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At least 883 records · Page 49Linked to original sources
PubMed2001

Kinetics of acetyl coenzyme A: arylamine N-acetyltransferase from rapid and slow acetylator human benign prostatic hyperplasia tissues.

N-acetyltransferase (NAT) activity was determined in 40 human benign prostatic hyperplasia tissues using 2-aminofluorene (AF) and p-aminobenzoic acid (PABA) as substrates. These were then assayed by high performance liquid chromatography for determining the amounts of acetylated AF and PABA and non-acetylated AF and PABA. The activities (mean +/- SD) of AF-NAT from human benign prostatic hyperplasia tissues were divided into rapid (2.06 +/- 0.08 nmol/min per milligram protein), intermediate (1.25 +/- 0.26 nmol/min per milligram protein), and slow (0.58 +/- 0.30 nmol/min per milligram protein) acetylator groups. The activities (mean +/- SD) of PABA-NAT from human benign prostatic hyperplasia tissues were also divided into rapid (2.00 +/- 0.00 nmol/min per milligram protein), intermediate (1.25 +/- 0.18 nmol/min per milligram protein), and slow (0.48 +/- 0.29 nmol/min per milligram protein) acetylator groups. Kinetic constants for arylamine NAT activities were determined for each of these acetylator groups. Apparent differences in Km and Vmax for AF were found. Therefore, there seems to be a polymorphism in NAT activity with two rapid, five intermediate, and 33 slow acetylators among the 40 samples assayed. This is the first demonstration of acetyl CoA-arylamine NAT activity in human benign prostatic hyperplasia tissues.

4-Aminobenzoic Acid↗
PubMed2000

Virilizing adrenal adenoma and primary amenorrhea in a girl with adrenal hyperplasia.

We report a 14-year-old girl with primary amenorrhea and virilization. The chromosomal analysis showed a normal 46,XX female karyotype and the hormonal assays disclosed high serum levels of testosterone (T): 450 ng/dL (normal 5-90), dehidroepiandrosterone-sulfate (DHEA-S): 690 microg/dL (normal 30-450) and 17-hydroxiprogesterone (17-OHP) >20 ng/mL (normal <2). A pelvic ultrasound disclosed a small uterus and bilateral enlargement of the ovaries, a computed axial tomographic scan of the abdomen identified a large right mass in the adrenal gland and a norcholesterol-I 131 adrenal gammagraphy revealed a functional adrenal tumor. The histological analysis of the surgical removed tumor revealed and adrenal adenoma. After surgery, a steep decline to normal serum levels of T and DHEA-S was observed, remaining an elevated level of 17-OHP: 5.4 ng/mL. During the first three months of follow up, the hirsutism declined sharply and spontaneous mammary development occurred, remaining elevated the 17-OHP serum level: 4.8 ng/mL. Prednisone 5 mg/day, was initiated decreasing the 17-OHP to normal level: 1.4 ng/mL, appearing the menarche followed by cyclical menses. One year after surgery, prednisone was withdrawn during one week, and an ACTH test and HLA typing were done, disclosing a 17-OHP response of an heterozygote for adrenal hyperplasia, and identifying B65 a subtype of B14, and DR1, that are frequently associated to adrenal hyperplasia. Previous reports have informed silent adrenal tumors associated to adrenal hyperplasia, but this is the first report of a functional adrenal tumor associated to adrenal hyperplasia.

Adenoma↗
PubMed2000

Alveolar epithelial type II cell apoptosis in vivo during resolution of keratinocyte growth factor-induced hyperplasia in the rat.

