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PubMed2006

[Endometrial hyperplasia: A review].

Endometrial hyperplasias can be divided into two categories based on the presence or absence of cytological atypia and further classified as simple or complex according to the extent of architectural abnormalities. They are usually diagnosed because of irregular bleeding in perimenopause. Hysteroscopy with a biopsy gives a more accurate diagnosis than transvaginal ultrasonography, sonohysterography, or blind curettage. Endometrial hyperplasias with no cytological atypia, regarded as a response to unopposed endogenous estrogenic stimulation, are normally treated with progestins. The intra-uterine route (levonorgestrel intra-uterine system) is more effective and better tolerated than the oral route. Either conservative surgery (endometrial resection, thermal ablation) or radical surgery (hysterectomy) in the case of other genital diseases is performed on women who did not respond to medical treatment. Endometrial hyperplasias with cytological atypia, considered as intra-epithelial neoplasias, are traditionally treated by hysterectomy. The absence of management protocols in the literature offers various treatment options and indications. Gonadotropin-releasing hormone agonists, danazol, or aromatase inhibitor are effective, but have adverse effects and are expensive. Endometrial ablation can be performed as a first line therapy in women suffering from bleeding related to hyperplasia without cytological atypia. Medical treatment may be offered to young women suffered from hyperplasias with cytological atypia and desiring pregnancy.

Biopsy↗

PubMed1998

New approaches to the quantitation of hypertrophy and hyperplasia in hepatomegaly.

A histological method utilizing the optical dissector principle has been developed for determining the contribution of hypertrophy and hyperplasia to the hepatomegaly induced by the peroxisome proliferator gemfibrozil. The optical dissector is a technique derived from the 'new stereology' and has been used to estimate the number of hepatocyte nuclear profiles, that are present in a reference volume of tissue. The overall changes due to hypertrophy and hyperplasia in the rat liver after gemfibrozil treatment, did not reach significance, although the zonal hypertrophy change did. This indicated that although there was a 20% increase in liver weight with treatment, the hepatomegaly was caused by a combination of hypertrophy and hyperplasia, neither of which, on its own, was significantly different from the control values. The distinction of hyperplasia from hypertrophy, using a purely histological method, will be useful in assessing whether treatment related sustained hyperplasia is occurring in the liver.

Animals↗

PubMed2003

P53 expression in spontaneous and estradiol-induced endometrial hyperplasia during menopause.

OBJECTIVE: To determine the percentage of endometrial hyperplasia positive for p53 expression in both spontaneously occurring cases or following the use of unopposed estradiol. METHODS: Fifty-four postmenopausal patients with endometrial hyperplasia diagnosed by endometrial biopsy and hysteroscopy were recruited to this study. Thirty-three patients had used unopposed estradiol for periods of time from 1 to 3 years. P53 expression was detected in paraffin-embedded endometrial specimens by immunohistochemical methods. RESULTS: The percentage of endometrial hyperplasia positive for p53 expression was significantly greater in spontaneously occurring hyperplasia than in cases induced by the unopposed use of estradiol. CONCLUSION: Endometrial hyperplasia caused by the unopposed use of estradiol during menopause probably harbors fewer genomic errors than those cases occurring spontaneously.

Aged↗

PubMed1998

Endothelin-B receptors mediate intimal hyperplasia in an organ culture of human saphenous vein.

