplasia, and 98.3% in SCC, respectively. The positive rates of COX-2 and iNOS were significantly higher in SCC than in normal epithelium (P < 0.001); the positive rate of iNOS was also significantly higher in hyperplasia than in normal epithelium (P < 0.001). The overexpression of COX-2 and iNOS was positively correlated with pathologic grade of the lesions (r = 0.418, P < 0.001; r = 0.607, P < 0.001). COX-2 expression was positively correlated with iNOS expression (r = 0.245, P < 0.001). CONCLUSOIN: The overexpression of COX-2 and iNOS is closely related to the carcinogenesis of the tongue.

Adult↗
PubMed1998

Determinants of villous trophoblastic hyperplasia in spontaneous abortions.

The diagnosis of complete and partial mole with its subsequent risk of trophoblastic malignancy relies on histologic criteria that are sometimes seen in nonmolar conceptuses. We performed karyotypic analysis on 1054 spontaneous abortions during a 43-month period. Villous trophoblastic hyperplasia was graded from 0 to 3 in successfully karyotyped cases of complete mole, triploidy, tetraploidy, monosomy X, trisomy, normal 46,XY, and normal 46,XX without contaminating maternal tissues (n = 649). Parental origin of the extra chromosome was analyzed by polymerase chain reaction in 64 trisomic cases. We also evaluated for each case the developmental stage, presence of uniformly hydropic villi, amnion, villous nucleated red blood cells, and fetal tissue. Villous trophoblastic hyperplasia was increased in spontaneous abortions with abnormal karyotype as a group and in the subgroup with trisomy compared with those of a normal karyotype. Hyperplasia and particularly high-grade hyperplasia (Grades 2-3), equivalent in severity to that seen in proliferative partial and complete moles was most frequent in a subgroup of trisomies involving chromosomes 7 (60% hyperplasia, with 30% of high grade), 15 (50% hyperplasia, 15% high grade), 21 (22% hyperplasia, 11% high grade), and 22 (13% hyperplasia, 4% high grade). Frequency of paternal origin for the extra chromosome in these four trisomies was similar in cases with and without hyperplasia There was a nonsignificant increase in female sex chromosomes with hyperplasia in both trisomic and normal conceptuses. Hyperplasia was more common in trisomic abortions of late stage (> 8.5 wk, P = .013), in those that lacked uniformly hydropic villi (P < .001), and in those that lacked fetal tissue (P = .204). This latter phenotype was particularly common with trisomies 15, 21, and 22.

Abortion, Spontaneous↗
PubMed2003

Atypical lobular hyperplasia as a unilateral predictor of breast cancer risk: a retrospective cohort study.

BACKGROUND: Clinical decisions about atypical lobular hyperplasia are based on the belief that later invasive breast-cancer risk is equal in both breasts. We aimed to show laterality and subsequent risk implications of invasive breast cancer in women with atypical lobular hyperplasia. METHODS: We did a retrospective cohort study of 252 women who had undergone 261 benign surgical biopsies that showed atypical lobular hyperplasia from 1950 to 1985, as part of the Nashville Breast Studies. Primary outcomes were development of invasive breast cancer and laterality of cancer compared with side of the biopsied breast. FINDINGS: 50 (20%) of 252 women treated by biopsy only developed invasive breast cancer. Relative risk of breast cancer in women with atypical lobular hyperplasia was 3.1 (95% CI 2.3-4.3, p<0.0001). Of these 50 women, the breast with invasive cancer was the same breast diagnosed with atypical lobular hyperplasia (ipsilateral) in 34 (68%) and the contralateral breast in 12 (24%). The ratio of ipsilateral/ contralateral cancers for atypical lobular hyperplasia without other atypical lesions was 17/5. For six women with atypical lobular hyperplasia plus atypical ductal hyperplasia, the ratio was 1/1. INTERPRETATION: Invasive carcinoma after atypical lobular hyperplasia is about three times more likely to arise in the breast diagnosed with atypical lobular hyperplasia than in the opposite breast without these initial findings. Our findings suggest a model of premalignancy for atypical lobular hyperplasia intermediate between a local precursor and a generalised risk for both breasts. See Commentary page 96

Aged↗
PubMed1988

Relationship of intrahepatic bile duct hyperplasia to cholangiocellular carcinoma.