Keratinocyte growth factor (KGF) induces rapid and transient hyperplasia of alveolar epithelial type II cells. We sought to determine components of the apoptotic process involved in the resolution of this hyperplasia and the fate of the apoptotic cells. Rats received intrabronchial instillation of 5 mg KGF/kg body weight or diluent. Lungs were fixed 1, 2, 3, 5, and 7 days later. Apoptosis was identified by TdT-mediated dUTP nick-end labeling (TUNEL), double-labeling for TUNEL and the type II cell marker MNF116, and electron microscopy. Fas, FasL, Bax, Bcl-2, and pro- and active caspase-3 were studied by immunohistochemistry. Changes were quantified by stereology. Cell type specificity was investigated by immunofluorescence double staining. Type II cells exhibited Fas, FasL, Bcl-2, and procaspase-3 irrespective of treatment and time. Immunoelectron microscopy revealed Fas at the apical type II cell membrane. Bax staining was prominent in controls (45-95% of type II cell surface fraction), markedly decreased during hyperplasia at days 2 (20-40%) and 3 (0-10%), and reappeared at day 7 (25-45%) when apoptosis was prominent. Remnants of apoptotic type II cells were incorporated in membrane-bound vacuoles of type II cell neighbors as well as alveolar macrophages. The results indicate that type II cells can enter the Fas/FasL/caspase-3 pathway regulated by Bax and Bcl-2. High Bcl-2:Bax levels favor type II cell survival and a low rate of apoptosis during hyperplasia. Low Bcl-2:Bax levels favor type II cell apoptosis during resolution. Because of time-dependent changes that occur within a short time, the KGF-treated rat lung provides a useful in vivo model to investigate apoptosis in the context of tissue remodeling and repair.

Animals↗
PubMed1999

Hyperplasia of gastric mucosa in donor rats orally infected with Taenia taeniaeformis eggs and in recipient rats surgically implanted with the larvae in the abdominal cavity.

Rats heavily infected with Taenia taeniaeformis larvae in the liver show a remarkable increase in their stomach weight, hyperplasia, and hypergastrinemia. However, it is unknown what causes these phenomena. Hence, as a preliminary study to investigate the importance of larval parasitism in the liver, two experiments were done. In the first experiment, 14 donor rats were orally inoculated with 3,000 T. taeniaeformis eggs. In the second experiment, 136-300 of the larvae obtained from the rats were surgically implanted into the abdominal cavity of 7 recipient rats. Gastrin levels and histopathological changes in the gastric mucosa were investigated. In all, 11 donor rats showed hypergastrinemia and hyperplasia, 5 recipient rats showed gastric mucosal hyperplasia accompanied by excessive mucous cell proliferation, and 2 recipient rats showed hypergastrinemia. These results suggest that parasitism of the liver by the larvae is not essential for the development of hyperplasia and that factors from the larvae might cause these phenomena.

Animals↗
PubMed2006

[Hyperplasia of the coronoid process: diagnosis and treatment].

STUDY GOAL: As it is an unusual and infrequent clinical entity, hyperplasia of the coronoid process is often overlooked or diagnosed too late. The aim of this study was to characterize the morphology, etiology, and clinical picture of coronoid hyperplasia as well as to discuss its diagnosis and treatment. MATERIALS AND METHODS: All cases of histologically confirmed hyperplasia of the coronoid process treated in our center between 1995 and 2004 were analyzed. Patient data were evaluated with respect to age, gender, clinical symptoms, diagnostic work-up, and treatment. The extracted data were compared to those found in the literature. RESULTS: The study included 14 new cases and 101 cases already published: 96 with bilateral and 19 with unilateral hyperplasia. At the time of diagnosis, the subjects' mean age was 23.7 years. The patients in Bonn were all treated by coronoidectomy and appropriate physiotherapy. An improvement in mouth opening could be achieved in 86% of our patients. CONCLUSIONS: In comparison to the somewhat disappointing results of previously published studies with regard to mouth opening and mandibular mobility, our treatment concept seems to offer the possibility for improvement. Our study emphasizes the significance of three-dimensional CT techniques for diagnosis and surgical planning, the superiority of coronoidectomy over coronoidotomy, and the importance of dynamic physiotherapy to prevent postoperative scar formation.

Adult↗
PubMed2005

Reduction of vascular intimal-medial hyperplasia in polytetrafluoroethylene arteriovenous grafts via expression of an inhibitor of G protein signaling.