OBJECTIVE: Although a number of pharmacologic agents have been shown to reduce intimal hyperplasia in animal models of restenosis, to date no systemic agent has conclusively been shown to be effective in humans. Recently, considerable attention has been directed towards endothelin (ET), a potent vasoconstrictor and a powerful mitogen for vascular smooth muscle cells, as a mediator of intimal hyperplasia. Endothelin-1 has been shown to be mitogenic for human saphenous vein smooth muscle cells, and expression also is elevated in human vein graft stenosis. The aim of this study was the investigation of whether ET receptor antagonists can attenuate neointima formation in a laboratory model of vein graft intimal hyperplasia and the determination of whether the effects are mediated by a specific ET receptor subtype. METHODS: We used an organ culture of human saphenous vein, a well-validated model of vein graft intimal hyperplasia. Paired segments of human long saphenous vein were cultured with and without the following antagonists: bosentan, a nonselective ET receptor antagonist; BQ 123, a specific endothelin-A antagonist; or BQ 788, a specific endothelin-B (ETB) antagonist. After 14 days in the culture, the segments were fixed and processed and the sections were immunostained to facilitate the measurements of neointimal thickness with a computerized image analysis system. RESULTS: The nonselective antagonist bosentan and the ETB selective antagonist BQ 788 significantly reduced neointima formation by 70% (P = .001) and 50% (P = .03), respectively, but the ETA antagonist BQ 123 had no significant effect on the reduction of neointima formation (P = 1.0). CONCLUSION: The results of this study imply an important role for ET as a mediator of human vein graft intimal hyperplasia and imply further that a specific ETB antagonist may have a therapeutic potential for the prevention of vein graft stenosis.

Bosentan↗

PubMed1989

Distal anastomotic intimal hyperplasia: histopathologic character and biogenesis.

Although thrombogenicity of the prosthetic graft, progression of the atherosclerotic disease and distal anastomotic intimal hyperplasia are known etiologic factors of late graft failure, its occurrence is frequently encountered in the late graft occlusion. Forth-two canine PTFE iliofemoral grafts (all with end-to-side distal anastomosis) were studied. Computer digitization revealed that distal anastomotic intimal hyperplasia occurred exclusively at the heel and the toe of the graft and the floor of the host artery. The distal anastomotic intimal hyperplasia was 80-130 cells thick. Light microscopy and transmission electron microscopy revealed a similar architecture of interlamination of cellular elements and extracellular matrix in the hyperplastic cells. Transmission electron microscopy further defined a gradual cell transformation and orientation from the graft to the lumen. The cells near the graft were characterized by a gradual reduction of rough endoplasmic reticulum with a concomitant acquisition of myofilaments, transforming ovoid mesenchymoid cells to slender myofibroblasts. The orientation of cells in distal anastomotic intimal hyperplasia was embodied by random cell distribution at the periphery to a well-organized interlamination of myofibroblasts and extracellular matrix near the lumen. Distal anastomotic intimal hyperplasia is a biologic entity with active cellular and subcellular events. Its biogenesis appears to be influenced by the hemodynamics of blood flow at the distal anastomosis.

Animals↗

PubMed1988

Distal anastomotic intimal hyperplasia: biogenesis and etiology.

Anastomotic intimal hyperplasia occurred exclusively at the heel and the toe plus the floor of the distal end-to-side anastomosis of canine autologous femoro-femoral bypass (n = 14) and not in the end-to-end carotid or femoral interposition graft (n = 14). The occurrence of anastomotic intimal hyperplasia in the absence of compliance mismatch in an autologous bypass suggests that the geometry of the end-to-side anastomosis is primarily responsible for intimal hyperplasia formation. It is believed that because an end-to-side distal anastomosis is not a natural occurrence it is conductive to turbulent flow. The latter causes endothelial injury which in turn allows platelet growth factor to incite subendothelial myoblasts in extracellular matrix synthesis and intimal hyperplasia formation. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) identify myofibroblasts and fibrocollagenous matrix as the dominant cellular and extracellular substances in anastomotic intimal hyperplasia.

Anastomosis, Surgical↗

PubMed2001

Complete inhibition of intimal hyperplasia by perivascular delivery of paclitaxel in balloon-injured rat carotid arteries.

