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 145 records · Page 8Linked to original sources
PubMed1999

Pituitary hyperplasia.

Comprehensive article summarizing more than 25 years of experience with pituitary hyperplasia in surgical material. Morphologic forms of hyperplasia--diffuse and nodular--are defined and, for comparison, the normal morphology, frequency and intraglandular distribution of cell types are briefly reviewed. All cell types can give rise to hyperplasia, although their frequency, extent and clinical importance widely vary. Somatotroph hyperplasia is rare; it is limited to cases of GHRH overproduction by extrapituitary endocrine neoplasms and sporadic examples of gigantism. Prolactin cells display the highest propensity for non-neoplastic proliferation. Physiologic hyperplasia occurs in pregnancy and lactation. Pathological hyperplasia is mostly secondary to other, neoplastic or non-neoplastic, space occupying processes. Idiopathic lactotroph hyperplasia is very rare. The much-disputed corticotroph hyperplasia is infrequent cause of pituitary dependent Cushing's disease. Despite difficulties of diagnosis in fragmented biopsies, several well-documented cases prove the existence of corticotroph hyperplasia which is nearly always nodular. Thyrotroph hyperplasia, secondary to hypothyroidism, a treatable condition, is not expected to occur in surgical material, yet several cases have been identified. Operated lesions are massive nodular leading to significant pituitary enlargement thereby mimicking TSH- or PRL-producing adenoma. Hyperprolactinemia is a frequent concomitant of severe thyrotroph hyperplasia. Gonadotroph hyperplasia and proliferation of pars intermedia derived POMC cells are not likely to occur in surgical material and have no clinical significance. Adenoma formation may rarely be associated with any type of pituitary hyperplasia.

Adrenocorticotropic Hormone↗
PubMed2002

Clonal analysis and mutations in the PTEN and the K-ras genes in endometrial hyperplasia.

The patterns of X chromosome inactivation and mutations of PTEN and K-ras were evaluated in cases of endometrial hyperplasia to determine the presence of potentially premalignant neoplastic versus polyclonal benign cell populations. Endometrial glandular epithelial cells were collected by laser capture microdissection, and genomic DNAs were extracted. Following treatment with the methylation sensitive restriction endonuclease Hha I, polymerase chain reaction amplification was performed targeting a highly polymorphic short tandem repeat of the human androgen receptor gene (HUMARA). PTEN and K-ras gene mutations were evaluated by analysis of single-strand conformation polymorphism. Two pathologists performed histologic diagnosis of the lesions independently. Monoclonal composition was demonstrated in 13 of 15 (87%) endometrial hyperplasias with atypia and 17 of 31 (55%) complex hyperplasias without atypia. Cytological atypia is significantly associated with the clonal status of the endometrial hyperplasia (13/15 vs 17/31, P = 0.049). In contrast, all 14 normal endometrial tissue samples were polyclonal. PTEN gene mutations were detected in 4 of 13 (30%) monoclonal endometrial hyperplasias with atypia and 2 of 17 (12%) monoclonal endometrial hyperplasias without atypia but were not detected in polyclonal endometrial hyperplasias, with or without atypia. K-ras gene mutations were present in 3 of 13 (23%) monoclonal endometrial hyperplasias with atypia but not in 2 cases of polyclonal endometrial hyperplasia with atypia or in 26 cases of endometrial hyperplasia without atypia. K-ras mutation is thus significantly more frequently found in endometrial hyperplasias with atypia than those without atypia (3/15 vs 0/31, P = 0.030). This study indicates that most cases of endometrial hyperplasia with atypia and a high proportion of cases of endometrial hyperplasias without atypia originate from a single progenitor cell, possibly as a result of genetic alterations, rather than as a result of benign reactive processes.

Cell Transformation, Neoplastic↗
PubMed2004

Molecular analysis of endometrial hyperplasia in HNPCC-suspicious patients may predict progression to endometrial carcinoma.

