Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPERPLASIA”

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

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

At least 235 records · Page 13Linked to original sources

Oral metronidazole does not improve cyclosporine A-induced gingival hyperplasia.

Recently, resolution of cyclosporine A (CSA)-induced gingival hyperplasia was reported with antibiotic treatment. We therefore assessed the oral status of 45 children on CSA after renal transplantation and evaluated the effects of metronidazole treatment in children with high-grade gingival hyperplasia. Gingival hyperplasia was absent in 19 (42%), mild in 5 (11%), moderate in 13 (29%), and severe in 8 (18%) children. There was no significantly different incidence in high-grade gingival hyperplasia (moderate and severe) between children with (16 of 30) or without (5 of 15) concomitant treatment with calcium channel blockers. The mean trough level of CSA was not different between children with varying severities of gingival hyperplasia. We treated 13 children with high-grade CSA-induced gingival hyperplasia (9 boys, 4 girls, mean age 14.2 +/- 3.4 years) with 750 mg metronidazole in three divided doses (10-25 mg/kg) for a total of 7 days. All 13 children were concomitantly treated with calcium channel blockers for hypertension; their mean monoclonal CSA trough level was 246 +/- 34 ng/ml. Oral examination and photographic documentation were performed by the same examiner on all patients before and 1 and 3 months after metronidazole treatment. We found no changes in gingival hyperplasia; gingival inflammation improved in 5 children (P = ns). We conclude that synergistic effects of calcium channel blockers and high concentrations of CSA in our population may outweigh beneficial effects of metronidazole treatment of CSA-induced gingival hyperplasia after renal transplantation.

Adolescent↗

Angiogenesis in endometrial hyperplasia and stage I endometrial carcinoma.

OBJECTIVE: To evaluate angiogenesis in endometrial hyperplasia and stage I endometrial carcinoma, and to investigate the relationship between angiogenesis and tumor grade and depth of invasion. METHODS: Three groups of patients were analyzed: control patients who underwent hysterectomy for benign conditions (n = 19), patients with endometrial hyperplasia (n = 24), and patients with stage I endometrial carcinoma (n = 34). All hysterectomy specimens were stained immunohistochemically for factor VIII-related antigen as a sensitive and specific marker for vascular endothelium. Areas close to the deepest myometrial invasion or those with the highest grade of endometrial hyperplasia and the highest angiogenic intensity were selected. Three fields (x 400) were selected for each slide, and the mean microvessel count was calculated. Statistical analysis included Mann-Whitney U test or Kruskal-Wallis analysis of variance and Dunn post hoc procedure. P < .05 was considered significant. RESULTS: A significant difference was found between the microvessel count of controls versus the group with complex endometrial hyperplasia (median 21, range 16-80, versus median 38, range 20-130; P < .05). Microvessel counts of complex endometrial hyperplasia were significantly higher than those of simple hyperplasia (median 25, range 16-42; P < .05) and significantly lower than counts of endometrial carcinoma (median 77.5, range 19-189; P < .05). Microvessel counts in complex hyperplasia were not significantly different than those of noninvasive stage I endometrial carcinoma (median 38, range 20-130, versus median 44, range 19-119; P = .5). In cases of stage I endometrial carcinoma, a higher number of microvessels was noted in specimens with myometrial invasion than in those without myometrial invasion (median 44, range 19-119, versus median 83, range 19-189; P < .01). A higher number of microvessels was noted in cases with grade 2 than in those with grade 1, stage I endometrial carcinoma (median 44, range 19-98, versus median 96, range 63-189; P < .001). CONCLUSION: Complex endometrial hyperplasia and endometrial carcinoma are angiogenic. Furthermore, in stage I endometrial carcinoma, greater depth of invasion and higher tumor grade are directly correlated with angiogenic intensity.

Endometrial Hyperplasia↗

The management of endometrial hyperplasia: an evaluation of current practice.

