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PubMed1998

Prevention of focal intimal hyperplasia in rat vein grafts by using a tissue engineering approach.

The present study focused on the role of blood flow in the formation of focal intimal hyperplasia in vein grafts, as well as the development of an engineering approach that can be used to eliminate disturbed blood flow and prevent blood flow-related focal intimal hyperplasia. A rat vein graft model was constructed by interposing a jugular vein into the abdominal aorta with end-to-end anastomoses. Locally disturbed flow was identified by analyzing particle streak-lines in methyl salicylate-cleared and perfused vein grafts in vitro with a physiological Reynolds number. At day 10, 20, and 30 after surgery, focal intimal hyperplasia of the vein grafts was examined using a histological approach and the density of alpha-actin positive cells was determined using immunohistological and fluorescent approaches. Results showed that apparent eddy blood flow formed at the proximal, but not at the distal, end of the vein grafts due to graft-host diameter mismatch and local geometric distortions, and was associated with apparent focal intimal hyperplasia. The thickness of the alpha-actin positive layers of the proximal vein grafts was significantly higher than that of the distal grafts (192 +/- 27 vs. 94 +/- 18 microm, 278 +/- 55 vs. 124 +/- 20 microm, and 288 +/- 24 vs. 131 +/- 23 microm for day 10, 20. and 30, respectively). The density of the alpha-actin positive cells, however, was similar between the proximal and the distal regions (3569 +/- 361 vs. 3285 +/- 343 cells/mm2, 5540 +/- 650 vs. 5376 + 887 cells/mm2, and 5465 +/- 791 vs. 5278 +/- 524 cells/mm2 for day 10, 20, and 30, respectively). When eddy blood flow was eliminated by matching the graft-host diameters using a tissue engineering approach, the average thickness of the alpha-actin positive layers of the proximal (71 +/- 15, 86 +/- 16, and 85 +/- 14 microm for day 10, 20, and 30, respectively) and the distal vein grafts (68 +/- 13, 80 +/- 14, and 79 +/- 13 microm for day 10, 20, and 30, respectively) was reduced significantly. The density of the alpha-actin positive cells was also reduced significantly in the proximal (2946 +/- 359, 3261 +/- 295, 3472 +/- 599 cells/mm2 for day 10, 20, and 30, respectively) and in the distal regions (3151 +/- 511, 3466 +/- 687, 3593 +/- 688 cells/mm2 for day 10, 20, and 30, respectively). The thickness of the alpha-actin positive layers and the density of the alpha-actin positive cells were not significantly different between the proximal and distal regions of the engineered vein grafts at each observation time. These results suggest that eddy flow may develop in vein grafts and may facilitate the formation of focal intimal hyperplasia, and the vascular tissue engineering approach developed in this study may be used to prevent blood flow-related focal intimal hyperplasia in vein grafts.

Actins↗
PubMed2003

Parathyroid hormone immunohistochemistry in dogs with primary and secondary hyperparathyroidism: the question of adenoma and primary hyperplasia.

In primary hyperparathyroidism, calcium homeostasis is disrupted by excessive synthesis and secretion of parathyroid hormone (PTH), which is usually caused by a solitary adenoma, or less often by nodular hyperplasia or carcinoma of the parathyroid glands. So far, the distinction between these forms of primary hyperparathyroidism has been made by histological examination. In this report clinical and histological findings, including PTH immunohistochemistry, are described in five dogs with primary hyperparathyroidism, three dogs with secondary hyperparathyroidism due to chronic renal failure, and eight control dogs. In the dogs with primary hyperparathyroidism, nodular adenomatous hyperplasia was found in two animals and parathyroid adenoma in three. The dogs with chronic renal failure had diffuse parathyroid gland hyperplasia. The parathyroid glands of the control dogs and the inactive cells surrounding the hyperplastic nodules showed slight to moderate, localized, paranuclear PTH immunolabelling. In the primary nodular and secondary diffuse hyperplasia, all parathyroid cells had a diffuse cytoplasmic PTH labelling pattern, sometimes in combination with localized paranuclear labelling. In parathyroid adenoma, areas with either paranuclear labelling or diffuse cytoplasmic labelling were observed. As both parathyroid adenoma and primary nodular parathyroid gland hyperplasia have characteristics of intrinsic autonomy (i.e., suppression of the remaining endocrine tissue), there would seem to be no functional difference between the two abnormalities. It is argued that primary (multi)nodular hyperplasia is a multiple form of parathyroid adenoma.