To investigate the relationship between intrahepatic bile duct hyperplasia and cholangiocellular carcinoma, 27 patients with cholangiocellular carcinoma (including biliary cystadenocarcinoma) and 303 controls were histologically examined. Livers with cholangiocellular carcinoma were closely associated with hyperplasia (100%), atypical hyperplasia (77.8%), and carcinoma in situ (51.9%). Transition from hyperplasia to atypical hyperplasia, and from atypical hyperplasia to carcinoma, was often observed. In the controls, hyperplasia was frequent in those older than 30 years of age, whereas carcinoma was frequent in patients from 50 to 80 years of age. Of the intrahepatic bile ducts examined, the large duct showed the highest incidence of hyperplasia, atypical hyperplasia, and carcinoma in situ. All 27 cases of cholangiocellular carcinoma originated in, or near, the hilus of the liver. These findings suggest that cholangiocellular carcinoma frequently develops from bile duct hyperplasia.

Adenoma, Bile Duct↗
PubMed1997

Increased expression of LH/hCG receptors in endometrial hyperplasia and carcinoma in anovulatory women.

Endometrial hyperplasias and carcinomas are well documented to occur in anovulatory women with or without polycystic ovarian syndrome (PCO), which is characterized by hypersecretion of luteinizing hormone (LH). Although overexpression of LH/human chorionic gonadotropin (hCG) receptors has been demonstrated in endometrial carcinomas, whether LH/hCG receptors are also expressed in the endometrial hyperplasias is not known. In this study, the expression of LH/hCG receptors as well as that of progesterone receptors (PR) was analyzed by immunohistochemistry in 20 cases of normal endometria and 24 cases of endometrial hyperplasia and carcinoma (9 simple hyperplasias, 6 complex hyperplasias, 6 atypical hyperplasias, and 3 well-differentiated carcinomas). Fifteen of the 24 patients were 40 years old or younger, presumably anovulatory by BBT chart. Serum levels of LH, follicular stimulating hormone (FSH), prolactin, estradiol, and testosterone were measured by radioimmunoassay. Expression of LH/hCG receptors was detected in 19 of the 21 hyperplasias with a relatively stronger staining intensity in the glandular cells of complex or atypical hyperplasia as compared with normal endometrial glands or simple hyperplasia. In addition, all of the 3 carcinoma specimens showed stronger expression of LH/hCG receptors compared with normal endometria. The expression of LH/hCG receptors was well correlated with the staining for PR. Hormonal assay revealed 3 women to have the typical endocrinological profile of PCO. These findings suggest that the increased expression of LH/hCG receptors is a feature of endometrial hyperplasia and carcinoma developing in younger anovulatory women including those with PCO.

Adult↗
PubMed1980

The biological significance of atypical hyperplasia of the prostate.

In tissue biopsies and resection material (TUR) of the prostate a high coincidence (49.4%) was found between atypical primary hyperplasia with atypical-dysplastic microglandular, adenomatous and cribriform structures on the one hand and carcinomas on the other. The frequency of atypical hyperplasia in prostatic tissue without carcinoma was 2.8%. Microglandular pattern predominates in atypical hyperplasia combined with differentiated adenocarcinomas. A high coincidence between cribriformly structured glands of atypical primary hyperplasia and solid anaplastic-cribriform carcinomas can be observed. Autoradiographically the labeling index of atypical hyperplasia was three times as high as that of simple hyperplasia. The mean labeling index of atypical hyperplasia, however, was similar to that of poorly differentiated adenocarcinomas and cribriform carcinomas. The similar proliferation pattern of atypical hyperplasia and carcinomas as well as the high coincidence between both indicate that severe atypical primary hyperplasia is a precancerous lesion. Therefore, those patients with primary atypical hyperplasia with distinct cellular and structural atypia but without manifest carcinomas in prostatic biopsy or resection material should be followed up at short intervals.

