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At least 1,099 records · Page 61Linked to original sources
PubMed1997

Congenital adrenal hyperplasia in Turkey: a review of 273 patients.

In this study the clinical and epidemiological characteristics of congenital adrenal hyperplasia were evaluated retrospectively from the records of 273 patients managed in our clinic over a 25-year period. 21-Hydroxylase deficiency was present in 234 patients (85.7%), simple virilizing form in 134 (110 F, 24 M), salt-losing form in 85 (71 F, 14 M) and late on-set form in 15 girls. 11 beta-Hydroxylase deficiency was diagnosed relatively frequently (13.5%) among our patients with congenital adrenal hyperplasia; one girl had 17 alpha-hydroxylase deficiency and one boy had 3 beta-hydroxy steroid dehydrogenase deficiency. The median chronological age of diagnosis was 12 months (1 day-16.6 years) in patients with classical congenital adrenal hyperplasia. Chromosomal sex was 46, XX in a total of 221 patients and 46, XY in 52. Ninety-one girls were considered to be male before diagnosis was established and male sex was assigned in 31 of them due to development of male gender identity at diagnosis. Parental consanguinity rate among families of patients was higher than the general population in Turkey (56.4% vs 21%). Our overall figures show that the incidence of congenital adrenal hyperplasia is expected to be high due to a high rate of consanguinity in our populations and the patients remain frequently undiagnosed during the neonatal period. Therefore screening may be beneficial in our population.

Adolescent↗
PubMed1988

Hyperplasia of the mesenterial windows precedes that of the small gut in the streptozotocin-diabetic rat.

Hyperplastic growth of the mesenterial windows abutting the small gut occurs in lactating rats (Bergström and Norrby 1988) and chronically diabetic rats (Norrby et al. 1983). In the present study, early events in the mesenterial windows and the small gut in streptozotocin-diabetic rats were examined. The area of the mesenterial windows had already increased significantly on day 1 and hyperplasia in terms of increased DNA content, as well as an increase in histamine content (a mast-cell marker), was established from day 2 of diabetes. The increase in total mesenterial window content of DNA, histamine and protein was roughly linear and parallel from day 2 to day 19. The small-gut circumference increased transiently on day 1, but the small-gut mucosal volume was unaffected on days 1 and 2. The small-gut wet weight increased significantly from day 5, whereas elongation was not observed until day 19. The difference in time between the appearance of hyperplasia and the growth of the mesenterial windows and their adjoining gut and the rate with which the hyperplasia proceeds in the two tissues indicate that the regulatory mechanisms of early hyperplastic growth in these tissues are not identical. The factor(s) causing mesenterial window growth and hyperplasia is/are as yet unknown.

Animals↗
PubMed2001

Intimal hyperplasia and wall shear in arterial bypass graft distal anastomoses: an in vivo model study.

The observation of intimal hyperplasia at bypass graft anastomoses has suggested a potential interaction between local hemodynamics and vascular wall response. Wall shear has been particularly implicated because of its known effects upon the endothelium of normal vessels and, thus, was examined as to its possible role in the development of intimal hyperplasia in arterial bypass graft distal anastomoses. Tapered (4-7 mm I.D.) e-PTFE synthetic grafts 6 cm long were placed as bilateral carotid artery bypasses in six adult, mongrel dogs weighing between 25 and 30 kg with distal anastomotic graft-to-artery diameter ratios (DR) of either 1.0 or 1.5. Immediately following implantation, simultaneous axial velocity measurements were made in the toe and artery floor regions in the plane of the anastomosis at radial increments of 0.35 mm, 0.70 mm, and 1.05 mm using a specially designed 20 MHz triple crystal ultrasonic wall shear rate transducer Mean, peak, and pulse amplitude wall shear rates (WSRs), their absolute values, the spatial and temporal wall shear stress gradients (WSSG), and the oscillatory shear index (OSI) were computed from these velocity measurements. All grafts were harvested after 12 weeks implantation and measurements of the degree of intimal hyperplasia (IH) were made along the toe region and the artery floor of the host artery in 1 mm increments. While some IH occurred along the toe region (8.35+/-23.1 microm) and was significantly different between DR groups (p<0.003), the greatest amount occurred along the artery floor (81.6+/-106.5 microm, mean +/- S.D.) (p < 0.001) although no significant differences were found between DR groups. Linear regressions were performed on the paired IH and mean, peak, and pulse amplitude WSR data as well as the absolute mean, peak, and pulse amplitude WSR data from all grafts. The mean and absolute mean WSRs showed a modest correlation with IH (r = -0.406 and -0.370, respectively) with further improvements seen (r = -0.482 and -0.445, respectively) when using an exponential relationship. The overall best correlation was seen against an exponential function of the OSI (r = 0.600). Although these correlation coefficients were not high, they were found to be statistically significant as evidenced by the large F-statistic obtained. Finally, it was observed that over 75 percent of the IH occurred at or below a mean WSR value of 100 s(-1) while approximately 92 percent of the IH occurred at or below a mean WSR equal to one-half that of the native artery. Therefore, while not being the only factor involved, wall shear (and in particular, oscillators wall shear) appears to provide a stimulus for the development of anastomotic intimal hyperplasia.