Women predisposed to hereditary nonpolyposis colorectal cancer are at high risk of developing endometrial carcinoma at a young age. Hereditary nonpolyposis colorectal cancer-associated endometrial carcinomas are of the endometrioid type, usually arise from complex atypical hyperplasia, and often show microsatellite instability. To identify occult hereditary nonpolyposis colorectal cancer individuals among endometrial carcinoma patients, we examined complex atypical hyperplasias and endometrial carcinomas of 60 women < or =50 years of age (mean age: 35.7 years) using microsatellite instability, immunohistochemistry, and DNA sequence analysis. Three patient groups were recruited: group 1, patients with complex atypical hyperplasia exclusively (n = 27); group 2, patients with complex atypical hyperplasia and synchronous or metachronous endometrial carcinoma (n = 15); group 3, patients with endometrial carcinoma only (n = 18). Overall, 13 of 33 endometrial carcinomas (39%) displayed high-level microsatellite instability. None of the complex atypical hyperplasias in group 1 had high-level microsatellite instability or loss of hMLH1/hMSH2 protein expression. In group 2 patients, 33% of complex atypical hyperplasias and 53% of endometrial carcinomas had high-level microsatellite instability. Loss of hMSH2 protein expression was found in six endometrial carcinoma patients, five of them with verified hMSH2 germline mutations, including four patients with high-level microsatellite instability in complex atypical hyperplasia. Among group 3 patients, 28% of endometrial carcinomas displayed high-level microsatellite instability; three of those five endometrial carcinomas were from patients with multiple extrauterine hereditary nonpolyposis colorectal cancer-associated tumors. We conclude that young women (< or =50 years of age) with concurrent complex atypical hyperplasia and multiple hereditary nonpolyposis colorectal cancer-associated carcinomas are at risk of developing high-level microsatellite instability endometrial carcinoma. Combined microsatellite instability and immunohistochemistry analysis allows the identification of a high proportion of hereditary nonpolyposis colorectal cancer patients among young women with endometrial carcinoma and complex atypical hyperplasia. All complex atypical hyperplasias with high-level microsatellite instability progressed to endometrial carcinoma. Only one third of the complex atypical hyperplasias with microsatellite stability progressed to high-level microsatellite instability endometrial carcinoma, while seven complex atypical hyperplasias progressed to microsatellite stability endometrial carcinoma. Microsatellite analysis of complex atypical hyperplasia in young patients may therefore be a useful prognostic marker for predicting possible progression to high-level microsatellite instability endometrial carcinomas.

Adenocarcinoma↗
PubMed2002

[Expression of telomerase genes in mamary atypical ductal hyperplasia].

OBJECTIVE: To investigate the relationship of telomerase genes and the malignant transformation of atypical mammary ductal hyperplasia. METHODS: Telomerase genes hTR and hTRT in 50 cases of mammary hyperplasia (the cases included 6 benign hyperplasia, 9 mild atypical hyperplasia, 12 medium atypical hyperplasia, 23 severe atypical hyperplasia) and 26 cases of breast carcinoma were detected by in situ hybridization. RESULTS: The expression of hTR and hTRT mRNA were weak or negative in benign hyperplasia (1/6, 0), weaker in mild-moderate atypical hyperplasia (2/9, 1/9, 4/12, and 3/12), strong in severe atypical hyperplasia (14/23, 60.9% and 12/23, 52.1%), while very strong expression (23/26, 88.5% and 21/25, 80.8%) in carcinoma of the breast. The difference between mild-moderate atypical hyperplasia, invasive ductal carcinoma and severe atypical hyperplasia was significant (P < 0.05) and the difference between severe atypital hyperplasia and intraductal carcinoma was not significant (P > 0.05). CONCLUSIONS: Telmerase genes (hTR, hTRT) expression is closely related to the malignant transformation of atypical hyperplasia. The reactivated telomerase may play a crucial role in the development of breast cancer.

Breast Neoplasms↗
PubMed2002

Expression of telomerase genes in cancer development in atypical hyperplasia of the mammary duct.

OBJECTIVE: To investigate telomerase gene expression in precancerous mammary lesion, such as atypical ductal hyperplasia and breast cancer and to study the relationship between expression and malignant transformation. METHODS: Expression of human telomerase genes (hTR) and human reverse transcriptase gene (hTRT) in 76 cases of mammary tissue was evaluated using in situ hybridization and included 50 cases of mammary hyperplasia, 6 of which were benign hyperplasia, 9 were mild atypical hyperplasia, 12 were moderate atypical hyperplasia, 23 were severe atypical hyperplasia and 26 were mammary cancer. RESULTS: The expressions of hTR and hTRT mRNA were much weaker or negative in benign hyperplasia (16.6%, 0), weak to mild moderate in atypical hyperplasia (22.2%, 11.1%, 33.3%, 25.0%), strong in severe atypical hyperplasia (60.9%, 52.1%), and significantly strong in mammary cancer (88.5%, 80.8%). The difference between mild-moderate atypical hyperplasia, invasive ductal carcinoma and severe atypical hyperplasia was significant (P < 0.05) and the difference between severe atypical hyperplasia and intraductal carcinoma was not significant (P > 0.05). CONCLUSION: Telomerase genes (hTR and hTRT) expressions are related to the transformation of atypical hyperplasia. Activated telomerase may play a role in mammary cancer development.