PURPOSE: To determine whether perivascular delivery of paclitaxel prevents luminal narrowing after balloon injury by inhibiting intimal hyperplasia. MATERIALS AND METHODS: Immediately after balloon injury of the entire left common carotid artery, three slow-release formulations of paclitaxel or control formulations without drug were applied around a distal segment of the artery. The noninjured right carotid arteries were evaluated as a control. The animals were maintained for 14 and 28 days (n = 5 in each group at each time interval). Histology, immunohistochemistry, and morphometric analysis were performed. RESULTS: Injured nontreated arteries exhibited a pronounced intimal hyperplasia (0.185 +/- 0.01 mm2 at 14 days and 0.189 +/- 0.01 mm2 at 28 days) and a marked reduction in luminal area (44% at 14 days and 43% at 28 days). Medial area and the number of medial cells increased by 44% and 45%, respectively, at 14 days, and by 22% and 37%, respectively, at 28 days. Injured arteries treated with perivascular paclitaxel did not show any intimal hyperplasia, and luminal area was increased in five of six groups and was unchanged in one group. These arteries had an increased medial area but they had fewer medial cells than noninjured arteries. Injured arteries treated with control implants without paclitaxel exhibited intimal hyperplasia and luminal narrowing. CONCLUSION: Perivascular slow release of paclitaxel totally inhibits intimal hyperplasia and prevents luminal narrowing after balloon injury. Because of its efficacy, perivascular paclitaxel represents a possible approach for prevention of restenosis in humans.

Angiogenesis Inhibitors↗

PubMed2002

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

STUDY OBJECTIVE: To evaluate the role of resectoscopic surgery in the diagnosis and treatment of women with abnormal uterine bleeding and endometrial hyperplasia without atypia. DESIGN: Retrospective analysis (Canadian Task Force classification II-2). SETTING: University-affiliated teaching hospital. PATIENTS: Twenty-five women with simple and seven with complex hyperplasia. INTERVENTION: Hysteroscopic endometrial ablation. MEASUREMENTS AND MAIN RESULTS: In patients with simple hyperplasia, average age, parity, body mass index, and mean arterial pressure were 53.2 years, 2.4 pregnancies, 30 kg/m2, and 99.5 mm Hg, respectively; in those with complex hyperplasia corresponding figures were 48 years, 2 pregnancies, 36 kg/m2, and 100 mm Hg. Nineteen of 32 women had postmenopausal bleeding, 9 of whom were taking combined hormone replacement therapy. Two had subsequent hysterectomies, one for pain and the other for incomplete resection due to an enlarged uterus. Resection could not be completed in one morbidly obese woman. One patient died from heart disease. During the follow-up of 1 to 8 years (mean 4 yrs) all patients remained amenorrheic with no evidence of recurrent disease or progression to cancer. CONCLUSION: Resectoscopic surgery by experienced hysteroscopists may be effective therapy for endometrial hyperplasia without atypia, especially in women at high risk for medical therapy or hysterectomy. Patient surveillance is mandatory for early detection and management of recurrent disease and progression to cancer.

Adult↗

PubMed2002

[Endometrial hyperplasias resistant to progestins: alternatives to traditional treatments].

Endometrial hyperplasias are mainly regarded as a response to unopposed endogenous estrogenic stimulation and concern 12% of perimenopausal women. They are usually diagnosed because of irregular bleeding. They are divided into two categories based on the presence or absence of cytological atypia and further classified as simple or complex according to the extent of architectural abnormalities. Endometrial hyperplasias with cytological atypia are classically treated by hysterectomy. Endometrial hyperplasias without cytological atypia are classically treated by progestins. The bad observance (25% spontaneously stopping), the 30% recurrence rate after stopping progestin and the 12-53% resistance rate to treatment lead to propose a second-line therapy after endocrinological check-up, exploration of haemostasis, pelvic ultrasonography, hysteroscopy and endometrial biopsies. Standard treatments include uterine curettage which is not very effective and hysterectomy. Medical alternatives (gonadotropin-releasing hormone agonists, levonorgestrel-releasing intrauterine device) and surgical alternatives (endometrial resection, thermal balloon endometrial ablation) were developed to avoid treating functional pathology radically. These conservative procedures correct 80% of endometrial hyperplasia symptoms with a low rate of lateral effects. However, these results need to be confirmed by long-term studies. Some economical, legal or material factors can also limit carrying out the procedures. Clinical trials need to be performed to better define the place of medical and surgical alternatives to hysterectomy in the treatment of endometrial hyperplasias resistant to progestins.

