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PubMedDate not supplied

The effects of clopidogrel and calcium dobesilate on intimal hyperplasia following vascular injury.

BACKGROUND: Neo-intimal hyperplasia is one of the most common causes of failure of arterial patency following cardiovascular interventions. It has been proposed that clopidogrel and calcium dobesilate may play an important role in the amelioration of intimal hyperplasia. The aim of this study is to examine the effect of these agents on intimal hyperplasia occurring after experimental balloon catheter injury. MATERIAL AND METHODS: Twenty-four male New Zealand rabbits were divided into three groups. Endothelial injury was caused by introducing a 2.5 x 20 mm balloon angioplasty-catheter into the left iliac artery. After the procedure, clopidogrel (25 mg/kg/day/orally) or calcium dobesilate (100 mg/kg/day/orally) were given for 2 weeks. Eight rabbits were given a placebo and served as controls. The contralateral non-injured iliac arteries of the control group were considered as normal iliac artery samples. Iliac artery specimens were examined planimetrically and the intima/media ratio was obtained for each vessel. RESULTS: In the control group, the intima/media ratio was still significantly higher (p < 0.05) than the contralateral normal artery 14 days after the balloon catheter injury. In the clopidogrel and calcium dobesilate groups, this ratio had significantly decreased when compared with the control group (p < 0.05). No significant difference was found when the clopidogrel and calcium dobesilate groups were compared. CONCLUSION: The anti-agregant agent clopidogrel, and the venous endothelial regulator calcium dobesilate, ameliorate intimal hyperplasia after experimentally induced vascular injury in rabbit iliac arteries.

Angioplasty, Balloon↗
PubMed2006

Magnetic resonance imaging comparison of intra-articular cavernous synovial hemangioma and cystic synovial hyperplasia of the knee.

PURPOSE: To identify and compare magnetic resonance imaging (MRI) characteristics, with and without intravenous contrast medium, of cavernous synovial hemangiomas and cystic synovial hyperplasia. MATERIAL AND METHODS: Four cases of cavernous synovial hemangioma and five of cystic synovial hyperplasia of the knee were studied retrospectively. The patients (5 F and 4 M; 15-25 years of age) all had long-standing knee pain. At clinical examination we observed elastic swelling and pain without significant joint effusion. The patients underwent conventional radiography and MRI without and following intravenous contrast medium before arthroscopic biopsy. RESULTS: The radiographs were interpreted as negative in all patients. MRI examination without contrast medium revealed a similar multicystic appearance for both lesions. Following intravenous contrast agent administration, cavernous synovial hemangiomas demonstrated avid, rather homogenous enhancement, whereas cystic synovial hyperplasia demonstrated less intense, peripheral enhancement only. Arthroscopy with histological examination of the lesions confirmed the MRI diagnosis in every case. CONCLUSION: In our experience, cavernous synovial hemangioma and cystic synovial hyperplasia have a similar appearance on unenhanced MRI, but can be reliably differentiated on the basis of enhancement characteristics following intravenous contrast administration.

Adolescent↗
PubMed2003

Local methylprednisolone delivery using a BiodivYsio phosphorylcholine-coated drug-delivery stent reduces inflammation and neointimal hyperplasia in a porcine coronary stent model.

Phosphorylcholine (PC)-coated stents have shown excellent blood and tissue biocompatibility in porcine coronary arteries. The purpose of this study was to determine the efficacy of local methylprednisolone (MP) delivery using PC-coated stents to inhibit inflammatory response and in-stent neointimal hyperplasia in an overstretched porcine coronary model. BiodivYsio (Biocompatibles, Farnham, Surrey, UK) PC-coated drug delivery (DD) stents and DD stents loaded with a high dose of MP (269 microg) were implanted in the coronary arteries of 20 pigs with a balloon/artery ratio of 1.2 : 1. At five days the peri-strut inflammatory response score and thrombus score of the MP-loaded DD stents were lower than in the control stents. The neointimal hyperplasia of MP-loaded DD stents was significantly reduced (0.80 +/- 0.10 versus 0.48 +/- 0.10 mm(2), p < 0.01). At four-week follow-up, the inflammatory response of MP-loaded stents was lower than the control stents, but without significant difference. The MP-loaded stents showed decreased peri-strut arterial injury and in-stent neointimal hyperplasia (2.42 +/- 0.87 versus 1.62 +/- 0.71 mm(2), p < 0.05). It is concluded that local vascular delivery of a high dose of MP from PC-coated DD stents could effectively decrease inflammatory response and thrombus formation after oversized stent deployment and result in a significant reduction of neointimal hyperplasia.

