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PubMed1990

Clinical characteristics and surgical treatment of sporadic primary hyperparathyroidism with emphasis on chief cell hyperplasia.

In 570 patients with sporadic primary hyperparathyroidism, the age, sex, symptoms, and preoperative serum calcium values were related to the histopathologic diagnoses, operative findings, and the extent and outcome of parathyroid surgery. Renal stone formation was especially prevalent in younger patients with slight hypercalcemia and parathyroid chief cell hyperplasia, whereas neuromuscular and psychiatric disturbances were overrepresented among older women with higher serum calcium values. Serum calcium concentration was inversely correlated to the proportional incidence of chief cell hyperplasia and positively correlated to the glandular weight of both adenomas and hyperplasias. Glandular size was markedly irregular in chief cell hyperplasia, with increased gland weights of no more than two glands in 78% of patients. During follow-up, for as long as 27 years, normocalcemia was obtained in 91% of patients with adenomas, with failures mainly depending on difficulties in identifying the parathyroid glands. The rate of normocalcemia was lower (80%) among patients with hyperplasia, but an inability to visualize the glands was not a major cause of failure. In patients with hyperplasia with asymmetric and more markedly enlarged glands, it appeared sufficient to remove only the enlarged glands, whereas the findings advocated a subtotal 3- to 3.5-gland resection in patients with more symmetrically or less enlarged hyperplastic glands.

Adenoma↗
PubMed1989

[Pheochromocytoma and adrenomedullary hyperplasia].

A comparison was made on the main clinical features between 6 cases of benign pheochromocytoma and 4 cases of adrenomedullary hyperplasia admitted in to our hospital from 1981 to 1986. It is found that differentiation between pheochromocytoma and adrenomedullary hyperplasia with symptoms or signs alone is difficult, since both may have the same symptoms such as paroxysmal or sustained hypertension elevation and shock. Moreover, the laboratory findings of the former were also similar to those of the latter. So the diagnosis of both was suspected upon clinical manifestations and confirmed with biochemical investigation. If an enlarged adrenal silhouetteis shown on one side or both sides with no tumor mass, as evidenced by retroperitoneal pneumography, computerized tomography, nuclear magnetic resonance, ultrasonography or 131I-meta-iodobenzyl-guanidine (131I-mIBG), adrenomedullary hyperplasia might be considered. Confirmatory differential diagnosis between the pheochromocytoma and adrenomedullary hyperplasia perhaps can only be made after surgical exploration and pathological examination. Pheochromocytoma is usually benign and can be excised totally after medical preparation with an alpha-adrenergic antagonist as we have done; adrenomedullary hyperplasia can only be treated with subtotal adrenalectomy. We also agree with the idea that preoperative alpha-adrenergic blockage would reduce surgical complication and mortality. It is generally recommended that a beta-adrenergic antagonist, such as propranolol, be given only after effective alpha-adrenergic blockade is established because beta-adrenergic blockade alone may exacerbate hypertension as a result of unopposed alpha-adrenergic stimulation. Besides operation, 131I-mIBG administration seems to be a promising alternative method for malignant pheochromocytoma or adrenomedullary hyperplasia.

Adolescent↗
PubMed1987

Expression of tumor-associated antigen (DF3) in atypical hyperplasias and in situ carcinomas of the human breast.

