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PubMed1995

Verumontanum mucosal gland hyperplasia.

Prostatic adenocarcinoma of the small acinar type can be mimicked by benign proliferative lesions, such as atypical adenomatous hyperplasia (adenosis), sclerosing adenosis, nodular hyperplasia (cellular areas), lobular hyperplasia, basal cell hyperplasia, mesonephric hyperplasia, and nephrogenic adenoma. In our study, we describe another microacinar proliferation, which we have termed verumontanum mucosal gland hyperplasia (VMGH) because it occurs exclusively in the verumontanum and adjacent posterior urethra where the ejaculatory ducts and utricle empty into the urethra. We reviewed 341 radical prostatectomies and cystoprostatectomies done from 1988 through 1993 for prostate and bladder carcinoma, respectively. Forty-nine prostates (14%) from patients aged 47 to 87 contained foci of VMGH. Of a total of 88 foci, a single lesion was present in 19 cases and multiple lesion in 30 cases. Fifty-nine of the foci arose around the ejaculatory or prostatic ducts, 17 from around the utricle, and 13 from adjacent posterior urethral mucosa. Individual lesions were quantified as to the number of acini per focus as follows: 6 to 10 in 28 (1+), 11 to 25 in 29 (2+), 25 to 50 in 16 (3+), and more than 50 in 15 (4+). No crystalloids or intraluminal mucin were seen, but; intraluminal corpora amylacea, usually numerous, were present in 57 of the 88 voci. The microacini were frequently "back to back" architecturally. The lining epithelium consisted of bland cuboidal to columnar luminal cells with underlying basal cells. VMGH, a previously undescribed benign microacinar proliferation, occurs in a very restricted and specific location and appears to be unrelated to other lesions with which it may be confused.

Aged↗

PubMed1987

Lectin binding to human endometrial hyperplasias and adenocarcinoma.

Arias-Stella change, cystic glandular hyperplasia, adenomatous hyperplasia, atypical hyperplasia, and adenocarcinoma of the human endometrium were stained with different fluorescein-conjugated lectins. The lectins used were Concanavalin A, Triticum vulgaris, Arachis hypogaea, Glycine maximum, Dolichos biflorus, Ulex europaeus, and Ricinus communis. The results showed that the lectin staining of Arias-Stella change differed from the other conditions and resembled more closely the staining properties of normal late secretory endometrium. Cystic glandular hyperplasia resembled the normal proliferating endometrium and even had features of atrophic endometrium. The staining properties of adenomatous hyperplasia and atypical hyperplasia resembled more those of endometrial adenocarcinoma. These similarities may be considered as support for the clinical findings that these conditions are potentially premalignant.

Adenocarcinoma↗

PubMedDate not supplied

Reversal by medical treatment of endometrial hyperplasia caused by estrogen replacement therapy.

OBJECTIVE: Endometrial hyperplasia, an entity considered a precursor to endometrial carcinoma, frequently develops in women receiving unopposed estrogens. Progestins used concomitantly with estrogens can largely prevent endometrial hyperplasia and carcinoma. However, the ability of progestins to reverse endometrial hyperplasia induced by estrogens is less well recognized. The purpose of this study was to assess the medical reversal rate of endometrial hyperplasia that develops in women receiving unopposed estrogen replacement therapy (ERT). DESIGN: Review of recent literature (1990-2000). RESULTS: Based on four large series, more than 90% of endometrial hyperplasia caused by ERT can be reversed by medical treatment. Discontinuation of estrogen and oral administration of 10 mg/day of medroxyprogesterone acetate continuously for 6 weeks or cyclically for 3 months (2 weeks of each month) are the two regimens most widely used. Other progestins also have been shown to be effective. CONCLUSIONS: Progestins are highly successful in reversing endometrial hyperplasia caused by ERT.

Clinical Trials as Topic↗

PubMed2003

Investigation of benign prostatic hyperplasia.

