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PubMed2000

Inhibition of 12(S)-hydroxyeicosatetraenoic acid (12-HETE) production suppressed the intimal hyperplasia caused by poor-runoff conditions in the rabbit autologous vein grafts.

The efficacy of OPC-29030, a newly developed inhibitor of 12(S)-hydroxyeicosatetraenoic acid (12-HETE) production, was evaluated on intimal hyperplasia of experimental autologous vein grafts in a distal poor-runoff model and a hyperlipidemic model in rabbits. First, rabbits were divided into two groups, the distal poor-runoff group (PR group) and the hyperlipidemic group (HL group). After 4 weeks preparing the PR model and the HL model, the femoral vein was implanted into the ipsilateral femoral artery. Then they were subdivided into two groups, depending on the diet provided; diet group with 0.1% OPC-29030 (OPC-29030 group) and normal diet group (control group). At 4 weeks, the grafts were harvested, and intimal hyperplasia of the graft was measured with an ocular cytometer. Intimal cell proliferation was determined by bromodeoxyuridine (BrdU) incorporation at 2 weeks after surgery. In addition, the effect of OPC-29030 on the proliferation or migration of rat aortic smooth muscle cells in culture was investigated. In the in vivo study in the PR group, the intimal hyperplasia and the plasma 12-HETE levels in the OPC-29030 group were significantly inhibited, compared with those of the control group. However, in the HL group, the intimal hyperplasia in both the OPC-29030 and control groups showed a remarkable degree of intimal hyperplasia. There was no significant difference between those two groups. Furthermore, there was no significant difference in the plasma 12-HETE levels in the HL group irrespective of the presence of OPC-29030. The BrdU labeling index at 2 weeks after grafting was significantly lower in the OPC-29030 group compared with that in the control group in the PR group. In the in vitro study, OPC-29030 did not inhibit smooth muscle cell proliferation; however, OPC-29030 inhibited the migration. These results demonstrate the efficacy of OPC-29030 in reducing the degree of intimal hyperplasia under PR conditions, but not under hyperlipidemic conditions. The mechanism of reducing the intimal hyperplasia may be that OPC-29030 inhibited 12-HETE production, which did not inhibit proliferation while inhibiting migration of the smooth muscle cell. These results suggested the possible involvement of 12-HETE with the intimal hyperplasia under PR conditions.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

Discriminant and criterion validation of the US-Spanish version of the SF-36 Health Survey in a Cuban-American population with benign prostatic hyperplasia.

OBJECTIVES: The study tested the validity of the Medical Outcomes Study 36-Item Short-Form (SF-36) Health Survey (originally validated in the Mexican-American population) in a different Spanish subgroup to determine whether the Spanish version is equally applicable to the Cuban-American population. METHODS: Individuals with and without benign prostatic hyperplasia served as the study sample. The SF-36 scores of 264 individuals with benign prostatic hyperplasia were compared with those of 273 individuals without benign prostatic hyperplasia to determine discriminant and criterion validity. These individuals were assigned to one of the following groups: non-Hispanic subjects, Cuban subjects who took the English version, and Cuban subjects who took the Spanish version. MANOVA with planned comparisons was used for this analysis. RESULTS: In all three culture/language groups, the quality-of-life scores of individuals without benign prostatic hyperplasia were significantly different than those of benign prostatic hyperplasia individuals. These results demonstrated that the English and Spanish versions can differentiate between individuals with and without benign prostatic hyperplasia. Moreover, the quality-of-life scores of Cuban subjects with and without benign prostatic hyperplasia who took the English version were statistically similar to those of their counterparts who took the Spanish version. CONCLUSIONS: The US-Spanish version of the SF-36 appears to be valid when used to measure health status in Cuban-American subjects with benign prostatic hyperplasia. Further studies should be conducted to verify the validity of the US-Spanish version of the SF-36 for other health conditions.

Aged↗
PubMed2004

Basal cell proliferations of the prostate other than usual basal cell hyperplasia: a clinicopathologic study of 23 cases, including four carcinomas, with a proposed classification.