The monoclonal antibody (MoAb) DF3 prepared against a membrane-enriched fraction of human breast carcinoma has previously shown a differential reactivity to cytoplasmic antigen in carcinomas versus antigen concentrated on apical borders in benign lesions of the breast. In the present report the cytoplasmic reactivity of MoAb DF3 within a spectrum of benign and malignant breast lesions was studied to define whether the DF3 antigen is expressed in the cytoplasm of potentially premalignant lesions, i.e., atypical hyperplasias, or early malignant lesions, i.e., in situ carcinomas. Biopsy specimens of breast lesions from 108 women, including 28 patients with invasive carcinoma, 12 with in situ carcinoma, 17 with atypical hyperplasia, 25 with proliferative lesions without atypia, and 26 with nonproliferative lesions, were examined for DF3 antigen expression with the use of an indirect immunohistochemical method. Atypical hyperplasias were less reactive with MoAb DF3 than invasive carcinomas (P = .05 by Wilcoxon rank sum test). No significant statistical differences were observed, however, between invasive carcinomas and in situ carcinomas or between in situ carcinomas and atypical hyperplasias on the basis of cytoplasmic DF3 reactivity. Invasive carcinomas, in situ carcinomas, and atypical hyperplasias, however, demonstrated significantly higher reactivity with MoAb DF3 in the cytoplasm than proliferative lesions without atypia and nonproliferative lesions (P less than .01). These studies demonstrate that atypical hyperplasias express elevated levels of a given tumor-associated antigen and thus provide further immunologic evidence that these lesions are premalignant.

Antibodies, Monoclonal↗
PubMed1987

Epithelial hyperplasia in human polycystic kidney diseases. Its role in pathogenesis and risk of neoplasia.

The importance of tubular epithelial hyperplasia in polycystic kidney diseases has become apparent during the last decade. Micropapillary hyperplasia occurs in autosomal dominant polycystic kidney disease, in localized cystic disease, and in acquired cystic disease. Neoplastic or severely dysplastic epithelial hyperplasia occurs in von Hippel-Lindau disease. A histopathologically distinctive epithelial hyperplasia occurs in tuberous sclerosis. In each of these conditions, epithelial hyperplasia may be related to cyst formation and may also impose an increased risk of malignancy--a risk that seems to be highest in patients under treatment with long-term hemodialysis for end-stage kidney disease. Although hyperplasia in some of these diseases may share a common pathway of development, it is more probable that the histopathologic differences reflect different pathogenetic pathways that converge on a common endpoint.

Epithelium↗
PubMed1986

[Morphological aspects of parathyroid hyperplasia in patients with chronic renal insufficiency on dialysis].

The authors present an anatomic study of parathyroid hyperplasia in 15 patients presenting chronic renal failure treated by hemodialysis (mean time 6 years). The light microscopic examination (n = 56) confirms diffuse hyperplasia so occur in patients submitted to dialysis for a period inferior to 4 years while nodular hyperplasia occurs in patients submitted to dialysis for longer a time. Mixed hyperplasia may be considered a transitional form between diffuse and nodular hyperplasia. Electron microscopic examination (n = 31) reveals the secretory ability of chief cells containing lots of secretory granules, and the energetic power of oxyphil cells filled with mitochondria. The great amount of oxyphil and of vacuolized cells after long periods of dialysis means degenerative transformation of ancient chiefs cells. The authors emphasize the interest of per-operative identification of the type of hyperplasia in order to choose the fitting procedure of parathyroidectomy.

Adult↗
PubMed1979

[Atypical adenomatous hyperplasia of the endometrium].

By women in climacterium and postmenopause the authors found 30 adenomatous atypical hyperplasias out of a total of 909 active hyperplasias. They also detected 68 endometrial carcinomas and 65 other changes. Out of 30 patients with adenomatous atypical hyperplasia, 23 had been subjected to curettage earlier but at that time had revealed only milder forms of hyperplasia. Surgery was performed in 21 patients: in 15 patients the diagnosis based on the operative preparation agreed with that based on curettage findings, in 2 patients endometrial carcinoma and in 2 patients glandular hyperplasia were detected, while in 2 patients there was no functional endometrium. Out of 9 patients who for various reasons were not surgically treated and represented an unintentional prospective study, 5 subsequently developed endometrial carcinoma, 3 mild forms of hyperplasia, and 1 atrophia cystica. In the authors' opinion, the histogenesis of endometrial carcinoma in late postmenopause is still an open question.

Adult↗
PubMed1984

Cytological evaluation of endometrial hyperplasia in relation to histological pictures.