PURPOSE OF REVIEW: This is a concise and timely update of the most recent developments in the clinical research on the investigation of benign prostatic hyperplasia. RECENT FINDINGS: Analysis of the peer-review literature confirms a high level of consensus as to the management of prostatic hyperplasia; analysis of practice trends suggests a satisfactory degree of adoption of the proposed guidelines. The evaluation of lower urinary tract symptoms remains the mainstay in the investigation of prostatic hyperplasia although problems concerning the evaluation of nocturia and the differential diagnosis between hyperplasia and chronic prostatitis were identified. Lower urinary tract symptoms confirmed their value as predictors of disease progression. The extent of patient involvement in the decision making process is increasing and new tools to elicit patient preference have been developed. A growing consensus as to the concept of disease progression has been reached concerning prostatic hyperplasia. Analysis of patient sexual function is now considered an important part of patient's interview. More sophisticated instruments, such as time trade-off values were successfully tested to elicit patient preference in the management of prostate disease. The value of serum prostate specific antigen as a predictor on prostate volume growth has recently been confirmed also in unselected male population. SUMMARY: Current research into the investigation of benign prostatic hyperplasia provides new insight into the pathophysiology of lower urinary tract symptoms and identifies parameters to predict the natural history of the disease in the individual patient, particularly regarding progression of the disease and the onset of adverse events.

Aged↗

PubMed2005

Cutaneous lymphoid hyperplasia and other lymphoid infiltrates of the breast nipple: a retrospective clinicopathologic study of fifty-six patients.

This study characterizes the clinicopathological spectrum of lymphoproliferations involving the breast nipple and/or areola. Morphologic, immunohistochemical, molecular-genetic, and clinical features of 58 specimens from 56 patients were analyzed. They were re-diagnosed as cutaneous lymphoid hyperplasia (CLH, n = 44); other benign lymphoid infiltrates (OBLI, n = 8); peripheral T-cell lymphoma, not otherwise specified (n = 1); cases with overlapping features of CLH and B-cell lymphoma (n = 3), one of them composed of spindle cells. Cutaneous lymphoid hyperplasia infiltrates were dense, composed mainly of B cells forming follicles with germinal centers (GC). Cutaneous lymphoid hyperplasia frequently showed features suggesting a malignancy as coalescing follicles with non-polarized germinal centers lacking mantle zones, and smudged infiltrates of lymphoid cells spreading into collagen (often as "Indian files"), smooth muscle, vessel walls, and nerve sheaths. Only two cutaneous lymphoid hyperplasias recurred; otherwise all patients are without disease (mean follow-up 62 months). Monoclonal rearrangement of immunoglobulin heavy chain gene was detected in five, and of T-cell receptor gamma gene in two cutaneous lymphoid hyperplasias using polymerase chain reaction (PCR), but the patients fared well too. In 47% of cases Borrelia burgdorferi was detected by polymerase chain reaction and/or serology, of which one was monoclonal. We conclude that cutaneous lymphoid hyperplasia is the most common lymphoproliferation of the breast nipple, rarely recognized clinically, and often overdiagnosed histologically as lymphoma.

Adolescent↗

PubMed1978

Circumscribed sebaceous gland hyperplasia: autoradiographic and histoplanimetric studies.

Circumscribed sebaceous gland hyperplasia (sebaceous hyperplasia) is a common benign facial tumor found in adults and aged. Seventeen biopsies of sebaceous hyperplasia from 10 patients, females and males aged 57-87 years were secured which were injected 45 min or up to 15 days prior with tritiated thymidine, and prepared for autoradiography. Specimens were evaluated by cell counts (labeling index, labeled total cells), and histoplanimetric techniques (sagittal section areas and circumference of sebaceous hyperplasia, of sebocytes, and of sebocyte nuclei). Controls were uninvolved sebaceous follicles from the same subjects, from an age-matched group, and from young male adults. In sebaceous hyperplasia the labeling index of basal cells is low with 5.7% +/- 2.3 vs uninvolved sebaceous follicles from the same subject (8.6% +/- 2.4) and the younger subjects with a value of 10.1% +/- 2.0). Labeled cells are retained in the acini much longer than in young adults (slowed down transit and turnover time). The glands of sebaceous hyperplasia are very large, their sebocytes are small, and many more basal cells are found per unit basement membrane length.

Adenoma↗

PubMedDate not supplied

Which surgical procedure for patients with atypical endometrial hyperplasia?