Basaloid proliferations of the prostate with morphologic patterns other than usual basal cell hyperplasia are rare, and the distinction between benign and malignant lesions has been difficult. We describe 23 such lesions and classify them into two groups: adenoid cystic-like hyperplasia and adenoid cystic or basaloid carcinoma. Adenoid cystic-like hyperplasia (n = 19) was characterized by an older age at presentation (mean, 71.8 years), transition zone location with background of nodular hyperplasia, multifocality, lobulation, circumscription, and small acini with occasional hyalinization. A cribriform pattern limited to small- and medium-sized glands, squamous metaplasia, and hypercellular myxoid stroma were occasionally seen. Adenoid cystic carcinoma (n = 3) was characterized by a younger age at presentation (mean, 46.0 years), peripheral zone involvement, and large acini that were often dilated and exhibited extensive interanastomoses, prominent intraglandular hyalinization, perineural invasion, and extraprostatic extension. Basaloid carcinoma (n = 1) showed infiltration between normal glands, perineural invasion, and extraprostatic extension but lacked a cribriform architecture. The degree of cytologic atypia and mitotic rate overlapped between the hyperplasia and carcinoma cases. Both hyperplastic lesions and adenoid cystic carcinomas showed a basal cell phenotype with strong immunoreactivity to cytokeratins 14 and 34betaE12, but the basaloid carcinoma was negative for these markers. In all cases, the proliferating basal cells were nonreactive for myoepithelial and prostatic secretory cell markers. The 8 patients with adenoid cystic-like hyperplasia with available follow-up information had no progression of disease (mean follow-up period, 8.6 years). One patient with adenoid cystic carcinoma died with widespread metastases, but the 3 other patients with carcinomas had no disease progression (mean follow-up period, 7.0 years). In conclusion, most florid basaloid proliferations of the prostate fall into one of two categories. In the first, there is a clear association with nodular hyperplasia (adenoid cystic-like hyperplasia) and, although cytologic atypia and mitoses may be seen, they are present within a lesion that retains an orderly, vaguely nodular (noninfiltrative) pattern. The second group of cases (adenoid cystic and basaloid carcinoma) shows a widespread, haphazard infiltrative growth pattern. This study suggests that adenoid cystic carcinomas are biologically indolent following prostatectomy but have a low risk of distant metastasis.

Adult↗
PubMed2005

VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) induced intimal hyperplasia in carotid arteries.

BACKGROUND: The role of vascular endothelial growth factors (VEGFs) in intimal hyperplasia and atherogenesis remains unknown. Several studies have suggested that some members of the VEGF family reduce intimal hyperplasia, but others have proposed that VEGFs accelerate restenosis and atherosclerosis. This investigation conducted a comparative study with adenoviruses encoding different VEGFs in a rabbit carotid artery collar model of intimal hyperplasia in order to analyze the role of VEGFs in the formation of intimal hyperplasia. MATERIALS AND METHODS: Intimal hyperplasia was induced in the carotid arteries of cholesterol fed New Zealand White rabbits using a silastic collar. Adenoviral vectors encoding VEGF-A, VEGF-B, VEGF-C, VEGF-C(DeltaNDeltaC), VEGF-D and VEGF-D(DeltaNDeltaC) were delivered to the adventitia using the collar as a gene delivery device. Adeno-LacZ was used as a control. RESULTS: A significant (P < 0.01) increase in the intima/media ratio was observed in the arteries transduced with VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC). There was a significant increase in the number of proliferating cells in the adventitia, media and intima of the VEGF-A, VEGF-D and the VEGF-D(DeltaNDeltaC) transduced arteries. The majority of medial smooth muscle cells in these arteries had a synthetic phenotype. The presence of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the VEGF-A, VEGF-D and the VEGF-D(DeltaNDeltaC) transduced arteries was significantly increased. A significant positive correlation was observed between adventitial angiogenesis and intimal hyperplasia. CONCLUSIONS: Adventitial delivery of adenoviruses encoding VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) increased intimal hyperplasia in the rabbit collar model. Adventitial angiogenesis correlated positively with the intimal hyperplasia. These results indicated that efficient adventitial production of VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) can cause thickening of the inner layer of the artery in rabbits.