The Authors analyse possible parameters of cytological evaluation which can be used for the grading of endometrial hyperplasias and the diagnostic differentiation between atypical hyperplasia and adenocarcinoma. They consider 77 women who underwent endometrial cytology by aspiration just before diagnostic examination of the uterine cavity. Results show that in atrophic endometrium desquamation in clusters of less than 100 cells prevails whereas proliferative and secretory endometrium presents mainly clusters of 100-500 regularly stratified cells. Hyperplasia show progressive increase in isolated cells; "branched" glands appear rarely in hyperplasia with minimal atypia while prevailing in hyperplasia with severe atypia and adenocarcinoma. Simple layers prevail in atrophic endometrium, stratified regular layers prevail in proliferative and secretory endometrium; three-dimensional clusters appear in hyperplasia with minimal atypia and become significant with severe atypia. Adenocarcinoma is characterized by haematic and necrotic background, high percentage of isolated cells and prevalence of clusters of less than 100 cells, mainly three-dimensional. In addition it shows a significant incidence of papillary and rosette-like arrangements and abnormal cytoplasmic vacuolization.

Adenocarcinoma↗
PubMed1980

Modification of early dimethylhydrazine carcinogenesis by colonic mucosal hyperplasia.

The interaction of colonic mucosal hyperplasia with early 1,2-dimethylhydrazine (DMH) carcinogenesis was studied in random-bred NIH Swiss mice utilizing hyperplasia-inducing Citrobacter freundii. Mice inoculated with this bacterium developed significantly more DMH focal atypia than did mice without hyperplasia following a single dose of DMH (20 mg/kg). Mice with hyperplasia also developed DMH focal atypia with diminished doses of DMH (10 and 5 mg/kg), while normal mice did not. The effect of C. freundii on early DMH carcinogenesis was shown to be due to the hyperplasia rather than to a direct interaction of the bacterium with DMH. Focal atypia arose in high incidence 1 month after a single dose of DMH (20 mg/kg) but did not appear to progress to later stages of neoplasia, since significantly fewer atypia were present at 2 to 4 months among a randomized population. Colonic focal atypia may represent a reversible preneoplastic or precursor lesion as seen in other tissues, with features more aligned to neoplasia than to hyperplasia.

Animals↗
PubMed1981

Comparison of experimental and spontaneous bladder urothelial hyperplasias occurring in BALB/c mice.

Spontaneously occurring hyperplasia of urothelium of mice was compared morphologically to hyperplasia induced with 2-acetylaminofluorene (2-AAF) and 4-ethylsulfonylnaphthalene-1-sulfonamide (ENS). Simple and nodular hyperplasias were seen in all groups. Nodular downward hyperplasia was more commonly located in the vertex of the bladder of the 2-AAF treated mice but was more commonly located in the neck region of the ENS and control mice. The 2-AAF induced hyperplasia appeared to be capable of regression or progression to neoplasia. The ENS induced and the spontaneously occurring downward hyperplasia appeared to be secondary to a chronic cystitis and did not appear to progress to neoplasia.

Animals↗
PubMed1993

Impact of previously unrecognized benign prostatic hyperplasia on the daily activities of middle-aged and elderly men.

To assess the importance of benign prostatic hyperplasia on activities of daily living, a cross-sectional survey of 1627 men aged 40-79 years (representing a 65% response rate) registered with two health centres in central Scotland was carried out, using a urinary symptom questionnaire and uroflowmetry to identify men more likely to have benign prostatic hyperplasia. The condition was defined as a prostate gland of more than 20 g in the presence of symptoms of urinary dysfunction and/or a peak flow rate of less than 15 ml s-1, without evidence of malignancy. Transrectal ultrasonography was used to measure the volume (and by inference weight) of prostate glands. A total of 410 men satisfied the criteria for benign prostatic hyperplasia. Overall, 51% of men with benign prostatic hyperplasia reported interference with at least one of a number of selected activities of daily living as a result of urinary dysfunction, compared with 28% of men who did not have this condition. In 17% of men of working age (40-64 years) with benign prostatic hyperplasia, this interference occurred most or all of the time for at least one activity of daily living compared with only 3% of men in the same age group who did not have this condition. If the criteria of unmet need for treatment of benign prostatic hyperplasia constitutes interference by urinary dysfunction most or all of the time in at least one activity of daily living, then the findings of this survey suggest that a substantial number of middle aged and elderly men living in the United Kingdom may be in need of assessment and treatment for this condition.