Breast↗
PubMed2002

Expert system support using a Bayesian belief network for the classification of endometrial hyperplasia.

Accurate morphological classification of endometrial hyperplasia is crucial as treatments vary widely between the different categories of hyperplasia and are dependent, in part, on the histological diagnosis. However, previous studies have shown considerable inter-observer variation in the classification of endometrial hyperplasias. The aim of this study was to develop a decision support system (DSS) for the classification of endometrial hyperplasias. The system used a Bayesian belief network to distinguish proliferative endometrium, simple hyperplasia, complex hyperplasia, atypical hyperplasia and grade 1 endometrioid adenocarcinoma. These diagnostic outcomes were held in the decision node. Four morphological features were selected as diagnostic clues used routinely in the discrimination of endometrial hyperplasias. These represented the evidence nodes and were linked to the decision node by conditional probability matrices. The system was designed with a computer user interface (CytoInform) where reference images for a given clue were displayed to assist the pathologist in entering evidence into the network. Reproducibility of diagnostic classification was tested on 50 cases chosen by a gynaecological pathologist. These comprised ten cases each of proliferative endometrium, simple hyperplasia, complex hyperplasia, atypical hyperplasia and grade 1 endometrioid adenocarcinoma. The DSS was tested by two consultant pathologists, two junior pathologists and two medical students. Intra- and inter-observer agreement was calculated following conventional histological examination of the slides on two occasions by the consultants and junior pathologists without the use of the DSS. All six participants then assessed the slides using the expert system on two occasions, enabling inter- and intra-observer agreement to be calculated. Using unaided conventional diagnosis, weighted kappa values for intra-observer agreement ranged from 0.645 to 0.901. Using the DSS, the results for the four pathologists ranged from 0.650 to 0.845. Both consultant pathologists had slightly worse weighted kappa values using the DSS, while both junior pathologists achieved slightly better values using the system. The grading of morphological features and the cumulative probability curve provided a quantitative record of the decision route for each case. This allowed a more precise comparison of individuals and identified why discordant diagnoses were made. Taking the original diagnoses of the consultant gynaecological pathologist as the 'gold standard', there was excellent or moderate to good inter-observer agreement between the 'gold standard' and the results obtained by the four pathologists using the expert system, with weighted kappa values of 0.586-0.872. The two medical students using the expert system achieved weighted kappa values of 0.771 (excellent) and 0.560 (moderate to good) compared to the 'gold standard'. This study illustrates the potential of expert systems in the classification of endometrial hyperplasias.

Bayes Theorem↗
PubMed2001

Increasing levels of dietary homocystine with carotid endarterectomy produced proportionate increases in plasma homocysteine and intimal hyperplasia.

