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At least 523 records · Page 29Linked to original sources
PubMed1997

MIB-1 proliferative index in parathyroid adenoma & hyperplasia.

A retrospective study on 22 cases of parathyroid adenoma, 9 cases of primary parathyroid hyperplasia and 14 specimens of normal suppressed glandular tissue was undertaken to determine the usefulness of proliferative index (PI) for discriminating adenoma from hyperplasia, as an adjunct to the existing histological criteria. PI was determined by avidin-biotin-complex immunostaining after high temperature microwave antigen retrieval in paraffin sections, using monoclonal MIB-1 antibody which detects paraffin resistant analogue of cell cycle-associated Ki-67 antigen. PI expressed as percentage positive cell nuclei, was 1.36 +/- 0.62 (range 0.04-2.72) in adenoma, 1.17 +/- 0.83 (0.02-1.98) in hyperplasia and 0.03 +/- 0.02 (0.00-0.06) in normal suppressed glandular tissue. While the difference between normal suppressed glandular tissue and adenoma and hyperplasia was significant (P < 0.001), that between adenoma and hyperplasia was not. We conclude that although PI could distinguish between normal suppressed glandular tissue versus glands with primary hyperparathyroidism, it failed as an additional useful parameter for discriminating between adenoma and hyperplasia, both of which have low but similar proliferative activity.

Adenoma↗
PubMed1997

[Endometrial hyperplasias: histology, classification, prognostic significance and therapy].

Carcinomas of the endometrium are the most frequent neoplasias of the female genital tract. Precancerous lesions of the endometrium, including simple hyperplasia with and without atypism, complex hyperplasias as well as atypical complex hyperplasias occur 4.5 times more. The existence of hyperplastic or precancerous lesions of the endometrium is well established, but differences in terminology and difficulties in interpretation have complicated the communication between morphologists and clinicians. The risk of a metachronous endometrial carcinoma increases from about 1% in simple hyperplasia to 29-45% in atypical complex hyperplasia. Therapeutic procedures include the gestagen-therapy, depending from age and reproductive status of the women. Atypical complex hyperplasia requires the hysterectomy with bilateral salpingo-oophorectomy to treat a possible simultaneous carcinoma. Transvaginal sonography, hysteroscopy and pulsed Doppler sonography give additional informations and allows to distinguish a pathological from a normal endometrium. These methods may reduce the number of unnecessary diagnostic dilatation and curettage procedures, especially in patients with additionally cardio-vascular and other risk factors. But the histological examination of curettage material is still the "gold standard" for distinguishing between a normal and a pathologic endometrium. The classification and histologic criterias of precancerous lesions of the endometrium is presented and the need for better communication between pathologists and gynecologists is emphasised.

Adenocarcinoma↗
PubMed1998

Effects of diabetes and difluoromethylornithine treatment on hyperplasia, activity of MAP-kinase, and activity and association with cyclin B of p34cdc2 kinase in rat jejunal mucosa.

BACKGROUND: The different signal transduction pathways of rapidly proliferating cells of the intestine are not clearly understood. We report here a possible signaling pathway that involves regulation of activity of two closely related kinases, MAP-K (mitogen-activated protein kinase) and p34cdc2 kinase, during hyperplasia of diabetic jejunal mucosa. Our aim was to investigate the activity and phosphorylation of MAP-K and activity and association of p34cdc2 kinase with cyclin B during diabetes-induced jejunal mucosal hyperplasia in vivo. METHODS: We studied untreated and difluoromethylornithine (DFMO) treated control rats and rats with streptozotocin-induced type I diabetes. Assays were done 10 days after the induction of diabetes. In diabetic rats there was jejunal hyperplasia as indicated by increases in the jejunal mucosal weight/cm and DNA content as well as increased activities of MAP-K and p34cdc2 kinase and association of the latter with cyclin B as compared to corresponding values in control rats. Administration of DFMO, an irreversible inhibitor of the proliferation-associated enzyme ornithine decarboxylase (ODC), prevented diabetes-I induced jejunal hyperplasia and decreased all of the above enzymic parameters in both diabetic and control rats. In our previous in vivo study, DFMO administration also blocked diabetic jejunal hyperplasia and in addition decreased ornithine decarboxylase and tyrosine kinase activities jejunal and tyrosine phosphorylation of proteins. CONCLUSION: Thus the jejunal mucosal hyperplasia found in diabetes appears to involve activation of signal transduction pathways involving tyrosine kinases, MAP-K, p34cdc2 kinase, and cyclin B.