Activities of Daily Living↗
PubMed1978

An outbreak of cecal mucosal hyperplasia in hamsters.

Cecal mucosal hyperplasia associated with diarrhea, runting, and high mortality in suckling and weanling hamsters occurred as a natural disease outbreak in a production colony. Young hamsters were runted, and their perineal hair was stained and matted with liquid feces. Their ceca were thickened, contracted, congested, and had scant luminal content. There were severe hyperplasia of cecal crypts, accompanied by increased mitotic activity, inflammation, and focal mucosal erosion. A variety of bacteria was isolated, but none was considered pathogenic. No relationship of cecal hyperplasia to transmissible ileal hyperplasia of hamsters was found. Hyperimmune serum from hamsters with transmissible ileal hyperplasia did not react by immunofluorescence against hyperplastic cecal mucosa. Electron microscopy did not reveal a caustive agent. Transmission attempts have been unsuccessful. Cecal mucosal hyperplasia is apparently a newly discovered disease entity in hamsters with the clinical sign of diarrhea.

Animals↗
PubMed1994

Consultation patterns in a community survey of men with benign prostatic hyperplasia.

BACKGROUND: The Stirling benign prostatic hyperplasia natural history group have previously reported a prevalence of this condition of 255 per 1000 in a community study of 1610 men aged 40-79 years. AIM: It was decided to examine the consultation patterns of men with benign prostatic hyperplasia in greater detail. METHOD: All participating men were invited to complete a previously validated lifestyle questionnaire including questions on consultations with their general practitioner during the previous year and previous history of prostatic problems. The men who had a urinary symptom score greater than 11, or who had a urinary flow rate of less than 15 ml per second were examined by transurethral ultrasonography for prostate size. RESULTS: Of 364 men with benign prostatic hyperplasia, 89% had not consulted their doctor about urinary symptoms in the year prior to the study. Men with moderate to severe urinary symptoms were six times more likely to have consulted their doctor than those with mild symptoms. Moderate to severe symptoms and greater interference with daily living activities were both associated with a greater likelihood of consultation, independent of age. Of all the men in the study referred to the specialist clinic for assessment of prostate size by transurethral ultrasonography, two thirds were referred because of low urinary flow rate and one third because of high urinary symptom scores. The reported consultation data showed a reverse ratio of one third of those consulting having a low urinary flow rate and approximately two thirds having urinary symptoms. CONCLUSION: While mass screening is unjustified, there is a need for patient education about benign prostatic hyperplasia in general and the recognition of declining strength of urinary flow as a symptom of benign prostatic hyperplasia and not of ageing alone. Furthermore, evaluation of primary care use of urinary flowmeters and the development of local protocols are suggested as elements of a case finding strategy for benign prostatic hyperplasia based on patient led consultation.

Adult↗
PubMedDate not supplied

[Atypical hyperplasia and endometrial carcinoma (author's transl)].

Data on 167 cases of atypical hyperplasia of the endometrium and 292 cases of adenocarcinoma of the endometrium from 1966 to 1977 are presented. In 41 cases of atypical hyperplasia (24.5%) also adenocarcinoma of the endometrium coexisted. The age distribution revealed that atypical hyperplasia was much frequent in the age group from 40--59, and adenocarcinoma of the endometrium from 59--69. Out of 61 cases of theca- and granulosa-cell tumors of the ovary, 13 cases (21.3%) related to atypical hyperplasia or adenocarcinoma of the endometrium. Out of 27 cases of the Stein-Leventhal syndrome, 3 cases were atypical hyperplasia, one case adenocarcinoma of the endometrium. The data presented suggest that atypical hyperplasia might be a stage in the development of endometrial carcinoma.

