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PubMed2007

Holmium laser treatment of benign prostatic hyperplasia: an update.

PURPOSE OF REVIEW: The surgical treatment of benign prostatic hyperplasia is a dynamic, evolving field. Holmium laser enucleation of the prostate has been one of the most rigorously analyzed interventions for benign prostatic hyperplasia. In the 12 months since July 2005, a number of important studies have been published concerning this technique. RECENT FINDINGS: In the 12-month period of this review, there have been a number of articles published on holmium laser enucleation of the prostate. Among these are five randomized controlled trials. These studies emphasize the unique advantages of holmium laser enucleation of the prostate over other surgical treatments for benign prostatic hyperplasia. SUMMARY: Holmium laser enucleation of the prostate is a more efficient procedure than competitor techniques, when grams of tissue removed per unit time are quantified. Additionally, holmium laser enucleation of the prostate is associated with a reduced length of catheterization and hospitalization when compared with other surgical therapies for men with benign prostatic hyperplasia. Outcome measures for men undergoing holmium laser enucleation of the prostate are in many cases superior to those of other modalities. It is likely that the completeness of adenoma removal with holmium laser enucleation of the prostate confers many of these advantages.

Holmium↗
PubMed2007

Prostatic stents for the treatment of benign prostatic hyperplasia.

PURPOSE OF REVIEW: The insertion of prostatic stents in the treatment of lower urinary tract symptoms in men secondary to benign prostatic obstruction from benign prostatic hyperplasia has proven to be an effective modality in properly selected patients. We review the current literature on the role of prostatic stents in the treatment of bladder outlet obstruction secondary to benign prostatic hyperplasia. RECENT FINDINGS: Permanent stents such as the Urolume and the Memokath offer efficacious and safe treatment alternatives for men with bladder outlet obstruction from benign prostatic hyperplasia who are deemed high surgical risks for traditional transurethral resection of the prostate. When removal of permanent prostatic stent is necessary, the design of the Memokath allows for an easier removal than that of the Urolume. Temporary stents are being investigated as a means to treat the transient bladder outlet obstruction frequently observed after minimally invasive thermotherapy procedures aimed at treating benign prostatic obstruction, with both biodegradable and retrievable stents shown as successful modalities for this indication. SUMMARY: Prostatic stents remain an option to treat men with benign prostatic obstruction/bladder outlet obstruction; however, stent migration remains an obstacle to their widespread use. The key to obtaining optimal outcomes in men with benign prostatic hyperplasia is careful patient selection and experience with proper stent deployment.

Humans↗
PubMed1997

trans-4-(Aminomethyl)cyclohexane carboxylic acid (T-AMCHA), an anti-fibrinolytic agent, accelerates barrier recovery and prevents the epidermal hyperplasia induced by epidermal injury in hairless mice and humans.

Because wounding the epidermis increases proteolytic activity and because disorders associated with barrier dysfunction have elevated protease activity, we studied the effect of protease inhibitors on the time course of barrier recovery and on the development of epidermal hyperplasia induced by repeated injury. After injuries to the epidermis produced by tape stripping, acetone treatment, or detergent (SDS) treatment that disrupt the barrier, a single application of 5% tranexamic acid [4-(aminomethyl)cyclohexane carboxylic acid, t-AMCHA], a well known anti-plasmin reagent, accelerated barrier recovery in both hairless mouse and human skin. In contrast, neither aminocaproic acid nor aminobutyric acid, inactive analogs of t-AMCHA, affected the time course of barrier recovery. Several trypsin-like serine protease inhibitors, e.g., leupeptin, TLCK, and PMSF, also accelerated barrier repair. In contrast other types of protease inhibitors, e.g., EDTA, pepstatin, N-ethylmaleimide, chymostatin, and TPCK, did not accelerate barrier recovery. We next evaluated the effects of daily topical application of t-AMCHA on epidermal hyperplasia, induced by repeated tape stripping or acetone treatment for 7 d. The degree of hyperplasia, quantified by the measurement of epidermal thickness, was reduced in both models by repeated applications of t-AMCHA. Finally, proteolytic activity in both human and mouse epidermis increased 1-2 h after epidermal injuries that disrupt the barrier. These results demonstrate that the inhibition of plasmin, a serine protease, accelerates barrier recovery and inhibits the epidermal hyperplasia induced by repeated barrier disruption, perhaps by decreasing the extent of attendant epidermal injury.