Adenoma↗
PubMed1988

Urodynamic and histological correlates of benign prostatic hyperplasia.

The tissue obtained from transurethral prostatectomies was evaluated histologically and correlated to the clinical findings in 81 patients with benign prostatic hyperplasia. A median of 9 hematoxylin and eosin-stained tissue slides per patient were examined, each containing from 1 to 15 curettings. The patients were divided into 3 groups according to the following histology: predominantly stromal hyperplasia (39 patients), predominantly glandular hyperplasia (29 patients), and equal proportions of stromal and glandular hyperplasia (mixed group, 19 patients). There was no significant difference among the groups in patient age and duration of symptoms. The weight of resected tissue was significantly lower in the stromal group (median 16 mg.), compared to the glandular group (median 20 gm.) and the mixed group (median 25 gm.). Additionally, 29 of the 81 patients had chronic inflammation characterized by multifocal infiltrates of lymphocytes. These patients had significantly larger prostates (median 25 gm.) compared to those without lymphocytic infiltration (median 15 gm.). Sixty-five patients had a 3-month followup examination. Preoperatively there was no difference among the groups in maximum flow at uroflowmetry but at 3-month followup the stromal group had a median maximum flow of 13 ml. per second compared to 16.8 ml. per second in the glandular group and 21.5 ml. per second in the mixed group. These findings document histologically what has been reported from a clinical perspective: the clinical prostatism/benign prostatic hyperplasia complex is a spectrum of histological entities, and the small prostate with predominantly stromal hyperplasia responds less favorably to transurethral resection as determined by urodynamic evaluation.

Aged↗
PubMed1987

Light-microscopic stereologic analysis of spontaneous and steroid-induced canine prostatic hyperplasia.

A combined light-microscopic and stereologic analysis of the canine prostate was performed under the following experimental conditions: intact and castrated dogs, spontaneous benign prostatic hyperplasia, intact and castrated dogs after treatment with testosterone, 5 alpha-dihydrotestosterone or 3 alpha-androstanediol in combination with estradiol. Regarding the absolute amounts of the glandular and stromal parts of the prostate as well as the glandular cells, no difference was found among the testosterone, 3 alpha-androstanediol and 5 alpha-dihydrotestosterone treated castrated dogs. Treatment with 5 alpha-dihydrotestosterone or 3 alpha-androstanediol in combination with 17 beta-estradiol induced a four-fold increase in glandular and a two-fold increase in stromal tissue. The glandular to stromal tissue ratio equals that found in spontaneous canine hyperplasia, which is indicative of the glandular type of spontaneous canine hyperplasia. Therefore, it can be stated that treatment with 5 alpha-dihydrotestosterone or 3 alpha-androstanediol combined with 17 beta-estradiol not only induces prostatic overgrowth but also leads to prostatic hyperplasia of the glandular type. However, the stereologic analysis of canine prostates following steroid administration shows that canine hyperplasia is primarily a glandular disease, while human benign prostatic hyperplasia shows more stromal activation.

Androstane-3,17-diol↗
PubMed1983

Estrogen receptor in human benign prostatic hyperplasia.

Estrogens have been proposed as a major etiological factor in the pathogenesis of benign prostatic hyperplasia in man. The presence of estrogen receptor in benign prostatic hyperplasia would support this concept. Using the receptor stabilizer, sodium molybdate, and a hydroxylapatite assay we assayed human benign prostatic hyperplasia for the presence of cytosolic estrogen receptor. For comparison, we assayed estrogen receptor in cytosols of prostatic cancer and normal tissue, and we also measured androgen receptor and progesterone receptor concentrations in the 3 tissue types. Estrogen receptor was present in 8 of 15 benign prostatic hyperplasia specimens at a mean concentration of 9.2 fmol./mg. protein for the estrogen-receptor-positive samples. Sucrose gradient analysis of the estrogen receptor of benign prostatic hyperplasia revealed that it sedimented in the region of 8S, and steroid specificity studies confirmed that the binding to estrogen receptor was estrogen-specific. Estrogen receptor was also found in normal (3 of 3) and malignant (4 of 6) tissues, and all tissues were positive for androgen receptor. The presence of estrogen receptor in human benign prostatic hyperplasia supports the proposal that circulating estrogens may have a role in the pathogenesis of this disorder.