Animals↗
PubMed1976

The dexamethasone-modified adrenal scintiscan in hyporeninemic aldosteronism (tumor versus hyperplasia). A comparison with adrenal venography and adrenal venous aldosterone.

The dexamethasone-modified adrenal scintiscan, a noninvasive procedure, is described for the preoperative distinction between primary aldosteronism (aldosterone-producing ademona) and idiopathic aldosteronism (bilateral hyperplasia) and for the preoperative localization of aldostersone-producing adenomas. This procedure has been carried out on 17 subsequently proved cases of primary aldosteronism and nine cases (four unexplored) of idiopathic aldosteronism. In the tumor cases, it indicated correctly the side of the tumor in 88 per cent. It was correct in predicting the existence of bilateral hyperplasia in all of the five cases explored. It produced the same response in four more cases believed to have bilateral hyperplasia, in which surgical exploration has not been carried out. Many of the same patients had, in addition, standard adrenal scintiscans (SS), adrenal venography, and determinations of aldosterone in adrenal venous blood. These results are compared with those of the dexamethasone scintiscan (DS). In tumor localization, the 88 per cent figure for the DS was only moderately better than that of the other three (71 per cent, SS; 80 per cent, venography; 80 per cent, adrenal venous aldosterone levels). However, in predicting bilateral hyperplasia, the DS was 100 per cent correct, as were the levels of aldosterone in adrenal venous blood. The SS and adrenal venography failed in bilateral hyperplasia and gave many false-positive results indicating tumor. The DS, a relatively simple outpatient procedure, appears to be at least as effective, both in lateralizing tumors and distinguishing between tumor and bilateral hyperplasia, as the more difficult, expensive, and sometimes hazardous invasive procedure of bilateral adrenal vein catheterization.

Adolescent↗
PubMed1998

[Idiopathic hypophyseal hyperplasia: diagnosis by magnetic resonance].

INTRODUCTION: Hypophyseal hyperplasia is an uncommon disorder in which the gland increase in size due to excessive proliferation of strings of normal cells, which usually secrete prolactin. Different aetiologies may cause this disorder of the hypophyseal gland. However, in a small number of cases the hyperplasia is not due to any of these aetiologies and is therefore known as idiopathic hypophyseal hyperplasia. There are few references in the literature to idiopathic hypophyseal hyperplasia with hyperprolactinaemia. Usually diagnosis is reached after treatment for a hypophyseal adenoma, since the clinical features are similar. CLINICAL CASES: We present three cases seen in our department, in which hormone and endocrine studies were done to exclude known causes of hyperplasia, together with CT and MR scans. We analyzed the behaviour of hypophyseal hyperplasia by using imaging techniques, and the differential aspects with regard to hypophyseal adenomas. Firm diagnosis is only made on anatomopathological study of the hypophysis. However, we consider that sound knowledge of the characteristics of this condition may help to establish the correct diagnosis and thus avoid unnecessary surgery. CONCLUSIONS: We review the information published in the literature on this subject, emphasizing the importance of differential diagnosis by means of imaging techniques.

Adenoma↗
PubMed1998

Selective targeting and photodynamic destruction of intimal hyperplasia by scavenger-receptor mediated protein-chlorin e6 conjugates.