Animals↗
PubMed1989

Patterns of reactivity with the monoclonal antibodies HMFG1 and HMFG2 in normal endometrium, endometrial hyperplasia and adenocarcinoma.

Using an indirect immunoperoxidase technique the expression of the epitopes in human milk fat globule (HMFG) membranes detected by the monoclonal antibodies HMFG1 and HMFG2 was studied in the normal endometrium and in cases of cystic glandular hyperplasia, glandular hyperplasia with architectural atypia (complex hyperplasia), glandular hyperplasia with cytological atypia (atypical hyperplasia) and invasive adenocarcinoma. Luminal reactivity with HMFG1 was seen in cases of normal endometrium, cystic glandular hyperplasia and glandular hyperplasia with architectural atypia. In contrast most cases of glandular hyperplasia with cytological atypia and invasive adenocarcinoma also showed areas of cytoplasmic reactivity. Reactivity with HMFG2 was scanty.

Adenocarcinoma↗
PubMed2006

Steroid receptor expression and HER-2/neu (c-erbB-2) oncoprotein in the uterus of cats with cystic endometrial hyperplasia-pyometra complex.

The presence of oestrogen-alpha receptor (ER), progesterone receptor (PR), and HER-2/neu (c-erbB-2) oncoprotein in the uterine walls of 10 healthy cats and 20 subjects with cystic endometrial hyperplasia-pyometra (CEH-P) were evaluated. Lesions were graded according to the severity of cystic dilation, hyperplasia and inflammation, and were classified as normal, mild uterine hyperplasia and severe uterine hyperplasia. The ER, PR and c-erbB-2 expression in the endometrium, glandular epithelium, stromal fibroblasts and myometrial smooth muscle cells was quantified by immunohistochemistry. The ER, PR and c-erbB-2 staining patterns differed between normal uteri and uteri with CEH-P. The ER expression was tended to be higher in the endometrial surface and glandular epithelium in the severe hyperplasia group (P > 0.05) and significantly lower in the mild hyperplasia cases compared with normal endometrium (P < 0.05), whereas the PR expression in both severe and mild hyperplasia cases tended to be higher in stromal cells and glandular epithelium than those in the normal uteri. C-erbB-2 immunoreactivity was observed only in the endometrial surface and glandular epithelium of the uterine wall and immunostaining was found to be highest in cases with severe hyperplasia. As a conclusion, we suggest that c-erbB-2 oncoprotein may play a role in the pathogenesis of the CEH together with the ER and PR in cats, and that ER does not have a role in the mechanism of pyometra, whereas PR plays a role in the pathogenesis of both CEH and pyometra.

Animals↗
PubMed1992

Epithelial hyperplasia of the breast. Comparison of incidence between cases of breast carcinoma and control autopsy specimens with immunohistochemical observation of blood group antigens.

Epithelial hyperplasia in the duct, ductule or lobule of the breast is a very common lesion and has been considered to carry a risk of subsequent invasive carcinoma. However, it is not known whether epithelial hyperplasia can transform into carcinoma or whether malignant change occurs de novo. We analyzed the incidence of epithelial hyperplasia of the breast by making a comparison between cases of breast carcinoma and control autopsy specimens, and studied differences in the membrane antigens of the constituent cells using immunohistochemical staining of blood group antigens. It was found that the frequency of epithelial hyperplasia was higher in the cases of breast carcinoma. The lesions showed loss of A, B and H antigens at high frequency, and the proportion of lesions showing loss of these antigens became higher as the atypia of the lesion increased. On the other hand, expression of Lea antigen was observed more frequently in atypical epithelial hyperplasia or in situ carcinoma than in ordinary epithelial hyperplasia. These findings suggest possible transformation from epithelial hyperplasia to carcinoma, and indicate that atypical epithelial hyperplasia may be precancerous in nature.