Anastomosis, Surgical↗
PubMed1980

Fetal thyroid hyperplasia, rhesus isoimmunisation, and amniography.

Thyroid hyperplasia was identified at necropsy in 16 of 70 cases of haemolytic disease of the newborn due to rhesus isoimmunisation dying in the years 1959--76. No hyperplasia was found in the thyroids from 140 nonrhesus-affected infants matched for date of birth, bodyweight and length, and gestation, or in cases of haemolytic disease born before 1966. All 16 infants with thyroid hyperplasia had received intrauterine transfusions and the iodine-containing contrast media used for preliminary amniography were the only goitrogenic factors identified. Lipiodol, first used in 1966, was considered to have the greatest effect. The 16 infants with hyperplastic thyroids were less mature and smaller than 22 infants with normal thyroids who had been similarly exposed to contrast media. The high incidence of hyperplasia may be due to immaturity of the adaptive mechanisms which allow most normal individuals to escape the goitrogenic effects of iodine compounds.

Adult↗
PubMed1996

Role of epithelial hyperplasia in regression following photorefractive keratectomy.

AIM: To determine the relation between epithelial hyperplasia and regression of effect after photorefractive keratectomy (PRK). METHODS: Seventy unilaterally treated patients with PRK were examined. All eyes had been treated with the Summit excimer laser 27 (SD 7) months previously with zone diameters of 4.1 to 5.0 mm. The untreated fellow eyes served as controls. Epithelial thickness was measured centrally with a thin slit optical pachometer and manifest subjective refraction was performed. RESULTS: The epithelium was 21% thicker in the treated eye (p < 0.0001). The relation between refractive regression and epithelial hyperplasia was significant (r = 0.41; p < 0.001). CONCLUSIONS: Epithelial hyperplasia after PRK correlated with the myopic shift (including hyperopia reduction) after treatment with the Summit laser. A model is proposed suggesting that both subepithelial and epithelial layers contribute to regression in the Summit treated eyes with 18 microns of epithelial hyperplasia contributing each dioptre of regression.

Adult↗
PubMed1999

Familial occurrence of nodular regenerative hyperplasia of the liver: a report on three families.

BACKGROUND/AIMS: Nodular regenerative hyperplasia of the liver is a histological lesion usually associated with systemic diseases, haematological malignancies, or drugs. Its prognosis depends on portal hypertension, which usually is well tolerated and requires medical management only. PATIENTS: Three unrelated families, in which two sibling adult male patients presented with nodular regenerative hyperplasia of the liver, were studied. METHODS: Complete clinical charts and liver biopsy specimens were available for all patients. In addition, explanted livers were available for examination for the two transplanted patients. RESULTS: There was no evidence of any of the various clinical situations known to be associated with nodular regenerative hyperplasia of the liver. Portal hypertension was severe, requiring surgical treatment in two cases. Renal lesions were present in three patients. In two patients, progressive evolution to liver atrophy and hepatic failure, associated with renal failure, led to combined liver and renal transplantation. CONCLUSIONS: This report describes the existence of familial cases of nodular regenerative hyperplasia of the liver, occurring without underlying or associated systemic disease, characterised by a poor clinical course and often associated with progressive renal failure.

Adult↗
PubMed2004

Methotrexate loaded SAE coated coronary stents reduce neointimal hyperplasia in a porcine coronary model.