Polytetrafluoroethylene (PTFE) arteriovenous (AV) grafts are performed routinely for vascular access. The limited life span of PTFE grafts is a major cause of morbidity. Graft failure is attributed to venous outflow tract vascular smooth muscle (VSM) hyperplasia, which is linked to heterotrimeric G protein signaling. We proposed that expression of a peptide inhibitor of G(betagamma) signaling (betaARKct) in the venous outflow of PTFE grafts would reduce hyperplasia and prolong graft patency. Left carotid to right external jugular vein PTFE AV grafts were placed in swine. The isolated external jugular vein was treated with an adenovirus encoding betaARKct, empty adenovirus, or phosphate-buffered saline for approximately 25 min. After 7 or 28 days, flow probe analysis was performed and the vein was harvested and analyzed for cross-sectional area comparison. After both 7 and 28 days, when compared to controls, treated animals demonstrated a statistically significant reduction in VSM hyperplasia with a reduction in cross-sectional intimal and medial areas of >40% (p < 0.05). Flow was maintained in treated grafts, while control groups demonstrated a >50% reduction (p < 0.05) at 7 days. Further, treated grafts demonstrated significant improvement in graft patency at 28 days (100% vs. 12% for treated and untreated grafts, respectively). The inhibition of G(betagamma) signaling reduces intimal-medial hyperplasia and prolongs graft patency in PTFE AV grafts. This represents a novel molecular therapeutic strategy for improving the patency of vascular access grafts.

Anatomy, Cross-Sectional↗
PubMed1998

Irradiation for the treatment of intimal hyperplasia.

Intimal hyperplasia represents a serious complication limiting the long-term benefits of vascular interventions such as balloon angioplasty and stent placement. Although pharmacological interventions have attempted to curtail restenosis, they have not been shown to be effective to date. Radiotherapy is one alternative that has shown promise as an inhibitor of intimal hyperplasia in several animal models. Irradiation causes cell death by producing irreparable damage to DNA. This is believed to be the mechanism of inhibition of VSMC proliferation. Delivery of irradiation can be either intraluminal via an angiographically directed catheter or extraluminal using an external radiation source such as an x-ray device. Intraluminal irradiation has generally utilized either gamma or beta-emitting sources. Both have been effective in producing a dose response, although some studies advocate the use of beta-type irradiation as a safer, more efficient means of delivery. Extraluminal irradiation also has been an effective inhibitor of intimal hyperplasia. Studies suggest that this form of irradiation provides a more even-dose distribution to vessel walls than an intravascular delivery system. The use of radiotherapy has more recently been extended to clinical trials, and initial studies have shown promising results. The success of irradiation must be balanced with its potential complications including radiation-induced arteritis, coronary artery stenosis, and secondary development of malignancy. Although these have been associated with irradiation, the dose used in these cases was often considerably higher than those used in the treatment of intimal hyperplasia. Finally, with the advent of gene therapy, irradiation may provide an additional means of supplementing this new type of therapy through radiation-inducible gene therapy.

Animals↗
PubMed2006

Postnatal epithelial growth of the small intestine in the rat occurs by both crypt fission and crypt hyperplasia.

Studies of growth of the small intestine have largely concentrated on crypt hyperplasia rather than crypt fission. The aim of this study was to investigate quantitatively both crypt fission and crypt hyperplasia. DAxPVG/c rats were killed at 7, 11, 14, 17, 19, 21, 25, 55, and 72-73 days of life. Samples of jejunum at one third of the intestinal length were taken for morphometry (villous area, crypt area, percentage of bifid crypts, and crypt mitotic count) by microdissection. Growth factors and their receptors were assessed by oligonucleotide microarray. Crypt fission was 10.5%, 5.2%, and 1.5% at days 11, 25, and 72-73 of life, respectively. Crypt hyperplasia increased from day 21. No conventional growth factor was identified during crypt fission. We conclude that crypt fission contributes to growth of the small intestine prior to weaning and crypt hyperplasia to growth after weaning.

Animals↗
PubMed2005

Pituitary hyperplasia secondary to primary hypothyroidism: a case report and review of the literature.

Pituitary hyperplasia secondary to primary hypothyroidism has been reported in the literature in both adults and children. We report a case of a young woman who was diagnosed with hypothyroidism in her teenage years. Despite frequent follow-up, her TSH levels remained greater than 100 mIU/ml. A few years later, pituitary enlargement was found on an MRI at a time when her TSH was 177 mIU/ml and her free T4 was 0.2 ng/dl. Observed administration of 600 mcg of L-thyroxine was performed to determine the effectiveness of hormone absorption. Total T4 levels of 0.2 rose to 7.1 mcg/dl at two hours with a decrease in her TSH levels from 88.6 to 66.8 mIU/ml at 24 hours. With the exception of one short period, her TSH levels have remained elevated over eight years of observation without change in the size of the pituitary mass. In our review of the literature, primary uncontrolled hypothyroidism has been described as a precursor to pituitary hyperplasia. In these patients, TSH-secreting adenomas were distinguished from pituitary hyperplasia by a blunted TRH stimulation test, elevated alpha subunit concentration values, and elevated alpha subunit concentration/TSH ratios. TSH levels ranged from 98 to 732 mIU/ml in adults, and even higher values in children. Following adequate hormone replacement with L-thyroxine doses of 25 to 300 mcg/day, both symptoms and pituitary hyperplasia regressed on average within a few months.