OBJECTIVE: To identify current management practices and evaluate subsequent outcomes of treatment for women diagnosed with endometrial hyperplasia. STUDY DESIGN: All women with a histological diagnosis of endometrial hyperplasia at the Birmingham Women's Hospital were identified between October 1998 and September 2000. A retrospective case note review was performed for each woman using a standardised data abstraction sheet. Baseline characteristics including clinical presentation and treatment strategy were obtained. Results of subsequent endometrial tissue examinations were used to assess histological response to treatment and the need and indication for hysterectomy was used to assess clinical response. RESULTS: There were 351 women diagnosed with endometrial hyperplasia during the study period of which 84% presented with symptoms of abnormal uterine bleeding and 54% were postmenopausal. Complex endometrial hyperplasia was the most common diagnosis accounting for 60% of all cases. Eighty percent of women with atypical endometrial hyperplasia were treated by hysterectomy compared with 30% without evidence of cytological atypia (relative hysterectomy rate of 2.6, 95% CI 2.0-3.3). Hysterectomy was avoided in 138/172 (80%, 95% CI 74-86%) women managed conservatively during the study period. Overall 35/108 (36%, 95% CI 27-46%) of women managed conservatively had persistent or progressive disease identified (mean follow up 36 months). 20/143 (14%) women initially diagnosed with endometrial hyperplasia who subsequently underwent hysterectomy were found to have endometrial cancer, the majority of whom had been diagnosed with atypical disease (14/20, 70%). CONCLUSION(S): The majority of women with atypical endometrial hyperplasia were managed by hysterectomy and the substantial risk of diagnostic under-call supports this approach to treatment. In contrast, there is no consensus regarding the initial management of women with endometrial hyperplasia without cytological atypia.

Aged↗

Resectoscopic surgery may be an alternative to hysterectomy in high-risk women with atypical endometrial hyperplasia.

STUDY OBJECTIVE: Endometrial hyperplasia is found in 2% to 10% of women with abnormal uterine bleeding (AUB). Up to 43% of patients with cytologic atypia harbor coexisting adenocarcinoma, and approximately 20% to 52% of atypical hyperplasias, if untreated, progress to cancer. The objective of this study was to estimate the incidence of atypical endometrial hyperplasia encountered during routine resectoscopic surgery in women with AUB and to evaluate the role of resectoscopic surgery in the management of women with AUB and atypical endometrial hyperplasia who refused and/or were at high risk for hysterectomy. DESIGN: Prospective cohort study (Canadian Task Force classification II-3). SETTING: University-affiliated teaching hospital. PATIENTS: From January 1990 through December 2005, the senior author (GAV) performed primary resectoscopic surgery in 3401 women with AUB. Among these, there were 22 women with atypical (17 complex, 5 simple) endometrial hyperplasia. INTERVENTIONS: All women underwent hysteroscopic evaluation and partial (n = 3) or complete (n = 19) endometrial electrocoagulation and/or resection. Subsequently, 6 women had hysterectomy and bilateral salpingo-oophorectomy (BSO). MEASUREMENTS AND MAIN RESULTS: The median (range) for age, parity, and body mass index were 55 years (24-78 years), 2 (0-4), and 30.1 kg/m2 (22.5-52.2 kg/m2), respectively. Among the 3401 women, there were 22 cases of atypical endometrial hyperplasia, 12 of which were incidentally diagnosed at the time of hysteroscopy (complex 10, simple 2, incidence 0.35%). After hysteroscopic diagnosis or confirmation of diagnosis, 6 women underwent hysterectomy and BSO. Of the remaining 16 women, followed for a median of 5 years (range 1.5-12 years), 1 was lost to follow-up, 1 had only a biopsy to preserve fertility, 1 died from lung cancer after 4 years, and 1 died from colon cancer after 5 years. One patient developed endometrial cancer after 10.5 years with postmenopausal bleeding. She remains alive and well 3.5 years after hysterectomy and BSO. The remaining 11 patients are amenorrheic at a median follow-up of 6 years (range 1.5-12 years). CONCLUSIONS: Resectoscopic surgery in 3391 women with AUB detected 12 incidental cases of atypical endometrial hyperplasia (incidence 0.35%). Skillful resectoscopic surgery may be an alternative to hysterectomy in women with AUB and atypical endometrial hyperplasia, who refuse or are at high-risk for hysterectomy and who are compliant with regular and long-term follow-up.