OBJECTIVE: To determine the occult coexistence of endometrial carcinoma in patients with atypical endometrial hyperplasia and to compare histological prognostic factors according to lymph node status in occult endometrial carcinoma. MATERIALS AND METHODS: Two hundred and four patients from two referral centers (during the period 1990-2003) who were operated on within 1 month of endometrial biopsy for symptomatic endometrial hyperplasia without receiving any medical treatment were included retrospectively. Patients having preoperative endometrial biopsy results of concomitant endometrial hyperplasia and carcinoma were excluded from the study. Fifty-six patients having atypia in preoperative biopsy (group I) were compared with 148 patients without atypia (group II). Chi-square and Mann-Whitney U-tests were used for statistical analyses. RESULTS: No significant difference was observed between the two groups according to age or menopausal status. Patients in group II had significantly higher parity than patients in group I. In group I, 62.5% of the patients had endometrial carcinoma, 21.4% had endometrial hyperplasia, and 16.1% had normal endometrium in hysterectomy specimens. In group II, the percentages were 5.4, 38.5, and 56.1%, respectively. Complete surgical staging was performed in 20 patients. Four patients had metastatic lymph nodes. All of them had grade 2 tumors with lymphovascular space involvement. Three of them had nonendometrioid tumors. CONCLUSION: Careful intraoperative and preoperative evaluation of the endometrium must be the sine qua non for patients with atypical endometrial hyperplasia. It is reasonable to do frozen section at the time of hysterectomy for atypical endometrial hyperplasia, and if grade 2/3 of nonendometrioid cancer with lymphovascular space involvement is found, complete surgical staging should be performed.

Adult↗

PubMed1999

Clonal emergence in uremic parathyroid hyperplasia is not related to MEN1 gene abnormality.

It is difficult to differentiate between parathyroid neoplasia and hyperplasia. In an attempt to elucidate the clonality of uremic parathyroid hyperplasia and the molecular genetic abnormalities accounting for clonal emergence, we analyzed 20 cases of uremic parathyroid hyperplasia. Clonalities were determined using the X-chromosome-linked human androgen receptor (HUMARA) gene and the phosphoglycerate kinase (PGK) gene, and multiple endocrine neoplasia type 1 (MEN1) gene abnormality was analyzed by studying loss of heterozygosity (LOH) in 11q13 and somatic mutations in the MEN1 gene. As a positive control, a case of MEN1 with Zollinger-Ellison syndrome was analyzed simultaneously. Our analysis revealed that a majority (75%) of the uremic parathyroid hyperplasia tissues, including an autograft with recurrent hyperparathyroidism, was of monoclonal origin. Clonality did not correlate with serum carboxyl-terminal parathyroid hormone (C-PTH) level, calcium level, hemodialytic duration, gland weight or pathological features. Neither LOH in 11q13 nor somatic mutation in the MEN1 gene was detected. For the MEN1 case, a germline mutation (W198X) was detected in exon 3. We concluded that a majority of the uremic parathyroid hyperplasia cases was in fact monoclonal neoplasia. MEN1 gene abnormality played a minor role, if any, in the clonal emergence in uremic parathyroid hyperplasia.

Clone Cells↗

PubMed2006

Kimura's disease and angiolymphoid hyperplasia with eosinophilia: two disease entities in the same patient: case report and review of the literature.

BACKGROUND: Much controversy has existed with regard to the relationship between Kimura's disease and angiolymphoid hyperplasia with eosinophilia. They were initially thought to represent the same disease spectrum, but it has now been widely accepted that they are two separate disease entities. To our knowledge, there have been no reports to date describing a case of both Kimura's disease and angiolymphoid hyperplasia with eosinophilia coexisting in the same patient. METHODS: We describe a patient presenting initially with a right postauricular subcutaneous swelling and subsequently developing multiple erythematous facial papules and nodules. The medical literature is reviewed. RESULTS: Clinical features of the right postauricular subcutaneous swelling and multiple erythematous facial papules/nodules suggest Kimura's disease in the former and angiolymphoid hyperplasia with eosinophilia in the latter. Histopathological examinations of these lesions helped to confirm the diagnosis of Kimura's disease and angiolymphoid hyperplasia with eosinophilia, respectively. CONCLUSIONS: Kimura's disease and angiolymphoid hyperplasia with eosinophilia can coexist in the same patient. Coexistence of the two types of lesions in one patient may also be considered evidence that Kimura's disease and angiolymphoid hyperplasia with eosinophilia form a spectrum in one disease.