Adolescent↗
PubMed1984

Sclerosing lobular hyperplasia manifesting as a palpable mass of the breast in young black women.

Sclerosing lobular hyperplasia is defined as a lesion of the breast characterized solely by prominent hyperplasia of the lobules and sclerosis of the intralobular stroma. The extra-lobular connective tissue may or may not be fibrosed. To ascertain the frequency of this condition, the histologic sections of all benign breast lesions diagnosed at Howard University Hospital between January 1, 1980, and June 30, 1982, were reviewed. The patient population of the hospital is almost entirely black. Among a total of 590 benign breast lesions, 18 cases of sclerosing lobular hyperplasia were found. The mean age of the patients was 28.3 years. The patients generally complained of a painless or slightly tender lump in the breast, of one or two month's duration. The masses appeared finely nodular and varied in size from 0.8 X 1.2 cm to 3.5 X 5.0 cm. Some microscopic sections from patients with sclerosing lobular hyperplasia revealed incipient (lobule-sized) fibroadenoma. On re-examination of the available sections of 101 fibroadenomas, 47 (46.5 per cent) were found to be surrounded by breast tissue exhibiting focal sclerosing lobular hyperplasia. Apparently, sclerosing lobular hyperplasia is often overgrown by fibroadenoma, and the presenting symptoms are those of the dominant tumor rather than those of the preceding condition.

Adenofibroma↗
PubMed1997

Significance of AgNOR counts for distinguishing carcinoma from adenoma and hyperplasia in parathyroid gland.

Nucleolar organizer region proteins, which can be stained and visualized by an argyrophil technique (AgNORs), are markers of cell activities, such as DNA transcription and proliferation, and they are useful for differential diagnosis between benign and malignant tumors. We counted both AgNOR numbers in 25 parathyroid lesions (three carcinomas, 11 adenomas, 10 hyperplasias, and one hyperplasia with carcinoma) to determine if the AgNOR number could be useful as a diagnostic aid in parathyroid neoplasms and hyperplasias, because it is often difficult to histopathologically distinguish among these lesions. The AgNOR numbers were significantly higher in carcinomas (3.18 +/- 0.05) than in adenomas (1.67 +/- 0.30, P < .001) or hyperplasias (1.85 +/- 0.16, P < .001), but there was no significant difference between adenomas and hyperplasias. These results suggest that AgNORs may be useful as an adjunct to discriminating carcinomas from adenomas or hyperplasias in the parathyroid gland.

Adenoma↗
PubMed1997

Pancreatic-polypeptide cell hyperplasia associated with pancreatic or duodenal gastrinomas.

An immunohistochemical investigation of pancreatic-polypeptide (PP) cells in the PP-rich region of the pancreas, of ventral embryological origin, was performed in three female patients affected by or previously operated on for functioning duodenal or pancreatic gastrinomas not associated with multiple endocrine neoplasia syndrome. A pronounced PP-cell hyperplasia showing histological patterns of endocrine cell dysplasia and focal adenomatosis as defined by Jaffe et al was found in all cases. Morphometric analysis showed that in these patients the fraction of ventral-type pancreatic lobules occupied by PP-immunoreactive cells was 14.77 +/- 5.73%, 8.94 +/- 2.92%, and 10.83 +/- 5.64%, respectively. These values were three to five times higher than the upper values found in controls (mean, 2.20%; range, 1.54 to 2.93%; P < .0001). PP-cell hyperplasia may contribute for the increased circulating levels of PP found in gastrinoma patients. In this regard, elevation of fasting blood PP was found in one of four determinations done in one patient, indicating that PP-cell hyperplasia may be responsible for, at least, transient PP hypersecretion. In one of our patients, PP-cell hyperplasia was found 15 years after normalization of gastrin levels by removal of a single pancreatic gastrinoma. This finding is against a trophic role for hypergastrinemia in the development of PP-cell hyperplasia. In one of two patients in whom the pancreatic regions of dorsal embryological origin (ie, body and tail of the gland) were examined, ventral-type, PP-rich islets were frequently encountered, a finding at variance with their exceptional detection in control cases. This finding suggests that PP cell hyperplasia of the PP-rich pancreatic region may be a feature of a more diffuse disorder of PP cell development in the pancreas of gastrinoma patients.