Drug Resistance↗

PubMed2002

Gastric hyperplasia and parietal cell loss in Taenia taeniaeformis inoculated immunodeficient mice.

Immunodeficient mice were studied to determine their suitability as models in investigating the role of Taenia taeniaeformis larval products in the development of gastric hyperplasia. Recombinant active gene 2 (RAG2)-deficient and severe combined immune-deficient (SCID) mice were studied as candidate animal models. RAG2-deficient mice inoculated orally with T. taeniaeformis eggs developed gastric hyperplasia with alcian blue-periodic acid-Schiff-positive cell proliferation similar to those of rats. SCID mice inoculated with different doses and routes of T. taeniaeformis in vitro-hatched oncospheres and those orally inoculated with eggs resulted also in different degrees of gastric hyperplasia. Influence of inoculation forms of parasite, doses and routes of inoculation on initiation of hyperplastic gastropathy was suggested to be dependent on number and size of developed larvae. Both RAG2-deficient and SCID mice with hyperplastic mucosa were observed with significant loss of parietal cells. Apparent decrease in parietal cell number was observed in SCID mice at 2 weeks after intraperitoneal inoculation with oncospheres before hyperplastic lesions developed. Earliest occurrence of gastric hyperplasia in SCID mice was observed at 3 weeks after oral inoculation of in vitro-hatched oncospheres, sooner than orally inoculated rats. The results suggested that these immunodeficient mice could be used as animal models to study factors involved in T. taeniaeformis-induced gastric mucous cell hyperplasia.

Animals↗

PubMedDate not supplied

Comparability of the external vs internal location of radiation in inhibiting neointimal hyperplasia.

PURPOSE: One of the most controversial issues in utilizing radiation to inhibit restenosis is the importance of the location of the radiation source. The experimental results from using external forms of radiation have been contradictory and conflicting. In this study, we undertook to externally place a brachytherapy catheter source and to determine if a dose-response effect could be observed, as has been demonstrated with endovascular locations. MATERIALS AND METHODS: Neointimal hyperplasia was created in a rat carotid artery model by a balloon catheter technique. Immediately following injury, treatment groups received irradiation via an externally located high-dose rate (HDR) 192Ir brachytherapy catheter. This system allows for a more uniform dose delivery compared with endovascular radiation sources. Radiation was delivered to a 2-cm length of the injured vessel at doses of 5, 10, or 15 Gy and the animals were sacrificed at various time points following treatment (24 h to 6 months). Serial sections of tissue were stained immunohistochemically with primary antibodies for CD11b, platelet-derived growth factor (PDGF), and alpha-smooth muscle actin. RESULTS: Radiation doses of 5, 10, and 15 Gy inhibited the appearance of neointimal hyperplasia in a dose- and time-dependent manner. That is, doses of 5-15 Gy allowed for varying degrees of neointimal hyperplasia at 3 weeks posttreatment, with a greater resurgence of monocyte/macrophage activity at 5 Gy than at 10 or 15 Gy, where an absence of macrophage activity and PDGF expression was noted. From 2 to 6 months, the 10 and 15 Gy doses were again more suppressive of neointimal hyperplasia than 5 Gy, and at 6 months posttreatment the doses were approximately 25% and 50% effective, respectively. CONCLUSIONS: The demonstrated effectiveness of external brachytherapy provides "proof of principle," that it is the radiation dose delivered to the arterial wall, and not the location of the source, which is critical to a successful outcome. Ablation of the resident monocyte/macrophage population (or prevention of their activation) occurs with low to moderate doses of irradiation, leading to the absence of a cytokine cascade as evi denced by a lack of PDGF expression. A favorable therapeutic ratio exists, therefore, for radiation treatment of the arterial vasculature to prevent neointimal hyperplasia postangioplasty.