BACKGROUND: Photosensitizers, such as Photofrin II or Chloroaluminum-sulfonated phthalocyanine accumulate at sites of arterial injury. We have exploited this property to develop a model of photodynamic therapy (PDT) for intimal hyperplasia. The fluorescent probe [maleylated-bovine serum albumin (mal-BSA) conjugated with Texas-red] can be selectively targeted to intimal macrophages and smooth muscle cells recruited during formation of hyperplasia via a receptor-mediated mechanism. METHODS: In this study, the photosensitizer chlorin e6 (Cle6) was conjugated to mal-BSA in a rat model of intimal hyperplasia, then tested the efficacy of the ligand conjugation to photosensitizer (mal-BSA/Cle6) in PDT of intimal hyperplasia. Arterial wall injury was produced by a balloon catheter pulled through the abdominal aorta of the rat to create a model of intimal hyperplasia. Fluorescent compounds were injected two weeks after injury. RESULTS: Four hours after injection, the intensity of fluorescence achieved with injection of mal-BSA/Cle6 was higher for intimal hyperplastic lesions as compared to control areas. BSA-Cle6 unconjugated did not demonstrate such delivery. Two weeks after balloon injury, the injured aorta was irradiated externally with an argon pumped dye laser four hours following the photosensitizer injection. We employed two total radiant exposures: 20 J/cm2 and 40 J/cm2. Forty-eight hours after PDT, the arteries were examined histologically. Intimal hyperplastic cells were significantly reduced by PDT in the mal-BSA/Cle6 injected group (40-100%) versus the Cle6 group (0-20%). CONCLUSIONS: Mal-BSA/Cle6 is taken up efficiently by a scavenger pathway, localizes in areas of intimal hyperplasia, and functions as a photosensitizer for PDT.

Animals↗
PubMed2004

Saratin (an inhibitor of platelet-collagen interaction) decreases platelet aggregation and homocysteine-mediated postcarotid endarterectomy intimal hyperplasia in a dose-dependent manner.

BACKGROUND: This study investigated Saratin's (Merck KGaA, Darmstadt, Germany) prevention of platelet adhesion and intimal hyperplasia at different doses and in the hyperhomocystinemia rat carotid endarterectomy (CEA) model. METHODS: Rats were divided into two groups: (1) platelet adhesion or (2) luminal stenosis because of intimal hyperplasia. At CEA, rats received 0, 0.5, 5.0, 10.0, or 20.0 microg Saratin on the artery. Post-CEA platelet aggregation was evaluated by standard error of the mean. Intimal hyperplasia group received either (1) control or (2) 4.5 g/kg DL-homocystine diets for two weeks followed by CEA and treated with diluent or 5.0 microg Saratin. Endpoints included platelet adhesion, intimal hyperplasia, plasma homocysteine (HCys), and its metabolic enzymes cystathionine beta-synthase (CBS) and methylenetetrahydrofolate reductase (MTHFR). RESULTS: Platelet adhesion: post-CEA, platelet adhesion was reduced by 63%, 67%, and 67% in Saratin doses > or =5.0 microg. Intimal hyperplasia: 5.0 microg Saratin in the HCys group decreased intimal hyperplasia by 45% compared with the non-Saratin-treated HCys group. Plasma HCys levels were not altered with Saratin treatment in the HCys groups nor were CBS or MTHFR. CONCLUSIONS: Saratin significantly inhibited platelet adhesion at > or =5.0 microg, and Saratin at 5.0 microg attenuated luminal stenosis in a hyperhomocysteinemic rat CEA model.

Analysis of Variance↗
PubMed1997

Inhibition of the intimal hyperplasia in an arterial autograft model by blockade of the N-terminal of the integrin beta3 subunit by monoclonal antibody P37.