Adolescent↗
PubMed2002

Foveolar hyperplasia at the gastric cardia: prevalence and associations.

AIMS: In the gastric antrum and body, foveolar hyperplasia is a feature of reactive gastritis resulting from--for example, duodenogastric bile reflux and the use of non-steroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to examine the occurrence and clinical relevance of gastric cardiac foveolar hyperplasia. METHODS: The study population was drawn from a consecutive series of 1698 patients sent for upper gastrointestinal endoscopy. Only cases without chronic gastritis or Barrett's oesophagus were included. The final study population consisted of 307 patients. RESULTS: Foveolar hyperplasia was seen in the gastric cardiac mucosa in 31 (10%) patients with histologically normal stomach mucosa, but none had endoscopically noticeable hyperplastic polyps. Compared with patients without gastric cardiac hyperplasia, those with hyperplasia more often had chronic inflammation and complete intestinal metaplasia in the junctional biopsies (48% v 77% and 9% v 26%, respectively). Logistic regression analysis revealed that chronic cardiac inflammation (odds ratio (OR), 3.2; 95% confidence interval (CI), 1.3 to 7.8) and intestinal metaplasia of the complete type (OR, 2.8; 95% CI, 1.1 to 7.1) were independent risk factors for cardiac foveolar hyperplasia. In univariate analysis, endoscopic erosive oesophagitis (endoscopy positive gastro-oesophageal reflux disease) and the use of NSAIDs were not related to the presence of foveolar hyperplasia. CONCLUSIONS: Foveolar hyperplasia in the gastric cardiac mucosa occurs in patients with histologically normal non-gastritic stomachs and may develop as a consequence of chronic inflammation limited to the gastro-oesophageal junction ("junctitis"). It is not associated directly with endoscopy positive gastro-oesophageal reflux disease or the use of NSAIDs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Relationship between gingival hyperplasia and class II histocompatibility antigens in renal transplant recipients.

Gingival hyperplasia, a well-known side effect of ciclosporin A (CS-A), is much more prominent when CS-A is used in combination with calcium channel blockers, especially dihydropyridines. On the other hand, it is interesting to note that this complication is not observed in all patients using this drug combination. This study was conducted in order to investigate the relationship (if any) between major histocompatibility complex antigens and gingival hyperplasia. Seventy-six renal transplantation patients were evaluated by an experienced dentist for gingival hyperplasia. The patients were then divided into two groups according to the presence (group 1, n = 18) or absence (group 2, n = 58) of gingival hyperplasia. There was no significant difference between the two groups regarding age, sex, transplant age, donor type, antihypertensive and immunosuppressive therapy protocols, and CS-A levels. HLA-DR2 antigen was present in 63% of the patients with gingival hyperplasia and in 34% of the patients without gingival hyperplasia. However, the HLA-DR1 antigen frequencies were found to be 11 and 22% in group 1 and group 2, respectively. In patients receiving nifedipine as an antihypertensive therapy, gingival hyperplasia developed more often than in patients receiving verapamil or diltiazem. As a result, in renal allograft recipients with HLA-DR1 antigen, gingival hyperplasia was seen less frequently than in HLA-DR2-positive patients. It is believed that the presence of these antigens regulates the response of the patients to either CS-A and/or calcium channel blockers.

Adult↗
PubMedDate not supplied

The influence of lesion length on intimal hyperplasia after Fogarty balloon injury in the rabbit carotid artery: role of endothelium.