Animals↗
PubMed2003

Local infusion of the nitric oxide donor Sin-1 after angioplasty. Effects on intimal hyperplasia in porcine coronary arteries.

PURPOSE: To investigate the development of intimal hyperplasia in response to percutaneous transluminal coronary angioplasty (PTCA) followed by local delivery of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1). MATERIAL AND METHODS: Overdilation PTCA was performed in coronary arteries in 20 healthy pigs. One of the dilated segments was additionally treated with local delivery of SIN-1 for 10 min. Segments distal to the treated part of the arteries served as controls. Arteries were radiographically depicted and analyzed after 1 and 8 weeks for actin, myosin and intermediate filaments (IF), nitric oxide synthetase (NOS) and histological evaluation. RESULTS: Segments treated with PTCA+SIN-1 showed a significantly (p=0.03) larger luminal diameter compared with PTCA only treated segments. The luminal loss after SIN-1 was not significant compared with the diameter prior to treatment. Endothelial NOS content was significantly lower in the PTCA+SIN-1 group compared with the PTCA group after 1 (p=0.03) and 8 weeks (p=0.013). IF/actin ratio after 1 week was significantly increased in PTCA-treated segments compared with untreated controls (p=0.004), and compared with PTCA+SIN-1-treated segments (p=0.004). CONCLUSION: PTCA-induced intimal hyperplasia was potently inhibited by local delivery of the NO donor SIN-1. Momentary events at the time of injury play a significant role in the development of intimal hyperplasia and long-lasting down-regulation of the endothelial NOS expression after SIN-1 exposure is suggested. The IF/actin ratio can be useful as an early marker of intimal hyperplasia.

Angioplasty, Balloon, Coronary↗
PubMed1976

Isolated lymphoid hyperplasia of the bone marrow simulating malignant lymphoma.

Lymphoid hyperplasia of the bone marrow occasionally resembles malignant lymphoma and may lead to confusion in bone marrow interpretation. The case of a patient with an unusual variant of isolated bone marrow lymphoid hyperplasia in which histologic overlap with lymphoma was found is presented. The case illustrates the difficulties in bone marrow interpretation that lymphoid hyperplasia can present. One cannot always rely on the number, size, or general pattern of lymphoid nodules to determine whether a lesion is benign or malignant. We suggest that when isolated lymphoid hyperplasia is composed of mature lymphocytes and confined to the marrow, a diagnosis of malignant lymphoproliferative disease should not be made.

Aged↗
PubMed1980

Nodular regenerative hyperplasia of the liver. Report of three cases and review of the literature.

Nodular regenerative hyperplasia of the liver is characterized grossly by diffusely nodular liver resembling micronodular cirrhosis. Viewed microscopically, the nodules consist of regenerative parenchyma without fibrosis, which are usually smaller than the hepatic lobule. Nodular regenerative hyperplasia is distinct from other nodular lesions of the liver such as cirrhosis, partial nodular transformation, focal nodular hyperplasia, and adenoma. Although nodular regenerative hyperplasia is seldom reported, it may occur more frequently than it is recognized.

Aged↗
PubMed1991

Immunoglobulin gene rearrangement in abnormal lymph node hyperplasia.