Adult↗

Effects of azithromycin on cyclosporine-induced gingival hyperplasia in renal transplant patients.

BACKGROUND: Gingival hyperplasia is a well-known complication of cyclosporine therapy, affecting 21% to 35% of renal transplant patients. Metronidazole, clarithromycin, and azithromycin, all azalid antimicrobial agents derived from the macrolide antibiotic erythromycin, have been used for treatment. Marked improvements in gingival hyperplasia have been recorded in particular with azithromycin. The aim of the present study was to investigate histopathological features of cyclosporine-induced gingival hyperplasia and to evaluate the quantitative efficacy of short-term azithromycin therapy. METHODS: Eighteen renal transplant patients with cyclosporine-induced gingival hyperplasia were included in the study. All patients received azithromycin with a dose of 500 mg/d for 3 consecutive days. Changes in gingival hyperplasia were evaluated by measuring the gingival sulcus depth to the cementum-enamel junction of every tooth in each of the four quadrants on days 0, 7, 30, 90, 180. Gum biopsies were obtained on days 0 and 30; the degree of inflammation was classified as "mild," "intermediate," and "severe". RESULTS: Gingival hyperplasia was reduced in all treated patients throughout the study. The degree of improvement was more significant between 0 to 7 and 7 to 30 days than at other times (respectively, P < .0001 and P < .002). Histopathologically, eight patients had severe and one patient moderate chronic inflammation at the beginning of therapy. Three other biopsies were reported as papilloma, mucosal hyperplasia, and normal gingival tissue biopsy. CONCLUSIONS: Azithromycin appears to be useful to treat cyclosporine-induced gingival hyperplasia in renal transplant patients. Treatment is inexpensive and free from known adverse effects.

Adult↗

High rates of prostate-specific antigen testing in men with evidence of benign prostatic hyperplasia.

PURPOSE: Benign prostatic hyperplasia is common among men who may be candidates for prostate cancer screening using prostate-specific antigen (PSA) testing. Patterns of PSA testing among men with evidence of benign prostatic hyperplasia have not been studied. METHODS: We examined the prevalence and correlates of a self-reported history of PSA testing. In 1994, 33,028 US health professionals without prostate cancer aged 47 to 85 years provided information on prior PSA testing, lower urinary tract symptoms characteristic of benign prostatic hyperplasia, history of prostatectomy, and prostate cancer risk factors. In 1995, a subset of 7,070 men provided additional information on diagnosis and treatment of benign prostatic hyperplasia. RESULTS: From 39% of men in their 50s to 53% of men in their 80s reported PSA testing in the prior year (P <0.0001 for trend with age). Men were more likely to report PSA testing if they had lower urinary tract symptoms characteristic of benign prostatic hyperplasia (age-adjusted odds ratio for severe symptoms 2.2, 95% confidence interval 1.8 to 2.6), a prior history of prostatectomy (age-adjusted odds ratio 1.1, 95% confidence interval 1.02 to 1.2), or a physician diagnosis of benign prostatic hyperplasia (odds ratio 1.9, 95% confidence interval 1.7 to 2.2; adjusted for age, signs or symptoms of benign prostatic hyperplasia, and prostate cancer risk factors). CONCLUSIONS: These US health professionals reported preferential use of PSA testing among men least likely to benefit from early cancer detection (older men) and among men most likely to have a false-positive PSA result (men with benign prostatic hyperplasia). Physician and patient education are needed to promote more rational and selective use of this screening test.

Aged↗

The effect of low molecular weight heparin on intimal hyperplasia in vein grafts.