OBJECTIVE: To evaluate the effect of stent based methotrexate delivery on neointimal hyperplasia. METHODS: Stainless steel coronary stents and biological polymer coated (SAE) stents were randomly implanted in coronary arteries of pigs with a stent to artery ratio of 1.1:1. The pigs were killed after five days (10 stents) or four weeks (20 stents). Second, stainless steel coronary stents were dip coated in a 10 mg/ml methotrexate-SAE polymer solution, resulting in a total load of 150 microg methotrexate/stent. SAE coated stents and methotrexate loaded stents were randomly implanted in porcine coronary arteries with a stent to artery ratio of 1.2:1 and followed up to four weeks. RESULTS: SAE coated stents and bare stents elicited a similar tissue response at five days. At four weeks, neointimal hyperplasia induced by the coated stents was less pronounced than with the bare stents (1.32 (0.66) v 1.73 (0.93) mm2, p > 0.05). In vitro drug release studies showed that 50% of the methotrexate was released in 24 hours, and all drug was released within four weeks. No impact on vascular smooth muscle cell proliferation or viability was observed in in vitro cell cultures. At four weeks the arteries with methotrexate loaded stents had decreased peristrut inflammation and neointimal hyperplasia (1.22 (0.34) v 2.25 (1.28) mm2, p < 0.01). CONCLUSIONS: SAE coating had an excellent biocompatibility with vascular tissue. Stent based delivery of methotrexate in the SAE coating effectively reduced neointimal hyperplasia in a porcine coronary stent model, potentially due to reduced peristrut inflammation.

Animals↗
PubMed1995

Vimentin and cytokeratin expression in nodular hyperplasia and carcinoma of the prostate.

AIM: To assess the value of vimentin and cytokeratin (CK) intermediate filament proteins (IFPs) in distinguishing between nodular hyperplasia and carcinoma of the prostate and in predicting prognosis in prostatic cancer. METHODS: Fifteen carcinomas and 49 cases of nodular hyperplasia were studied using frozen sections and monoclonal antibodies to CK and vimentin IFPs. RESULTS: There was no statistically significant difference in vimentin expression between nodular hyperplasia and carcinoma. The luminal epithelium in both also reacted with antibodies which detect CK8, 18 and 19. CK 7 expression was found in 57% of cases of nodular hyperplasia and was not identified in any carcinoma. There was a reaction with antibodies to CK1, 2, 3, 4, 10, 11, and 13 in only a minority of cases. There was no statistically significant difference in vimentin and CK reactivity in high and low grade carcinomas. CONCLUSION: Neither vimentin nor CK expression assists in establishing whether a prostatic lesion is benign or malignant or in predicting the biological behaviour of a prostatic carcinoma.

Diagnosis, Differential↗
PubMed1999

Malignant mesothelioma eight years after a diagnosis of atypical mesothelial hyperplasia.

The separation of mesothelial hyperplasia from early malignant mesothelioma remains one of the most difficult problems in histopathology. Inconclusive cases are termed "atypical mesothelial hyperplasia" and treated expectantly. A 49 year old male pipeline engineer was diagnosed as having atypical mesothelial hyperplasia in appendiceal serosa by the US-Canadian Mesothelioma Panel. Eight years later, he developed overtly malignant peritoneal and pleural mesothelioma. In hindsight, histological similarities between the diffuse malignant mesothelioma and the atypical mesothelial proliferation suggested malignancy from the outset. The most important of these features were the degree of mesothelial proliferation, micronodularity, architectural complexity, superficial invasion, uniform mild cytological atypia, and the absence of a clinical cause for a benign mesothelial proliferation. Ancillary investigations including immunohistochemistry were of no benefit in determining whether the atypical mesothelial hyperplasia was benign or malignant. Careful histological examination remains the mainstay of the diagnosis of early mesothelioma.

Appendiceal Neoplasms↗
PubMed2005

Tissue hyperplasia: influence of a paclitaxel-eluting covered stent--preliminary study in a canine urethral model.