Adenocarcinoma↗
PubMed2006

Tonsillotomy or tonsillectomy?--a prospective study comparing histological and immunological findings in recurrent tonsillitis and tonsillar hyperplasia.

We evaluated the differences in histological and immunological findings in children with recurrent tonsillitis and tonsillar hyperplasia and assessed the risk for relapsing tonsillar hyperplasia or recurrent tonsillitis after tonsillotomy in a prospective clinical study. Sixty-four children with recurrent tonsillitis underwent traditional (total) blunt dissection tonsillectomy between October 2003 and July 2004. Partial tonsillectomy (tonsillotomy) using CO(2)-laser technique was performed on 49 children with tonsillar hyperplasia and no history of recurrent tonsillitis between August 2003 and March 2005. The present study compares preoperative serum anti-streptolysin-O antibody and immunoglobulin levels (IgG, IgA and IgM), C-reactive protein levels (CRP) and blood leukocyte counts of the two study groups. Additionally the tonsillar tissue removed by tonsillotomy or tonsillectomy was histologically examined in order to determine the grade of hyperplasia, chronic inflammation and fibrosis. Furthermore, the grade of fresh inflammation within the tonsillar crypts of the specimens was analysed. The parents of 40 patients treated by laser tonsillotomy were surveyed in average 16 months. There was no statistically significant difference in preoperative serum anti-streptolysin-O antibody and immunoglobulin levels, C-reactive protein levels and blood leukocyte counts between the two study groups. All specimens showed the histological picture of hyperplasia. There was no statistically significant difference in the grades of hyperplasia between the two study groups. Signs of fresh but mild inflammation within the tonsillar crypts could be found in over 70% of both study groups. Fibrosis only occurred in children with recurrent tonsillitis (9%). In all specimens signs of chronic inflammation could be detected. The histological examinations of specimens from children with repeated throat infections more frequently showed a moderate chronic inflammation of the tonsillar tissue. Two of forty patients treated by tonsillotomy required a subsequent tonsillectomy due to a recurrence of tonsillar hyperplasia but no recurrent tonsillitis occurred. Tonsillotomy with CO(2)-laser technique is an effective surgical procedure with a long-lasting effect in patients with tonsillar hyperplasia. The benefits over conventional tonsillectomy are a lower risk for postoperative haemorrhage, reduced postoperative morbidity and accelerated recovery. Even in children with no history of recurrent tonsillitis signs of chronic inflammation histologically can be found in specimens after tonsillotomy. The occurrence of recurrent tonsillitis after tonsillotomy is rare, however. A low incidence of relapsing tonsillar hyperplasia after tonsillotomy should be expected. Preoperative laboratory investigations show few differences in patients with tonsillar hyperplasia and recurrent tonsillitis. Components of the antimicrobial defense system are also produced by chronically infected tonsils. Therefore tonsillotomy with CO(2)-laser could also be an option in some patients with mild symptoms of recurrent tonsillitis.

Analgesics↗
PubMed2004

Intimal hyperplasia and expression of transforming growth factor-beta1 in saphenous veins and internal mammary arteries before coronary artery surgery.