The histologic designation "abnormal lymphoid hyperplasia" is applied to lymph nodes demonstrating varying degrees of architectural effacement and/or cytologic atypia. Although some of these cases may be suggestive of non-Hodgkin's lymphoma, a definitive diagnosis is not possible despite careful morphologic and immunophenotypic studies. Because the demonstration of immunoglobulin and T-cell receptor gene rearrangements by Southern blot analysis provides a sensitive marker of lineage and clonality in lymphoid malignant conditions, the frequency with which such gene rearrangements could be identified in abnormal hyperplasia and their significance were studied. DNA samples from lymph node biopsy samples of 11 patients with abnormal lymphoid hyperplasia were analyzed for rearrangements of immunoglobulin and T-cell receptor genes by Southern blot hybridization. Six of these patients had monoclonal B-cell populations identified by immunoglobulin gene rearrangements; all were found subsequently to have non-Hodgkin's lymphoma by repeated biopsy from 8 days to 46 months later. Two patients with negative Southern blot studies also developed lymphoma, one a T-cell non-Hodgkin's lymphoma and one a cutaneous B-cell non-Hodgkin's lymphoma. Three patients without detectable gene rearrangements showed no evidence of malignant lymphoma at 36-, 45-, and 60-month follow-up evaluations. Southern blot analysis thus identified monoclonal B-cell lymphoid populations in a subset of patients with abnormal lymphoid hyperplasia; the presence of clonal immunoglobulin gene rearrangement predicted progression to overt non-Hodgkin's lymphoma.

Aged↗
PubMed1992

Genetic alterations in the 61st codon of the H-ras oncogene isolated from archival sections of hepatic hyperplasias, adenomas and carcinomas in control groups of B6C3F1 mouse bioassay studies conducted from 1979 to 1986.

In order to better understand the molecular events in murine hepatocarcinogenesis, the frequency and types of mutations in the murine H-ras proto-oncogene isolated from 184 independent, spontaneously occurring hepatic lesions were determined. Hepatocellular foci, hyperplasias, adenomas and carcinomas were obtained from archival samples of control male (134 samples) and female (50 samples) B6C3F1 mice used in oncogenicity studies that were conducted at Lilly Research Laboratories from 1979 to 1986. The 61st codon region of the H-ras oncogene from these sections was amplified using the polymerase chain reaction. Mutation frequencies were determined by restriction fragment length polymorphism analysis. The types of mutations were characterized by allele-specific oligonucleotide hybridization and confirmed by DNA sequencing. Forty-two per cent of the carcinomas, 44% of the adenomas, 42% of the hyperplasias and 29% of the foci contained mutations at the 61 codon. The mutation spectra for the carcinomas, adenomas and hyperplasias consisted of mostly CAA-AAA transversions, followed by CAA-CGA transitions, followed by CAA-CTA transversions. These results demonstrate that: (i) the frequency of spontaneous mutations in the H-ras 61st codon is equivalent in murine hyperplasias, adenomas and carcinomas, and (ii) sex was not a determining factor in either the mutation frequency or mutation spectrum for the spontaneous lesions. If these lesions represent successive stages in the carcinogenic process, then these results suggest that mutations in the 61st codon of H-ras are early events in spontaneous murine hepatocarcinogenesis.

Adenoma↗
PubMed1996

Monoclonal development of squamous cell carcinomas from polyclonal papillary or nodular hyperplasias in the forestomach of C3H/HeN<-->BALB/c chimeric mice treated with N-methyl-N-nitrosourea or diethylnitrosamine.