Intimal hyperplasia due to smooth muscle cell proliferation is a well recognised cause of vascular graft failure. In experimental studies heparin and its low molecular weight derivatives can inhibit this proliferative response. This study examines the effect of subcutaneous low molecular weight heparin (LMWH) therapy on intimal hyperplasia in a model of arterial vein grafting. Twenty-four New Zealand White rabbits underwent interposition vein grafting of the carotid artery. Animals were randomly assigned to a control or treated group. Treated animals received 60 anti Xa units/kg of subcutaneous LMWH daily for 1 month. Animals were then sacrificed, graft patency assessed and the vessels then harvested for analysis of intimal hyperplasia. Intimal hyperplasia in carotid arteries and vein grafts was measured using a computerised image analysis system and was expressed as an intimal:medial area ratio. A statistically significant reduction in the degree of intimal hyperplasia seen in the arterial component of the distal anastomoses of carotid vein grafts was achieved using subcutaneous LMWH [Control 0.44 (0.37-0.55): LMWH 0.27 (0-0.37) p < 0.05]. There was no difference in the degree of intimal hyperplasia seen in the vein grafts themselves. [Control 0.21 (0-0.54): LMWH 0.23 (0-0.72)]. This study suggests that subcutaneous LMWH can inhibit the development of intimal hyperplasia in arteries undergoing vascular grafting but does not influence intimal hyperplasia within vein grafts. This has important implications for the further evaluation of antithrombotic agents following vascular surgery.

Animals↗

Resectoscopic surgery in 10 women with abnormal uterine bleeding and atypical endometrial hyperplasia.

STUDY OBJECTIVE: To evaluate the role of the resectoscope in the diagnosis and treatment of women with abnormal uterine bleeding (AUB) and atypical endometrial hyperplasia. DESIGN: Retrospective case series (Canadian Task Force classification III-3). SETTING: University-affiliated teaching hospital. PATIENTS: Ten women. Intervention. Hysteroscopic evaluation after preoperative endometrial biopsy indicated simple hyperplasia without atypia, complex hyperplasia with atypia, or inadequate specimen. MEASUREMENTS AND MAIN RESULTS: Atypical hyperplasia was confirmed in eight patients after total endomyometrial resection. Hysterectomy was offered to all patients but accepted by only two: one for bilateral ovarian serous cystadenomas and the second for a granulosa cell ovarian tumor. No residual endometrium was found in hysterectomy specimens. Seven women were amenorrheic and well 1 to 9 years after resection. An additional patient with amenorrhea died from colon cancer 2 years after resection. CONCLUSION: Resectoscopic surgery confirmed or detected atypical endometrial hyperplasia in eight women and excluded it in two patients with AUB and a previous diagnosis of simple hyperplasia, atypical hyperplasia, or inadequate specimen. Skillful resectoscopic surgery may be an alternative to hysterectomy in selected patients with atypical hyperplasia who are compliant with regular and long-term follow-up.

Aged↗

Evaluation of parathyroid hyperplasia by ultrasonographic examination in patients with end-stage renal failure before and at initiation of dialysis.

Secondary hyperparathyroidism (2HPT), which is related to renal osteodystrophy (ROD), may occur in patients in the comparatively early stage of chronic renal failure (CRF). Secondary hyperparathyroidism patients with parathyroid hyperplasia showed resistance to vitamin D(3) treatment during long-term dialysis. At present, evaluation by ultrasonography is considered to be useful for confirming parathyroid hyperplasia. There are no clinical data associated with imaging evaluation of 2HPT in CRF patients. In the present study, the relationship among clinical and biochemical data, and parathyroid hyperplasia by ultrasonography, was evaluated in 12 patients (six males and six females) with end-stage renal failure (ESRF) before and at initiation of dialysis. Five patients showed an enlargement of parathyroid glands in ultrasonography. Levels of serum-intact parathyroid hormone (PTH) in patients with parathyroid hyperplasia (positive group) were significantly higher than in those without hyperplasia (negative group; 97.6 +/- 36.65 vs 17.4 +/- 4.45 pmol/L; P < 0.05). The levels of intact PTH were above 35.0 pmol/L in all five patients with hyperplasia. All patients in the positive group had never taken vitamin D(3) supplements. Calcium-containing phosphate binders were not prescribed before the present study, except in one patient. Parathyroid hyperplasia caused by 2HPT was recognized in patients before and at initiation of dialysis in this study. It appears that untreated 2HPT in CRF patients may progress to advanced 2HPT in ESRF before and/or after the early stage of dialysis. The levels of serum intact PTH are useful in predicting parathyroid hyperplasia.