BACKGROUND: The development of fibromuscular intimal hyperplasia and subsequent graft failure remains an urgent problem in cardiac surgery. Transforming growth factor-beta1 (TGF-beta1) is involved in the pathogenesis of arteriosclerosis through induction of extracellular matrix proteins. We tested the hypothesis that intimal hyperplasia is already present in human saphenous veins and left internal mammary arteries before coronary artery bypass surgery and is associated with an increased expression of TGF-beta1. METHODS: Forty-six segments of saphenous veins and 27 of left internal mammary arteries were collected from 50 patients undergoing coronary artery bypass surgery. Morphometric analysis was performed by microscopic computer analysis. Immunohistochemistry was performed with antibodies directed against TGF-beta1, its latent binding protein (LTBP-1) and its type 2 receptor (RII). RESULTS: The incidence of intimal hyperplasia was significantly higher in saphenous veins (67.4%) than in mammary arteries (29.6%; p < 0.05). Saphenous veins and mammary arteries with intimal hyperplasia expressed more TGF-beta1 (endothelial and intimal layers) and LTBP-1 (intimal and medial layers) when compared with corresponding vessels without hyperplasia (both groups p < 0.05). Endothelial and intimal RII expression was significantly higher in saphenous veins with intimal hyperplasia as compared with saphenous veins without hyperplasia (p < 0.05). Transforming growth factor-beta1 staining in the intima correlated with the presence of an intimal hyperplasia in saphenous veins (rho = 0.317) and mammary arteries (rho = 0.428). CONCLUSIONS: Local TGF-beta1 expression is associated with the presence of intimal hyperplasia in the examined vessels. Preexisting intimal hyperplasia is more prevalent and serious in saphenous veins than in left internal mammary arteries, giving further explanation to the superior long-term results of left internal mammary grafts.

Aged↗
PubMed1992

Histological and clinical features of non-familial primary parathyroid hyperplasia.

Relations between histopathological characteristics and clinical data were retrospectively investigated in patients with sporadic primary hyperparathyroidism due to hyperplasia. The study comprised 100 patients with chief cell hyperplasia and nine with hyperplasia of the water-clear cell type operated on during the period of 1959-1989. The chief cell hyperplasia was associated with a renal stone disorder as the predominant symptom in 41 patients, psychiatric/neuromuscular manifestations in 26 patients, while 23 patients were apparently asymptomatic. The remaining ten patients had miscellaneous symptoms. Patients with renal stones were more frequently of the male sex and generally had lower serum calcium values and less marked increments in total parathyroid glandular weights than patients with other symptoms or those who were overtly asymptomatic. Two main morphological patterns, diffuse and nodular hyperplasia, were encountered in chief cell hyperplasia. Diffuse hyperplasia was usually found in moderately enlarged glands, with a less variable size and morphology. It was also more prevalent among young patients having moderate hypercalcaemia and either recurrent renal stones or neuromuscular/psychiatric symptoms. The glands affected by nodular hyperplasia were asymmetric in size with a variable cellular arrangement and a high proportion of oxyphil cells. Nodular hyperplasia was irrespective of symptoms more frequent in the elderly patients. Water-clear cell hyperplasia was not encountered during the last decade of the study and until then it was an occasional finding in patients with marked hypercalcaemia. In this histological entity the glands were greatly and asymmetrically enlarged.

Adult↗
PubMed2001

Reversible transdifferentiation: interconversion of somatotrophs and lactotrophs in pituitary hyperplasia.

Previous studies conclusively demonstrated transformation of somatotrophs into bihormonal mammosomatotrophs in gestational lactotroph hyperplasia during pregnancy. Similar transdifferentiation of somatotrophs into thyrotrophs through bihormonal intermediate thryrosomatotrophs was documented during thyrotroph hyperplasia in both rodent and human pituitaries in hypothyroidism. The cessation of the stimulation resulted in reversal of the process in both conditions. The conversion of lactotrophs into somatotrophs was suggested but not documented previously in the human gland. The present study was undertaken to investigate cases of somatotroph hyperplasia by transmission electron microscopy, immunoelectron microscopy using double immunogold labeling for growth hormone and prolactin, as well as combined immunocytochemistry and in situ hybridization. Adenohypophysial tissue was removed from a 38-year-old man and a 29-year-old woman with long-standing acromegaly due to ectopic overproduction of growth hormone-releasing hormone (GRH) by bronchial carcinoid tumors. For comparison, two pituitary biopsies were studied: one from a 38-year old woman with idiopathic lactotroph hyperplasia and one from a 14-year-old boy with secondary lactotroph hyperplasia due to a suprasellar craniopharyngioma. In the patients with somatotroph hyperplasia, the prevailing cell type was the hyperplastic somatotroph joined by mammosomatotroph deriving from lactotrophs, whereas monohormonal lactotrophs were rare. The predominance of mammosomatotrophs and active lactotrophs was documented in the patient with idiopathic lactotroph hyperplasia, whereas the case of the patient with secondary lactotroph hyperplasia was characterized by monohormonal lactotrophs and somatotrophs, but mammosomatotrophs were rare. That finding in the pituitary of the boy suggests that participation of mammosomatotrophs in lactotroph hyperplasia is not unconditional Our findings conclusively demonstrate conversion of lactotrophs into mammosomatotrophs during somatotroph hyperplasia, providing further evidence for the potential of reversible transdifferentiation between somatotrophs and lactotrophs in response to functional demand.