After balloon angioplasty, retarded endothelial cell recoverage of the injured segment may lead to enhanced intimal hyperplasia. We tested the hypothesis that long lesions result in more intimal hyperplasia than short lesions due to a prolonged time to complete endothelial cell recoverage. A 2-french Fogarty balloon was used to create 2.5- and 5-cm-long lesions in the rabbit carotid artery. After termination, the injured arteries (n = 9 for all groups) were serially processed for histochemistry. Endothelial cell coverage was assessed with an antibody to CD31 and cell proliferation with a monoclonal antibody to Ki-67 nuclear antigen. The intimal hyperplasia cross-sectional area was measured morphometrically. All data are mean +/- SEM. At 21 days, endothelial cell recoverage was almost complete in the 2.5-cm lesions. In the 5-cm lesions, endothelial cell recoverage was 66 +/- 6% in the middle segments (p = 0.04, 2.5 vs. 5 cm) and 100% at the cranial and caudal ends of the lesion. At 42 days, endothelial cell coverage had increased to 81 +/- 7% in the middle segments of the 5-cm lesions. The intimal hyperplasia area was similar in the 2.5- and the 5-cm lesions both at 21 days (0.19 +/- 0.02 and 0.20 +/- 0.01 mm2, respectively) and 42 days (0.27 +/- 0.02 and 0.26 +/- 0.03 mm2, respectively). The increase in intimal hyperplasia from 21 to 42 days was significant for both lesion lengths (p = 0.004). At 21 days, intimal proliferation was similar for the 2.5- and 5-cm lesions. After 42 days postinjury, intimal proliferation had decreased (p < 0.001) equally for both lesion lengths. Earlier recoverage by endothelium in the 2.5-cm lesions did not inhibit intimal hyperplasia compared to the 5-cm lesions which were still incompletely reendothelialized. We conclude that in the rabbit, rapid endothelial cell recoverage of Fogarty balloon-injured arteries may not limit intimal hyperplasia in the center of the lesion. It is conceivable that the inability of regenerated endothelium to inhibit intimal hyperplasia is due to its initially dedifferentiated and possibly dysfunctional phenotype.

Angioplasty, Balloon↗
PubMedDate not supplied

Mediastinal masses diagnosed as thymus hyperplasia by fine needle aspiration cytology.

OBJECTIVE: Thymic hyperplasia in the anterior mediastinum can occur in healthy children as idiopathic thymic hyperplasia or as a rebound effect after administration of chemotherapy in patients with malignancies. Thymic hyperplasia after chemotherapy is a well-documented phenomenon, particularly in children and less frequently in adults. Both forms of thymic hyperplasia are a diagnostic challenge, and most patients undergo surgical exploration. Fine needle aspiration cytology (FNAC) has supposed to be inadequate to diagnose benign thymic hyperplasia and to separate it from malignant disease. STUDY DESIGN: We report the cytologic findings on eight patients presenting with a mass in the anterior mediastinum that was diagnosed as thymic hyperplasia on FNAC. In five patients the masses developed after chemotherapy. The remaining three patients were healthy children. Three patients underwent ultrasound-guided aspiration; in five cases the procedure was performed under computerized guidance. RESULTS: In all eight patients the cytologic smears showed a mixed population of lymphoid cells. Cytologic diagnosis of thymic hyperplasia was confirmed by immunophenotyping in three patients and by follow-up studies in all of them (median, 68 months; range, 8-113). CONCLUSION: In contrast to previous reports, this study demonstrated the utility of FNAC as a front-line investigative procedure in diagnosing thymic hyperplasia.

Adolescent↗
PubMed1979

Concentration of dihydrotestosterone and 3 alpha-androstanediol in naturally occurring and androgen-induced prostatic hyperplasia in the dog.

