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PubMed2002

Contaminants from the transplant contribute to intimal hyperplasia associated with microvascular endothelial cell seeding.

OBJECTIVES: seeding prosthetic grafts with fat-derived microvascular endothelial cells (MVEC) results not only in a non-thrombogenic EC layer, but also in intimal hyperplasia. Here we investigated incidence, composition, progression, and cause of this intimal hyperplasia. DESIGN: EPTFE grafts with MVEC were implanted as carotid interpositions in six dogs with 1 month, and in three dogs with 4, 8 and 12 months follow-up. Grafts seeded without cells, implanted in the contralateral carotid, served as a control. In another three dogs labelled cells were seeded to investigate the contribution of the seeded cells (2-3 weeks). MATERIALS AND METHODS: MVEC were isolated from the falciform ligament. Cells were pressure seeded on ePTFE grafts. Labelling was performed using retroviral gene transduction. The grafts were analysed with immunohistochemical techniques. RESULTS: after 1 month, all patent non-seeded grafts (5/6) showed fibrin and platelet deposition, and all patent seeded grafts (5/6) were covered with a confluent endothelial monolayer on top of a multilayer of myofibroblasts, elastin and collagen. After long term follow-up, all non-seeded grafts were occluded, all patent seeded grafts (4 and 12 months) were covered with an EC-layer with intimal hyperplasia underneath. The thickness of the intima did not progress after 1 month. Transduced cells were found in the endothelial monolayer, hyperplastic intima and luminal part of the prosthesis. CONCLUSIONS: MVEC seeding in dogs results in intimal hyperplasia in all patent grafts, which contains myofibroblasts. Contaminants from the transplant contribute to this intimal hyperplasia.

Animals↗
PubMed2000

Risk factors for hyperplasia-associated versus atrophy-associated endometrial carcinoma.

OBJECTIVE: Endometrial cancer can be divided into atrophy-associated and hyperplasia-associated subtypes. It has been suggested that these subtypes have different pathologic features and prognoses. This preliminary study explores whether these subtypes are associated with different risk factors. STUDY DESIGN: Hysterectomies performed in cases of endometrial carcinoma with evaluable benign endometrium on routine processing were reviewed, and clinical data were abstracted from medical records. Forty-eight subjects with atrophy-associated and 28 subjects with hyperplasia-associated cancers were studied. RESULTS: We found younger age, higher weight, absence of cigarette smoking, and earlier menarche in subjects with hyperplasia-related cancers. CONCLUSIONS: Our findings support the idea that hyperplasia-associated endometrial cancer is estrogen-related but also suggest that atrophy-associated cases may result from a different causal pathway. Epidemiologic studies may yield more precise and accurate measures of association if atrophy-associated and hyperplasia-associated endometrial cancers are considered separately.

Adenocarcinoma↗
PubMed2002

Flow cytometric DNA analysis of benign hyperfunctioning parathyroid glands: significant difference in the S phase fraction and proliferative index between adenomas and hyperplasias.

AIMS: Flow cytometric DNA analysis was performed to measure the DNA content of benign parathyroid tumours in patients with primary hyperparathyroidism. METHODS: DNA analysis of paraffin-embedded parathyroid samples was performed on 51 parathyroid glands from 29 patients after parathyroidectomy. Histopathology showed parathyroid adenoma in 25 cases and hyperplasia in four patients. DNA ploidy status, DNA index (DI), percentage of cells in S phase and proliferative index (PI) were determined. RESULTS: Normal cells from normal glands were all diploid. DNA cytometry showed 12 aneuploid and 13 diploid adenomas. There were 12 diploid and four aneuploid hyperplastic glands. Incidence of aneuploid DNA histograms did not show a statistically significant difference between adenomas and hyperplasias (P=0.216). Mean S phase fraction was 3.45% in adenomas and 1.53% in hyperplasias (P= 0.015). Mean PI was 6.48% in adenomas and 2.78% in hyperplastic parathyroid glands. This difference was statistically significant (P=0.006). Diploid cases had a mean PI of 4.78% and aneuploid glands a mean PI of 7.7% (P=0.08). Aneuploid DNA content did not reveal statistically significant correlation with age, gender, pre-operative Ca, alkaline phosphatase, i-PTH levels, and tumour size. The mean S phase fraction and PI were 2.25% and 4.78% in diploid glands, and 4.5% and 7.7% in aneuploid cases. CONCLUSION: Aneuploid DNA content may be present in benign parathyroid diseases, but not in normal parathyroid glands. Aneuploid DNA histograms and higher PI occur more often in adenomas compared with hyperplasias, but the nuclear DNA analysis is unable to make a distinction between adenomas and hyperplasias.