PURPOSE: The role that homocysteine may play in post-carotid endarterectomy (CEA) restenosis due to intimal hyperplasia is not well understood. This study was designed to investigate the effects of different levels of dietary homocystine on: (1) plasma homocysteine; (2) post-CEA intimal hyperplasia; and (3) levels of the methyl donor S-adenosylmethionine (SAM) and its counterpart S-adenosylhomocysteine (SAH) in the homocysteine pathway. METHODS: Male rats were fed specialized diets for 2 weeks pre- and post-CEA. Groups included control (0 homocystine added, n=9), 1.5 (1.5 g/kg homocystine added, n=10), 3.0 (3.0 g/kg homocystine added, n=9), and 4.5 (4.5 g/kg homocystine added, n=11). The rats underwent a surgical carotid endarterectomy. Endpoints included; plasma homocysteine, intimal hyperplasia, replicative index using with alpha-SM actin and BrdU, hepatic SAM levels, SAH levels, and the hepatic activities of methylenetetrahydrofolate reductase (MTHFR) and cystathionine beta-synthase (CBS). RESULTS: Increasing dietary homocystine produced a proportionate increase in plasma homocysteine and an increase in intimal hyperplasia. Regression analysis of plasma homocysteine levels and intimal hyperplasia showed a significant correlation (r=0.71,P=0.003). Plasma homocysteine levels above 15 microM were associated with significant increases in intimal hyperplasia above 6.5% (P=0.04). Elevation of plasma homocysteine levels to moderate levels (5-25 microM) resulted in significant post-CEA intimal hyperplasia. Cellular analysis of the area of intimal hyperplasia in all diet groups showed comparable amounts of cells positive for alpha-SM actin. However, with increasing levels of dietary homocystine and plasma homocysteine there was an increase in replicative index (P<0.001) as determined by BrdU staining. Increasing dietary homocystine increased plasma homocysteine and was followed by increases in the replicative index thus producing increased intimal hyperplasia and lumenal stenosis. In hepatic measurements the 1.5 and 3.0 g/kg homocystine diets caused: increased liver activity of MTHFR (P=0.03) and decreased hepatic levels of SAM, SAH and SAM/SAH ratios compared to controls. Homocystine treatment did not cause significant alterations in CBS levels (P=0.992). These studies also showed no correlation of the MTHFR and CBS enzymes with plasma homocysteine levels or intimal hyperplasia. However, hepatic levels of SAM showed significant negative correlations with plasma homocysteine (r=-0.58; P=0.006) and with BrdU percentages of cellular proliferation (r=-0.69; P=0.06). CONCLUSION: The degree of post-CEA intimal hyperplasia in a rat model is directly related to the plasma level of homocysteine. The hyperplastic effects of homocysteine may be mediated in part by a physiological insufficiency of methyl donors as shown by decreases in SAM. Thus, increasing levels of plasma homocysteine enhanced and accelerated the smooth muscle cell response after CEA which led to increased intimal hyperplasia and lumenal stenosis.

Animals↗
PubMed1999

Lymphonodular hyperplasia as a sign of food allergy in children.

BACKGROUND: Lymphonodular hyperplasia of the gastrointestinal tract in children is a rare endoscopic finding of uncertain clinical significance. In this study, 12 children with lymphonodular hyperplasia of the duodenum from a series of 63 children were studied for recurrent abdominal pain. Four additional children with lymphonodular hyperplasia of the colon are described. All the patients with lymphonodular hyperplasia were also evaluated for food allergy. METHODS: A gastroduodenoscopy was performed in the patients with recurrent abdominal pain and in the four in whom lymphonodular hyperplasia of the colon had been diagnosed by colonoscopy. An open oral elimination and challenge test to diagnose food allergies was scheduled for all subjects with lymphonodular hyperplasia or any suspicion of food allergy. The study design also included skin prick tests with common allergens and determination of serum immunoglobulin A and immunoglobulin E concentrations. RESULTS: Lymphonodular hyperplasia of the duodenal bulb was the main finding in 12 (19%) of the 63 children. The condition was found to be associated with food allergy in nine subjects (75%), which was significantly more often than among the remaining 51, 12 (24%) of whom had food allergy by the same criteria. In an oral challenge, food allergy first manifested gastrointestinal symptoms in the subjects of both groups and, in all except one, on days 2 through 5 after the foodstuffs were administered in minimal doses. In a histologic study, the duodenal specimens revealed significantly more eosinophilic cells in the children with food allergy and lymphonodular hyperplasia than in the children with food allergy but no lymphonodular hyperplasia. The major symptoms in the four patients with lymphonodular hyperplasia of the colon had been anemia and blood in stool in two and abdominal pains with mucous loose stools in the remaining two. Colonoscopic examination showed one to have diffuse and the other three patchy lymphonodular hyperplasia of the colon. In an oral challenge, three reacted to milk and two to cereals. CONCLUSIONS: Preliminary observations showed that lymphonodular hyperplasia of the duodenum or the colon is related to the gastrointestinal type of food allergy to basic foodstuffs. Further research is needed to define this finding as a separate entity.

Abdominal Pain↗
PubMed1991

[Correlation of atypical hyperplasia and latent carcinoma of the prostate].