Previous studies have suggested that dihydrotestosterone accumulation in the prostate may be involved in the pathogenesis of prostatic hyperplasia in man and dog. However, the fact that the administration of 10 mg dihydrotestosterone/d to castrated, mongrel dogs (0.5 mg/kg body wt) causes little growth in the prostate, whereas identical doses of 3alpha- androstanediol regularly induce prostatic hyperplasia (> 14 g weight) has raised the possibility that the dihydrotestosterone accumulation may be the result rather than the cause of the pathology. To investigate the mechanism of this phenomenon, we measured the levels of dihydrotestosterone and 3alpha-androstanediol in prostates from 75 dogs. In both naturally occurring and 3alpha-androstanediol-induced prostatic hyperplasia, the levels of dihydrotestosterone were high (>5 ng/g), whereas in immature glands and glands from dihydrotestosterone-treated animals, levels were similar (2.1 and 2.6 ng/g, respectively). 3alpha-Androstanediol levels were no different in animals treated with dihydrotestosterone or 3alpha-androstanediol.Therefore, because exogenous 3alpha-androstanediol is a better precursor of prostatic dihydrotestosterone than exogenous dihydrotestosterone itself, the effects of treatment with larger doses (2.5 mg/kg per d) of dihydrotestosterone and 3alpha-androstanediol for 12 wk were examined. In these amounts, dihydrotestosterone was as effective as 3alpha-androstanediol in inducing the development of prostatic hyperplasia and in elevating prostatic dihydrotestosterone concentration. Because dihydrotestosterone accumulates in spontaneous prostatic hyperplasia, because the administration of sufficient amounts of dihydrotestosterone to the castrated dog can induce the development of prostatic hyperplasia, and because 3alpha-androstanediol induces the development of hyperplasia via conversion to dihydrotestosterone, we conclude that accumulation of dihydrotestosterone is the cause of canine prostatic hyperplasia.

Androstenediols↗
PubMed2006

Effect of D-004, a lipid extract from the Cuban royal palm fruit, on atypical prostate hyperplasia induced by phenylephrine in rats.

BACKGROUND AND OBJECTIVE: Benign prostatic hyperplasia (BPH) is a non-malignant enlargement of the prostate that results in obstructive lower urinary tract symptoms. Saw palmetto (Serenoa repens), the dwarf American palm (Arecaceae family), is commonly used to treat BPH. The Cuban royal palm (Roystonea regia) also belongs to the Arecaceae family, and 200-400mg of D-004, a lipid extract from its fruits, administered orally for 14 days has been shown to prevent testosterone- but not dihydrotestosterone-induced prostatic hyperplasia in rats. D-004 (125-250 microg/mL) added to preparations of rat vas deferens caused a marked, dose-dependent and significant inhibition of noradrenaline-induced smooth muscle contraction, a response mediated through alpha(1)-adrenoceptors, and was more effective in these respects than Saw palmetto. However, the in vivo effects of D-004 and Saw palmetto on the hypertensive response induced by noradrenaline were modest (albeit significant), and neither treatment affected resting blood pressure or heart rate in rats. The differential effects of D-004 in in vitro and in vivo models could be related to a differential affinity for adrenoceptor subtypes or to different bioavailabilities in vascular and urogenital targets. Phenylephrine injected into rodents induces prostatic hyperplasia with all the characteristic morphological changes of the condition but does not result in enlargement of the prostate. Therefore, this phenylephrine-induced change in rat prostate tissue is called atypical prostatic hyperplasia. It serves as an in vivo model of prostatic hyperplasia induced by stimulation of alpha(1)-adrenoceptors. The objective of this study was to determine whether D-004 can inhibit induction of atypical prostatic hyperplasia by phenylephrine in rats. METHODS: Rats were randomly distributed into five groups (ten rats/group). One group was a negative control and received oral vehicle only. The other four groups were injected subcutaneously with phenylephrine (2 mg/kg): of these groups, one was a positive control receiving the vehicle, and the other three groups were treated with D-004 or Saw palmetto (both 400 mg/kg) or tamsulosin 0.4 mg/kg. All active treatments were given orally for 28 days. After completion of treatment, rats were placed unrestrained in metabolic cages and micturition studies were performed. The rats were later killed and their prostates removed and weighed. Prostate samples were processed for histological study, with histological changes being assessed according to a scoring system. Bodyweight was measured at baseline and at weekly intervals. RESULTS: Histological examination of positive control rats revealed features of atypical prostatic hyperplasia, with piling-up, papillary and cribiform patterns and budding-out of epithelial cells. Micturition assessment revealed that phenylephrine significantly lowered both the total volume of urine in 1 hour and the volume per micturition; the latter was considered the main efficacy variable. D-004 and Saw palmetto extracts significantly prevented this reduction in volume per micturition by 70.5% and 68.6%, respectively, while tamsulosin totally abolished the reduction in micturition induced by phenylephrine (100% inhibition). Tamsulosin, D-004 and Saw palmetto significantly reduced the histological changes of atypical prostatic hyperplasia induced by phenylephrine by 73.1%, 61.2% and 50.0%, respectively. CONCLUSIONS: Administration of D-004 resulted in marked and significant prevention of phenylephrine-induced impairment of micturition and histological changes in rat prostate. These findings indicate that, in vivo, D-004 effectively opposes these responses to phenylephrine, which are mediated through urogenital alpha(1)-adrenoceptors. In this respect, D-004 was moderately more effective than Saw palmetto, a phytotherapeutic standard used to treat BPH, but less effective than tamsulosin, a selective alpha(1A)-adrenoceptor antagonist.