Adenoma↗
PubMed2001

Clara-cell hyperplasia after quartz and coal-dust instillation in rat lung.

Bronchiolo-alveolar hyperplasia of type II cells in rat lungs after particle exposure is a well-known preneoplastic lesion. The Clara cell, stem cell of the bronchiolar epithelium and the main carrier of cytochrome P-450 isoenzyme system in the lung, has barely been evaluated with regard to this effect. The aim of this study was to examine Clara-cell hyperplasia after particle exposure and to characterize cell proliferation and its normal function. Female Wistar rats were intratracheally instilled with coal dust samples of variable quartz content, quartz (DQ12), titanium dioxide, or saline solution containing 0.5% Tween 80. After 126-129 wk, all coal mine dust- and quartz-exposed animals developed Clara-cell hyperplasia: up to 0.48% of the total lung area, which was significantly increased compared to titanium dioxide (p <.05) and control (p <.03) animals. Proliferation and hyperplasia of bronchiolar Clara cells by coal dusts was independent of their quartz content. The lack of proliferating cell nuclear antigen staining in most of the hyperplastic Clara cells suggests that following damage of alveolar epithelial cells, Clara cells migrate in and remodulate the alveolar epithelium. After the migration they keep their function in the xenobiotic metabolism, as shown by expansion of CYP2E1 active Clara cells. The minor development of Clara-cell hyperplasia in titanium dioxide-treated rats indicates that this is not a general particle effect, and is possibly due to its lower toxicity to epithelial cells.

Animals↗
PubMed2003

Treatment of atypical endometrial hyperplasia with an insulin-sensitizing agent.

Endometrial cancer and hyperplasia have long been associated with diabetes. Hyperinsulinemia may have a direct mitogenic effect on the endometrium and may inhibit the effect of progestogen therapy. This case report describes the treatment of a patient with atypical endometrial hyperplasia with an insulin-sensitizing agent. A 37-year-old patient presented after failed treatment of endometrial hyperplasia with progestogen therapy. One month after initiating metformin therapy the patient's endometrial biopsy demonstrated proliferative endometrium. This patient's atypical endometrial hyperplasia regressed after the initiation of treatment with an insulin-sensitizing agent. This relatively new class of drugs may provide an adjunct to the therapy of endometrial hyperplasia.

Administration, Oral↗
PubMed1999

Basic fibroblast growth factor and myointimal hyperplasia after experimental polytetrafluoroethylene arterial grafting.

OBJECTIVE: To assess the role of polyclonal antibodies to basic fibroblast growth factor (bFGF) in inhibiting myointimal hyperplasia after insertion of polytetrafluoroethylene (PTFE) grafts in rats. DESIGN: Experimental study. SETTING: University laboratory, Italy. ANIMALS: 24 inbred Lewis rats. INTERVENTIONS: A segment of PTFE I cm long was interposed in the abdominal aorta. The animals were randomised in two groups, n = 12 in each. The first were given polyclonal antibodies to bFGF at the time of operation, and for the first two postoperative days; and the second were given non-specific IgG at the same time periods. MAIN OUTCOME AND MEASURES: Two animals died during the immediate postoperative period of anaesthetic complications. 12 animals (6 in each group) were killed 7 days postoperatively (24 hours after injection of 5-bromo-deoxyuridine BrdU) to assess smooth muscle cell proliferation. The remaining 10 animals (5 in each group) were killed after 1 month to assess the degree of anastomotic myointimal hyperplasia. RESULTS: Antibodies to bFGF resulted in less smooth muscle cell proliferation at the anastomoses as well as anastomotic myointimal hyperplasia. Smooth muscle cell proliferation was reduced to about half in animals treated with anti-bFGF antibodies. Neointimal thickness was reduced in treated animals. CONCLUSIONS: We conclude that after PTFE arterial grafting there is increased production of bFGF at the anastomotic regions that leads to smooth muscle cell proliferation and formation of myointimal hyperplasia. Agents that reduce the production of bFGF may also reduce the development of myointimal hyperplasia after PTFE arterial grafting.

Analysis of Variance↗
PubMed2004

Inhibition of neointimal hyperplasia by a specific thrombin inhibitor.