Animals↗
PubMed1992

"Giant" senile sebaceous hyperplasia.

Although the usual size of senile sebaceous hyperplasia is 2 to 3 mm in diameter, we report one "giant" nodular case on the face. The patient is a 75-year-old Japanese man with a dome-shaped, skin-colored nodule on his right cheek. The lesion was 10 mm in diameter and had multiple small umbilications on its surface. He also had several small, yellow-colored, asymptomatic papules with central umbilication on his cheeks. Histologically, the giant nodule and the papule on the right cheek showed the same architectural pattern, a sharply demarcated hyperplasia of grouped mature sebaceous glands with a sebaceous converging duct, whose opening to the surface epithelium corresponded to the clinical umbilication. The reason for the giant growth of this senile sebaceous hyperplasia in our case is obscure; the patient had not been stressed by inductive agents or factors such as systemic corticosteroid and hemodialysis except for electrocoagulation on the lesion. In spite of the extraordinarily large size of the nodule, the conservative proliferating pattern seemed to show the benign hyperplastic character of senile sebaceous hyperplasia.

Age Factors↗
PubMed1992

Reversibility of carcinogen-induced rat forestomach basal cell hyperplasia is due to squamous cell differentiation.

The mechanisms of reversibility of basal cell hyperplasia in the rat forestomach were investigated. Male F344 rats were given an initial single gastric intubation of N-methyl-N'-nitro-N-nitorosoguanidine and then received 2% butylated hydroxyanisole in the diet from the third week to the 26th week. Rats were killed at weeks 26 and 46 after return to basal diet and their forestomachs were removed. Bromouracil deoxyriboside (BUdR) was administered as a single i.p. injection 1 h before death or by osmotic minipump (120 micrograms/h) continuously for 7 days before death. Additional animals were maintained for 2 or 4 weeks after removal of osmotic minipumps to allow assessment of the fate of proliferating populations. In each case BUdR-labeled cells were demonstrated by immunohistochemistry by immunohistochemistry. At week 26, hyperplastic changes were more pronounced than at week 46. Squamous cells above basal cell hyperplasias were strongly labeled even 4 weeks after cessation of continuous BUdR Three-dimensional reconstruction of persisting basal cell hyperplasias showed almost all basal cells limited to a thin sheet in direct contact with the squamous cell layer, occasional separate islands demonstrating differentiation to squamous cells and formation of epidermal cysts. The results thus showed that the mechanism of reversibility of basal cell hyperplasia involves differentiation of basal cells to squamous cells.

Animals↗
PubMed1999

Multiple K-ras mutations in hyperplasia and carcinoma in cases of human pancreatic carcinoma.

Mucous cell hyperplasia (MCH) has been considered an important precursor of pancreatic ductal carcinoma based on histological and molecular research, although various K-ras mutations rates are seen among cases with pancreatic carcinoma, chronic pancreatitis and normal pancreas, with a wide range of histological characters. To investigate the premalignant potential of MCH and the multicentricity of pancreatic carcinoma, we analyzed K-ras mutation at codon 12 in carcinoma foci of 82 cases of surgically-resected pancreatic carcinoma [67 solid-type carcinomas (SCs) and 15 ductectatic-type carcinomas (DCs)], as well as in both MCH and carcinoma foci in 42 cases (30 SCs and 12 DCs), using an enriched polymerase chain reaction (PCR)-enzyme linked mini-sequence assay (ELMA). K-ras mutation was recognized in 85% (57/67) of SCs and 73% (11/15) of DCs, and multiple K-ras mutations in 12% (8/67) of SCs and in 20% (3/15) of DCs. Multiple K-ras mutations were also recognized in MCHs in 47% (14/30) of SCs and in 42% (5/12) of DCs. Moreover, the same sequence at K-ras codon 12 in MCH and carcinoma was identified in 76% (32/42) of carcinoma cases and it was more frequently recognized in hyperplasias with histological atypia (51%, 37 of 72 foci) than those without atypia (24%, 16 of 68 foci) (P<0.0007). These results further support the idea of multicentric carcinogenesis and premalignant potential of atypical hyperplasia in the human pancreas, although about half of the hyperplasias around carcinomas were not thought to be direct precursors.