Animals↗
PubMed1995

Sclerosing lobular hyperplasia of the breast: imaging features in 15 cases.

OBJECTIVE: Sclerosing lobular hyperplasia is an infrequent benign lesion of the breast, defined as prominent hyperplasia of the lobules with sclerosis of the interlobular stroma. It commonly presents as a tumorlike mass clinically. Sclerosing lobular hyperplasia has been identified at biopsy at our institution with rare but increasing frequency. We reviewed the imaging features of 15 patients with biopsy-proven sclerosing lobular hyperplasia to determine if a characteristic imaging pattern could suggest this diagnosis. MATERIALS AND METHODS: The mammograms and sonograms of all women with pathologically proved sclerosing lobular hyperplasia seen between January 1986 and June 1993 were retrospectively reviewed by two of the authors who were familiar with the pathologic diagnosis. Imaging findings that led to biopsy or were present on the preoperative studies were reviewed. The study included 15 patients ranging in age from 21 to 46 years old, with a mean age of 32 years. Seven were black, and eight were white. All women had mammograms, three patients had prior mammograms for comparison, and sonography was done in all but one case. Presenting symptoms included a recently discovered breast lump in eight patients, breast tenderness in one patient, and a clear nipple discharge in one patient. The other five were asymptomatic and had screening mammograms. RESULTS: Eight patients (53%) had a well-defined mass on mammography, varying in size from 1.0 cm to 8.0 cm (mean, 3.7 cm). In one of these patients, the nodule was proved to be a fibroadenoma; sclerosing lobular hyperplasia was found only microscopically. Microcalcifications were present within the mass on mammography in one patient. Mammograms in two women showed asymmetric increased density compared with the opposite breast, and in five cases, the mammographic findings were interpreted as normal. Sonograms showed a solid, well-defined mass with either homogeneous or mixed echoes in 10 of 14 patients (71%). In only one of these nodules was acoustic enhancement present. In the other four women, sonograms were normal. No characteristic findings were identified that would suggest sclerosing lobular hyperplasia as a likely diagnosis preoperatively, and, in fact, in many cases a diagnosis of fibroadenoma was considered most probable. CONCLUSION: The imaging findings of sclerosing lobular hyperplasia are not sufficiently characteristic to distinguish the lesion from fibroadenomas and well-circumscribed carcinomas.

Adult↗
PubMed1999

Management of endometrial hyperplasia: a retrospective analysis.

OBJECTIVE: To determine the incidence of endometrial hyperplasia and to analyse the management of patients with this disorder. METHOD: Retrospective descriptive study at the Department of Obstetrics and Gynecology, Ramathibodi Hospital. The medical records of patients with endometrial hyperplasia from 1990 to 1995 were analysed. Descriptive statistic was used. RESULT: Medical records could be obtained in 87 per cent of cases. Incidence of endometrial hyperplasia was 1 per cent of gynecological out-patients and 11 per cent of uterine curettage. Half of the patients had cystic hyperplasia. Main treatment options of patients with cystic hyperplasia were expectant and progestogen therapy. The major treatments of adenomatous hyperplasia were progestogen and hysterectomy. Most patients with atypical hyperplasia underwent hysterectomy. Most of the patients with expectant or hormonal therapy have recurrence of abnormal uterine bleeding. CONCLUSION: Endometrial hyperplasia is not uncommon in gynecological practice. All gynecologists should be familiar with the pathophysiology and the natural history of this disorder. The unopposed estrogen stimulation should be investigated and corrected. Treatment options should be tailored to individuals according to disease grading, age of the patient and desire of pregnancy. Long-term follow-up until menopause is mandatory to prevent the excessive uterine blood loss and the progression to carcinoma.