Atypical hyperplasia and latent carcinoma of the prostate from 310 prostates of all age obtained at autopsy were studied. Atypical hyperplasia was graded into 3 groups based on the frequency of nucleoli and cell arrangement. The results were as follows: the origin of both atypical hyperplasia and latent carcinoma was considered to be in the peripheral zone. The frequency of atypical hyperplasia increased with age. Atypical hyperplasia was found in younger generation than latent carcinoma. Grade of atypical hyperplasia increased with age. Atypical hyperplasia was often coincident with latent carcinoma: 74% of atypical hyperplasia were associated with latent carcinoma. Atypical hyperplasia was significantly associated with multicentric latent carcinoma. All these findings supported the assumption that atypical hyperplasia was a premalignant lesion. Clinically, in a case in which atypical hyperplasia is found in biopsy, intense follow-up will be necessary. In particular, in cases of grade 3 atypical hyperplasia, further study for detection of probable coexistent carcinoma is recommended.

Adult↗
PubMed1987

[Benign hyperplasia of the prostate--an autopsy analysis].

The great number of the forms of hyperplasia of the prostate gland which became known recently requires a systematic histological investigation concerning their incidence and age distribution and as preliminary performance for the clarification of the problems of the frequency of prostate gland carcinoma. For this purpose we investigated by means of the serial section technique on macrosections the prostate glands of 450 males from the 40th year of age. Taking as a basis a new subdivision of the hyperplasias worked out in accordance with Dhom (1985) we found the following average frequencies: simple hyperplasia 37% (macroscopically) and 69% (histologically), fibromatous hyperplasia 29%, adenomatous hyperplasia 21%, parvicellular hyperplasia 27.3%, cribriformous hyperplasia 7%, lobular postatrophic hyperplasia 40%, panacinous postatrophic hyperplasia 58%, focal (intra)acinous postatrophic hyperplasia 26.4%. An age-depending increase of frequency is common to all forms of hyperplasia. The importance of the knowledge of the various forms of hyperplasia develops from the necessity of their differential-diagnostic delimitation from the carcinoma and their probably precancerous potency.

Adult↗
PubMed1994

Failure of down-regulation of estrogen receptors and progesterone receptors after medroxyprogesterone acetate administration for endometrial hyperplasias.

BACKGROUND: To determine the biologic difference between normal endometrium and endometrial hyperplasias, the authors assessed the expression of estrogen receptors (ER) and progesterone receptors (PR) in the subjects before and after oral administration of medroxyprogesterone acetate (MPA) (Hysron-H, Kyowa Hakko Kogyo Co., Ltd., Tokyo, Japan). METHODS: The authors studied the expression of ER and PR in pathologic conditions of the endometrium such as cystic, adenomatous, and atypical hyperplasias before and after MPA treatment, 600 mg daily, for 8-14 weeks, and compared this expression with that of normal endometrium. RESULTS: Stromal and epithelial components of the normal endometrium in the proliferative phase were positive for ER and PR. In the secretory phase and after MPA treatment, the epithelial component showed either negative or faint staining for ER and PR, but the stromal component showed positive staining for PR and negative or faint staining for ER. All hyperplasias exhibited ER and PR in the stromal and epithelial components, although the intensity of the staining was variable in atypical hyperplasias. After MPA treatment, in the epithelial component of cystic and adenomatous hyperplasias, down-regulation of PR was prominent, but many cells continued to express ER. The epithelial component usually was surrounded by PR-positive decidual cells. In atypical hyperplasia, many cells continued to express ER and PR in the epithelial component surrounded by both ER and PR positive stromal cells after MPA treatment. CONCLUSIONS: Among the pathologic conditions of the endometrium, cystic and adenomatous hyperplasias have mechanisms of down-regulation of PR but not ER in the glandular component after MPA treatment, whereas in atypical hyperplasia, down-regulation of ER and PR does not occur in the epithelial component. Compared with normal endometrium, the majority of endometrial hyperplasias have an impairment of down-regulation of ER in the epithelial component by MPA treatment, and atypical hyperplasia has an impairment of down-regulation of ER and PR. Endometrial hyperplasias seem to have an abnormality of down-regulatory mechanisms of sex steroid receptors in the epithelial component when treated with exogenous progesterone.

Adult↗
PubMed2002

Mutation of beta-catenin gene in endometrial cancer but not in associated hyperplasia.