Adult↗
PubMed1990

'Atypical adenomatous hyperplasia' in liver cirrhosis: low-grade hepatocellular carcinoma or borderline lesion?

Adenomatous hyperplasia, defined as a sizable parenchymal nodule in cirrhosis, was examined morphologically. Ninety-seven nodules of adenomatous hyperplasia were obtained from 47 cirrhotic livers and were divided into 'ordinary' (44 nodules) and 'atypical' (53 nodules) types. The former consisted of hepatocytes similar to those of the surrounding liver, and showed regularly distributed portal tracts. The latter type was composed of hepatocytes showing nuclear atypia, relative to the surrounding liver, and showed irregular or sparse portal tracts. Atypical nodules were histologically heterogeneous, possessing areas of normo-trabecular, compact, pseudoglandular and/or scirrhous patterns. Several cytological changes, such as clear cell change, small or large cell change and fatty change, were intermingled variably within a given nodule. Atypical nodules showed expansive and/or replacing growth into the surrounding liver. Atypical hepatocytes also infiltrated into the fibrous septa and portal tracts. Foci of overt hepatocellular carcinoma were found in 11 of the 53 atypical nodules. These findings suggest that ordinary adenomatous hyperplasia may be a large-sized regenerative nodule, while atypical adenomatous hyperplasia may be a hepatocellular neoplasm, a peculiar form of low-grade hepatocellular carcinoma or borderline lesion, in which overt hepatocellular carcinoma is likely to evolve through multiple steps.

Adult↗
PubMed1995

Association between mucosal hyperplasia of the appendix and adenocarcinoma of the colon.

Mucosal hyperplasia of the appendix is a seemingly benign change of poorly understood significance, at times found in patients with colorectal malignancy. To determine the incidence of this change and its association with colonic adenocarcinoma, we have examined the appendiceal mucosa in 122 ileocolectomy specimens gathered between 1987 and 1990, and in 273 consecutive appendectomies carried out during 1990 at The Methodist Hospital in Houston, Texas. We found that 23 out of 122 ileocolectomies (18.8%) showed mucosal hyperplasia of the appendix and, of these, 17 (77%) were associated with colorectal malignancy, predominantly of the right side. Moreover, 24 of 273 appendectomies (8.8%) exhibited the presence of mucosal hyperplasia and, of these, six (25%) also were associated with adenocarcinoma of the colon. On the basis of this significant rate of association, we feel that a concomitant colorectal carcinoma should be ruled out in patients who exhibit mucosal hyperplasia of the appendix.

Adenocarcinoma↗
PubMed2005

Relationship between Candida infection and immune cellular response in inflammatory hyperplasia.

OBJECTIVES: To analyze and quantify the CD8(+) and CD4(+) T-lymphocyte populations in inflammatory hyperplasia and to establish the relationship between the frequency and location of these cells and Candida infection. METHODS: Samples of inflammatory hyperplasia were stained with PAS for evidence of Candida sp. and were classified in two groups, infected and control, according to the presence or absence of infection. After immunoreaction with specific anti-CD4 and anti-CD8 monoclonal antibodies, the distribution and frequency of the positive cells were analyzed in 41 cases (19 controls without Candida sp. and 22 infected cases). Lymphocytes were quantified in the three consecutive fields where the inflammatory infiltration was concentrated. RESULTS: There was no relationship between the frequency and location of CD4(+) T cells and Candida sp. infection. The number of CD8(+) cells close to the fungi hyphae as well as the total number of CD8(+) T cells present in inflammatory hyperplasia were higher in the Candida sp. group than in the control noninfected group (P < 0.05). CONCLUSION: Since the CD8(+) T cells were distributed according to the location of Candida sp. hyphae, and since a higher CD8(+)/total lymphocytes ratio was observed in the infected group, we suggest a role for CD8(+) T cells in the defense against Candida in oral infections associated with inflammatory hyperplasia in immunocompetent individuals.