OBJECTIVE: Restenosis secondary to neointimal hyperplasia remains the major limiting factor after vascular interventions. Thrombin generated in high concentrations at the site of vascular injury plays a central role in thrombosis and hemostasis. Thrombin has also been implicated as a mitogen for smooth muscle cell proliferation that contributes to restenosis. This study was designed to determine the effects of a specific thrombin inhibitor on neointimal hyperplasia after balloon injury in a rat carotid artery model. DESIGN: A total of 47 male Sprague-Dawley rats were divided into five groups. All groups underwent balloon injury of the left carotid artery. A specific thrombin inhibitor, inogatran, was given in four different regimens: low and high dose injections, short-term infusion for 3 h, and long-term infusion for 1 week. After 2 weeks the animals were killed and the carotid neointima/media area ratio and the luminal narrowing were calculated. RESULTS: All treatments significantly reduced the neointimal hyperplasia. Inogatran given as a long-term infusion for 1 week had the lowest neointima/media ratio compared with the other groups. The percentage of lumen narrowing was also significantly lower in all treatment groups compared with the control group. CONCLUSION: A specific direct thrombin inhibitor, inogatran, reduces neointimal hyperplasia after arterial injury in rats. A more prolonged administration of the thrombin inhibitor gave a further reduction of the neointimal hyperplasia. It seems that inhibition of thrombin activity is not only important early after injury, but also later. This could have clinical implications in the treatment of restenosis and needs to be further evaluated.

Animals↗
PubMed2006

Inhibition of testosterone-induced hyperplasia of the prostate of sprague-dawley rats by pumpkin seed oil.

The oil from the pumpkin (Cucurbita pepo) seed is claimed to be useful in the management of benign prostatic hyperplasia. This investigation seeks to examine the effect of pumpkin seed oil on testosterone-induced hyperplasia of the prostate of rats. Hyperplasia was induced by subcutaneous administration of testosterone (0.3 mg/100 g of body weight) for 20 days. Simultaneous oral administration of either pumpkin seed oil (2.0 and 4.0 mg/100 g of body weight) or corn oil (vehicle) was also given for 20 days. The weights of the rats were recorded weekly, and the influence of testosterone and pumpkin seed oil on the weight gain of the rats was examined. On day 21, rats were sacrificed, and the prostate was removed, cleaned, and weighed. The prostate size ratio (prostate weight/rat body weight) was then calculated. Neither testosterone nor pumpkin seed oil had any significant influence on the weight gain of the rats. Testosterone significantly increased prostate size ratio (P < .05), and this induced increase was inhibited in rats fed with pumpkin seed oil at 2.0 mg/100 g of body weight. The protective effect of pumpkin seed oil was significant at the higher pumpkin seed oil dose (P < .02). We conclude pumpkin seed oil can inhibit testosterone-induced hyperplasia of the prostate and therefore may be beneficial in the management of benign prostatic hyperplasia.

Animals↗
PubMed1991

Aberrant MT2 positivity distinguishes follicular lymphoma from reactive follicular hyperplasia in B5- and formalin-fixed paraffin sections.

Often, it is difficult to distinguish follicular lymphoma from reactive follicular hyperplasia histologically. Immunotypic evidence of monoclonality cannot be demonstrated routinely or reliably in routine paraffin-embedded sections. To determine whether a panel of monoclonal antibodies reactive with lymphoid cells in paraffin-embedded sections might be useful in distinguishing these confusing proliferations, the authors examined 45 follicular lymphomas and 30 follicular hyperplasia with the following antibodies; L26, B2, MT1, MT2, and UCHL-I. All sections were routine paraffin preparations from formalin- or B5-fixed tissue and were immunostained with the avidin-biotin immunoperoxidase technique. Ninety-two percent of the B5-fixed and 77% of the formalin-fixed lymphomas were MT2 positive. None of the reactive hyperplasias stained positively, and none of the other antibodies demonstrated consistent differences between these benign and malignant proliferations. MT2 marks interfollicular T cells and mantle-zone B cells in normal lymph nodes but does not mark normal germinal centers; this staining pattern is retained in reactive hyperplasia. However, paradoxically, in most follicular lymphomas the neoplastic germinal centers show aberrant MT2 positively. The authors conclude that MT2 may be useful in distinguishing follicular lymphoma from follicular hyperplasia in paraffin sections.

Antibodies, Monoclonal↗
PubMed1993

Hypertrophy or hyperplasia in cardiac muscle. Post-mortem human morphometric study.