Adult↗

Basaloid/follicular hyperplasia overlying connective tissue/mesenchymal hamartomas simulating basal cell carcinomas.

BACKGROUND: Basaloid hyperplasia has been described overlying dermatofibromas as well as in the epidermis overlying nevus sebaceus. Although the morphology of these areas may resemble that of basal cell carcinoma (BCC), in the majority of cases aggressive behavior of the proliferation is not seen. In fact, the basaloid proliferation often shows follicular differentiation and may be stimulated and maintained by its relationship with the underlying stromal cells. OBJECTIVE: We wanted to determine whether immunohistochemical staining for antibodies, which may suggest differences in pathogenesis, were different in basaloid hyperplasia overlying connective tissue/mesenchymal hamartomas and BCC. METHODS: We report 3 cases of connective tissue/mesenchymal hamartomas with overlying basaloid hyperplasia, in which the areas of the basaloid proliferation showed follicular differentiation. Immunohistochemical stains included Ber-EP4, PCNA, Ki-67, Bcl-2, p53, SM-Actin, CD31, factor XIIIa, KP-1, and CD34. RESULTS: There was a diffuse positive reaction for Ber-EP4 in all specimens and there was increased nuclear staining for PCNA and Ki-67. There was focal cytoplasmic staining for Bcl-2 in the areas of basaloid hyperplasia. Immunohistochemical staining for p53 showed only scattered positive cells except in a small focus in the areas of basaloid hyperplasia. The connective tissue component of all lesions showed diffuse staining for CD34 surrounding areas of basaloid hyperplasia in the mesenchymal component as well as in abundant S-100(+) nerves. CONCLUSION: The areas of basaloid hyperplasia in these hamartomas exhibited an immature phenotype similar to that seen in both BCCs and follicular tumors; however, the patterns of proliferation markers, p53, Bcl-2, and the surrounding stromal cell markers were similar to those of benign follicular tumors. Thus the staining pattern for this group of antibodies suggests that areas of basaloid hyperplasia are not BCC.

Adult↗

Saratin, an inhibitor of von Willebrand factor-dependent platelet adhesion, decreases platelet aggregation and intimal hyperplasia in a rat carotid endarterectomy model.