Aged↗
PubMed1998

Inhibition of chronic vessel wall intimal hyperplasia following acute anticoagulant treatment: relative effects of heparin and dermatan sulphate.

Surface-bound thrombin which contributes to vessel wall hyperplasia, is resistant to inhibition by heparin/antithrombin III (/ATIII) but not to inhibition by dermatan sulphate/heparin cofactor II (/HCII). To determine the effects of heparin and dermatan sulphate on vessel wall hyperplasia after a first or second injury, rabbit carotid arteries first were injured, using a standard procedure (first injury). Half of the first-injury rabbits were given heparin, dermatan sulphate, or saline, 5 minutes before and at 30-minute intervals over 2 hours post-injury, and then allowed to recover. Four weeks later, the first-injury treated animals were killed and their injured carotid arteries were processed histologically. The remaining untreated first-injury rabbits were also allowed to recover. At 4 weeks, those rabbits were re-anesthetized and their first-injury arteries (which were occluded >75%), were isolated, and vessel wall lumen patency was re-established by endarterectomy (second injury). During this second injury, the animals were treated with heparin, dermatan sulphate, or saline as described above. Four weeks after this second injury, these rabbits were killed and their second injury arteries were processed histologically. Intimal hyperplasia determined histologically, was expressed as an x-fold increase in vessel wall cross-sectional area (i.e., [(media+intima area) media area]). Vessel wall lumen occlusion was expressed as [1-(lumen area/internal elastic lamina area) x 100; % occlusion]. Vessel wall area in the saline-treated animals, increased 2.6+/-1.2 and 2.4+/-1.0 fold respectively, means+/-SD, n = 12, within 4 weeks of the first and second injuries. These increases were due to intimal hyperplasia and associated with 75+/-19% and 79+/-21% occlusion of the vessel wall lumen, respectively. Heparin had little effect, whereas dermatan sulphate (1) decreased hyperplasia by 45% after the first injury and by 47% after the second injury, p<0.008 and <0.03, respectively, and (2) decreased vessel wall occlusion 47+/-12% and 33+/-5% after the first and second injury, respectively. We conclude that (1) dermatan sulphate/HCII may be a useful inhibitor of vessel wall hyperplasia following vessel wall injury, and (2) this effect can be achieved by an acute anticoagulant treatment at the time of injury, unlike heparin/ATIII.

Animals↗
PubMed1996

Sebaceous hyperplasia in organ transplant recipients: shared aspects of hyperplastic and dysplastic processes?

BACKGROUND: Patients receiving kidney or heart transplants are subject to a wide range of cutaneous changes attributed largely to the immunosuppression required to prevent rejection of their transplant. In addition to infection, they have an increased incidence of dysplastic lesions, some of which are malignant. OBJECTIVE: Our purpose was to determine the incidence of sebaceous hyperplasia in heart and kidney transplant recipients and its association with neoplasia. METHODS: Patients undergoing heart transplantation from a single transplant center were examined during a 30-month screening period to establish the prevalence of cutaneous abnormalities. RESULTS: Sixteen of 104 (16%) heart transplant recipients had sebaceous hyperplasia in comparison with 1% of an age- and sex-matched control group. Those with sebaceous hyperplasia did not have a significantly higher incidence of hypertrichosis than those without sebaceous hyperplasia. CONCLUSION: Sebaceous hyperplasia is seen in heart transplant recipients. It does not appear to be connected with hypertrichosis, in which it is believed that the pilosebaceous unit is the target of the direct effect of cyclosporine. We propose that the development of sebaceous hyperplasia is related to the process of dysplastic epithelial proliferation in transplant recipients.

Child↗
PubMed2003

Clinical over- and under-estimation in patients who underwent hysterectomy for atypical endometrial hyperplasia diagnosed by endometrial biopsy: the predictive value of clinical parameters and diagnostic imaging.