Myointima formation or intimal hyperplasia is a major undesirable problem at the anastomotic ends of narrow bore arterial autografts and in other arterial wall injuries, which often leads to late restenosis and thrombosis and whose pathogenesis is still not understood. Platelets are suspected to intervene at some stages of its development, together with endothelial and muscle cells, the extracellular matrix and, most probably, adhesion receptors. To ascertain whether and at what stage beta3 integrins are involved, a rat arterial autograft model was used, together with monoclonal antibody P37, which is directed to the sequence 101-109 of the beta3 subunit of the human platelet fibrinogen receptor (integrin alphaIIbbeta3) and inhibits platelet aggregation in vitro and acute thrombosis in vivo. Three groups of animals were used: group I underwent an arterial autograft of a 5-mm segment of the right common iliac artery; group II received, intravenously, a single dose (0.8 mg/kg) of P37 at 15 min before the graft implantation; and group III was treated as group II but a similar dose of antibody was additionally given on day 14 after the operation. Animals in each group were sacrificed on days 7, 14, 21, 30 and 50 after the operation, and the grafts were removed for light and electron microscopy observation and further time-dependent morphometric analysis. By day 14, group I autografts already showed intimal hyperplasia and secretory smooth muscle cells, while group II and II autografts presented only some degenerative changes in the medial layer, with no signs of hyperplasia. Intimal hyperplasia was observed on day 21 in group II and on day 30 in group III, although less pronounced than in the corresponding controls. However, by day 50, the three groups had the same thickness of myointima. The immunohistochemical determination of metalloproteases suggests no role for these enzymes in the immunoinhibition of myointima formation. We conclude that P37 inhibits the onset of the intimal hyperplasia in the arterial autografts and that this onset in treated animals seems to be related to the decay of the circulating antibody. Further work is required to decide whether a higher or longer presence of circulating P37 can definitively prevent the development of intimal hyperplasia, as well as to ascertain which cells and which beta3 integrin receptors intervene.

Journal Article↗
PubMed2000

Nodular lymphoid hyperplasia of the lung: a clinicopathologic study of 14 cases.

Nodular lymphoid hyperplasia is a controversial entity in which its existence in the lung has been doubted. The current opinion is that most, if not all, such cases represent extranodal marginal zone B-cell lymphomas masquerading as reactive lesions. We found 14 cases of nodular lymphoid hyperplasia in the files of the Pulmonary Department at the Armed Forces Institute of Pathology from 1974 through 1998. All had clinical histories and hematoxylin-eosin slides. In 12 of 14 with paraffin blocks, we applied immunohistochemical antibodies for CD20, CD3, CD43, CD5, bcl-2, bcl-1, CD45RA, and kappa and lambda immunoglobulin light chains. Molecular genetic analysis was performed on paraffin sections in 10 of 14 by the polymerase chain reaction for rearrangements of the immunoglobulin heavy chain gene and the minor and major break-point regions of the chromosomal translocation t (14;18). There were eight women and six men ranging in age from 19 to 80 years (median, 65 yrs). Most lesions (71%) were incidental findings on routine chest x-rays. Most patients (64%) had a single lesion by chest x-ray whereas the remainder had two to three lesions, except for one patient who had "multiple" lesions. There was associated regional lymphadenopathy in five of 14 cases (36%) which, on biopsy, proved to be reactive follicular hyperplasia. The only treatment was surgical excision. Of the seven patients with follow-up information from 8 months to 6 years (mean, 30 mos), none had clinical recurrence and no patient died of disease. The histology and immunophenotype of the lesions were strikingly similar, including abundant reactive germinal centers, intense interfollicular polyclonal plasmacytosis, and a variable degree of interfollicular fibrosis. No case showed a molecular rearrangement of the immunoglobulin heavy chain gene or the minor or major break-point region of the t (14;18). We conclude that nodular lymphoid hyperplasia of the lung, although rare, does exist and deserves its place in the spectrum of reactive pulmonary lesions that ranges from follicular hyperplasia to diffuse hyperplasia of the bronchus-associated lymphoid tissue (lymphoid interstitial pneumonitis).

Adult↗
PubMedDate not supplied

Flow cytometrical DNA measurements in endometrial hyperplasias. A prospective follow-up study after abrasio only or additional high-dose gestagen treatment.