Acromegaly↗
PubMed1999

Autogenous artery grafts in hypertensive (SHR) rats do not have increased smooth muscle cell hyperplasia in the graft neointima, compared with grafts in normotensive rats.

Vein-to-artery graft surgery is used widely to by-pass arterial stenoses, but such grafts can fail over a prolonged period as a result of excessive neointimal hyperplasia causing thrombosis and graft occlusion. It has been suggested that neointimal hyperplasia, in vein grafts, is a result of the vessel wall adapting to the higher intraluminal pressure of the arterial circulation, compared with the venous circulation. Autologous artery grafts have been used to bypass arterial stenoses. Initially it was assumed that donor artery segments would not develop neointimal hyperplasia as they are already adapted to the arterial circulation but this is not so. In this study we postulated that surgical or postsurgical trauma was the cause of neointimal hyperplasia in autologous artery-to-artery grafts. In addition, as artery grafts are pre-adapted to the arterial circulation, autologous artery-to-artery grafts in hypertensive rats should develop similar levels of neointimal hyperplasia as seen in normotensive rats. Artery-to-artery grafts were placed in a series of 20 spontaneously hypertensive rats (SHR). In a separate series of sham grafting experiments the effects of anoxia and clamp trauma were assessed in SHR and WKy normotensive control rats. Finally, clamping, anoxia and anastomosis trauma were assessed in a similar series of rats. In the artery-to-artery graft series there was no difference in neointimal thickness between the SHR and that previously reported for normotensive rats. Minimal neointimal hyperplasia was demonstrated in the sham grafted series of rats and only slightly more in the single anastomosis series. It was only in the full grafting procedure that considerable neointimal hyperplasia developed. These data demonstrate that neointimal hyperplasia in artery-to-artery grafts is not exacerbated by the hypertension. In addition, trauma appears to be the initiator of neointimal hyperplasia and the extent of trauma correlates with the degree of neointimal hyperplasia.

Animals↗
PubMed1986

[Medroxyprogesterone acetate in adenomatous hyperplasia of the uterine endometrium. Clinical and morphologic studies on the duration and dosage of gestagen therapy].

To learn how effective medroxyprogesterone-acetate is for treating adenomatous hyperplasia of the endometrium, we prescribed a controlled therapy in a randomly selected group of 60 women in whom we had diagnosed adenomatous hyperplasia histologically. The endometria of these women were histologically evaluated before therapy was started and again after three months of therapy. The greatest rate of regression was shown by the 40-59 year old women with adenomatous hyperplasia of grade I (15 of 23 patients). The regression occurred with 50 mg/day within three to eight months. For the women with adenomatous hyperplasia of grade II severity, 100 mg per day were required to obtain a similarly good result. For those with adenomatous hyperplasia of grade III severity, 150 mg per day were needed. The over 60-year old patients required higher doses of MPA over longer time periods for equally good therapeutic results. The patients younger than 40 years of age received lower doses (10-40 mg daily) to maintain or regain their fertility. Their adenomatous hyperplasias regressed with 20-40 mg of MPA daily, whereas with a daily dose of 10 mg their adenomatous hyperplasias recurred. The number of cases here, however, is too small for a statistical analysis. Summarising our results we recommend treating patients with adenomatous hyperplasias of grade I and II severity with MPA until it can be proved histologically that the hyperplasia has regressed. The daily dose needed for grade I hyperplasias is between 50 and 100 mg per day, whereas for grade II between 100 and 150 mg are needed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Regression of endometrial hyperplasia after treatment with the gonadotrophin-releasing hormone analogue triptorelin: a prospective study.