CD4-Positive T-Lymphocytes↗
PubMedDate not supplied

Leydig cell hyperplasia due to a testicular embryonal carcinoma producing human chorionic gonadotropin.

Report of the case of a 21-year-old man who presented with gynecomastia and was found to have a testicular embryonal carcinoma producing human chorionic gonadotropin (HCG), associated with massive hyperplasia of Leydig cells. While the morphologic features of Leydig cell hyperplasia have been documented with excess endogenous luteinizing hormone (LH), as in Klinefelter's syndrome, and following administration of exogenous HCG, to our knowledge, this is the first description of the histologic and ultrastructural changes in Leydig cells associated with increased secretion of endogenous HCG. The Leydig cell stimulation which results from excess endogenous HCG is unusual in that it causes an elevation of estrogens which may be greater than the rise in androgens. It is concluded that embryonal cell carcinoma of the testis, producing HCG, may lead to Leydig cell hyperplasia with morphologic features similar to those seen in other conditions with such hyperplasia, and that there is no correlation between those morphologic features and testosterone production.

Adult↗
PubMed1990

Effect of anti-androgen (TZP-4238) on steroid-induced canine prostatic hyperplasia. Light and electron microscopic investigations.

The effect of a synthetic steroidal anti-androgen, TZP-4238, on steroid-induced canine prostatic hyperplasia was studied by light and electron microscopy. Male beagle dogs (1-2 years old) were divided into four experimental groups. Group 1 consisted of intact controls. The other animals were castrated. The castrated animals were treated for 25 weeks with 1) 5 alpha-androstane-3 alpha, 17 beta-diol (A-diol) plus 17 beta-estradiol (E2) (Group 2), 2) A-diol plus E2 + TZP-4238 0.5 mg/kg (Group 3) and 3) A-diol plus E2 + chlormadinone acetate (CMA) 2.5 mg/kg (Group 4). TZP-4238 and CMA were administered orally for 21 weeks after 4 weeks treatment with A-diol plus E2. In group 2, glandular hyperplasia of the prostate was clearly noted. In contrast, combined treatment with TZP-4238 (Group 3) or CMA (Group 4) produced marked atrophy of the glandular epithelium. Loss of secretory and metabolic activities was confirmed by ultrastructural investigations. Our data indicate that TZP-4238 is a potent anti-androgen for the prevention of canine prostatic hyperplasia in the steroid-induced benign prostatic hyperplasia (BPH) model.

Administration, Oral↗
PubMed1998

Pleomorphic adenoma of the minor salivary gland with pseudoepitheliomatous hyperplasia of the overlying oral mucosa: report of two cases.

Two cases of intra-oral pleomorphic adenoma with marked pseudoepitheliomatous hyperplasia of the overlying oral mucosa are reported. Incisional biopsy specimens, taken a few weeks before surgical excision of the tumor, showed no squamous cell element. Surgically excised specimens revealed pseudoepitheliomatous hyperplasia with hyperortho- and para-keratinization, which extended from overlying oral squamous epithelium, where an incisional biopsy was performed into the deep tumor area. Approximately half of the tumor area in case 1 and one-third in case 2 were occupied by hyperplastic squamous epithelium of the oral mucosa. Although the induction mechanism of such prominent pseudoepitheliomatous hyperplasia of the overlying oral mucosa occupying more than one-third of the tumor area could not be understood, it is thought that surgical injury and/or focal anesthesia during the incisional biopsy played an important role. To the best of our knowledge, these two cases represent the first reported association between benign salivary gland tumor and marked pseudoepitheliomatous hyperplasia of the overlying oral mucosa.