As part of a prospective study on endometrial hyperplasias the DNA content in individual cells was measured by flow cytometry in 109, 35 and 12 cases of cystic glandular, adenomatous and atypical hyperplasias respectively. About 20% of all types of hyperplastic endometria revealed a non-diploid DNA index compared to 6% in normal endometria and 29% in well differentiated carcinomas. Increasing severity of hyperplasia was accompanied by increased proliferative activity as reflected by increased S-phase-and (S + G2)-fractions. The findings emphasise a previous suggestion that all types of hyperplasias are predecessors to endometrial carcinomas. Examination after 3 months following abrasio alone or in combination with high-dose gestagen treatment revealed a still high frequency of non-diploid cells. This was the case in endometria without histologic signs of hyperplasia as well as in those still demonstrating hyperplastic changes. Hypothetically chromosomal aberrations could be the main reason for the development of hyperplasias.

Adenoma↗
PubMed1987

Inheritance of susceptibility to phototumorigenesis and persistent hyperplasia in F1 hybrids between SENCAR mice and BALB/c or C57BL/6 mice.

SENCAR mice are selectively bred for hypersusceptibility to two-stage chemical skin carcinogenesis. They are also hypersusceptible to UV radiation tumorigenesis with single high-dose, but not chronic low-dose, exposures. In addition, SENCAR mice exhibit an exaggerated and persistent epidermal hyperplasia (due to sustained proliferation of the basal cells) in response to UV-induced tissue damage. In the present study, we have examined the inheritance of susceptibility to both phototumorigenesis and persistent hyperplasia in the F1 offspring of SENCAR mice crossed with either of two inbred strains (BALB/c or C57BL/6) which are relatively resistant to phototumorigenesis. A total of 428 mice from the parental strains and reciprocal F1 crosses were given a single high dose (8.64 x 10(4) J/m2) of UV radiation (FS40 sunlamps) which causes persistent hyperplasia and tumorigenesis in many SENCAR, but no BALB/c or C57BL/6, mice. F1 hybrids between SENCAR and C57BL/6 mice did not develop persistent hyperplasia or skin tumors, which indicates that susceptibility to both traits is completely recessive to the C57BL/6 genotype. In contrast, F1 hybrids between SENCAR and BALB/c mice developed both persistent hyperplasia and skin tumors, although at a much lower incidence than the SENCAR mice, indicating that susceptibility to both traits is only partially (incompletely) recessive to the BALB/c genotype. Thus, in either F1 cross, susceptibility to phototumorigenesis decreased in parallel with persistent hyperplasia. These results are consistent with the hypothesis that the two characteristics are mechanistically related.

Animals↗
PubMed1987

Murine epidermal xanthine oxidase activity: correlation with degree of hyperplasia induced by tumor promoters.

Topical application of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) to SENCAR mouse skin results within 48 h in a 3-fold elevation of xanthine oxidase (XO) activity, an enzyme capable of generating the reactive oxygen species superoxide and hydrogen peroxide. The antiinflammatory steroid fluocinolone acetonide, an inhibitor of TPA-induced hyperplasia, as well as the multiple stages of tumor promotion as defined in SENCAR mice (Stages I and II), inhibited the TPA-dependent elevation of epidermal XO activity. Neither tosylphenylalanyl chloromethyl ketone nor retinoic acid, inhibitors of promotion Stages I and II, respectively, had significant effects on TPA-induced hyperplasia or elevated XO activity. The nonpromoting but hyperplasiogenic agents ethyl phenylpropiolate and acetic acid significantly elevated XO activity within 48 h of topical application. The non-phorbol ester tumor promoter benzoyl peroxide also elevated XO activity consistent with the degree of induced hyperplasia. Multiple treatments with TPA or ethyl phenylpropiolate resulted in a sustained elevation of XO activity which peaked at five treatments and then declined. Sustained inhibition of XO activity by p.o. administration of allopurinol did not inhibit the TPA-induced hyperplasia as determined histologically. These results suggest that the TPA-dependent elevation of epidermal XO activity is associated with the hyperplasia induced by the agent, and is a consequence of the hyperplasia rather than the cause of it.