Animals↗

PubMed2001

Accuracy of outpatient endometrial biopsy in the diagnosis of endometrial hyperplasia.

BACKGROUND: To determine the accuracy of outpatient endometrial biopsy in diagnosing endometrial hyperplasia in women with abnormal uterine bleeding. DESIGN: Systematic quantitative review of published medical literature. DATA SOURCES: Relevant papers were identified through electronic scanning of MEDLINE (1980-1999) and EMBASE (1980-1999), manual searching of bibliography of known primary and review articles and contact with manufacturers. REVIEW METHODS: Studies were selected if accuracy of outpatient endometrial biopsy, in women with abnormal pre or postmenopausal uterine bleeding, was estimated compared to a reference standard, which was endometrial histology obtained by tissue sampling under anesthesia. Quality assessment and data extraction were performed in duplicate. Diagnostic accuracy was determined by pooled likelihood ratios (LR) for positive and negative test results for endometrial hyperplasia. RESULTS: There were 881 subjects in 8 diagnostic evaluations reported in 6 primary studies. Postmenopausal women represented 25% of the participants studied. There were 43 patients in whom outpatient sampling was inadequate. A positive test result on outpatient biopsy diagnosed endometrial hyperplasia with a pooled LR of 12.0 (95% CI 7.8-18.6) while a negative test result had a pooled LR of 0.2 (95% CI 0.1-0.3). With a positive test result, the posttest probability of endometrial hyperplasia was 57.7% (95% CI 41.1%-72.7%) while it was 2.2% (95% CI 0.9%-4.1%) with a negative test. CONCLUSION: Outpatient endometrial biopsy has modest accuracy in diagnosing endometrial hyperplasia. Therefore, additional endometrial assessment should be undertaken, especially if symptoms persist or intrauterine structural abnormalities are suspected.

Ambulatory Care↗

PubMed2005

Endocervical adenocarcinomas associated with lobular endocervical glandular hyperplasia: a report of four cases with histochemical and immunohistochemical analyses.

We report on four cases of endocervical adenocarcinoma associated with lobular endocervical glandular hyperplasia using histochemical and immunohistochemical analyses. The patients ranged in age from 59 to 67 years (mean 62 years). Chief complaints were watery vaginal discharge in two cases, genital bleeding in one and no subjective symptoms in one. Cytological examinations of the cervical smears revealed adenocarcinoma cells and benign-looking glandular cells with intracytoplasmic golden-yellow mucin in all cases. Radical hysterectomy was performed in three patients, and simple total hysterectomy was performed in one. From surgical specimens, three tumors were diagnosed as mucinous adenocarcinoma and one was adenocarcinoma in situ. All adenocarcinomas were located proximally on the cervix, and did not involve the transformation zone. Adjacent to carcinoma tissues in the cervix, lobular endocervical glandular hyperplasia was detected. The cells of lobular endocervical glandular hyperplasia were dominantly positive with neutral mucin, and immunohistochemistry revealed that these cells had prominent pyloric gland mucin (HIK1083). Focal immunopositivity for pyloric mucin was also observed in three adenocarcinomas. Either CEA or p53 were immunopositive in all adenocarcinomas and negative in the tissues of lobular endocervical glandular hyperplasia. Histopathological features of the present cases suggest that some endocervical adenocarcinomas may originate from lobular endocervical glandular hyperplasia.

Adenocarcinoma↗

PubMed2002

Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue.