Adenoma, Pleomorphic↗
PubMed2005

Cinacalcet HCl attenuates parathyroid hyperplasia in a rat model of secondary hyperparathyroidism.

BACKGROUND: Secondary hyperparathyroidism (HPT) in chronic kidney disease (CKD) is a physiologic response to kidney failure characterized by elevated serum parathyroid hormone (PTH) levels and parathyroid gland enlargement. Calcimimetic agents acting through allosteric modification of the calcium-sensing receptor (CaR) can attenuate parathyroid hyperplasia in rats with secondary HPT. The present study explores the effects of the calcimimetic cinacalcet HCl on parathyroid hyperplasia, apoptosis, and PTH secretion in a rat model of secondary HPT. METHODS: Cinacalcet HCl was gavaged daily (1, 5, or 10 mg/kg) for 4 weeks starting 6 weeks post-5/6 nephrectomy. After dosing, hyperplasia was determined using parathyroid weight and proliferating cell nuclear antigen (PCNA) immunochemistry. Apoptosis was determined using in situ techniques. Serum PTH((1-34)) and blood chemistries were determined throughout the course of the study. RESULTS: Administration of cinacalcet HCl (5 or 10 mg/kg) significantly reduced the number of PCNA-positive cells and decreased parathyroid weight compared with vehicle-treated 5/6 nephrectomized rats. There was no difference in apoptosis from cinacalcet HCl-treated or vehicle-treated animals. Serum PTH and blood ionized calcium levels decreased in cinacalcet HCl-treated animals compared with vehicle-treated controls. CONCLUSION: The results confirm previous work demonstrating that calcimimetic agents attenuate the progression of parathyroid hyperplasia in subtotally nephrectomized rats, extending earlier observations to now include cinacalcet HCl. These results support a role for the CaR in regulating parathyroid cell proliferation. Therefore, cinacalcet HCl may represent a novel therapy for improving the management of secondary HPT.

Animals↗
PubMed2004

Sebaceous hyperplasia treated with a 1450-nm diode laser.

BACKGROUND: Sebaceous hyperplasia is a benign proliferation of the sebaceous gland. Previous treatment options have included isotretinoin, destructive modalities, and pulsed-dye laser. OBJECTIVE: To evaluate the efficacy of a 1450-nm diode laser for the treatment of sebaceous hyperplasia. METHODS: Ten patients with sebaceous hyperplasia were treated one to five times with a 1450-nm diode laser. Fluences of 16 to 17 J/cm2 were used, with cooling durations of 40 to 50 ms. Patients and physicians evaluated treated lesions for improvement. Measured areas of treated lesions were also recorded. RESULTS: In most cases, patients and physicians rated improvement as "very good" or better. After two to three treatments, 84% of lesions shrunk greater than 50%, and 70% shrunk greater than 75%. Adverse effects were unusual; one atrophic scar and one case of transient hyperpigmentation were observed. CONCLUSION: The 1450-nm diode laser is effective and safe for the treatment of sebaceous hyperplasia.

Humans↗
PubMedDate not supplied

Expression of estrogen receptors ERalpha and ERbeta in endometrial hyperplasia and adenocarcinoma.

We assessed the expression of estrogen receptors (ER)alpha and ERbeta in 114 human endometrial hyperplasia and adenocarcinomas. The aim of this study was to determine the expression of both ER isoforms in human endometrial tissue by immunohistochemistry. From normal proliferation to simple and complex hyperplasia, the expression of ERalpha was increased (P < 0.05), while ERbeta did not change much (P > 0.05). In atypia hyperplasia and adenocarcinoma, both ERalpha and ERbeta were decreased significantly (P < 0.05). Most endometrial adenocarcinomas expressed ERalpha, either alone or in combination with ERbeta, and the ERbeta/ERalpha ratio was decreased when compared to normal proliferation (P < 0.05). Also, we found that the expression of ERalpha and ERbeta has no relationship with the status of lymph node of adenocarcinoma (P > 0.05). Both ERalpha and ERbeta play an important role in endometrial hyperplasia and carcinomas, the levels of ERalpha and ERbeta appear be used as prognostic indicators.