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, and density of myocyte nuclei. The values of all histometric parameters correlated well with left ventricular (LV) weight up to 350 g. In heavier hearts these parameters remained approximately of the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g. The influence on LV weight of age, coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue was also evaluated. On the basis of a linear discriminant function, hearts were divided into three classes: (1) LV weight < or = 250 g (absence of hyperplasia, hypertrophy only); (2) LV weight 251-350 g (hypertrophy+signs of hyperplasia); (3) LV weight > 350 g (marked signs of hyperplasia). The percent of fibrosis increased proportionally to LV weight. Where LV weight was above 250 g there was a subsequent increase in the mean percent of fibrosis (approx. 26%). This phenomenon (plateau of percent fibrosis) is the result of an increased number of myocytes (myocyte hyperplasia). We suggest that, independent of aetiology, in all hearts above 350 g (patients with congestive heart failure) hyperplasia phenomenon exists.

Adult↗
PubMed1998

Natural history and prognosis of adenomatous hyperplasia and early hepatocellular carcinoma: multi-institutional analysis of 53 nodules followed up for more than 6 months and 141 patients with single early hepatocellular carcinoma treated by surgical resection or percutaneous ethanol injection.

BACKGROUND: The natural history and posttherapeutic outcome of adenomatous hyperplasia and early hepatocellular carcinoma have rarely been analyzed. METHODS: Fifty-three hepatic tumors diagnosed as adenomatous hyperplasia or early hepatocellular carcinoma and followed up for more than 6 months and 141 patients with single early hepatocellular carcinoma treated by surgical resection or ethanol injection were collected retrospectively and analyzed. RESULTS: Some of the adenomatous hyperplasias developed to early and to advanced hepatocellular carcinoma. Tumors tended to grow faster in the order adenomatous hyperplasia, early hepatocellular carcinoma and advanced hepatocellular carcinoma, with respective mean (SD) tumor volume doubling times of 21.2 (10.7), 13.9 (11.7) and 6.0 (5.2) months. Overall survival rates at 5 years in 53 patients treated by surgery and 88 patients treated by ethanol injection were 89.6 and 71.9%, respectively. CONCLUSION: Progression of adenomatous hyperplasia and early HCC was confirmed pathologically. Early HCC was shown to have a good prognosis.

Adenoma↗
PubMed2006

Paclitaxel-coated expanded polytetrafluoroethylene haemodialysis grafts inhibit neointimal hyperplasia in porcine model of graft stenosis.

BACKGROUND: The main pathology of haemodialysis graft stenosis is venous neointimal hyperplasia at graft-venous anastomoses. Neointimal hyperplasia is also observed in cases of coronary artery in-stent restenosis. Paclitaxel is a chemotherapeutic agent used to treat cancer, and has been proven to inhibit neointimal hyperplasia of coronary artery in-stent restenosis. In this study, we examined whether a paclitaxel-coated haemodialysis graft could inhibit neointimal hyperplasia and prevent stenosis. METHODS: We dip-coated paclitaxel on expanded polytetrafluoroethylene (ePTFE) grafts at a dose density of 0.59 microg/mm(2). In vitro release tests showed an initial paclitaxel burst followed by a long-term slow release. Using ePTFE grafts with (coated group, n = 8) or without a paclitaxel coating (control group, n = 11), we constructed arteriovenous (AV) grafts connecting the common carotid artery and the external jugular vein in Landrace pigs. RESULTS: After excluding seven pigs for technical failure, cross-sections of graft-venous anastomoses obtained 6 weeks after placing the AV grafts were analysed. Percentage luminal stenosis, ratios of intima to media in whole cross-sections, areas of intima in the peri-junctional areas (within 2 mm above and 2 mm below the graft-venous junction), and the mean thickness of intima within venous sides of cross-sections, were 60.5% (range, 41.5-60.7), 13.0 (range, 8.6-20.4), 23.7 mm(2) (range, 10.8-32.1) and 2.1 mm (range, 1.1-3.0), respectively, in the control group, whereas corresponding median values in the coated group were 10.4% (range, 1.0-17.8), 1.0 (range, 0.7-5.1), 1.6 mm(2) (range, 0.2-8.0) and 0.3 mm (range, 0.1-2.2). All parameters were significantly different between the two groups (P<0.05 by Mann-Whitney test). CONCLUSION: Paclitaxel-coated ePTFE grafts could prevent neointimal hyperplasia and the stenosis of AV haemodialysis grafts.

Animals↗
PubMed1996

Liver regeneration versus direct hyperplasia.