OBJECTIVE: The aim of this study was to analyze the clinical and imaging characteristics in patients diagnosed with atypical endometrial hyperplasia based on endometrial biopsy in comparison with the final diagnosis from resected uteri; i.e. to determine the rates of underestimation (endometrial cancer), equivalent diagnosis (atypical hyperplasia), and overestimation (hyperplasia without atypia or non-hyperplastic lesion). MATERIALS AND METHODS: We reviewed 33 patients who were diagnosed with atypical endometrial hyperplasia by endometrial biopsy using a small curette and then underwent total abdominal hysterectomy between September 1992 and May 2002. Clinical parameters obtained from patients' charts, and imaging analyses using transvaginal ultrasonography (TUS) and magnetic resonance (MR) imaging were retrospectively re-examined. RESULTS: Among 33 patients who underwent hysterectomy due to a diagnosis of atypical hyperplasia, nine cases (27.2%) were underestimated (cancer), nine cases (27.2%) were equivalent and 15 cases (45.6%) were overestimated as indicated by examination of the endometrium of the resected uterus. There was no difference among these groups in either clinical parameters or diagnostic images obtained by TUS or MR. CONCLUSION: Diagnosis of atypical endometrial hyperplasia by endometrial biopsy often resulted in under- or over-estimation, as shown by examination after hysterectomy. As there is neither a reliable clinical parameter nor imaging feature to distinguish between these groups, hysterectomy is still the best treatment for these patients if they are willing to give up their fertility.

Adult↗
PubMed1990

Nucleolar organiser regions in endometrial hyperplasia and neoplasia.

Nucleolar organiser regions (NORs) were counted in the nuclei of both epithelial and stromal cells in cases of endometrial hyperplasia and carcinoma. The scores for each case were expressed as a ratio. No significant difference was found between the ratios for cystic hyperplasia and hyperplasia with architectural atypia, confirming the view that these are morphological variants of the same benign hyperplastic process. The ratios for hyperplasia with cytological atypia and adenocarcinoma differed significantly from the benign hyperplasias. This adds support to the view that hyperplasia with cytological atypia should be considered a neoplastic condition.

Adenocarcinoma↗
PubMed1996

Diagnostic accuracy of hysteroscopy in endometrial hyperplasia.

OBJECTIVES: To determine the diagnostic accuracy of hysteroscopy in the diagnosis of endometrial hyperplasia in women with abnormal uterine bleeding. METHODS: From 1993 through 1995, 980 women referred to our institution for abnormal uterine bleeding underwent diagnostic hysteroscopy with eye direct biopsy of the endometrium in case of macroscopic abnormalities. Hysteroscopic features were compared with pathologic findings in order to detect the reliability of the endoscopic procedure. Statistical analysis was performed with the McNemar test. RESULTS: Positive predictive value of hysteroscopy in the diagnosis of endometrial hyperplasia accounted for 63%. In fact hysteroscopic diagnosis of endometrial hyperplasia was confirmed at pathologic examination in 81 out of 128 patients. Sensitivity and specificity of the endoscopic procedure accounted for 98% and 95%, respectively. Negative predictive value accounted for 99%, as only two cases of atypical hyperplasia were missed at hysteroscopy. Positive predictive value was higher in postmenopausal patients compared to women in the fertile age (72 vs. 58%). CONCLUSIONS: Overall, results appear encouraging, since no case of endometrial hyperplasia was missed by hysteroscopy. The high diagnostic accuracy, associated with a minimal trauma, renders hysteroscopy the ideal procedure for both diagnosis and follow-up of conservative management of endometrial hyperplasia.

Adult↗
PubMed1997

Pulmonary endocrine cell hyperplasia and papilloma in rats induced by intratracheal injections of extract from particulate air pollutants.