Adenocarcinoma↗
PubMed1995

Pharmacologic suppression of intimal hyperplasia: a dose-response suppression by enalapril.

Intimal hyperplasia is an exaggerated proliferative response to arterial intimal injury. A successful means of limiting this hyperplastic response would significantly improve patency rates of vascular reconstruction. Angiotensin-converting enzyme (ACE) inhibitors decrease the proliferation and synthetic function of vascular smooth muscle cells in vitro, which have been implicated in the production of intimal hyperplasia. We performed a dose-response study of enalapril to assess the level at which maximal suppression of intimal hyperplasia occurs. Seventy male Sprague-Dawley rats weighing 250-300 grams underwent standardized carotid artery balloon catheter endothelial denudation to induce intimal hyperplasia. Six groups of ten animals each were treated with daily intramuscular injections of one of the following doses of enalapril (mg/kg): 0.025, 0.050, 0.075, 0.100, 0.125, and 0.150. A control group (n = 10) was treated with saline. Injections were started two days before injury and continued for 4 weeks, at which time the injured arteries were pressure-fixed in vivo and harvested. EVG-stained histologic cross-sections were measured by planimetry to determine the amount of intimal hyperplasia, which was calculated as the percentage of the arterial lumen replaced by the lesion. Enalapril suppresses the development of intimal hyperplasia in a dose-responsive manner in this model. No further suppression is achieved above a dose of 0.125 mg/kg.

Animals↗
PubMed1995

Inhibition of parathyroid hormone-related protein release by extracellular calcium in dispersed cells from human parathyroid hyperplasia secondary to chronic renal failure and adenoma.

The relationship between parathyroid hormone-related protein (PTHrP) release from parathyroid cells and extracellular calcium ion concentration was investigated in three cases of parathyroid hyperplasia secondary to chronic renal failure and in four cases of parathyroid adenoma. Amounts of PTHrP released from individual parathyroid cells dispersed from surgical specimens were estimated by cell immunoblot assay. Parathyroid cells from both hyperplasias and adenomas showed significant suppression in the release of PTHrP with increase in extracellular calcium ions, but the amounts of PTHrP released from adenoma cells were significantly larger than from hyperplasia cells. The maximal value for PTHrP released within 120 minutes from adenoma cells was 2.91 +/- 2.11 x 10(-2) fmol/cell ([Ca2+], 0.4 mmol/L), and the minimal value was 1.32 +/- 0.35 x 10(-2) fmol/cell ([Ca2+], 2.0 mmol/L). On the other hand, the maximal value for PTHrP released from hyperplasia cells was 1.79 +/- 1.56 x 10(-2) fmol/cell ([Ca2+], 0.4 mmol/L), and the minimal value was 0.32 +/- 0.19 x 10(-2) fmol/cell ([Ca2+], 2.0 mmol/L). These results demonstrate actual release of PTHrP from abnormal parathyroid tissues into the extracellular space with the response to extracellular calcium ions depending on the cell status. Given the lack of definite histological criteria to differentiate between hyperplasias and adenomas in the parathyroid gland, the presently demonstrated significant difference in the ability to release PTHrP is important in pointing to parathyroid hyperplasia secondary to chronic renal failure as a distinct pathological entity separate from parathyroid adenoma.

Adenoma↗
PubMedDate not supplied

Diagnosis of endometrial hyperplasia in women with abnormal uterine bleeding.

BACKGROUND: Reliability of hysteroscopy in diagnosing endometrial hyperplasia in women with abnormal uterine bleeding. METHODS: Out of 105 patients with abnormal uterine bleeding 47 showed structural abnormalities. Comparative analysis between hysteroscopic and histological results in 58 women without gross abnormalities has been performed in order to verify sensitivity and specificity of hysteroscopy in the diagnosis of endometrial hyperplasia. RESULTS: Specificity of hysteroscopy in diagnosing endometrial hyperplasia was 84.7% while sensitivity resulted to be 80%. CONCLUSIONS: Women with abnormal uterine bleeding and normal uterine cavity has a low rate (3.4%) of false negative endometrial hyperplasia. On the contrary findings of endometrial hyperplasia at hysteroscopy has a high incidence of false positive (25.8%). In conclusion, abnormal uterine bleeding could cause an increased thickness in endometrium, appearing as hyperplasia on hysteroscopic examination.