Liver cell growth can be induced in two distinct patterns: compensatory regeneration and direct hyperplasia. In the former, DNA synthesis is preceded by a loss of liver cells such as seen after partial resection of the liver or cell necrosis, whereas in direct hyperplasia, DNA synthesis is stimulated without cell loss. During the past decade, considerable advances have been made in understanding molecular mechanisms of the compensatory regeneration. There is increasing evidence that hepatocyte proliferation induced by some primary mitogens is mediated by patterns of growth factor modulation and signal transduction different from those of compensatory regeneration. Indeed, whereas activation of transcription factors such as NF-kappa B and increased expression of immediate early genes such as c-fos, c-jun, egr-1, and c-myc are induced during compensatory regeneration, such changes are not observed during hyperplasia induced by certain primary mitogens. In addition, although experimental evidence suggests a critical role for growth factors such as hepatocyte growth factor and transforming growth factor-alpha for the progression into cell cycle of competent hepatocytes in compensatory regeneration, these growth factors do not appear to play a major role in direct hyperplasia. One class of primary mitogens may trigger their actions through tumor necrosis factor-alpha, and the other by activation of nuclear hormone receptors. The differences in molecular events observed between liver regeneration and direct hyperplasia may affect differently the initiation step of chemical hepatocarcinogenesis. Whereas the former supports initiation by chemicals, the latter does not. A similar lack of effect on promotion of carcinogen-altered cells has also been observed after acute treatment with some primary mitogens. Definition of the mechanisms by which primary mitogens stimulate liver cell proliferation may elucidate the nature of the signals responsible for triggering the entry into cell cycle. Furthermore, due to their low toxicity, primary liver mitogens could have significant clinical applications in gene transfer and liver transplantation.

Animals↗
PubMed1990

Mesonephric remnants, hyperplasia, and neoplasia in the uterine cervix. A study of 49 cases.

Hyperplasia of mesonephric remnants in the uterine cervix is an unusual condition that is often misdiagnosed as adenocarcinoma. The rare mesonephric carcinoma can be confused with more common forms of cervical adenocarcinoma. We studied 49 specimens of cervix containing mesonephric remnants, or lesions derived from them, in women 21 to 72 (mean, 38) years of age. Four cases were classified as mesonephric remnants, 31 as lobular mesonephric hyperplasia, eight as diffuse mesonephric hyperplasia, two as mesonephric ductal hyperplasia, and four as mesonephric carcinoma. In the nonneoplastic cases, the lesion was unrelated to symptoms that resulted from excision of cervical tissue and, except in one case, did not produce a detectable mass. In two cases of carcinoma, the patient presented with bleeding; in one case, the patient presented with pelvic relaxation. The manner of presentation was not known in the fourth case of carcinoma. Twenty-eight patients with mesonephric remnants or hyperplasia underwent hysterectomy; 15 had a cone biopsy; one underwent excision of the cervical stump; and one had only a cervical biopsy. None of these patients has had a recurrence. All four patients with carcinoma had a hysterectomy; three of them died of carcinoma 2 years and 10 months, 7 years, and 9 years after diagnosis, respectively. Correct classification of mesonephric lesions is imperative for appropriate patient management.

Adenocarcinoma↗
PubMed1991

Adenomatous hyperplasia of the rete testis. A clinicopathologic study of nine cases.

Adenomatous hyperplasia of the rete testis is an uncommon lesion that has recently been described. Nine cases of adenomatous hyperplasia were identified in two institutions from 1980 to 1989. At diagnosis the nine patients ranged in age from 30 to 74 years (mean, 59 years; median, 66 years). Three patients presented with a grossly identifiable solid or cystic testicular hilar mass. In six cases adenomatous hyperplasia was an incidental microscopic finding--five from orchiectomy specimens and one from an autopsy specimen. Microscopically, the hyperplasia consisted of a tubulopapillary epithelial proliferation of rete testis. The lining cells were cuboidal to low columnar and lacked nuclear pleomorphism or mitotic figures. The involvement of the rete testis was predominantly diffuse. In seven cases the seminiferous tubules showed atrophic changes. Ultrastructural and immunohistochemical (keratin, epithelial-membrane antigen: positive; vimentin, muscle-specific actin, desmin, and S-100: negative) studies done on one case showed similar features to those of nonhyperplastic rete testis epithelium. No patient with adenomatous hyperplasia showed local recurrence or metastasis. Possible pathogeneses include hormonal imbalance or stimulatory influence that remains as yet unidentified.

