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PubMed1976

Myeloid metaplasia in the spleen after acute haemolysis.

Copper sulphate, phenyl hydrazine and antiserum were administered to adult albino rats to produce equivalent haemolysis. Red pulp activity was studied for myeloid metaplasia after 24, 48 and 72 h, 5 and 7 days. Myeloid metaplasia was not related to the marginal zone proliferation. The activity rose rapidly with all the three agents and followed a similar curve despite the different patterns of haemolysis and erythrophagocytosis. Splenic erythrophagocytosis acts as a powerful feedback for splenic myeloid metaplasia. With copper, the release of reticulocytes and iron binding in haemoglobin is rapid as compared to the other agents, in spite of the initial lag phase, due to its effect on cellular metabolism.

Animals↗

PubMedDate not supplied

Mechanobiology of tendon adaptation to compressive loading through fibrocartilaginous metaplasia.

Tendons that wrap around bones often undergo fibrocartilaginous metaplasia. In this paper, we examine the biomechanical causes and consequences of this metaplasia. We propose an adaptation rule in which tissue permeability changes in response to local cyclic hydrostatic pressures associated with physical activity. The proposed rule predicts the development of a low-permeability region corresponding to the fibrocartilaginous region in a representative wrap-around tendon. A poroelastic finite element model is used to examine the time-dependent fluid pressures and compressive stresses and strains in the solid constituents of the tendon's extrafibrillar matrix. The low permeability in the adapted fibrocartilaginous region maintains fluid pressures, protecting the solid constituents of the tendon's extracellular matrix from high compressive stresses and strains that could disrupt the matrix organization. Adaptation through fibrocartilaginous metaplasia therefore allows wrap-around tendons to function effectively over a lifetime without sustaining excessive mechanical damage due to cyclic compressive loading.

Adaptation, Physiological↗

PubMedDate not supplied

Genetic versus environmental interactions in the oesophagitis-metaplasia-dysplasia-adenocarcinoma sequence (MCS) of Barrett's oesophagus.

The prevalence of Barrett's oesophagus has risen over a short time interval implying environmental in addition to genetic aetiological factors. Bile salt effects from duodenogastro-reflux are assuming increasing importance with deoxycholic and taurodeoxycholic acid being particularly associated with Barrett's oesophagus. The cellular biology changes appear to follow a progression from initial inflammation and oesophagitis to metaplasia and dysplasia through to adenocarcinoma. Mechanisms of restitution include epidermal growth factor mediated increases in epithelial thickness. This results in basal stem cells becoming superficially placed and exposed further to luminal refluxed bile salts. Immature stem cells result which undergo mutation to a metaplastic glandular phenotype with intestinal metaplasia. P53 mutation increasingly occurs in progression to dysplasia and carcinoma and may confer a survival advantage of these cell clones by delaying apoptosis. Cell cycling gene mutations occur with accumulation of cells in G2 phase. Disruption of cellular checkpoint mechanisms in the mitotic process result in loss of heterozygosity and aneuploidy including loss of the Y chromosome. Identical mutations between adjacent areas of dysplasia and adenocarcinoma supports clonal expansion as the mechanism of carcinogenesis. APC tumour suppressor gene mutations are conserved in synchronous carcinomas in Barrett's dysplasia and are associated with beta-catenin accumulation in the nucleus and cellular migration with invasion. Cumulative genetic errors result in abnormal clones with metastatic or angiogenic potential. When a clone with malignant potential occurs adenocarcinoma can result completing the progression from inflammation to metaplasia and dysplasia through to adenocarcinoma.

Adenocarcinoma↗

PubMed1975

Myelofibrosis-myeloid metaplasia in childhood.

A child with idiopathic myeloid metaplasia is described and her course contrasted with another child having myeloid metaplasia secondary to reticulum cell sarcoma. Despite prior reports the idiopathic form of illness may pursue a relatively indolent course in children. A thorough search should be made for underlying disease when myeloid metaplasia is first diagnosed.

Child↗

PubMedDate not supplied

p53 immunoreactivity in Barrett's metaplasia, dysplasia, and adenocarcinoma--a case report.

Barrett's esophagus is a condition in which the stratified squamous epithelium of the esophagus is replaced by a columnar epithelium with malignant potential. Mutations of the tumor-suppressor gene p53 have been implicated in the evolution of esophageal carcinomas. The aim of this study was to determine whether p53 immunoreactivity in Barrett's esophagus is a marker of neoplasia and, if so, when it occurs in the metaplasia-dysplasia-carcinoma sequence. We treated a patient with esophageal carcinoma arising from the Barrett's esophagus. Consecutive evidence existed for a metaplasia-dysplasia-carcinoma in the same specimen. Immunohistochemical staining with the monoclonal antibody was used to detect the intranuclear protein product of mutated p53. No p53 immunoreactivity was seen in specimen of Barrett's mucosa. p53 immunoreactivity was found only in specimen of dysplasia and carcinoma. Immunoreactivity occurs late in the metaplasia-dysplasia-carcinoma sequence, during the transition to high-grade dysplasia.