Endometrial hyperplasia is thought to be caused by the prolonged, unopposed oestrogenic stimulation of the endometrium. The regression of hyperplastic back to normal endometrium is the main purpose of any conservative treatment in order to prevent development of adenocarcinoma. The aim of this study was to evaluate the regression of hyperplastic to normal endometrium in patients with various forms of endometrial hyperplasia after treatment with the gonadotrophin-releasing hormone analogue (GnRHa) triptorelin for 6 months. Fifty-six patients with endometrial hyperplasia were enrolled in this trial; 39 patients (group I) presented simple hyperplasia, 14 (group II) complex hyperplasia and three (group III) atypical complex hyperplasia. All patients were treated with triptorelin for 6 months. Bleeding control during treatment was excellent. A post-treatment curettage for estimation of endometrial histology was performed on 54 out of 56 patients 100.1 +/- 44.7 days after the last triptorelin dose, following the restoration of pituitary function. Regression of hyperplastic to normal endometrium was observed in 32 (86.5%) out of 37 patients in group I and in 12 (85.7%) out of 14 in group II. Persistence of simple hyperplasia was found in five (14.5%) out of 37 patients in group I. Persistence of complex hyperplasia was found in 1 (7.1%) out of 14 patients and progression to atypical complex hyperplasia in another one (7.1%) woman in group II. In some of these cases, the presence of risk factors such as obesity, diabetes mellitus and ovulatory disturbances may contribute to the disease persistence despite therapy. On the other hand, in group III, none of the three patients had normal post-treatment endometrial histology. It seems, therefore, that in cases of endometrial hyperplasia without atypia, the administration of the GnRHa triptorelin is associated with high regression rates to normal endometrium. Conversely, the presence of atypia seems to be a poor prognostic factor. Treatment tolerance and bleeding control during therapy is excellent.

Adult↗
PubMed1981

Primary hyperparathyroidism: four- to eight-year postoperative follow-up demonstrating persistent functional insignificance of microscopic parathyroid hyperplasia and decreased autonomy of parathyroid hormone release.

Thirty-nine patients with primary hyperparathyroidism were studied four to eight years after their initial operation. In six patients, both the pathologist and surgeon agreed on the diagnosis of solitary adenoma; in 16 patients, the surgeon diagnosed solitary adenoma and the pathologist parathyroid hyperplasia (microscopic hyperplasia). In 16 patients, primary chief cell hyperplasia was agreed upon by the pathologist and surgeon. In the 16 patients with microscopic hyperplasia, there have been no long-term recurrences of hypercalcemia, but, in two patients, plasma parathyroid hormone levels are high. Parathyroid hormone--total calcium regression curves demonstrate significant preoperative correlation in solitary adenoma, p less than 0.01, and primary chief cell hyperplasia, p less than 0.05. After operation, significant correlations were not found between parathyroid hormone and total calcium. T-testing slope differences of pre- and postoperative parathyroid hormone--total calcium regression curves demonstrates a significant (p less than 0.01) shift to the right of the microscopic hyperplasia patients after operation, moving them to a broader range of total calcium per picogram parathyroid hormone. We conclude that 1) in primary hyperparathyroidism, positive regulation of total calcium by autonomously released parathyroid hormone exists in patients with solitary adenoma and chief cell hyperplasia; 2) autonomously functioning parathyroid tissue has been removed by operation for solitary adenoma with coexistent microscopic parathyroid hyperplasia. In this four- to eight-year follow-up period, it is clear that microscopic parathyroid hyperplasia is not associated with recurrent hypercalcemia. Two functionally distinct forms of parathyroid suppression are suggested; positively regulated microscopic hyperplasia and negatively regulated pathologically suppressed glands.