Endometrial hyperplasia is a recognized effect of excessive or unopposed estrogen stimulation and is considered to be a precancerous condition of endometrial adenocarcinoma. We have previously shown that the subcellular localization of beta-catenin in the human endometrium is changed according to cell proliferation, suggesting a role of intercellular transduction in cell-growth control in human endometrium, not only in the physiological condition but also in the carcinogenic endometrium. In the present study, to clarify at which stage of endometrial carcinogenesis molecular alteration of the beta-catenin gene occurs, we analyzed the subcellular localization of beta-catenin by immunohistochemistry, and we analyzed exon 3 of the beta-catenin gene, in 25 patients - with endometrial hyperplasia and 20 patients with endometrial cancers associated with endometrial hyperplasia, digesting DNA from the cancer and hyperplasia parts, separately. Fourteen of the 25 (56.0%) endometrial hyperplasia samples, 12 (60.0%) endometrial cancers, and 11 (55.0%) associated hyperplasias of the 20 endometrial cancers associated with hyperplasia showed nuclear localization of beta-catenin. Mutation in exon 3 of the beta-catenin gene was found in 2 of the 20 endometrial cancer samples; however, it was not found in the 25 endometrial hyperplasias or the 20 associated hyperplasias. The results suggest that molecular alteration of the beta-catenin gene occurs in atypical hyperplasia or cancer, rather than in simple or complex hyperplasia without atypia, during endometrial carcinogenesis.

Base Sequence↗
PubMed1993

Frequency and consequences of intimal hyperplasia in specimens retrieved by directional atherectomy of native primary coronary artery stenoses and subsequent restenoses.

Although intimal hyperplasia is a frequent occurrence after arterial interventional procedures, the overall frequency and significance of intimal hyperplasia in primary coronary lesions has not been previously addressed. The incidence of intimal hyperplasia was therefore examined using standard light microscopy in specimens obtained from native coronary arteries of patients undergoing directional coronary atherectomy. The associated clinical history, angiographic results and clinical outcomes were also tabulated. Intimal hyperplasia was identified in 51 of 55 patients (93%) treated with directional coronary atherectomy for restenosis after a prior intervention. These restenosis lesions had less acute gain in lumen diameter after directional coronary atherectomy, a smaller late lumen diameter, more severe late stenosis (p < 0.04), and tended to have more restenosis defined as late stenosis > or = 50% (restenosis rate 40% for prior restenosis vs 26% for primary lesions). Surprisingly, however, intimal hyperplasia was also identified in 45 of 102 (44%) primary stenoses. Primary lesions (n = 45) with intimal hyperplasia were more likely to occur in younger patients and in the left anterior descending artery than were either primary lesions without intimal hyperplasia (n = 57) or prior restenosis lesions. There were otherwise no differences in the baseline characteristics, angiographic findings or clinical outcome of primary lesions with or without intimal hyperplasia (restenosis rate 28 and 24%, respectively). The event-free survival (72% at 12 months) was similar in all 3 groups. Thus, even though intimal hyperplasia is an almost universal finding in restenosis lesions, intimal hyperplasia is not specific for restenosis since histologically identical hyperplasia may be found in nearly half of primary coronary artery stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Prevention of benign prostatic hyperplasia disease.

PURPOSE: We reviewed the evidence that benign prostatic hyperplasia is a progressive condition and men at risk for benign prostatic hyperplasia disease can be identified, treated and protected to a meaningful extent regardless of symptom status. MATERIALS AND METHODS: The MEDLINE database was searched in 4 areas of interest relating to benign prostatic hyperplasia, including 1) progression of clinical manifestations with age, especially in regard to baseline symptom status, 2) the incidence of complications due to disease progression, 3) the use of predictive factors that may help identify men at risk for disease progression and 4) the prevention of benign prostatic hyperplasia disease with medical therapy. RESULTS: Tissue changes in the prostate (benign prostatic hyperplasia) are inevitable consequences of aging. However, benign prostatic hyperplasia disease, which we define as a life altering urinary condition requiring medical intervention, is predictable and preventable. Benign prostatic hyperplasia disease progression is associated with increasing prostate volume, decreasing urinary flow, symptomatic deterioration often to the point of major life-style interference and serious complications, eg acute urinary retention and the need for surgery. The risk of benign prostatic hyperplasia disease progression was found to be directly related to prostate volume and its surrogate marker, serum prostate specific antigen, after prostate cancer is excluded. Other factors, eg baseline symptoms and the flow rate, were found to be less relevant compared with prostate specific antigen greater than 1.5 ng/ml for predicting benign prostatic hyperplasia disease morbidity. CONCLUSIONS: Men at risk for benign prostatic hyperplasia disease can be identified using prostate specific antigen greater than 1.5 ng/ml as a surrogate marker of prostate volume. In men at risk with prostate specific antigen greater than 1.5 ng/ml 5alpha-reductase inhibitors have potential value for benign prostatic hyperplasia disease prevention regardless of symptom status.