Animals↗
PubMed1992

Benign prostatic hyperplasia. Its natural history, epidemiologic characteristics, and surgical treatment.

Benign prostatic hyperplasia is a nonmalignant enlargement of the prostate that is due to both epithelial and stromal hyperplasia. Although the exact origin of this condition is not well defined, it is thought to arise as microscopic nodules in the periurethral tissue of the prostate gland as early as the late '20s. With advancing age and the presence of androgens, this histologically identifiable hyperplastic tissue progresses to a macroscopic state, which is a palpably enlarged prostate. This enlarged prostate causes clinically significant obstruction of the bladder outlet in many men, necessitating therapeutic intervention. Currently, prostatectomy is the standard treatment with successful long-term results. Nevertheless, much information has become available recently on its indications, outcomes, associated morbidity and mortality, and effect on quality of life. Because of these findings as well as the rising healthcare costs and the desire among patients to avoid surgery if possible, there is much enthusiasm for developing less expensive, less invasive, but effective treatments for symptomatic benign prostatic hyperplasia. To appreciate the tremendous advances being made with regard to the treatment of benign prostatic hyperplasia, it is necessary to have a complete understanding of the disease process itself and its traditional therapies. This clinical report provides a comprehensive review of the natural history, epidemiologic characteristics, and outcomes of both open and transurethral surgery for benign prostatic hyperplasia.

Age Distribution↗
PubMed1999

Benign lymphoid hyperplasia of the conjunctiva in children.

Benign lymphoid hyperplasia of the conjunctiva occurs infrequently in children, and its presentation, clinical course, and appropriate management are not well established. We describe 2 children with nasal conjunctival masses that on pathological examination demonstrated benign lymphoid hyperplasia. Local irradiation of residual tissue was deferred, and the lesions remained stable for 1 year in one case and for 3 1/2 years in the other case. No systemic involvement had occurred. Although the natural history of extranodal lymphoid hyperplasia in children is poorly documented, most cases of nodal lymphoid hyperplasia in children are at very low risk of malignant transformation. Careful observation for local and systemic disease is indicated for ocular adnexal lymphoid hyperplasia in children until a more complete understanding of its natural history is available.

Antigens, CD20↗
PubMed2000

Pharmacological effects of the lipidosterolic extract of Serenoa repens (Permixon) on rat prostate hyperplasia induced by hyperprolactinemia: comparison with finasteride.

BACKGROUND: The growth of the prostate gland is mainly dependent on androgens. Other hormones, like prolactin (PRL), also influence prostate development. Our purpose was to analyze and compare the effects of two drugs (5alpha-reductase inhibitor) used in the therapy of benign prostatic hyperplasia: lipidosterolic extract of Serenoa repens (LSESR), and finasteride in an in vivo model of rat prostate hyperplasia induced by hyperprolactinemia. METHODS: Hyperprolactinemia was induced by 30 daily injections of sulpiride. Wistar rats received daily gavages of LSESR or finasteride. We used the following groups: control, castrated, castrated with a substitute testosterone (T), or 5alpha-dihydrotestosterone (DHT) implant. RESULTS: Hyperprolactinemia increases the wet weight and induces hyperplasia in the lateral prostate (LP). Unlike finasteride, LSESR significantly reduced LP growth and hyperplasia in castrated, DHT-implanted, and sulpiride-treated rats. CONCLUSIONS: Finasteride was only capable of inhibiting the effect of androgens on rat prostate enlargement. LSESR inhibited not only the androgenic but also the trophic effect of PRL in rat LP hyperplasia.

Androgen Antagonists↗
PubMed1996

Physiologic versus neoplastic C-cell hyperplasia of the thyroid: separation of distinct histologic and biologic entities.