The RET proto-oncogene encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain. In human thyroid gland, the RET proto-oncogene is normally expressed in parafollicular C-cells. Thyroid C-cell hyperplasia is associated with inherited medullary thyroid carcinomas and is considered as a pre-neoplastic stage of C-cells disease. It has also been observed in thyroid tissues adjacent to follicular and papillary carcinomas. In order to study the relationship between a misfunctioning of the RET proto-oncogene and the presence of C-cell hyperplasia, we compared a series of thyroid glands presenting sporadic or radiation-associated tumours, as well as samples of unrelated normal thyroid tissues, for alteration in exons 10 and 11 of the gene and for the presence or absence of C-cell hyperplasia. Here we report a significantly higher frequency of C-cell hyperplasia present in peritumoural thyroid tissues of radiation-induced epithelial thyroid tumours, than in peritumoural of sporadic thyroid tumours or in control normal thyroid tissues (P=0.001). A G691S RET polymorphism was present with a higher frequency in radiation-induced epithelial thyroid tumours (55%) than in sporadic tumours (20%) and in control normal thyroid tissues (15%). Interestingly, this polymorphism was associated in the majority (88%) of radiation-induced tumours with a C-cell hyperplasia in the peritumoural tissues. Several explanations for this association are discussed.

Adenoma↗

PubMed2000

Suppression of arterial intimal hyperplasia by cilostamide, a cyclic nucleotide phosphodiesterase 3 inhibitor, in a rat balloon double-injury model.

The effects of cilostamide, a cyclic nucleotide phosphodiesterase 3 (PDE3) selective inhibitor, on vascular intimal hyperplasia were evaluated using a single-balloon injury model and a double-injury model in which the rat common carotid artery was subjected to a second injury at a site injured 14 days previously. In the double-injury model, the second balloon injury caused more severe intimal hyperplasia (intima/media (IM) ratio, 1.88+/-0.10) than in the single-injury model (1.09+/-0.08). Histopathological study revealed that vascular smooth muscle cells (VSMC) were the predominant cell-type in the affected neointimal area. Oral administration of cilostamide for 2 weeks after the second injury suppressed intimal hyperplasia in the double-injury model (30 mg kg(-1) bid, 83% inhibition in terms of the IM ratio, P<0.05; 100 mg kg(-1) bid, 69% inhibition, P<0.05). Similar effects were also observed in the single-injury model with oral administration of cilostamide for 2 weeks (100 mg kg(-1) bid, 36% inhibition, P<0.01). Cilostamide inhibited DNA synthesis of cultured VSMC stimulated by foetal calf serum or different kinds of growth factors, but did not affect their migration stimulated by platelet-derived growth factor (PDGF)-BB. Cilostamide significantly increased the cyclic AMP concentration of VSMC dose-dependently. These results indicate that cilostamide suppresses intimal hyperplasia both in the single- and double-injury models of rat, presumably by inhibiting proliferation rather than migration of VSMC. It is suggested that PDE3 inhibitors might find application in preventing intimal hyperplasia following angioplasty such as percutaneous transluminal coronary angioplasty (PTCA) or stent.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMedDate not supplied

Loss of heterozygosity and microsatellite instability in epithelial hyperplasia of the breast.

We evaluated loss of heterozygosity (LOH) and microsatellite instability (MSI) in epithelial hyperplasia of the breast by the PCR method using microsatellite markers. Seven loci of 16q, 17p, 17q, and 18q were examined in 35 lesions of epithelial hyperplasia observed in non-neoplastic breast tissue of eight breast carcinoma cases, and 29 lesions were observed within 19 fibroadenomas. These hyperplastic lesions were classified by standard criteria into three groups, namely, mild, moderate and atypical ductal hyperplasia (ADH). In the breast carcinoma cases, the frequency of loss of heterozygosity was 40% in mild, 50% in moderate, and 100% in ADH; while in the fibroadenoma cases, the frequency was 10% in mild, 27% in moderate, and 25% in ADH; total frequency of LOH was statistically higher in carcinoma cases than in fibroadenoma cases. On the other hand, the frequency of microsatellite instability was higher in fibroadenoma cases (28%) than in breast carcinoma cases (11%). Furthermore, we analyzed two cases of noninvasive ductal carcinoma arising in fibroadenoma, which had various types of hyperplasia along with carcinoma in situ, and many hyperplasias showed LOH at several of the same markers as carcinoma in situ. From those results, we speculated that LOH at these markers is an early event in mammary tumorigenesis, and some of the hyperplastic lesions with LOH have precancerous natures.