Adult↗
PubMed1991

Magnetic resonance imaging of the adrenal gland in women with late-onset adrenal hyperplasia.

To determine the presence of structural abnormalities of the adrenal in late-onset adrenal hyperplasia, four consecutive patients were studied by MRI before beginning glucocorticoid replacement therapy. Three women were diagnosed as 21-hydroxylase deficient late-onset adrenal hyperplasia by a 17-OHP level greater than 1,000 ng/dL 30 minutes after acute adrenal stimulation, and one patient was diagnosed as 11-hydroxylase deficient late-onset adrenal hyperplasia when her 11-deoxycortisol level was threefold the upper 95th percentile of normal. Two patients with 21-hydroxylase deficient late-onset adrenal hyperplasia had normal adrenal glands on MRI. Another 21-hydroxylase deficient late-onset adrenal hyperplasia patient was noted to have a 2.5 x 3.3-cm left adrenal nodule, which had been documented some 4 years earlier on CT scan and had not changed in size during that interval. This patient was 40 years of age when the diagnosis of late-onset adrenal hyperplasia was established. The patient with 11-hydroxylase deficient late-onset adrenal hyperplasia demonstrated a diffuse enlargement of the left adrenal gland consistent with hyperplasia, with no focal lesions. In conclusion, although patients with late-onset adrenal hyperplasia may often demonstrate nodular or diffuse adrenocortical hyperplasia on MRI, not all patients with endocrinologically evident disease demonstrate such abnormalities, consistent with a lesser degree of ACTH stimulation compared with women with classical congenital adrenal hyperplasia.

Adrenal Glands↗
PubMed2002

Prognostic significance of atypical papillary urothelial hyperplasia.

Typical papillary hyperplasia, a recently recognized precursor lesion to low-grade papillary urothelial neoplasms, consists of undulating folds of cytologically benign urothelium. Well-developed, branching fibrovascular cores of a papillary neoplasm are not evident. We have noted lesions with the architectural pattern of papillary hyperplasia; however, the overlying urothelium demonstrated varying degrees of cytologic atypia. We identified 15 cases of atypical papillary hyperplasia (13 males, 2 females, age 55 to 92) with overlying urothelium showing cytologic atypia. Of these cases, 8 (53%) were received in consultation. Of the 15 cases, 8 exhibited overlying flat carcinoma in situ (CIS), 4 had overlying dysplasia, and 3 were transitional between papillary hyperplasia with atypia and the earliest lesions of papillary neoplasia. Of these cases, 5 patients had multiple specimens with atypical papillary hyperplasia (range, 2 to 8) over time. Concurrent to the diagnosis of atypical papillary hyperplasia, there were 25 different urothelial lesions: CIS (n = 11), papilloma (n = 1), papillary neoplasm of low malignant potential with CIS (n = 1), high-grade papillary urothelial carcinoma (n = 10; 3 with CIS), small-cell carcinoma (n = 1), and infiltrating urothelial carcinoma (n = 1). Of 11 patients with known prior history, 2 had 12 prior urothelial neoplasms (9 low-grade papillary neoplasms, 2 papillary urothelial neoplasms of low malignant potential, and 1 high-grade papillary cancer). Of 10 patients with atypical papillary hyperplasia and a minimum of 1 year of follow-up, 9 had 19 recurrences: CIS (n = 4), papilloma (n = 1), papillary neoplasm of low malignant potential (n = 1), infiltrating urothelial carcinoma (n = 3; 1 with CIS), and high-grade papillary urothelial carcinoma (n = 10; 5 with invasion and 2 with CIS). Whether the papillary hyperplasia had overlying CIS or dysplasia did not affect the correlation with urothelial neoplasms. Immunohistochemical analysis of p53 and Ki-67 expression in 8 cases demonstrated overexpression of p53 (n = 2; 1 with overlying dysplasia and 1 with overlying CIS), and Ki-67 (n = 5; 2 with overlying dysplasia and 3 with overlying CIS). Taken together, these results suggest that atypical papillary hyperplasia is most frequently associated with CIS and high-grade papillary cancer. In some cases, CIS or dysplasia may evolve into atypical papillary hyperplasia, with further progression to high-grade papillary cancer. This process may be analogous to papillary hyperplasia without cytologic atypia progressing to low-grade papillary urothelial neoplasms.