Adenoma↗
PubMed1992

Atypical basal cell hyperplasia of the prostate.

Basal cell hyperplasia classically has been described as having bland cytologic features. During the past 2 years, we have seen 12 cases (11 in consultation) with atypical features that were confused with adenocarcinoma of the prostate. Eleven of these 12 cases contained prominent nucleoli mimicking carcinoma; in the 12th case, nuclei were enlarged, hyperchromatic, and moderately pleomorphic. Immunohistochemistry with antibodies against high-molecular-weight cytokeratin (34 beta E12) was performed in nine of the cases, verifying their basal cell nature. Additional findings in these cases were necrotic intraluminal secretions (two cases), immature squamous metaplasia (two cases), peculiar hyaline cytoplasmic globules (two cases), adenosis (one case), markedly atypical nuclei of uncertain nature occurring elsewhere in the specimen (one case), and intraluminal blue mucin (two cases). We analyzed nine cases of typical basal cell hyperplasia, all of which showed classic features of basal cell hyperplasia with benign cytology. Both atypical and classical basal cell hyperplasia were frequently infiltrated by lymphocytes such that the cytologic changes could not be attributable to inflammation. Atypical basal cell hyperplasia must be differentiated from ordinary adenocarcinoma of the prostate, prostatic intraepithelial neoplasia, and basaloid carcinoma (adenoid cystic carcinoma) of the prostate.

Adenocarcinoma↗
PubMed1997

Follicular basal cell hyperplasia overlying dermatofibroma.

Follicular basal cell hyperplasia (FBCH) overlying dermatofibroma represents aborted or impeded pilar differentiation. Historically, this hyperplasia has been misinterpreted as basal cell carcinoma. In a large series of dermatofibroma (258 cases), those that contained primitive or malformed follicular structures over the lesion (59 cases) were compared with those without such elements (199 cases). Statistical analysis of various clinicopathologic features showed that FBCH was significantly associated with younger age, trunk location, hypercellular dermatofibroma, loss of a Grenz zone, clear cell hyperplasia, and seborrheic keratosis-like change. There was an inverse correlation between epidermal atrophy, lichen simplex chronicus-like change, and lower extremity location with FBCH. Histologic features favoring a diagnosis of FBCH over basal cell carcinoma are the focal nature and superficial location of the lesion, lack of cytologic atypia and mitoses, recognizable components of hair follicle differentiation, focal condensation of mesenchymal cells around basal cell proliferation, and the association of epidermal hyperplasia. Our findings suggest that FBCH, clear cell hyperplasia, and seborrheic keratosis-like change all represent an expression of follicular differentiation overlying dermatofibroma.

Adult↗
PubMed1998

Lesions described as nodular mesothelial hyperplasia are primarily composed of histiocytes.

It is known that, on occasion, histiocytic proliferations can be confused with reactive mesothelial cell hyperplasia or with a malignant process. We report four cases of histiocytic proliferation, two occurring in the pleura in a 23-year-old woman and a 78-year-old woman, respectively, one in a hernial sac of a 2-year-old boy, and one in the lamina propria of the bladder of a 74-year-old man with a noninvasive papillary transitional cell carcinoma. The morphologic features of the pleural lesion of the 23-year-old woman and of the hernial sac lesion of the 2-year-old boy, as well as the bladder lesion, were similar to those reported in cases of the so-called nodular mesothelial hyperplasia. The pleural lesion in the 78-year-old woman consisted of a proliferation of cells with a signet ring-like morphology that was originally interpreted as either an unusual form of mesothelial hyperplasia or a metastatic signet ring cell adenocarcinoma. Because of mitotic activity and some cellular atypia in the bladder lesion, the possibility of invasive transitional cell carcinoma into the lamina propria was considered before immunohistochemical studies were performed. Staining for keratin showed only a few positive cells in the hernial sac and pleural lesions, whereas most cells reacted for the histiocytic marker CD68. Immunohistochemical studies on the bladder lesion also demonstrated strong staining for CD68, but no reactivity for keratin was observed. Based on these results, it is concluded that all of the lesions are primarily reactive histiocytic proliferations and because they may occur in other locations aside from the serosal membranes, the designation "nodular histiocytic hyperplasia" appears to be more appropriate than that of nodular mesothelial hyperplasia. It is important that the reactive nature of these lesions be recognized because on occasion they may present high mitotic activity or may show signet ring-like morphology and thus they can be confused with a malignancy.

Adult↗