The clonality of epithelial proliferative lesions of forestomach carcinogenesis was immunohistochemically investigated in C3H/HeN<-->BALB/c chimeric mice using a specific antibody to C3H strain specific antigen (CSA) and as well as in terms of microsatellite DNA polymorphism patterns. The C3H/HeN<-->BALB/c chimeric mice were produced by an aggregation procedure. Male chimeric, C3H/HeN, and BALB/c animals were given N-methyl-N-nitrosourea (MNU) 0.5 mg/mouse once a week for a total of 10 times by intragastric intubation or 30 p.p.m. diethylnitrosamine (DEN) in their drinking water for 20 weeks. Those treated with MNU were killed at weeks 11, 25 and 45 and with DEN at week 35. Normal chimeric forestomach epithelium was found to demonstrate mixtures of epithelial cell groups composed of either CSA positive or negative cells. The same was the case for all simple hyperplasias. Papillary and nodular (PN) hyperplasias increased with time even after cessation of MNU treatment and many of them consisted of both CSA positive and negative cell groups. In one case, a CSA positive and a negative cancer were observed to have developed independently in the same PN-hyperplasia consisting of both parental cell types. In 28 tumor bearing chimeric mice, all squamous cell carcinomas (SCCs) were composed entirely of either CSA positive or negative tumor cells. However, in two animals with advanced CSA positive cancers and negative cancers, tiny cancer nests composed of both parental type cells were found in association. Microsatellite DNA polymorphism patterns of DNAs sampled from histological sections completely conformed with the outcomes of immunohistochemical staining. The results suggest that PN-hyperplasias are aggregates (polyclonal) of preneoplastic changes from which monoclonal SCCs are derived. Polyclonal cancers may also arise secondarily at low incidence during progression, due to two or more lesions coalescing.

Animals↗
PubMed1999

Hepatic hyperplasia and cancer in rats: alterations in copper metabolism.

We previously demonstrated that rats exposed to the peroxisome proliferator (PP) diethylhexylphthalate (DEHP) had reduced serum ceruloplasmin (CP) oxidase activity, which suggests tissue copper deposition. Copper is highly toxic in excess, and results in cellular damage and hepatocellular carcinomas (HCC). This study addresses changes in expression of copper-related genes and metal accumulation in hyperplastic liver and tumors induced by PP. Male rats were fed diets containing DEHP or clofibrate (CLF) for 3-60 days (hyperplasia) and 4-chloro-6-(2,3 xylidino)-2-pyrimidinyl-thio(N-beta-hydroxyethyl) acetamide for 10 months (HCC). During hyperplasia, an immediate and progressive decrease in serum CP activity was observed (P < 0.05), as were reductions in mRNA levels for both CP and Wilson's disease gene (WD gene, a P-type ATPase) (P < 0.05). Tumor-bearing rats had lower serum CP activity (P < 0.05), and CP and WD gene mRNA levels were reduced in tumors (P < 0.05), and in liver surrounding tumors (SL) (P < 0.05). Metallothionein mRNA showed no consistent changes during hyperplasia. Tumors showed a 2.5-fold induction of metallothionein mRNA (P < 0.05), and a 1.2-fold increase in SL. Temporal increases in liver copper content occurred during hyperplasia, with increases of 2-fold (DEHP) and 3.3-fold (CLF) at 60 days (P < 0.05). Copper content was 2.2-fold higher in tumors (P < 0.05) and 1.7-fold higher in SL; iron did not increase and zinc decreased temporally. Thus, copper accumulation and changes in copper-related gene expression may be contributing factors in liver neoplasia in PP-treated rats. Loss of CP results in decreased free radical scavenger capacity and thus may enhance oxidative damage induced by PPs.

Animals↗
PubMed1988

sn-1,2-didecanoylglycerol effectively induces epidermal ornithine decarboxylase but only weak hyperplasia in mouse skin.