Adult↗

PubMed2001

Lobular endocervical glandular hyperplasia is a metaplastic process with a pyloric gland phenotype.

AIMS: Lobular endocervical glandular hyperplasia of the uterine cervix is a rare pseudoneoplastic lesion of the uterine cervix, described recently. Our aim was to characterize the clinicopathological and immunohistochemical features of lobular endocervical glandular hyperplasia, to elucidate its pyloric gland phenotype, and to distinguish it from adenoma malignum of the uterine cervix. METHODS AND RESULTS: Nine cases of lobular endocervical glandular hyperplasia were studied histologically and immunohistochemically. The average age of the nine patients was 48.8 years (range 38-64 years). Six cases were found incidentally, whereas in three cases a watery vaginal discharge and imaging studies suggested adenoma malignum preoperatively. Microscopically, lobular endocervical glandular hyperplasia ranged from 1 mm to 20 mm (mean 6.8 mm) in the largest horizontal extent and 1 mm to 10 mm (mean 3.9 mm) in depth, and was characterized by lobular arrangements of small glands composed of low columnar cells with pale eosinophilic cytoplasm and bland nuclei. Three cases showed a pseudo-invasive growth. Intracytoplasmic mucin was predominantly PAS-positive, and seven cases showed immunoreactivity for M-GGMC-1, an antibody that reacts with pyloric gland-type mucin. Only focal and faint reactivity for CEA was seen, and ER was negative in all cases. The cytokeratin profile was CK7+/20- in all cases, in keeping with their Müllerian derivation. All three lesions examined contained chromogranin-positive endocrine cells. After surgery all patients are well without recurrent disease (mean follow-up was 48.4 months). CONCLUSIONS: Lobular endocervical glandular hyperplasia is a morphologically distinct pseudoneoplastic glandular lesion, which has unique phenotypic characteristics shared by pyloric glands of the stomach. Although most are found incidentally, some cases may show clinical and radiological features resembling those of adenoma malignum.

Adenocarcinoma, Mucinous↗

PubMed1999

Immunohistochemical finding of alpha-1-antichymotrypsin in tissues of benign prostatic hyperplasia and prostate cancer.

BACKGROUND: Ratio of free to total (F/T) prostate-specific antigen (PSA) is higher in the blood of patients with benign prostatic hyperplasia than those with prostate cancer. To clarify the difference between ratios in these two, alpha-1-antichymotrypsin, the major component of the bound PSA in the blood, was immunohistochemically examined. METHODS: Tissues were obtained surgically via a retropubic approach from patients with benign prostatic hyperplasia (nine cases) and prostate cancer (27 cases). These samples were processed in paraffin blocks, cut into 5 mm sections and stained with antibodies against alpha-1-antichymotrypsin and PSA. RESULTS: The percentage of alpha-1-antichymotrypsin-stained cells in prostate cancer was higher than that in benign prostatic hyperplasia (P<0.05). Almost all of glandular and cancer cells were stained with PSA antibody. The percentage of alpha-1-antichymotrypsin-stained cells in prostate cancer did not correlate to histologic grade, although alpha-1-antichymotrypsin-stained cells were more widely scattered in high grade tissues. No correlation was found between alpha-1-antichymotrypsin-stained cells and ratio of F/T in the blood of cancer patients. In about 20% of cancer tissues, histiocytes with positive alpha-1-antichymotrypsin staining were found in stroma but not in that of benign prostatic hyperplasia. CONCLUSIONS: Prostate cancer tissues are shown to have a richer environment of alpha-1-antichymotrypsin than those of benign prostatic hyperplasia. Some cancer tissues contained alpha-1-antichymotrypsin-stained histiocytes. These local events may correlate to a high amount of the bound form among total PSA in the blood of prostate cancer patients.

Aged↗