Adult↗
PubMed1983

Long-term effect of megestrol acetate in the treatment of endometrial hyperplasia.

Fifty-two postmenopausal women who were poor surgical risks and had histologically proved adenomatous hyperplasia, atypical hyperplasia, or adenocarcinoma in situ of the endometrium were treated with megestrol acetate, 40 mg per day, continuously for 9 to 104 months (mean, 42 months). More than 90% of these women had complete remissions of the hyperplasia. Three women with carcinoma in situ were followed up for 57, 65, and 104 months, without recurrence of the disease. Four women required hysterectomy; none had invasive adenocarcinoma. No adverse side effects of the drug were observed. Thus, we conclude that the continuous use of megestrol acetate is an effective, safe, alternative form of therapy for endometrial hyperplasia in postmenopausal women.

Adenocarcinoma↗
PubMed1993

Mutation of the p53 tumor-suppressor gene is not a feature of endometrial hyperplasias.

OBJECTIVE: Mutation and overexpression of the p53 gene occur in approximately 20% of endometrial carcinomas. To determine whether alteration of the p53 gene is an early event in endometrial carcinogenesis, we examined the p53 gene in endometrial hyperplasias. STUDY DESIGN: Genomic deoxyribonucleic acid was extracted from 117 endometrial hyperplasias (36 simple, 40 complex, 41 atypical) and 30 endometrial cancers. Exons 5 through 8 of the p53 gene were amplified by means of the polymerase chain reaction. Mutations in the p53 gene were sought with single-stranded conformation polymorphism analysis and confirmed by direct deoxyribonucleic acid sequencing. RESULTS: None of 117 endometrial hyperplasias were found to have mutations in the p53 gene, whereas mutations were seen in three of 30 (10%) endometrial cancers (p < 0.02). The p53 mutations seen in three cancers were confirmed by direct sequencing (codons 157, 180, 272). CONCLUSION: Because it does not appear to be a feature of endometrial hyperplasias, mutation of the p53 gene may represent a relatively late event in endometrial carcinogenesis.

Base Sequence↗
PubMed1993

Massive thymic hyperplasia.

Massive thymic hyperplasia is an extremely rare form of true thymic hyperplasia most often described in infants and children. Hyperplasia of this order is not known to occur in any other organ, and its etiology and prognostic significance remain unknown. As there is no accurate way of preoperatively differentiating massive thymic hyperplasia from other tumors of the thymus and anterior mediastinum, we advise excision in all cases for histological analysis and relief of mediastinal compression. This description of 4 cases updates the 30 previously reported cases, and includes a literature review.

Child, Preschool↗
PubMed1990

Langerhans cells in human chronic gingivitis and phenytoin-induced gingival hyperplasia.

Langerhans cell numbers in oral epithelium increase as dental plaque accumulates. The anti-convulsant drug phenytoin predisposes to gingival hyperplasia in certain patients who take this medication for epilepsy and who also have poor oral hygiene. In this study 7 patients with phenytoin-induced gingival hyperplasia were compared with 5 subjects with chronic marginal gingivitis. On initial examination and on completion of the hygiene phase of periodontal therapy (a period ranging from 3.0 to 4.25 months), clinical indices of plaque and gingivitis were recorded and biopsies were taken from the lower anterior labial gingiva. Frozen sections were stained by an immunoperoxidase technique using the monoclonal antibody OKT6, and the number of Langerhans cells in a defined cross-sectional area was counted. In phenytoin-induced gingival hyperplasia there was a marked increase in Langerhans cells (13.8 +/- 0.45) when compared with chronic gingivitis (7.7 +/- 0.31; p less than 0.05). Both groups showed marked reductions in their plaque and gingival indices and numbers of Langerhans cells once treatment had been completed. However, levels of Langerhans cells in the drug-induced hyperplasia remained significantly higher (3.5 +/- 0.26) than in chronic gingivitis (1.5 +/- 0.22; p less than 0.05).