PURPOSE: Post-carotid endarterectomy, thrombosis, and intimal hyperplasia may be decreased by the inhibition of platelet adhesion and activation. In this study, a novel agent, saratin, was used to inhibit platelet-to-collagen adhesion in a rat carotid endarterectomy model. Saratin is a recombinant protein isolated from the saliva of the medicinal leech Hirudo medicinalis, which is thought to act by binding to collagen, and inhibits von Willebrand factor-collagen interaction under conditions of increased shear and therefore, the adherence and activation of platelets at the vessel wall. Saratin has the advantage of being a nonsystemic, site-specific topical application. METHODS: A rat carotid endarterectomy model was used in which an open technique with arteriotomy and intimectomy was used. Saratin was applied to the endarterectomized surface of the carotid artery before arterial closure. End point measurements included platelet adhesion, thrombosis rate, intimal hyperplasia development, bleeding times, and platelet counts. Electron micrographs of carotid arteries were used for quantitative analysis of platelet aggregation and platelet counts. Intimal hyperplasia and thrombosis were assessed with computer-assisted morphometric analysis of elastin-stained carotid artery sections with direct measurement of the intimal hyperplasia area. RESULTS: The topical application of saratin significantly decreased platelet adhesion compared with controls at 3 hours after carotid endarterectomy (64 +/- 17 vs 155 +/- 33 platelets per grid, P = .05), and 24 hours after carotid endarterectomy (35 +/- 11 vs 149 +/- 37 platelets per grid, P = .0110), respectively. A percent luminal stenosis, as a measure of intimal hyperplasia, was significantly decreased with saratin application compared with controls (10.9% +/- 1.8% vs 29.8% +/- 6.8%, P = .0042). This decrease in intimal hyperplasia formation correlated with the inhibition of platelet adhesion. Thirty-three percent of control arteries were found to be thrombosed 2 weeks after carotid endarterectomy compared with a 0% thrombosis rate in the saratin-treated group (P = .0156). No increased bleeding was encountered along the arterial suture line in the saratin group. Bleeding times and systemic platelet counts were not found to change significantly in the saratin-treated rats compared with control rats at 3 and 24 hours after endarterectomy. CONCLUSION: Saratin significantly decreased platelet adhesion, intimal hyperplasia, luminal stenosis, and thrombosis after carotid endarterectomy in rats. Saratin did not increase suture line bleeding or bleeding times, and did not decrease platelet counts. Saratin may serve as a topical agent to be used for the site-specific inhibition of thrombosis and intimal hyperplasia after vascular manipulation.

Administration, Topical↗

DNA ploidy, cell cycle kinetics, and low versus high grade atypia in endometrial hyperplasia.

There have been few studies of DNA ploidy and cell cycle kinetics in endometrial hyperplasia. The authors studied archival cases of proliferative endometrium, simple, complex and atypical endometrial hyperplasia and well, moderately, and poorly differentiated endometrial adenocarcinoma by flow cytometry and also evaluated the significance of the degree of cytologic atypia (low versus high) in endometrial hyperplasia relative to the occurrence of carcinoma. All proliferative endometria, all types of hyperplasia and well and moderately differentiated carcinomas were diploid. Two-thirds of poorly differentiated adenocarcinomas were aneuploid. Neither S-phase fractions or proliferative fractions (S+G2M) could distinguish among the different types of hyperplasia or predict which hyperplasias were associated with carcinomas. The degree of cytologic atypia in atypical hyperplasia was not predictive of the occurrence of carcinoma. Poorly differentiated carcinomas showed significant differences in DNA ploidy, S-phase, and proliferative fractions from endometrial hyperplasia and lower grade carcinoma. These results support the concept that there are two fundamentally different types of endometrial carcinoma.

Adenocarcinoma↗

A high body mass index and female gender are associated with an increased risk of nodular hyperplasia of parathyroid glands in chronic uraemia.