Adenoma↗
PubMed1983

Downstream anastomotic hyperplasia. A mechanism of failure in Dacron arterial grafts.

The precise location and progression of anastomotic hyperplasia and its possible relationship to flow disturbances was investigated in femoro-femoral Dacron grafts in 28 dogs. In 13 grafts, the outflow from the end-to-side downstream anastomosis was bidirectional (BDO), and in 15 it was unidirectional (UDO) (distally). Grafts were electively removed at intervals of two to 196 days or at the time of thrombosis. Each anastomosis and adjacent artery was perfusion-fixed and sectioned sagittally. The mean sagittal section was projected onto a digitized pad, and the total area of hyperplasia internal to the arterial internal elastic lamina and within the adjacent graft was integrated by computer. The location of the hyperplasia was compared with previously established sites of flow separation and stagnation. The observation was made that hyperplasia is significantly greater at the downstream, as compared with the upstream, anastomosis in both groups (BDO = p less than 0.001 and UDO = p less than 0.001) (analysis of variance for independent groups). Furthermore, this downstream hyperplasia was progressive with time (BDO p less than 0.01) (UDO p less than 0.01); Spearman Rank Correlation. There was no significant increase in the extent of downstream hyperplasia where flow separation was known to be greater (BDO). Five grafts failed (three BDO, two UDO), as a result of complete occlusion of the downstream anastomosis by fibrous hyperplasia. Transmission electron microscopy showed the hyperplasia to consist of collagen-producing smooth muscle cells. Anastomotic hyperplasia is significantly greater at the downstream anastomosis, is progressive with time, and is the primary cause of failure of Dacron arterial grafts in this model. Quantitative analysis of downstream anastomotic hyperplasia may be a valuable measure of the biocompatibility of Dacron grafts.

Animals↗
PubMedDate not supplied

Risk of progression in complex and atypical endometrial hyperplasia: clinicopathologic analysis in cases with and without progestogen treatment.

In most cases, the endometrioid adenocarcinoma of the endometrium is preceded by hyperplasia with different risk of progression into carcinoma. The original histologic slides from 560 consecutive cases with complex and atypical hyperplasia were re-examined to assess the interobserver-correlation. The hyperplasias were analyzed separately for their likelihood of progression to carcinoma in patients with and without progestogen hormonal therapy. In all cases, a fractional re-curreting was performed to establish the state of the disease. The leading symptom was vaginal bleeding in 65.5% of the cases in the postmenopausal period. Eighty-six percent of the patients presented with obesity (BMI > 30 kg/m(2)), 23% had had an exogeneous use of estrogens. Twenty-two cases were reclassified as simple hyperplasia and excluded from further analysis. The interobserver-correlation was 91% for complex, 92% for atypical hyperplasia, and 89% for endometrioid carcinoma, representing an overall correlation of 90%. Two percent of the cases with complex hyperplasia (8/390) progressed into carcinoma and 10.5% into atypical hyperplasia. Fifty-two percent of the atypical hyperplasias (58/112) progressed into carcinomas. In the case of progestogen treatment (n = 208; P < 0.0001) 61.5% showed remission confirmed by re-curetting, compared with 20.3% of the cases without hormonal treatment (n = 182; P < 0.0001). Endometrial hyperplasia without atypia is likely to respond to hormonal treatment. Especially in postmenopausal situation, atypical hyperplasia should be treated with total hysterectomy.

Adenocarcinoma↗
PubMedDate not supplied

Endothelial cell recoverage and intimal hyperplasia after endothelium removal with or without smooth muscle cell necrosis in the rabbit carotid artery.