BACKGROUND: Although hyperplasia of C-cells has been described in association with various pathologic and physiologic conditions, criteria for its diagnosis are poorly defined. Both neoplastic and physiologic C-cell proliferations have been lumped together under the umbrella designation of C-cell hyperplasia (CCH), creating considerable confusion among clinicians and pathologists. METHODS: in order to compare the morphologic and immunohistochemical characteristics of the two major types of CCH, we examined thyroid sections of 17 patients with familial forms of C-cell hyperplasia and/or neoplasia and tissue sections of 19 thyroid glands known to have reactive or physiologic CCH (at least 50 C-cells per one low power field, 100X). Hematoxylin and eosin (H & E) stained sections and immunohistochemical stains for calcitonin were assessed in each case. RESULTS: Physiologic or reactive CCH was not recognized with certainty on H & E stains in any of the cases due to morphologic similarities between C-cells and adjacent follicular cells. Detection of this form of hyperplasia, which was predominantly diffuse, required calcitonin immunostains and quantitative analysis. Conversely, nodular and diffuse neoplastic CCH was easily identified with conventional H & E stains at the periphery of 11/12 (92%) familial medullary thyroid carcinomas (MTC). In the other five cases, neoplastic C-cell hyperplasia was the only pathologic finding on thyroidectomy performed for elevated serum calcitonin levels detected via provocative biochemical screening or identification of the mutated RET proto-oncogene by genetic analysis. The C-cells in this neoplastic form of CCH were large, mildly to moderately atypical, and confined within the basement membrane of thyroid follicles. Moreover, these cells were cytologically indistinguishable from those of invasive MTC cells. CONCLUSIONS: Physiologic and neoplastic CCH are biologically and morphologically distinct entities. The former cannot be recognized with certainty with conventional stains and requires immunohistochemistry and quantitative analysis for diagnosis. The latter consists of mildly to moderately atypical C-cells that can be identified with H & E stained sections. Consequently, the number of C-cells is of no importance for the diagnosis of neoplastic CCH which is considered to be the precursor (medullary carcinoma in situ) of invasive medullary carcinoma.

Adolescent↗
PubMed1989

Binding of soybean agglutinin lectin to prostatic hyperplasia and adenocarcinoma.

The binding of soybean agglutinin (SBA) lectin to routinely processed surgical pathology material from cases of prostatic hyperplasia, atypical hyperplasia, and adenocarcinoma was studied using an immunoperoxidase technique. Positive staining was obtained in eight of eight cases of nodular hyperplasia, eight of eight cases of atypical hyperplasia, and ten of 11 cases of adenocarcinoma. This report indicates that this lectin is not useful in distinguishing prostatic hyperplasia from adenocarcinoma.

Adenocarcinoma↗
PubMed1992

Thymic hyperplasia with hemorrhage simulating recurrent Hodgkin disease after chemotherapy-induced complete remission.

BACKGROUND: Thymic hyperplasia after successful treatment of malignant disease is a well-documented phenomenon, particularly in younger patients with testicular carcinoma. However, it has been reported only sporadically in association with Hodgkin disease. The authors report the first instance of an adult with nodular sclerosing Hodgkin disease who had thymic hyperplasia develop after clinical and radiographic complete remission (CR) with chemotherapy alone. METHODS: In addition to the current case, 20 other instances of thymic hyperplasia have been culled from the literature and analyzed. RESULTS: The median age of these 21 patients was 23 years of age (range, 8-40 years of age). Thymic hyperplasia was noted after treatment was initiated or completed in all but two patients; and all did well, with one exception: a 17 year-old boy who was inadvertently treated for relapsed Hodgkin disease and who died of fibrinous pneumonitis and nocardia, with pathologic CR noted at autopsy. CONCLUSIONS: Thymic hyperplasia in association with Hodgkin disease appears to be a favorable prognostic phenomenon, restricted to younger patients in the first modal peak of Hodgkin incidence. Prospective studies have yet to be performed.

Adult↗