The abilities of sn-1,2-didecanoylglycerol (sn-1,2-DDG) to induce epidermal ornithine decarboxylase (ODC) activity and epidermal hyperplasia were tested using SENCAR, DBA/2 and C57BL/6 mice. Following a single application of 5000 nmol of sn-1,2-DDG, ODC activity reached a maximum at 4 h after treatment with a peak activity of 6.03 nmol CO2/mg protein/60 min in C57BL/6, 1.50 in SENCAR and 0.73 in DBA/2, respectively. The time course and magnitude for induction of ODC activity after multiple treatments was very similar to that after a single application in these three mouse lines. Interestingly, the induced ODC activity in C57BL/6 was always higher than that in SENCAR and DBA/2 mouse epidermis regardless of the treatment protocol. Induction of hyperplasia and dark basal keratinocytes (DCs) and changes in the labeling index (LI) of basal keratinocytes in DBA/2 and C57BL/6 mice following treatment with sn-1,2-DDG were investigated. Multiple treatments (twice weekly for 2 weeks) of 5000 nmol sn-1,2-DDG did not induce substantial increases in epidermal thickness or DCs 24 or 48 h after the last treatment. In contrast, TPA induced a marked increase in epidermal thickness in DBA/2 rather than C57BL/6 and a considerably higher induction of DCs in DBA/2 (37.3 +/- 2.2%) than in C57BL/6 (9.6 +/- 2.5%) 48 h after the last treatment. The LIs after topical application of sn-1,2-DDG were elevated at 24 h, but returned to basal levels by 48 h in both strains, whereas TPA treatment significantly elevated the LI in both strains at 48 h after the last application. In addition, the effects of various doses and frequencies of application of sn-1,2-DDG were investigated using SENCAR mice. High doses (20,000 nmol) or more frequent applications (5000 nmol once daily for 7 days) of sn-1,2-DDG still produced only weak hyperplasia. These results suggest that the induction of epidermal ODC activity can be dissociated from the induction of epidermal hyperplasia and may provide an explanation for the lack of complete promoting activity presently observed with membrane permeable diacylglycerol derivatives.

Administration, Cutaneous↗
PubMed1985

Intimal hyperplasia in autogenous vein grafts used for arterial bypass: a canine model.

Late vein graft occlusion following myocardial revascularisation is usually the result of progressive intimal hyperplasia which ultimately leads to vein graft thrombosis. Considerable attention has recently been directed towards the development of optimal platelet-inhibiting drug regimens designed to prevent intimal hyperplasia in autogenous vein grafts. This report describes an animal model that reliably reproduces short-term intimal hyperplasia in autogenous vein grafts, thus facilitating the study of platelet-inhibiting drug regimens for the prevention of intimal hyperplasia. 28 segments of undistended jugular vein were implanted end-to-end between bilaterally divided femoral arteries in 14 mongrel dogs. Seven control animals (CON) received a non-lipid diet one week before and for 6 weeks following vein implantation. A further seven animals received a 2% cholesterol diet throughout the study. Serum cholesterol was measured at 4.06 +/- 0.6 mmol X litre-1 in the CON and did not change significantly throughout the study. Serum cholesterol rose from 3.9 +/- 0.4 to 8.5 +/- 0.8 mmol X litre-1 in the lipid-supplemented animals (p less than 0.001). Vein grafts were harvested at 6 weeks and fixed in formaldehyde. Precise measurements of intimal thickness in microns were measured from multiple vein graft cross-sections with a Zeiss computerised interactive image analysing system. A mean of 102 +/- 15 measurements were made from each vein graft cross-section. Intimal thickness of autogenous vein grafts prior to implantation were similar in both groups and measured 4.15 +/- 0.4 micron. Intimal thickness increased in CON animals to 23.3 +/- 3 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Inhibition and reversal by beta-retinoic acid of hyperplasia induced in cultured mouse prostate tissue by 3-methylcholanthrene or N-methyl-N'-nitro-N-nitrosoguanidine.

The effect of beta-retinoic acid (RA) on carcinogen-induced hyperplasia was studied in organ cultures of mouse prostate gland. 3-Methylcholanthrene (MCA), requiring metabolic activation, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), not requiring activation, were used to induce hyperplastic changes. Treatment of cultures with MCA or MNNG stimulated cell proliferation and caused the alveolar epithelium to become hyperplastic. The development of this hyperplasia was inhibited when RA was added simultaneously with MCA or MNNG. However, RA had no significant effect on cell proliferation in untreated control cultures. Elimination of carcinogen from the hyperplastic cultures after 8 days of treatment did not reverse hyperplasia of the alveolar epithelium. When the withdrawal of MCA or MNNG was followed by treatment of the cultures with RA, hyperplasia was markedly reversed within 96 hours. Thus RA actively inhibited and reversed the effect of MCA and MNNG, two carcinogens that may have different mechanisms of action.