Adenocarcinoma↗

PubMedDate not supplied

Estrogen receptor-beta is expressed in Barrett's metaplasia and associated adenocarcinoma of the esophagus.

Estrogen receptor-beta (ER-B) has been identified in benign and malignant tissues of a variety of human organs including the colon. In breast carcinoma, ER-B was found to be a significant predictor of response to adjuvant hormonal therapy with tamoxifen. The aim of the present study was to determine whether esophageal adenocarcinoma, and its precursosr, Barrett's metaplasia, express ER-B. Sections of formalin-fixed and paraffin-embedded tissue from 31 esophagectomy specimens were immunostained for ER-B using the immunoperoxidase technique, and the percent of positive cells in areas of Barrett's metaplasia negative for dysplasia (ND), low-grade dysplasia (LGD), high-grade dysplasia (HGD) and adecocarcinoma, (CA) were recorded. Nuclear ER-B staining in >50% of the cells was seen in all 23 CA (100%), 10 out of 11 (91%) HGD, 8 out of 11 (83%) LGD and in 10 of 15 (66.6%) ND. It is concluded that all adenocarcinomas of the esophagus and most precursor lesions, Barrett's Metaplasia (BM) with or without dysplasia, express ER-B in a significantly high percentage of the cells. These findings raise the possibility that esophageal adenocarcinomas may benefit from treatment and/or chemoprevention with antiestrogens, such as tamoxifen.

Barrett Esophagus↗

PubMed2002

Does Helicobacter pylori eradication modify intestinal metaplasia evolution in the stomach?

BACKGROUND: We aimed to evaluate Helicobacter pylori eradication impact on the gastric carcinogenesis cascade following the evolution of intestinal metaplasia (IM) in gastric antrum after Helicobacter pylori (HP) eradication. METHODS: We followed yearly for a 5 year period after bacterial eradication, 69 HP positive patients with gastric or duodenal ulcers who showed antral gastric intestinal metaplasia at histology at time 0. All patients, eradicated by OAC triple short-term therapy and assessed both performing 13C-UBT 1 month after eradication and by Giemsa stain, persisted HP negative during follow-up. Upper endoscopy with 6 biopsies from gastric antrum at least 2 cm away from pylorus, was repeated every year in each patient involved in the study, in order to evaluate IM evolution and HP eradication persistence. During the follow-up histological specimens were examinated from the same pathologist and IM differentiated as complete (type I), incomplete (type II) or incomplete solphomucin-positive (type III). Statistical analysis between different groups after each year was performed by chi2 method. RESULTS: At time 0.48 cases out of 69 (69.7%) presented type I IM, 14 cases (20.2%) type II IM and 7 cases (10%) type III IM. IM presence in histological specimens after 1, 2, 3, 4 and 5 years from HP eradication were evaluated and statistical analysis between the 3 IM groups after each control showed a significant regression after HP eradication in type I versus III IM (p<0.001), mostly 2 and 3 years after HP eradication, but no significance in type I versus II IM (p=0.284) neither in type II versus III IM (p=0.981) also after 5 years. CONCLUSIONS: HP eradication permits complete intestinal metaplasia regression in gastric antrum 2 or 3 years after antibiotic treatment. Otherwise incomplete IM in gastric antrum, both type II and III, is not significantly modified after bacterial eradication.

Journal Article↗

PubMed1985

Myelofibrosis with myeloid metaplasia: pathophysiologic implications of the correlation between bone marrow changes and progression of splenomegaly.

We undertook a study of 35 cases of myelofibrosis with myeloid metaplasia to assess the histopathologic findings in the bone marrow of patients with this disorder, to ascertain if changes in morphology occurred with time, and to attempt to correlate marrow findings with splenic size. We reviewed 71 bone marrow biopsies and studied 13 splenectomy specimens. Sequential bone marrow biopsies were obtained in 21 cases over intervals ranging from two to ten years (mean, 4 1/2 years). We noted a patchy nature and variable degree of stromal proliferation in most marrow biopsies, and were unable to demonstrate a correlation between the extent of medullary fibrosis and duration of disease, splenic weight, or degree of splenic myeloid metaplasia. We were unable to document a progression of medullary fibrosis as a cause for increasing splenomegaly. However, the alteration in the marrow stroma in this disorder is responsible for the presence of distended marrow sinusoids with intravascular hematopoiesis, a phenomenon we observed in all cases. We believe that this morphological feature, not emphasized by previous investigators, is of significance in understanding the pathophysiology of myeloid metaplasia.

Adult↗

PubMed1978

Agnogenic myeloid metaplasia: a clonal proliferation of hematopoietic stem cells with secondary myelofibrosis.