Adrenal Cortex Hormones↗

PubMed1991

An autopsy case of metastatic foci of hepatocellular carcinoma in adenomatous hyperplasias of the liver.

Adenomatous hyperplasia of the liver is known as a preneoplastic or early developmental stage of hepatocellular carcinoma, in which overt malignant foci occasionally develop. We have recently experienced an autopsy case (a 70-year-old male) of liver cirrhosis with hepatocellular carcinoma and two nodules of adenomatous hyperplasia. The latter two nodules contained several microscopic foci of moderately differentiated hepatocellular carcinoma. There were a number of tumor microemboli in portal vein branches within areas of adenomatous hyperplasia in addition to areas surrounding cirrhotic liver, some of which grew into the parenchyma of adenomatous hyperplasia and cirrhotic regenerative nodules. These findings and the fact that adenomatous hyperplasia contained portal tracts including portal venous branches, suggest that malignant foci in adenomatous hyperplasia contained portal tracts including represent metastases from hepatocellular carcinoma in other parts of the liver via the intrahepatic portal venous system.

Aged↗

PubMed2005

On the relation of nitric oxide to nifedipine-induced gingival hyperplasia and impaired submandibular glands function in rats in vivo.

Calcium-channel blockers such as nifedipine could be associated with gingival overgrowth. The aim of this study was to examine the role of nitric oxide (NO) on nifedipine-induced gingival hyperplasia along with submandibular secretory function in rats. Animals in divided groups received nifedipine (250 mg/kg diet) alone and in combination with L-arginine (2.25% w/v) or N(omega)-nitro-L-arginine methyl ester (L-NAME) (0.7% w/v) in drinking water for 20 days. Controls received only tap water. Pure submandibular saliva was collected intraorally by micropolyethylene cannula and the mandibular gingiva was examined by means of dissecting microscope for signs of redness, thickness, inflammation and exuda. Twenty-day nifedipine treatment induced gingival hyperplasia accompanied with reduced salivary flow rate and concentrations of total protein, epidermal growth factor (EGF) and calcium in comparison with controls. Co-treatment of animals with nifedipine and L-arginine protected from gingival hyperplasia and retained flow rate, and concentrations of total protein, EGF and calcium in normal levels. Co-treatment of animals with nifedipine and L-NAME potentiated nifedipine-induced gingival hyperplasia and reductions in flow rate and concentrations of total protein, EGF, and calcium. It is concluded that nifedipine-induced gingival hyperplasia is associated with salivary dysfunction. Activation of cGMP-dependent positive signal-transduction mechanisms in salivary glands might be the mechanism for protective effects of NO against nifedipine-induced gingival hyperplasia.

Animals↗

PubMed2004

Inhibition of neointimal hyperplasia in vascular grafts by sustained perivascular delivery of paclitaxel.

BACKGROUND: Neointimal hyperplasia occurs commonly at the anastomoses of arteriovenous grafts for chronic hemodialysis, causing stenosis and occlusion. Antiproliferative drugs may be effective in inhibiting hyperplasia, but local drug delivery would be required to minimize systemic side effects. We examined the feasibility of local drug delivery to inhibit neointimal hyperplasia at dialysis grafts in a canine model. METHODS: Bilateral polytetrafluoroethylene loop grafts (10-cm length and 6-mm internal diameter) were placed between the femoral artery and ipsilateral femoral vein of five mongrel dogs. At the time of surgery or 1 to 5 weeks later, 2 mL of a thermosensitive biodegradable copolymer (ReGel) mixed with 0.26 mg or 0.65 mg paclitaxel were applied to the external surface of one graft around the anastomoses to provide a depot for sustained release of the drug. ReGel alone without paclitaxel was applied to the contralateral graft as a control. The grafts and the connecting vessels were explanted at eight or nine weeks, and the cross-sections were examined histologically. The degree of hyperplasia at the anastomoses was graded by five blinded independent reviewers, with scores ranging from 0 to 5. RESULTS: The median (25th-75th percentile) hyperplasia score of both arterial and venous anastomoses was 1.80 (0.90-3.05) in the grafts treated with ReGel alone, and 0.95 (0.70-1.50) in the grafts treated with ReGel/paclitaxel (N= 8; P < 0.05 by Wilcoxon signed rank test). There were no noticeable localized or systemic complications attributed to the treatments in these animals. Paclitaxel levels in the plasma obtained from forelimb veins were undetectable (<10 ng/mL). CONCLUSION: These results suggest that the local delivery of antiproliferative agents using a thermosensitive, injectable biodegradable copolymer (ReGel) for sustained delivery is a promising strategy to inhibit neointimal hyperplasia of arteriovenous hemodialysis grafts.