PURPOSE: To evaluate a paclitaxel-eluting covered stent in reduction of tissue hyperplasia after stent placement in a canine urethral model. MATERIALS AND METHODS: Procedures were performed in accordance with the National Institutes of Health guidelines for humane handling of animals; approval of the committee of animal research was obtained. Twenty paclitaxel-eluting polyurethane-covered stents (drug stents) and 20 polyurethane-covered stents (control stents) were placed alternately between the proximal and distal urethra in 20 male dogs. The dose of paclitaxel was approximately 1800 mug in each drug stent but absent in each control stent. Dogs were sacrificed either 4 (n = 10) or 8 (n = 10) weeks after stent placement. The percentage diameter of stenosis was assessed with follow-up retrograde urethrography and histologic findings obtained after sacrifice and compared between drug stents and control stents and between the proximal and the distal urethra. RESULTS: Two drug stents partially migrated during retrograde urethrography immediately after stent placement; they were removed and replaced with a second stent during the same procedure. There was a strong tendency toward a lower percentage diameter of stenosis and numeric mean values of the four histologic findings, which indicates less formation of tissue hyperplasia in the proximal urethra than in the distal urethra. In particular, thickness of the papillary projection denoting the entire thickness of hyperplastic reaction was significantly less in drug stents than in control stents in the proximal urethra in the 8-week group (P = .016, Mann-Whitney U test). CONCLUSION: Local delivery of paclitaxel via covered stents has the potential to reduce tissue hyperplasia secondary to stent placement in a canine urethral model. With stent placement, there are distinct differences of tissue hyperplasia between the proximal and distal urethra.

Animals↗
PubMed1985

Focal nodular hyperplasia and hepatic adenoma: comparison of angiography, CT, US, and scintigraphy.

The authors reviewed 23 cases of focal nodular hyperplasia and 13 cases of hepatic adenoma, all of which were confirmed pathologically. All solitary masses that exhibited normal or increased uptake of technetium 99m-sulfur colloid were shown to be hyperplasia; while previous criteria such as a central blood supply on angiograms or a central scar on computed tomography (CT) or ultrasound (US) scans were helpful, they were relatively infrequent. A mass that was slightly hypodense and homogeneous on a CT or US scan and highly vascular with an intense capillary stain on an angiogram was almost always hyperplasia. Acute hemorrhage within a focal hepatic tumor was common in adenoma but did not occur in hyperplasia.

Adenoma↗
PubMed1997

Morphological and biochemical evidence of muscle hyperplasia following weight-lifting exercise in rats.

We used a rat model of weight lifting to examine the serial biochemical and morphological changes following muscle fiber hyperplasia during 14 days of exercise. [3H]thymidine and [14C]leucine labeling were used to determine the serial changes in cellular mitotic activity and the level of amino acid uptake and myosin synthesis. Morphological changes were assessed with light and transmission electron microscopy, whereas proliferation of cells was evaluated immunohistochemically with 5-bromo-2'-deoxyuridine (BrdU). The intensity of the exercise and degree of muscle damage were monitored by serum creatine kinase (CK) activity. Damaged fibers were sparsely distributed, and a significant CK leakage was observed 30-60 min after exercise. Anti-BrdU-positive cells were observed in damaged fibers and at the periphery of undamaged fibers. Changes typical of muscle regeneration were observed; however, the formation of new fibers in the interstitial space was also evident. The mitotic activity also changed and reflected the appearance of anti-BrdU-positive cells and activated satellite cells. Amino acid uptake increased during the first week of exercise, probably reflecting muscle hypertrophy and synthesis of other noncontractile related proteins. The uptake also increased during the second week, probably due to hyperplasia, a finding also supported by electron microscopy. Our results suggest that one bout of weight-lifting exercise in untrained rats induced muscle hyperplasia following regeneration. The process of muscle hyperplasia was activated by muscle fiber damage in our model.

Animals↗
PubMed2006

Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner.

The adrenal gland is an essential stress-responsive organ that is part of both the hypothalamic-pituitary-adrenal axis and the sympatho-adrenomedullary system. Chronic stress exposure commonly increases adrenal weight, but it is not known to what extent this growth is due to cellular hyperplasia or hypertrophy and whether it is subregion specific. Moreover, it is not clear whether increased production of adrenal glucocorticoid after chronic stress is due to increased sensitivity to adrenocorticotropic hormone (ACTH) vs. increased maximal output. The present studies use a 14-day chronic variable stress (CVS) paradigm in adult male rats to assess the effects of chronic stress on adrenal growth and corticosterone steroidogenesis. Exogenous ACTH administration (0-895 ng/100 g body wt) to dexamethasone-blocked rats demonstrated that CVS increased maximal plasma and adrenal corticosterone responses to ACTH without affecting sensitivity. This enhanced function was associated with increased adrenal weight, DNA and RNA content, and RNA/DNA ratio after CVS, suggesting that both cellular hyperplasia and hypertrophy occurred. Unbiased stereological counting of cells labeled for Ki67 (cell division marker) or 4,6-diamidino-2-phenylindole (nuclear marker), combined with zone specific markers, showed that CVS induced hyperplasia in the outer zona fasciculata, hypertrophy in the inner zona fasciculata and medulla, and reduced cell size in the zona glomerulosa. Collectively, these results demonstrate that increased adrenal weight after CVS is due to hyperplasia and hypertrophy that occur in specific adrenal subregions and is associated with increased maximal corticosterone responses to ACTH. These chronic stress-induced changes in adrenal growth and function may have implications for patients with stress-related disorders.