Interventional-injury-induced intimal hyperplasia involves smooth muscle cell proliferation that may be limited by endothelial cell coverage. We hypothesized that endothelial cell coverage modulates intimal hyperplasia. Therefore rabbit carotid arteries were injured with (2-french Fogarty balloon) and without media necrosis (Prolene loop). After termination at 3, 7, 21, or 42 days, endothelial cell coverage was assessed with an antibody to CD31 and cross-sectional intimal hyperplasia area was measured morphometrically. At 21 and 42 days, maximal intimal hyperplasia thickness was measured at a site where endothelium was present and where endothelium was absent. Proliferating cells were identified with an antibody to the nuclear antigen Ki-67. From 3 to 42 days, endothelial cell coverage progressed from the caudal and cranial ends of the lesion towards the center and was slower in balloon- versus loop-injured arteries (p<0.001, Anova). At 21 and 42 days, intimal hyperplasia area was larger after balloon than after loop injury (21 days: 0.20 +/- 0.01 vs. 0.09 +/- 0.04 mm2, p<0.05; 42 days: 0.26 +/- 0.03 vs. 0.08 +/- 0.02 mm2, p<0.01). At 21 days, the intimal hyperplasia was maximal at the center of the lesion and diminished towards the edges in both balloon- and loop-injured arteries. Surprisingly, at 21 and 42 days, maximal intimal hyperplasia thickness was larger in CD31-positive compared to CD31-negative regions (104 +/- 8 vs. 72 +/- 12 micron, p<0.01, paired t test). At 3 and 7 days, more medial proliferation was found after balloon than after loop injury (3 days: 46.2 +/- 8.8 vs. 0.2 +/- 0.1%, p<0.01; 7 days: 18.5 +/- 6.4 vs. 1.0 +/- 0.4%, p<0.01). In the same period, abundant adventitial proliferation was found after balloon injury that was entirely absent after loop injury. We conclude, first, that endothelial cell recoverage proceeded at a lower rate over damaged than over normal media. This retarded endothelial cell recoverage may contribute to enhanced intimal hyperplasia. Second, at a late stage of vascular healing, when intimal hyperplasia had already been formed, reendothelialization seems to have been enhanced over areas with thick intimal hyperplasia. Third, dilation-induced medial damage was accompanied with massive adventitial cell proliferation.

Animals↗
PubMed1998

Fibroadenomatoid hyperplasia: a cause of suspicious microcalcification on mammographic screening.

OBJECTIVE: Fibroadenomatoid hyperplasia is a well-described but rare benign breast lesion with composite features of fibroadenoma and fibrocystic change. Because fibroadenomatoid hyperplasia has not to our knowledge been reported as a cause of suspicious microcalcifications and because several pathology reports of biopsies of mammographically detected microcalcification at our institution included fibroadenomatoid hyperplasia, we undertook this study to describe the features of mammographically detected microcalcification seen in patients with fibroadenomatoid hyperplasia. MATERIALS AND METHODS: Two breast pathologists reviewed the records of 54 mammographically detected lesions that were compatible with a diagnosis of fibroadenomatoid hyperplasia and that provoked subsequent core biopsy or surgical excision of microcalcifications. Eleven cases (20%) fulfilled the diagnostic criteria for fibroadenomatoid hyperplasia. The sites of all calcifications found at histology were documented, and the mammographic features were described. RESULTS: Eleven cases of fibroadenomatoid hyperplasia were identified in nine core biopsy samples and two surgical specimens. Calcification was present in all 11 pathologic specimens. Calcification was stromal in nine, subepithelial in two, and epithelial in none. The mammographic features of fibroadenomatoid hyperplasia in all 11 cases were granular microcalcifications that varied in shape, size, and density and had no associated mass; of these calcifications, 91% were in a localized, irregularly shaped cluster. Rod-shaped calcifications were also seen in 64% of cases. CONCLUSION: Fibroadenomatoid hyperplasia is a cause of suspicious, granular, clustered microcalcifications on screening mammography. Fibroadenomatoid hyperplasia can be confirmed using 14-gauge core biopsy in most cases.

Aged↗