We investigated the effect of intratracheal injections of an extract of suspended particulate matter (SPM) obtained from the urban ambient air of Tokyo, upon the development of proliferative lesions of pulmonary endocrine cells (PECs) in the rat. We also examined the modification effects of nitrogen dioxide, sulfur dioxide, or both of them on the PEC lesions. Male F344 rats were divided into six experimental groups of 5 animals each. Twenty animals were treated with intratracheal instillations of SPM admixed with carbon once a week for 4 weeks with or without additional gaseous exposure (6 ppm nitrogen dioxide or 4 ppm sulfur dioxide) 16 hrs a day for 11 months. Five animals were given intratracheal injections of carbon suspended in saline and the other five were untreated. The subcardiac lobes of the right lung were fixed with 4% paraformaldehyde, and embedded in paraffin. PEC hyperplasias and papillomas were counted in 200 serial sections, 4 microns thick. The average incidences of PEC hyperplasia in the untreated animals and in those treated with carbon were 194 and 200/cm3, respectively. The average incidences of PEC hyperplasia in the animals exposed to SPM tar only, SPM tar plus nitrogen dioxide and sulfur dioxide, SPM tar with nitrogen dioxide and SPM tar with sulfur dioxide were 376, 378, 372 and 349/cm3, respectively. These were significantly higher than the levels of the control animals, and additional gaseous stimuli had no effect on the incidence of PEC hyperplasia. Besides PEC hyperplasia, a few PEC papillomas were found in the animals treated with SPM tar, regardless of gaseous exposure, but in the control animals no papilloma was evident. Thus, compounds in airborne particulates are considered to be responsible for the development of PEC hyperplasias and papillomas.

APUD Cells↗
PubMedDate not supplied

Time course of the regression of intimal hyperplasia in experimental vein grafts.

A previous study in which vein grafts were removed from the arterial circulation and reimplanted into the venous circulation of the same animal demonstrated regression of vein graft intimal hyperplasia and medial thickening within 14 days. The present study was designed to characterize the kinetics of the morphological and ultrastructural changes over this 14-day period. Twenty-one male New Zealand White rabbits received a reversed vein interposition bypass graft of the right common carotid artery. Fourteen days after the procedure, 21 vein grafts were isolated, removed, and reimplanted into the contralateral external jugular venous system as veno-venous interposition bypass grafts (reversal grafts). The grafts were harvested at 60 minutes, 1 day, 3 days, 5 days, 7 days, and 14 days after reversal. Before insertion into the venous circulation, the vein graft had a confluent endothelial cell surface with multiple layers of smooth muscle cells representing intimal hyperplasia. After 1 hour, the reversal graft retained an intact endothelial cell layer with no evidence of tissue edema or cellular disruption. By 24 hours, there were a few blood cells on the endothelial cell surface. There was no inflammatory infiltrate seen in the subendothelium, and the smooth muscle cells were unaltered. At 3 days, the endothelial cell lining remained intact with no polymorphonucleocytes in the subendothelium or within the graft wall. Underlying smooth muscle cells at this time were noted to contain cytoplasmic vacuoles. At 5 days, there were no inflammatory cells seen on the surface or within the vein graft wall, but many of the underlying smooth muscle cells within the intimal hyperplasia were noted to be fragmented and to have clumping of chromatin. After 7 days, the endothelial cells remained intact and there was widespread evidence of apoptosis beneath the subendothelium with highly fragmented smooth muscle cells, some of which were histologically in the process of breaking up. At 14 days, the grafts retained uniform endothelial cell surfaces. Most of the smooth muscle cells that composed the intimal hyperplasia seen before implantation as a reversal graft were gone. Areas of newly laid down collagen could be observed. There were no acute inflammatory cells but for some mast cells seen in the graft wall. This study demonstrates that in this model, regression of intimal hyperplasia was associated with apoptosis of the smooth muscle cells and the deposition of collagen. There was no evidence that this process is mediated by an acute inflammatory response. Regression therefore appears to be due to induction of smooth muscle cell apoptosis by either a reduction in pressure or flow or a combination of both factors. The findings will enable a systematic cellular and molecular analysis of the biology of regression, which may afford clues to better understand the biology of the developing intimal hyperplasia.

Animals↗
PubMed1997

Growth factors and myointimal hyperplasia in experimental aortic allografts.