Adult↗
PubMed1994

Postmenopausal endometrial hyperplasia: role of danazol therapy.

OBJECTIVES: To confirm the effectiveness of danazol in the management of simple or complex endometrial hyperplasia without atypical features, as has been demonstrated previously. METHODS: Seventy-six patients affected by postmenopausal histologically-confirmed endometrial hyperplasia with uterine bleeding were submitted to danazol therapy at a dose of 400 mg/day for 3 consecutive months. RESULTS: After cessation of treatment, 82.8% of the patients (63/76 enrolled) showed a conversion of the hyperplasia into atrophic (65.8%), secretory (11.9%) or proliferative (4.2%) endometrium at the histological examination. Uterine bleeding disappeared, during the therapy, in 90% of the responders (59/63). CONCLUSIONS: Although 17.1% of the women had a persistence of the hyperplasia and 8.4% of the symptom-free women relapsed after 4 months of follow-up, this experience confirms the effectiveness of danazol therapy in hyperplastic endometrial lesions. Nevertheless, a study comparing danazol and progestin therapy is required.

Aged↗
PubMed1985

Gingival hyperplasia induced by nifedipine, an arterial vasodilating drug.

In a 32-year-old patient a relationship was suggested between the development of gingival hyperplasia and the vasodilating drug nifedipine (Adalat). The hyperplasia was clinically and histologically similar to the gingival hyperplasia previously noticed with diphenylhydantoin. The nifedipine-induced gingival hyperplasia may be caused by alterations in calcium metabolism.

Adult↗
PubMed1991

Adenomatoid hyperplasia of minor salivary glands.

Adenomatoid hyperplasia of minor salivary glands is an uncommon clinicopathologic entity. It comprises clinical swelling resembling a neoplasm with a histologic picture of aggregates of normal-appearing salivary gland tissue in excess of that anticipated for the anatomic site. The significance of this lesion is derived from its clinical resemblance to a neoplasm of salivary gland origin. This study adds 40 new cases to the literature and analyzes their clinical and histologic features. Most of the lesions were located on the hard and soft palates. The exact nature of the minor salivary gland hyperplasia is not clear. Some of the cases may represent a hamartoma or a reactive hyperplasia, but in most cases the nature of the hyperplasia is idiopathic.

Adolescent↗
PubMed1993

Intraoral sebaceous hyperplasia. Diagnostic criteria.

Surprisingly little is understood about the physiologic and pathologic processes that involve intraoral sebaceous glands. Neoplasms are rare. Hyperplasia of these glands is undoubtedly more common, but criteria for the diagnosis of intraoral sebaceous hyperplasia have not been established. These lesions are too often misdiagnosed as large "Fordyce granules" or, when very large, as sebaceous adenomas. On the basis of a series of 31 nonneoplastic sebaceous lesions and on published data, the following definition is proposed: intraoral sebaceous hyperplasia occurs when a lesion, judged clinically to be a distinct abnormality that requires biopsy for diagnosis or confirmation of clinical impression, has histologic features of one or more well-differentiated sebaceous glands that exhibit no fewer than 15 lobules per gland. Sebaceous glands with fewer than 15 lobules that form an apparently distinct clinical lesion on the buccal mucosa are considered normal, whereas similar lesions of other intraoral sites are considered ectopic sebaceous glands. Sebaceous adenomas are less differentiated than sebaceous hyperplasia.

Adenoma↗
PubMed1991

Atypical mesothelial hyperplasia associated with bronchogenic carcinoma.

Atypical mesothelial hyperplasia encountered in pleural fluid or in a pleural biopsy specimen raises the suspicion that one may be dealing with a diffuse malignant mesothelioma of the pleura. We studied eight cases with cytologic or histologic changes of mesothelial atypia thought to be suspicious for diffuse malignant mesothelioma. In each case, the hyperplasia was associated with a bronchogenic carcinoma in the lung subjacent to the mesothelial hyperplasia. Bronchogenic carcinoma should be added to the list of causes of atypical mesothelial hyperplasia. This combination of reactive and malignant processes should be appreciated, since pleural carcinomatosis and diffuse malignant mesothelioma must be separated for clinical and epidemiologic reasons.

Adenocarcinoma↗