Animals↗
PubMed1999

Two-dimensional gel analysis of human endometrial proteins: characterization of proteins with increased expression in hyperplasia and adenocarcinoma.

In the search for new markers of human endometrial hyperplasia and adenocarcinoma the method of quantitative two-dimensional gel electrophoresis was applied to study the protein expression profiles of metabolically [(35)S]-methionine-labelled proteins of endometrial explants. Approximately 1700 protein spots were resolved by the two-dimensional gel electrophoresis, and the expression pattern of each of these proteins was assessed for increased expression during hyperplasia or adenocarcinoma. In total, six protein spots showed increased expression in hyperplasia, 19 in carcinoma, and eight in both hyperplasia and carcinoma. Twelve of these 33 differentially expressed proteins were identified by peptide mass mapping combined with sequence database searching. Among the identified proteins were proteins involved in cellular transport and chaperoning, i.e. heat shock protein 27 kDa protein, heat shock 70 kDa protein, heat shock cognate 71 kDa protein, and serotransferrin. Other identified proteins were: regulatory chain protein of cAMP-dependent protein kinase, prohibitin, and heterogeneous nuclear ribonucleoprotein A2/B1. Finally we identified proteins associated with the cytoskeleton, vimentin and tropomyosin isoform 3, and the glycolytic pathway, alpha enolase, and phosphoglycerate kinase. The remaining unidentified proteins were either not contained in the database and must be assumed to be novel proteins, or were present in too low amounts to allow characterization.

Adenocarcinoma↗
PubMed2001

Sevelamer hydrochloride (Renagel), a non-calcaemic phosphate binder, arrests parathyroid gland hyperplasia in rats with progressive chronic renal insufficiency.

BACKGROUND: It has been demonstrated that dietary phosphate restriction suppresses parathyroid hormone (PTH) secretion and parathyroid cell proliferation in experimental animals with chronic renal insufficiency (CRI) independently of serum calcium and 1,25(OH)(2)D3 levels. This study was conducted to examine whether sevelamer hydrochloride (Renagel); hereafter referred to as sevelamer), a non-calcaemic phosphate binder could inhibit the parathyroid gland (PTG) hyperplasia in rats with progressive CRI. METHODS: Male Sprague-Dawley rats were injected twice with low doses of adriamycin (ADR). Two weeks after the last injection of ADR, rats were fed a diet containing 1 or 3% sevelamer for 84 days. Time course changes of serum levels of calcium, phosphorus, and PTH were measured. At the end of study, serum 1,25(OH)(2)D3 levels were measured and the maximal two-dimension area of the PTG in paraffin section was calculated using an imaging analyser. RESULTS: Dietary sevelamer treatment inhibited the elevations of serum phosphorus, calciumxphosphorus product, and PTH levels that occurred as the study progressed. Sevelamer also suppressed maximal PTG area and there existed positive strong correlation between maximal PTG area and serum PTH levels at the end of the study. Serum phosphorus levels positively correlated well with serum PTH levels and maximal PTG area. In contrast, serum calcium or 1,25(OH)(2)D3 levels did not show any correlation with serum PTH levels and maximal PTG area. CONCLUSIONS: Sevelamer treatment arrested hyperphosphataemia and PTG hyperplasia accompanied by the elevation of serum PTH levels. The correlation analysis suggests that reduced serum phosphorus levels contributed to the suppression of PTG hyperplasia and resulted in the reduction of PTH levels in this animal model after the sevelamer treatment. The management of phosphorus control started from early stage of CRI could prevent PTG hyperplasia and facilitate later management of secondary hyperparathyroidism.

Animals↗
PubMed2003

Idiopathic gingival hyperplasia and orthodontic treatment: a case report.