OBJECTIVES: To analyse the role of growth factors (platelet derived growth factor, PDGF; basic fibroblast growth factor, bFGF; interleukin 1, IL-1) in the genesis of myointimal hyperplasia in arterial allografts. MATERIALS: Two groups of experiments were performed: isografts and allografts. The isograft group consisted of 15 inbred Lewis rats in which a 1 cm long segment of aorta was inserted as an abdominal aortic interposition graft. The aortic segments were obtained from syngenic Lewis rats. The allograft group consisted of 15 inbred Lewis rats, in which a 1 cm long segment of aorta was interposed at the abdominal aorta level. The aortic segments were obtained from allogenic Brown-Norway rats. CHIEF OUTCOME MEASURES: The animals were killed 4 weeks after surgery and were analysed by morphometric analysis (n = 3 for each group). In addition, production of PDGF, bFGF and IL-1 by aortic segments (n = 12 for each group) in organ culture was assessed. MAIN RESULTS: Allografts had more myointimal hyperplasia, than isografts (p < 0.05). PDGF and bFGF production, generally considered to be the cause of myointimal hyperplasia, was not increased in allografts. IL-1 production was higher in allografts (p < 0.001). MAIN CONCLUSIONS: Myointimal hyperplasia in aortic allografts is dependent on growth factors produced by the graft itself. These growth factors are different from PDGF and bFGF that generally have been implicated in the genesis of naturally occurring myointimal hyperplasia and atherosclerosis. IL-1 may have a principal role in the genesis of myointimal hyperplasia in arterial allografts.

3T3 Cells↗
PubMed1998

Local effects of nitric oxide supplementation and suppression in the development of intimal hyperplasia in experimental vein grafts.

OBJECTIVES: The universal response of vein grafts after insertion into the arterial circulation is the development of intimal hyperplasia; smooth muscle cell proliferation and connective tissue deposition, which may be modulated in part by dysfunctional endothelial nitric oxide (NO) metabolism. This study examines the effects of single dose, local application by pluronic gel of a NO donor, S-nitroso-N-acetylpenicillamine (SNAP) and an NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME) on the formation of intimal hyperplasia. MATERIALS: Forty New Zealand white rabbits underwent jugular vein interposition grafting of the common carotid artery. DESIGN: Ten animals were controls, 10 animals had the outer surface of the vein graft coated with 30% pluronic gel (2.5 ml), and 10 each were immersed for 15 min prior to insertion in Ringer lactate containing 10(-3) M of SNAP or L-NAME and then had their vein grafts coated with 2.5 ml of gel containing either SNAP (10(-3) M) or L-NAME (10(-3) M), which allows for sustained delivery for up to 6 h. On the 28th post operative day, the animals were sacrificed and vein grafts were harvested for morphology by electron microscopy (SEM and TEM) and dimensional analysis by videomorphometry. RESULTS: All vein grafts developed intimal hyperplasia. On SEM the vein grafts had a confluent layer of endothelial cells with multiple layers of smooth muscle cells representing intimal hyperplasia in TEM. There were no demonstrable morphological differences between the four groups. Local treatment with SNAP produced a significant 36% decrease in mean intimal thickness (72 +/- 4 microns vs. 45 +/- 4 microns; mean +/- S.E.M.; p < 0.01) without a change in medial thickness compared to gel-only treated groups (58 +/- 6 microns vs. 61 +/- 7 microns; p = ns). Inhibition of NO synthase by L-NAME had no effect on the development of intimal hyperplasia (72 +/- 4 microns vs. 79 +/- 10 microns; p = ns); medial thickness was also unchanged. CONCLUSION: These data confirm the protective effect of NO in vascular injury and suggest that NO synthase activity is either absent or reduced to such a level that further inhibition in this short time course is not relevant to the pathophysiology of vein graft intimal hyperplasia.

Animals↗
PubMed1998

Intraductal proliferations of the breast: a review of histologic criteria for atypical intraductal hyperplasia and ductal carcinoma in situ, including apocrine and papillary lesions.

The proliferation of intraductal mammary epithelium forms a continuum that begins with intraductal hyperplasia and ends with ductal carcinoma in situ. Atypical intraductal hyperplasia is the midpoint between the benign and malignant poles of this proliferative continuum. By defining the histological criteria for atypical intraductal hyperplasia, distinction from ordinary intraductal hyperplasia and the noncomedo forms of ductal carcinoma in situ becomes easier. Histopathologic criteria for atypical intraductal hyperplasia, ductal carcinoma in situ, and intraductal hyperplasia and their relative risks for the development of invasive breast carcinoma are reviewed. Related topics of intraductal apocrine and papillary proliferative lesions also are discussed.

Breast↗