Adenocarcinoma↗
PubMed2006

Immunohistochemical analysis of Omi/HtrA2 expression in prostate cancer and benign prostatic hyperplasia.

The serine protease Omi/HtrA2 is released from mitochondria into the cytosol after apoptotic stimuli, inducing apoptosis in a caspase-independent manner through its protease activity and in a caspase-dependent manner by neutralizing the inhibition of inhibitor of apoptosis proteins (IAPs) on caspases. Alteration of apoptosis is essential for cancer development, and cancer cell death by radiation and chemotherapy is largely dependent upon apoptosis. Thus, analysis of the expression status of Omi/HtrA2, a regulator of apoptosis, in cancer tissues is needed for an understanding of cancer development. In the current study we analyzed the expression of Omi/HtrA2 in 65 prostate cancer, 40 benign prostatic hyperplasia and 10 normal prostate specimens by immunohistochemistry. Omi/HtrA2 mRNA levels of in vivo prostate cancer and benign prostatic hyperplasia samples were also assayed by semiquantitative reverse transcription-polymerase chain reaction. Immunopositivity (defined as > or =30%) was observed for Omi/HtrA2 in most of the prostate cancers, and the positive rate of Omi/HtrA2 was lower in the well-differentiated group than in the poorly and moderately differentiated groups (p<0.005). By contrast, the cells in the normal prostate and benign prostatic hyperplasia groups showed no or only weak expression of Omi/HtrA2. Meanwhile, the Omi/HtrA2 mRNA level of prostate cancer is much higher than that of benign prostatic hyperplasia (p<0.001). Taken together, these results suggest that prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

Aged↗
PubMed1993

The potential use of CO2-laser gingivectomy for phenytoin-induced gingival hyperplasia in mentally retarded patients.

Patients with hyperplastic states of the gingiva, i.e., phenytoin hyperplasia, nifedipine hyperplasia, cyclosporin hyperplasia, gingival fibromatosis and others may be treated by laser gingivectomy as no bone surgery is involved in these cases. Patients who are mentally retarded may represent special care problems postoperatively after conventional surgical gingivectomy i.e., unintentional removal of surgical dressing, postoperative bleeding etc. Therefore, the potential use of CO2-laser gingivectomy for mentally retarded persons was evaluated in a prospective study comprising 15 patients with fenytoin hyperplasia of the gingiva. No intra- or postoperative bleeding occurred and no surgical dressing was applied. The majority of the patients did not need any analgesics postoperatively. Healing was uncomplicated and the time needed for healing was of the same order of magnitude as after surgical gingivectomy.

Adolescent↗
PubMed1995

Basaloid folliculolymphoid hyperplasia with alopecia as an expression of mycosis fungoides (CTCL).

Follicular mucinosis, papules, cysts and comedones have been previously described as expressions of follicular involvement by mycosis fungoides. We report a patient with mycosis fungoides who developed extensive alopecia. Multiple scalp biopsies showed perifollicular and intrafollicular infiltrate of lymphocytes but no evident follicular mucinosis. On transverse sections many of the follicles showed an absence of differentiation towards hair sheath, canal, sebaceous gland or hair formation, but instead formed undifferentiated basaloid structures. These basaloid structures showed transition from atrophic telogen follicles to hypertrophic basaloid islands infiltrated by lymphocytes, resembling the pattern previously described in cutaneous lymphadenoma. Immunophenotyping showed a predominance of helper T-cells which, on ultrastructural examination, showed cerebriform nuclei. The unusual histological findings in our case may be analogous to the hyperplasia seen in sweat glands in syringotropic mycosis fungoides (syringolymphoid hyperplasia), and we propose the term basaloid folliculolymphoid hyperplasia to describe this feature. Basaloid follicular hyperplasia has been previously described as a component of follicular mucinosis but may apparently develop in the absence of overt mucinosis.

Aged↗