Animals↗

PubMed1994

Clinical assessment of gingival hyperplasia in patients treated with nifedipine.

Gingival hyperplasia caused by the use of nifedipine has been extensively reported. In this paper, the gingiva of 18 patients suffering from cardiopathy and treated with nifedipine were compared with those of 10 patients with cardiac disorders who had not been treated with calcium antagonists and with a no-treatment group of 12 patients. Nifedipine produced gingival hyperplasia, although patients who had not been treated with calcium antagonists also had mild hyperplasia. Hyperplasia first appeared in the interproximal areas, an observation which may be important for early detection. There was a direct correlation between the degree of hyperplasia and the bacterial plaque score. When we studied the influence of administration time and dose of nifedipine with the degree of hyperplasia, no statistically significant differences were found.

Dental Plaque Index↗

PubMed1984

Effects of the anti-inflammatory agents indomethacin, metiamide and acetylsalicylic acid on the induction of hyperplasia in hamster cheek-pouch epithelium and ear epidermis.

Previous studies have shown that agents such as indomethacin and hydrocortisone act to reduce the level of epidermal hyperplasia produced by various chemical, but little information is available about the effects of such anti-inflammatory agents on the induction of hyperplasia in oral mucosa. Hamster cheek-pouch epithelium and ear epidermis were treated with indomethacin, metiamide and acetylsalicylic acid prior to treatment with turpentine, podophyllin or TPA. The levels of hyperplasia induced were monitored by rates of epithelial glycolysis, protein synthesis and mitosis. The response of the metabolic assays to epinephrine was also examined. Alone, turpentine, podophyllin and TPA each caused a 3-5 fold increase in the metabolic assays and loss of the normal tissue response to epinephrine. Tissues pretreated with indomethacin showed significant reductions in the levels of hyperplasia produced and they retained a normal response to epinephrine. No reduction in hyperplasia was observed following pretreatment with acetylsalicylic acid, an alternative inhibitor or prostaglandin synthesis or with metiamide, a histamine blocker. The results indicate that the production of epithelial hyperplasia by turpentine, podophyllin and TPA can be inhibited by indomethacin.

Animals↗

PubMed1985

Pharyngeal lymphoid hyperplasia in Thoroughbred racehorses in training.

The prevalence of pharyngeal lymphoid hyperplasia in Thoroughbred racehorses in training was investigated using a fibre optic endoscope. Of the 70 horses examined, all but 8 showed evidence of pharyngeal lymphoid hyperplasia and the severity of the pharyngeal changes decreased with age. Two-year old horses had greater pharyngeal lymphoid hyperplasia (p less than 0.05) when compared to all other age groups. More horses (p less than 0.05) with Grade 3 or Grade 4 pharyngeal lymphoid hyperplasia experienced recent mild respiratory disease than did horses with Grade 2 or less pharyngeal lymphoid hyperplasia. None of the horses examined had a history of diminished racing performance although 30% had either Grade 3 or Grade 4 pharyngeal lymphoid hyperplasia.

Age Factors↗

PubMedDate not supplied

Reversion of gingival hyperplasia in a heart transplant patient upon interruption of cyclosporine therapy.