BACKGROUND: A persistent hyperphosphataemia represents one of the most important factors in the development of secondary hyperparathyroidism (sHPTH). The present prospective study was designed in order to test the hypothesis that a higher body mass index (BMI) may predispose to a larger body burden of phosphate (P), influencing by that way the severity of sHPTH. METHODS: Histological studies were performed on 168 parathyroid glands of 42 consecutive adult Caucasian haemodialysis patients (20 males and 22 females) referred for first parathyroidectomy (PTx): each parathyroid gland was graded as 0, when only or mainly diffuse hyperplasia was found, or as 1, when only or mainly nodular hyperplasia was found. Thus, parathyroid histology was scored on a 5-point scale: 0 = diffuse hyperplasia in the four glands; 1 = nodular hyperplasia in one gland; 2 = nodular hyperplasia in two glands; 3 = nodular hyperplasia in three glands; 4 = nodular hyperplasia in the four glands. For sake of simplicity, the three less severe histological gradings, i.e. scores 0-2 were grouped together and indicated as score group 2. RESULTS: The distribution of the patients was the following: 28.6% were in the score group 2, 23.8% in the score group 3 and 47.6% in the score group 4 (20 patients, 14 of whom were females). The output of the one-way ANOVA with the histological scores as grouping variable and age, dialysis duration, BMI and pre-PTx serum iPTH, alkaline phosphatase (ALP), calcium (Ca) and P as predictors showed that only BMI was different among the three histological scores (P = 0.001). By stratifying the analysis by gender, the relationship between BMI and histological scores was confirmed only in females (P = 0.006). The stratification of the entire cohort into two groups according to the cut-off value of BMI = 25 kg/m(2) showed that: (i) score 4 was more prevalent in the high-BMI group and score 2 in the normal-BMI group (P = 0.01); (ii) female gender was more represented in the high-BMI group (12 out of 18 patients, P = 0.04); and (iii) the pre-PTx serum P levels were significantly higher in the high-BMI group (P = 0.008). The output of the linear multiple regression analysis with pre-PTx serum P as dependent variable and BMI, pre-PTx serum ALP and Ca as independent variables (selected according to the statistical significance in the bivariate correlations) showed that only serum Ca and BMI were statistically significant predictors of serum P levels. CONCLUSIONS: A high BMI and female gender are associated with an increased risk of nodular hyperplasia of parathyroid glands in adult Caucasian haemodialysis patients. The two risk factors, above all if combined in the same patient, appear to predispose to a larger body burden of P, increasing by that way the severity of sHPTH.

Body Mass Index↗

Effect of estrogen and progesterone on the development of endometrial hyperplasia in the Fischer rat.

The effect of changing endocrine status on the uterine endometrium of the female Fischer rat was observed in vivo after neonatal androgenization, after aging, after estrogen (E) implant in ovariectomized (OVX) rats, and in vitro after progesterone (P) addition to monolayer cultures of uterine tumor cells. Neonatal androgenization produced cystic ovarian follicles and persistent vaginal cornification for 10-14 mo, indicative of an anovulatory, persistent E status. The constant estrous (CE) state, induced by androgenization, uniformly produced focal glandular hyperplasia of the endometrium at 9 mo of age. Focal glandular hyperplasia, which was absent in the cycling 6-mo-old estrous endometrium, was also apparent in the 12-mo-old rats which had ceased cycling and entered natural CE. Subcutaneous estradiol-17 beta (E2) implants in 12-mo-old OVX rats induced early cystic and adenomatous changes in the foci of hyperplasia. Acyclic control rats, 21 mo old, in persistent diestrus (PD) exhibited a 3-fold elevation of serum P associated with glandular atrophy of the endometrium. Ten nM P also inhibited proliferation of endometrial cells in cultures prepared from tumors of 21-mo-old rats. On the other hand, adenomatous hyperplasia was observed in 29-mo-old PD rats, despite the presence of low serum E and elevated serum P. These results indicate that either induced or natural constant E status leads to focal glandular hyperplasia in the Fischer rat. E2 implants in the 12-mo-old OVX Fischer rat induced early cystic and adenomatous changes in the focal hyperplasia. Inhibition of these focal hyperplasias was associated with elevated serum P at 21 mo. The development of adenomatous hyperplasia in the aged endometrium, on the other hand, occurred despite elevated serum P at 29 mo.

Aging↗

Cell biology of parathyroid hyperplasia in uremia.

Marked parathyroid hyperplasia of heterogeneous degrees is often seen in chronic dialysis patients with severe secondary hyperparathyroidism. In uremia, parathyroid cell proliferation is initially stimulated by decreased concentration of calcium ions and calcitriol and also by direct effect of phosphate accumulation, leading to diffuse hyperplasia of the parathyroid. Then, small nodules caused by monoclonal cell proliferation form within diffuse hyperplasia, which progress to form nodular hyperplasia. Cells in nodular hyperplasia have a lower density of calcitriol receptor and calcium-sensing receptor than diffuse hyperplasia and are thus more resistant to medical therapy, including calcitriol pulse therapy. One of these nodules may grow more vigorously than the others and may finally occupy a large part of the enlarged gland. Genetic mutations and rearrangements of these cells in nodular hyperplasia remain to be fully elucidated in the near future to establish an effective method for the prevention of parathyroid hyperplasia in uremia.