Aged↗
PubMed2006

Evaluation of histological techniques for quantifying haemodialysis arteriovenous (AV) graft hyperplasia.

BACKGROUND: Assessing treatment efficacies for preventing haemodialysis arteriovenous (AV) graft stenosis requires a reproducible method for quantifying intimal hyperplasia. We identified sources of variability in three histological methods for assessing hyperplasia in a porcine AV graft model. METHODS: Carotid-jugular synthetic grafts were placed in pigs. After explantation at 3-6 weeks, the tissue was stained with haematoxylin and eosin (H&E), Masson's trichrome or elastic tissue Van Gieson (EVG) stains and examined histologically. Hyperplasia at the anastomosis of 14 grafts was quantified using three different methods, each by four blinded observers. These methods were visual scoring, ratio of intima-to-media surface area (I/M ratio), and ratio of intra-graft hyperplasia to graft surface area (H/G ratio) at the graft-vessel interface. RESULTS: The EVG stain proved superior in delineation of the elastic lamina yet quantification of the intimal and medial layers was still often difficult. This is illustrated by the greater inter-observer median coefficient of variances (CV) found using the I/M ratio method (intimal area CV=13.7%; medial area CV=32.7%; I/M ratio CV=44.0%) than with the H/G method (intra-graft hyperplasia area CV=7.3%, graft area CV=5.3%; H/G ratio CV=6.9%) or by visual scoring (CV=26.8%). The H/G ratios correlated positively with visual scores (r=0.941; P=0.0007; n=14) and the I/M ratio (r=0.719; P=0.0095; n=14). While hyperplasia was seen in both native vessel and graft lumen, in only one of the 14 anastomoses was the degree of hyperplasia greater in the native vessel than in the graft lumen, suggesting that the degree of hyperplasia occurring within the graft lumen predicted the total hyperplasia around the anastomosis. CONCLUSIONS: The H/G method for assessing hyperplasia is preferred in a porcine model of AV graft because it is quantitative, less variable and does not require the delineation of the elastic lamina, although it infrequently underestimates the total hyperplasia that occurs.

Animals↗
PubMed2002

Atypical focal nodular hyperplasia of the liver: imaging features of nonspecific and liver-specific MR contrast agents.

OBJECTIVE: The objective of our study was to describe the functional and differential uptake features of atypical focal nodular hyperplasia using different MR contrast agents and to evaluate their potential role in the diagnosis and characterization of focal nodular hyperplasia. MATERIALS AND METHODS: Contrast-enhanced MR images of 45 patients with 85 focal nodular hyperplasia lesions were retrospectively reviewed. In these patients, sonographic findings were nonspecific (n = 37), or CT features were inconclusive (n = 8). Non-liver specific gadolinium chelates were used in 18 patients (48 lesions) suspected of having either focal nodular hyperplasia or hemangioma. The following liver-specific agents were used in patients with suspected focal nodular hyperplasia or metastases: mangafodipir trisodium, 30 patients (55 lesions); ferumoxides, six patients (16 lesions); and SHU 555 A, six patients (six lesions). Individual lesions were quantified by signal intensity and assessed qualitatively by homogeneity, contrast enhancement, and presence of a central scar. RESULTS: At unenhanced MR imaging, the triad of homogeneity, isointensity, and central scar was found in 22% of the focal nodular hyperplasia lesions. On mangafodipir trisodium-enhanced T1-weighted images, all focal nodular hyperplasia lesions showed contrast uptake: in 64% of the lesions, uptake was equal to parenchyma; 25%, greater than the parenchyma; and 11%, less than the parenchyma. On iron oxide-enhanced T2-weighted images, all focal nodular hyperplasia lesions showed uptake of the contrast agent, but contrast uptake in the lesions was less than in the surrounding parenchyma. Dynamic gadolinium chelate-enhanced MR imaging showed early and vigorous enhancement of focal nodular hyperplasia lesions with rapid washout in 88%. Atypical imaging features of the lesions included hyperintensity on T1-weighted images, necrosis and hemorrhage, and inhomogeneous or only minimal contrast uptake. CONCLUSION: For patients in whom the diagnosis of focal nodular hyperplasia cannot be established on unenhanced or gadolinium-enhanced MR imaging, homogeneous uptake of liver-specific contrast agent with better delineation of central scar may help to make a confident diagnosis of focal nodular hyperplasia.

Adult↗