Adrenal Cortex↗
PubMed1997

Cell proliferation contributes to PNEC hyperplasia after acute airway injury.

Pulmonary neuroendocrine cells (PNECs) are airway epithelial cells that are capable of secreting a variety of neuropeptides. PNECs are scattered throughout the bronchial tree either as individual cells or clusters of cells termed neuroepithelial bodies (NEBs). PNECs and their secretory peptides have been considered to play a role in fetal lung development. Although the normal physiological function of PNECs and neuropeptides in normal adult lungs and in repair from lung injury is not known, PNEC hyperplasia has been associated with chronic lung diseases, such as bronchopulmonary dysplasia, and with chronic exposures, such as hypoxia, tobacco smoke, nitrosamines, and ozone. To evaluate changes in PNEC number and distribution after acute airway injury, FVB/n mice were treated with either naphthalene or vehicle. Naphthalene is an aromatic hydrocarbon that, at the dose used in this study, selectively destroys nonciliated bronchial epithelial cells (Clara cells) through cytochrome P-450-mediated metabolic activation into cytotoxic epoxides. PNECs were identified by immunohistochemical analysis of calcitonin gene-related peptide-like immunoreactivity (CGRP-IR). Proliferating cells were marked with [(3)H]thymidine incorporation. Acute naphthalene toxicity results in PNEC hyperplasia that is detectable after 5 days of recovery. PNEC hyperplasia is characterized by increased numbers of NEBs without significant changes in the number of isolated PNECs and by increased [(3)H]thymidine labeling of CGRP-IR cells. These data show that cell proliferation contributes to PNEC hyperplasia after acute airway injury and suggest that PNECs may be capable of more rapidly increasing their number in response to injury than previously recognized.

Acute Disease↗
PubMed1987

Resistance to adipocyte hyperplasia in ground squirrels given high-fat diets.

Mammalian hibernators prepare for the winter by depositing fat in existing fat cells. There is little, if any, production of new fat cells. This is curious because equivalent fat deposition in rats is associated with substantial fat cell production. To determine whether degree of weight gain, diet composition, or some special mechanism militating against adipocyte hyperplasia may underlie the absence of adipocyte hyperplasia in hibernators, male Richardson's ground squirrels, Spermophilus richardsonii, were fed a fattening high-fat diet for either 5 mo or 1 yr. The 5-mo high-fat feeding period caused peak body weights to increase 36% relative to the peak body weights seen in control animals fed ordinary chow. Despite this increase, there was no apparent increment in fat cell number in any of the major fat depots. Animals fed the diet for 1 yr reached body weights similar to those of the 5-mo group but showed significant adipocyte hyperplasia in all fat depots studied. Thus adult ground squirrels are clearly capable of enlarging their pool of mature fat cells, but they fail to do so, at least at certain times, in response to conditions of weight gain that cause considerable adipocyte hyperplasia in rats.

Adipose Tissue↗
PubMed2005

A critical role for enhanced TGF-alpha and EGFR expression in the initiation of parathyroid hyperplasia in experimental kidney disease.