Calcitriol↗

Lymphoid hyperplasia of the gastrointestinal tract. A study of 26 cases and review of the literature.

Based on a study of 26 cases and a review of the literature, lymphoid hyperplasia of the gastrointestinal tract can be categorized into four clinicopathologic groups: focal lymphoid hyperplasia of the stomach, focal lymphoid hyperplasia of the small intestine, focal lymphoid hyperplasia of the rectum, and nodular lymphoid hyperplasia of the gastrointestinal tract. The focal lesions are single, variably circumscribed, and produce thickening of the wall of the affected part of the viscus. While a substantial number of the gastric lesions are associated with chronic peptic ulcers, ulceration is absent or insignificant in focal lesions located in the intestine. The extent of the infiltrate may range from involvement of the mucosa and submucosa only to infiltration of the full thickness of the wall. Nodular lymphoid hyperplasia of the gastrointestinal tract produces multiple discrete mucosal nodules in a variable segment of the small intestine, large intestine, or both. Gastric involvement is rare. The lymphoid infiltrate is confined to the lamina propria and superficial submucosa. Nodular lymphoid hyperplasia is most commonly encountered incidentally during radiologic examination or at autopsy, but it also occurs in association with hypogammaglobulinemia, especially late-onset acquired hypogammaglobulinemia. Lymphoid hyperplasia of the gastrointestinal tract can be distinguished from malignant lymphoma by the polymorphic nature of the infiltrate, the absence of significant cytologic atypia, and the presence of reactive follicles within the lesion.

Adult↗

Use of monoclonal antibodies MSN-1 and B72.3 in the prediction of the natural history of endometrial hyperplasia.

Forty patients, originally diagnosed as endometrial hyperplasia, were reviewed histopathologically and evaluated for immunohistochemical staining with antibodies directed against TAG-72 and MSN-1 antigens. All patients had follow-up endometrial biospies or hysterectomies from 1 to 13 years later. The extent of regression to normal of nonhyperplastic endometrium, persistence as any type of endometrial hyperplasia, or progression to endometrial adenocarcinoma was correlated with the histologic hyperplastic subtype and immunohistochemical staining. As expected, cases of complex or atypical hyperplasia more often progressed to carcinoma than cases of simple or no hyperplasia. Interestingly, MSN-1 positivity was more prevalent in cases of higher grades than lower grades of hyperplasia and was associated with the tendency to show persistent hyperplasia or progression to carcinoma. B72.3 positivity was uncommon in the hyperplastic endometrium and was not correlated with clinical regression or progression. Although the tendency for progression of endometrial hyperplasia to endometrial carcinoma is best judged histologically, MSN-1 may add prognostic information in subgroups of hyperplasia.

Adenocarcinoma↗

Mesonephric hyperplasia of the uterine cervix: a clinicopathologic study of 51 cases.

Lesions derived from remnants of the mesonephric (Wolffian) duct frequently occur in the wall of the uterine cervix and often cause diagnostic problems. Fifty-one cervical mesonephric lesions were studied. There were 40 lobular mesonephric hyperplasias and 11 diffuse mesonephric hyperplasias. Lobular hyperplasia was characterized by a distinctive clustering of mesonephric tubules, while diffuse hyperplasia was nonclustered. Fifteen patients with hyperplasia followed for a mean of 6.3 years were alive and well at last contact. In addition to morphologic differences between lobular and diffuse hyperplasia, there were statistically significant differences in patient age (means of 35 and 46 years, respectively) and lesion size (means of 11.8 and 15.7 mm, respectively), and less pronounced differences in proximity to surface epithelium and age-size correlations. Evidence suggests that the two types of mesonephric hyperplasias may be distinct entities. The morphologic appearances of the diffuse hyperplasias are emphasized to prevent their misinterpretation as variants of minimal deviation adenocarcinoma.

Adult↗