A heart transplant patient undergoing a combined cyclosporine and prednisone treatment was monitored during the 18 months following transplantation. A complete oral and dental examination was performed in each of the first six months after transplantation, and then in the 9th, 12th, 15th, and 18th months. The data collected included gingival hyperplasia secondary to cyclosporine use, and clinical and periodontal variables. Histological studies were also conducted on gingival tissue samples in months 1, 3, 9, 15, and 18. Cyclosporine treatment was replaced by azathioprine treatment in month 10 because the patient was experiencing nephrotoxicity. Between months 9 and 18, gingival hyperplasia regressed by 26.5% due to a reduction in the fibrous connective tissue mass, fibroblasts, and inflammatory infiltration. The control group included 13 heart transplant patients subject to equivalent conditions except discontinuance of cyclosporine treatment; seven of the patients had developed hyperplasia by month 9. Average hyperplasia in the control group increased by 2% between months 9 and 18; only one patient showed a 6.2% decrease in hyperplasia. This provides further evidence for the causal relationship between cyclosporine therapy and gingival hyperplasia, and suggests that this side-effect is reversible.

Child↗

PubMed1966

Hypertrophy versus hyperplasia.

Although all tissues and organs of the body are normally subject to the growth-regulating influences of functional demands, some are potentially capable of unlimited growth while others are not. This depends on whether hyperplasia of their functional units ceases prior to maturity or can continue throughout life. In the former case, further growth is limited by the extent to which hypertrophy can enhance physiological efficiency. Some of the body's most vitally essential organs (heart, brain, kidney, lung) lack the ability to make additional structural units in the adult and are therefore handicapped in compensating for the depreciations of advancing age. Theoretically, at least, other organs (glands, renewing tissues) possess unlimited powers of regeneration because they never lose the capacity (latent or expressed) for hyperplasia. There is a strategy in the way growth mechanisms have evolved. It may be significant that the so-called "hypertrophic" organs lose the capability for hyperplasia, because not to do so might jeopardize their growth regulation. If size is determined by functional demands, then the latter must not operate continuously lest growth go on without interruption and lead to overproduction of functional units. Only renewing tissues can tolerate perpetual growth because they get rid of excess structures as fast as they are formed. Endocrine and exocrine glands are in most cases known to function discontinuously and are thus not in danger of being overstimulated. The heart, lungs, and kidneys (and brain?), however, must work incessantly. Were their functional units capable of hyperplasia and at the same time subject to control by functional demand, then overgrowth would seem to be inevitable. By giving up the potential for hyperplasia in favor of the necessity for constant function, these organs have adopted a strategy that enables them to become hypertrophic to a limited extent while doing their jobs efficiently. It is a curious fact that the unrestricted proliferation of biological structures cannot occur at all levels of organization. The counterpart of cancer, which is a cellular phenomenon, does not exist among molecules or cytoplasmic organelles, nor is it known to occur at the histological level of organization. Even in organs made up of histological units of function and having the potential for unlimited hyperplasia (for example, liver, exocrine glands, thyroid, ovary), the population of functional units never exceeds the number needed to fulfil the physiological requirements of the body. Above and below the level of the cell, therefore, structures are not permitted to escape the constraints of functional demands which control their production. The fact that cells can occasionally do so when they become neoplastic may reveal as much as it conceals about the problem of growth regulation.

Cell Differentiation↗

PubMed1980

Congenital adrenal hyperplasia--a clinical and genetic survey. Are we detecting male salt-losers?

In a genetic and clinical study in Wales of congenital adrenal hyperplasia due to 21-hydroxylase deficiency, 26 cases were found in the period 1966 to 1977. No one was known to have died from the condition in the period. There were 14 female and 5 male salt-losers, and 5 female and 2 male nonsalt-losers. The discrepancy between the sexes suggests that some cases of congenital adrenal hyperplasia in males are not being detected. This is of concern as salt-losing cases may be dying without a diagnosis being established. The carrier incidence of the condition in females, assuming complete ascertainment, is 1:55. Salt-losers in Wales appear to be more than twice as common as nonsalt-losers. HLA typing of certain affected families confirmed a genetic linkage between the congenital adrenal hyperplasia gene and HLA. This linkage appears to exist in both forms of congenital adrenal hyperplasia and suggests that the genes for salt-losing and nonsalt-losing forms of congenital adrenal hyperplasia are alleles. The linkage between congenital adrenal hyperplasia and HLA provides a potential method for antenatal detection. However, only a few parents would wish to take advantage of this method if it were readily available.

Adolescent↗