Adult↗
PubMed1994

Modulation of oncogene and tumor suppressor gene expression in a hamster model of chronic lung injury with varying degrees of pulmonary neuroendocrine cell hyperplasia.

BACKGROUND: Intense pulmonary neuroendocrine cell (PNEC) hyperplasia occurs during preneoplastic lung injury in hamsters treated with diethylnitrosamine (DEN) plus hyperoxia. Alterations in oncogene and tumor suppressor gene expression during this process have not been explored. EXPERIMENTAL DESIGN: Our goals were: (a) to analyze expression of genes potentially involved in growth and differentiation of PNECs and/or nonneuroendocrine pulmonary epithelial cells (non-PNECs) in hamsters treated for up to 20 weeks with hyperoxia and DEN or the major tobacco-derived nitrosamine, 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone (NNK); and (b) as a corollary, to determine which cells were most mitotically active by immunostaining for c-myc and proliferating cell nuclear antigen. RESULTS: Immunohistochemical analyses demonstrated intense PNEC hyperplasia after treatment with either DEN/O2 or NNK/O2. Whereas DEN/O2-induced PNEC hyperplasia spontaneously regressed, NNK/O2-induced PNEC hyperplasia continued to increase up to 20 weeks. Rb transcripts were decreased similarly in lungs from all treatment groups (NNK/O2 = DEN/O2 = DEN alone) in spite of large differences in PNEC hyperplasia between these groups. c-myc was overexpressed in lungs from animals treated with NNK/O2, DEN/O2 and DEN alone, in which c-myc protein immunostaining occurred predominantly in non-PNECs. Proliferating cell nuclear antigen immunostaining confirmed that non-PNECs were most mitotically active. CONCLUSIONS: These data indicate that PNEC hyperplasia is primarily due to PNEC differentiation, suggesting that this model is ideal for studying mechanisms of neuroendocrine differentiation. Paracrine effects of PNEC-derived growth factors may then contribute to dysregulation of non-PNEC growth preceding the ultimate development of non-neuroendocrine lung tumors in nitrosamine-treated hamsters.

Animals↗
PubMed1993

[Aromatase activities of endometrial carcinomas and both basic and clinical analyses of endometrial hyperplasia as a premalignant disease].

Paraffin-embedded materials obtained from 117 cases of endometrial hyperplasia and 84 cases of carcinoma were used for measurement of both ki-ras and p53 gene mutation and aromatase (ARO) and TGF-alpha immunostaining. The overall incidence of ki-ras mutations in the hyperplasia specimens (16%) was similar to the incidence detected in carcinomas (18%). None of 117 endometrial hyperplasias were found to have mutations in the p53 gene, whereas mutations were seen in 3 (13.3%) endometrial carcinomas. The intensity of both ARO and TGF-alpha immunostaining was increased in glands of both hyperplasia and carcinoma, and also in the interstitium of carcinoma. The positive sites of both ARO and TGF-alpha were almost the same, with an incidence below 40% in both hyperplasias and carcinomas. The cultured cells of endometrial carcinoma showed aromatase activity below MCF-7 cells, because testosterone was converted to estradiol (E2). TGF-alpha induced cell growth with at an optimal concentration. In HEC-59 cells, TGF-alpha increased both ARO-activity and mRNA. Some promoters on ARO-exon 1 in HEC-59 cells were different from those in BeWo cells. Progesterone inhibited the E2-induced excretion of pre TGF-alpha in endometrial carcinoma cells. These findings suggest that endometrial hyperplasia can be a premalignant condition of carcinoma, and can be initiated by both ki-ras codon 12 mutation and abnormal activity of ARO induced by TGF-alpha. In addition, HEC-59 cells may possess autocrine/paracrine properties involving ARO, E2 and TGF-alpha.

Adult↗