Adolescent↗
PubMed1999

[Endometrial hyperplasia--diagnosis and treatment].

The International Society of Gynecological Pathologists recently agreed on a classification of endometrial hyperplasia into two main groups; hyperplasias with and without atypia. The lesions were further subdivided into simple and complex hyperplasia. These guidelines were subsequently adopted by the World Health Organization. The disease is a result of oestrogen/gestagen imbalance with oestrogen overexpression. The most important prognostic factor is cellular atypia. Progress to invasive cancer is seen in about 20% of the patients with atypical hyperplasia, and most frequently occurs in postmenopausal women. The treatment of endometrial hyperplasia depends on histologic type, patients' age and whether the hyperplasia is a result of endogenous or exogenous oestrogen overexpression. The risk for progression to invasive cancer is minimal in oestrogen treated patients with simple or complex hyperplasia without atypia. Women under 40 years of age in this group can safely be treated with gestagens. In postmenopausal women with simple or complex hyperplasia with atypia, the recommended treatment is surgery including removal of the uterus and the ovaries.

Adult↗
PubMedDate not supplied

Epithelial hyperplasia of the gallbladder in children with anomalous pancreaticobiliary ductal union.

BACKGROUND/AIMS: Few data are available on the fate and incidence of epithelial hyperplasia throughout the life of anomalous pancreaticobiliary ductal union (APBD) patients. The pathological study in pediatric APBD patients is less recognized. METHODOLOGY: Ten resected gallbladders obtained from children with APBD and control patients without APBD were examined histologically, and immunohistochemically for the detection of Ki-67 (as a proliferative marker) and p53. K-ras mutations in codon 12 were also examined. Epithelial hyperplasia was classified into high-grade and low-grade hyperplasia. RESULTS: Six (60%) of 10 patients with APBD had epithelial hyperplasia of the gallbladder, whereas no patients without APBD exhibited this lesion. Diffuse epithelial hyperplasia was observed in 1 (50%) of 2 undilated-type APBD and 5 (63%) of 8 dilated-type. Two (33%) of 6 patients with epithelial hyperplasia exhibited high-grade hyperplasia. Ki-67 labeling index (LI) was significantly higher in hyperplastic mucosa than in control gallbladder mucosa. K-ras mutations and p53 overexpression were not detected in hyperplastic and normal mucosa. CONCLUSIONS: Epithelial hyperplasia of the gallbladder accompanied by increased proliferative activity exists at birth or is acquired in childhood with APBD patients and may be an important factor predisposing to the development of gallbladder carcinoma.

Cell Division↗
PubMedDate not supplied

[Functional morphology of the hypophyseal-adrenal-gonad system in different variants of prostatic hyperplasia].

Two forms of prostatic hyperplasia are distinguished: fibro-glandular (FGH) and glandular-fibrous (GFH). An increase in the number of adenohypophysis cells producing gonadotrophic hormone, hyperplasia of the adrenal reticular zone, hyperplasia and hypertrophy of Leydig and Sertoli cells in the testis were observed in FGH. Signs of enhanced functional activity were observed in all cases of hyperplasia. In GFH there was an increase in the number of adenohypophyseal cells producing adrenocorticotrophic hormone, hyperplasia of the fascicular layer in the adrenals, atrophy of Leydig cells in the presence of Sertoli cell hyperplasia. The variant of prostatic hyperplasia is determined by the hormonal changes and this may help in choosing of approaches to therapeutic correction of prostatic hyperplasia and its early diagnosis.

Adult↗