There are many reasons for gingival hyperplasia. Mostly, proper oral hygiene is sufficient to achieve normal healthy gingiva. In some situations, however, gingival hyperplasia is drug-induced or can be a manifestation of a genetic disorder. In the latter, it may exist as an isolated abnormality or as part of a syndrome. If orthodontic treatment is needed in patients with gingival hyperplasia, both orthodontic and periodontal aspects need to be considered. Extreme hereditary gingival fibromatosis was periodontally treated, by removal of all gingival excess using flaps and gingivectomies. After a follow-up period, the orthodontic treatment started with fixed appliances. Monthly periodontal check-ups (scaling and polishing) were scheduled to control the gingival inflammation. After the orthodontic treatment, permanent retention was applied, once more followed by a complete gingivectomy in both maxilla and mandible. One of the most important keys to successful treatment of hyperplasia patients is the cooperation between the periodontist and the orthodontist.

Adolescent↗
PubMed1986

Risk factors for adenomatous endometrial hyperplasia: a case-control study.

A population-based case-control study of histologically confirmed endometrial neoplasia was conducted in Toronto, Canada, between 1977 and 1978. Pathologic slide review resulted in classification of patients to diagnostic categories of endometrial carcinoma, endometrial carcinoma in situ, and endometrial hyperplasia. This report concerns the subset of patients classified as having adenomatous endometrial hyperplasia. Two age-matched neighborhood controls were selected for each case, and analyses included only those case-control sets in which the case and at least one control were concordant on menopausal status. Among postmenopausal women (87 cases and 151 controls), noncontraceptive estrogen use was a statistically significant risk factor (adjusted odds ratio (OR) = 6.7), as was heavy body weight relative to height (Quetelet index) (adjusted OR = 3.2). Long-term (5+ years) estrogen use conferred an estimated relative risk of more than 20, but use of oral contraceptives did not alter risk significantly. Among premenopausal women (62 cases and 97 controls), a high Quetelet index appeared to be a significant protective factor, even when adjusted for oral contraceptive use (adjusted OR = 0.2). While oral contraceptive use was not associated with a change in risk, long duration of use was highly, but statistically not significantly, protective against hyperplasia. The data for pre- and postmenopausal women indicate that both endogenous and exogenous estrogen exposure are important factors in the etiology of adenomatous endometrial hyperplasia.

Adult↗
PubMed1994

Obesity and benign prostatic hyperplasia.

Abdominal obesity increases the estrogen-to-androgen ratio and may increase sympathetic nervous activity, both hypothesized to influence the development of benign prostatic hyperplasia and the severity of urinary obstructive symptoms. In 1986 and 1987, men aged 40-75 years who were participants in the Health Professionals Follow-up Study and who were without prior diagnosis of cancer or prostatectomy provided data on weight, height, and waist and hip circumferences. The men were followed for incidence of prostatectomy for benign prostatic hyperplasia up to January 1992. In addition, the frequency and severity of symptoms of urinary obstruction were assessed among respondents to a questionnaire in 1992. Among 25,892 men who provided complete information for both surgery and symptoms, 837 men had surgery for benign prostatic hyperplasia, and 2,581 of those without surgery reported frequent urinary symptoms. After adjustment for age, smoking, and body mass index, abdominal obesity was related to prostatectomy (odds ratio (OR) = 2.38, 95% confidence interval (CI) 1.42-3.99, for those with a waist circumference > or = 43 inches (109 cm) relative to those with a waist circumference < 35 inches (89 cm); p trend < 0.0001) and with frequent urinary symptoms among those without prostatectomy (OR = 2.00, 95% CI 1.47-2.72; p < 0.0001). Body mass index, hip circumference, and waist-to-hip ratio were not associated with benign prostatic hyperplasia independently of waist circumference. These results suggest that abdominal obesity in men may increase the frequency and severity of urinary obstructive symptoms and may increase the likelihood that such obese men will undergo a prostatectomy.

Anthropometry↗