The parathyroid hyperplasia secondary to kidney disease is associated with enhanced expression of the growth promoter transforming growth factor-alpha (TGF-alpha). TGF-alpha stimulates growth through activation of its receptor, the epidermal growth factor receptor (EGFR), normally expressed in the parathyroid glands. Because enhanced coexpression of TGF-alpha and EGFR causes aggressive cellular growth, these studies utilized highly specific inhibitors of EGFR tyrosine kinase, a step mandatory for TGF-alpha-induced EGFR activation, to assess the contribution of growth signals from enhanced expression of TGF-alpha exclusively or both TGF-alpha and EGFR to the rapid parathyroid growth induced by kidney disease and exacerbated by high-phosphorus (P) and low-calcium (Ca) diets in rats. The enhancement in parathyroid gland weight and proliferating activity (proliferating cell nuclear antigen/Ki67) induced by kidney disease and aggravated by either high P or low Ca intake, within the first week after 5/6 nephrectomy, in rats, coincided with simultaneous increases (2- to 3-fold) in TGF-alpha and EGFR content. Conversely, prevention of the increases in both TGF-alpha and EGFR paralleled the efficacy of either P restriction or high-Ca intake in ameliorating uremia-induced parathyroid hyperplasia. More importantly, suppression of TGF-alpha/EGFR signaling, through prophylactic administration of potent and highly selective inhibitors of ligand-induced EGFR activation, completely prevented both high-P- and low-Ca-induced parathyroid hyperplasia as well as TGF-alpha self-upregulation. Thus enhanced parathyroid TGF-alpha/EGFR expression, self-upregulation, and growth signals occur early in kidney disease, are aggravated by low-Ca and high-P intake, and constitute the main pathogenic mechanism of the severity of parathyroid hyperplasia.

Animals↗
PubMed1995

Subtotal but not unilateral nephrectomy induces hyperplasia and protooncogene expression.

It is generally accepted that renal compensatory growth after unilateral nephrectomy (Uni) is due to prominent hypertrophy with no involvement of protooncogenes. Neither the balance between hypertrophy and hyperplasia nor the expression of the early-growth-related genes has been studied after subtotal nephrectomy (Nx). The occurrence of cystic tubular dilatations after Nx may suggest an excessive cell proliferation in this model. We measured DNA, RNA, and protein content, number of nuclei per tubular section, as well as c-fos, c-jun, c-myc, c-H-ras, c-sis, and c-erb-B2 protooncogene expression in kidneys taken at time of surgery and 2, 7, and 14 days after sham operation (control rats), Uni, or Nx. After Uni, hyperplasia was greater than expected (+79% for DNA at day 14) and was associated with moderate hypertrophy (+11% for protein/DNA ratio). After Nx, compensatory growth was due only to hyperplasia (+117% for DNA at day 14), with unchanged protein/DNA ratio (vs. Uni, P < 0.02). The greater hyperplasia after Nx was confirmed by nuclei counting. The protooncogene mRNA expression was constantly absent in control and Uni rats, whereas that of c-fos and c-jun genes was detected in Nx rats at day 14 with a 2- to 12-fold increment. The c-fos and c-jun protein levels were also increased at that time in Nx rats. This suggests the following: 1) the cellular events following Uni and Nx are not the same, and 2) the late protooncogene expression in Nx exclusively could favor a particular type of cell proliferation possibly more related with cystic formation than with actual compensatory growth.

Adaptation, Physiological↗
PubMed2005

Serum concentrations of estrogens, sex hormone binding globulin, and androgens and risk of breast hyperplasia in postmenopausal women.

OBJECTIVE: We sought to determine whether serum concentrations of estrogens, androgens, and sex hormone binding globulin in postmenopausal women were related to the presence of mammary hyperplasia, an established breast cancer risk factor. METHODS: Study participants provided serum before breast biopsy or mastectomy in three hospitals in Grand Rapids, Michigan, between 1977 and 1987. A total of 179 subjects with breast hyperplasia were compared with 152 subjects with nonproliferative breast changes that are not associated with increased breast cancer risk. RESULTS: The odds ratios (OR) associated with the three upper quartiles of estradiol in comparison with the lowest quartile were 2.2 [95% confidence interval (95% CI) 1.1-4.6], 2.5 (95% CI, 1.1-5.3), and 4.1 (95% CI, 2.0-8.5; Ptrend = 0.007). The corresponding ORs for bioavailable estradiol, estrone, and estrone sulfate were of generally similar magnitude (Ptrend = 0.003 for bioavailable estradiol, 0.0004 for estrone, and 0.0009 for estrone sulfate). Relative to women concurrently in the lowest tertile for serum estradiol, estrone, and estrone sulfate, women concurrently in the highest tertile for all three hormones had an OR of 5.8 (95% CI, 2.2-15.2). Serum concentrations of sex hormone binding globulin, testosterone, dehydroepiandrosterone, androstenedione, and androstenediol were not associated with risk of hyperplasia. CONCLUSIONS: Serum concentrations of estrogens, but not of androgens or sex hormone binding globulin, were strongly and significantly associated with risk of breast hyperplasia in postmenopausal women, suggesting that estrogens are important early in the pathologic process towards breast cancer.

Androgens↗