The glucose-6-phosphate dehydrogenase (G-6-PD) types and chromosomes of hematopoietic and other tissues were determined in a woman with agnogenic myeloid metaplasia. The patient was heterozygous at the X-linked G-6-PD locus so that both B and A isoenzymes were found in nonhematopoietic cells. In contrast, only one G-6-PD type was found in granulocytes, red cells, and platelets. She also had a distinctive chromosome abnormality in blood cells but not in other tissues. These results indicate that agnogenic myeloid metaplasia is a disorder of a pluripotent stem cell and provide strong evidence that it is of clonal origin. In contrast to blood cells, the patient's cultured marrow "fibroblasts" had normal chromosomes and both B and A G-6-PD types, suggesting that the marrow fibrosis is a secondary abnormality. Thus, at least in this case of agnogenic myeloid metaplasia, the hematopoietic cell proliferation appears to be clonal, and, by inference, possibly neoplastic, whereas the marrow fibrosis is probably not clonal, and therefore appears to be secondary.

Aged↗

PubMed1994

Esophageal motor dysfunction and acid exposure in reflux esophagitis are more severe if Barrett's metaplasia is present.

OBJECTIVES: To compare esophageal motor function in patients with reflux esophagitis with controls, and identify patient characteristics that may have a bearing on the severity of esophageal motor dysfunction and acid exposure. METHODS: Esophageal motor function was assessed in 60 patients with reflux esophagitis. All patients had manometry, 50 had an esophageal transit test, and 23 had an acid clearance test. Forty-eight had dual site [5 and 10 cm above lower esophageal sphincter (LES)] esophageal pH monitoring, four had only distal pH monitoring, and one patient had only proximal pH monitoring. Thirty-four controls underwent the same tests. The association between the indices of esophageal function plus the degree of esophageal acid exposure and eight patient characteristics (age, sex, obesity, smoking, alcohol intake, hiatus hernia, grade of esophagitis, and Barrett's metaplasia) was examined in unifactorial and multifactorial analysis of variance. RESULTS: The patients had significantly lower LES pressure, lower distal and middle esophageal amplitudes, longer duration of contraction, and slower velocity of propagation. They had longer esophageal transit and acid clearance times. Barrett's metaplasia was the only factor that had an association with the magnitude of esophageal motor dysfunction and acid exposure, except age, which had a weak positive association with acid exposure (p = 0.03). Compared to the rest of the patients with esophagitis, patients with Barrett's had lower LES pressure (median = 10.5 vs. 17.5 mm Hg, p = 0.013), longer supine transit time (median = 180 vs. 13.5 s, p = 0.0001), and higher % of total time pH < 4 (median = 48.2 vs. 8.7 and 23.2 vs. 5.2; p < 0.0001 for distal and proximal esophageal acid exposure, respectively). Ten of the 12 patients with Barrett's had abnormal manometry, compared with 20 of the 48 without (chi 2 = 6.67; p < 0.01). There was a strong correlation between the degree of acid exposure in the proximal esophagus and the length of Barrett's segment (r = 0.846, 0.81, 0.725; and p < 0.001, 0.005, 0.018, for the % of times pH < 4 for total, supine, and upright periods, respectively). CONCLUSIONS: The development of Barrett's metaplasia may be determined by the degree of esophageal exposure to the refluxate which, in turn, may be a function of the severity of esophageal motor dysfunction. The length of Barrett's segment may be dependent on the extent of orad transport of the refluxate.

Analysis of Variance↗

PubMedDate not supplied

Subtotal splenectomy for treatment of patients with myelofibrosis and myeloid metaplasia.

Idiopathic myelofibrosis is a chronic myeloproliferative disorder that may course with myeloid metaplasia involving several organs. Occasionally, the spleen reaches giant proportions and must be withdrawn. However, this procedure is followed by greater morbidity and mortality. Partial splenectomies, preserving the splenic pedicle, have been proposed in order to reduce postoperative complications. After an early postoperative improvement, some patients present symptomatic recurrence of their disease. This communication presents a new alternative for the treatment of complicated myeloid metaplasia: subtotal splenectomy, preserving the upper splenic pole supplied only by the splenogastric vessels. We performed this procedure in three patients. Their almost two years postoperative follow-up and health improvement suggest that this operation should be considered for the treatment of huge spleens due to myelofibrosis with myeloid metaplasia.

Adult↗

PubMed1997

Microglandular endocervical hyperplasia and tubal metaplasia: pitfalls in the diagnosis of adenocarcinoma on cervical smears.

The detection of atypical glandular cells of undetermined significance (AGUS) has risen recently due to the use of new endocervical canal sampling devices, in particular the cytobrush. From April 1993-June 1994, a diagnosis of AGUS ranging from adenocarcinoma in situ (AIS) to invasive adenocarcinoma was initially made on cervical smears from 6 women for whom histologic follow-up data were available. The purpose of this study was to determine if benign cervical glandular lesions can be reliably distinguished from adenocarcinoma on cytology. Review of the smears and histologic slides from 3 patients showed microglandular endocervical hyperplasia on cervical cone specimens. Cervical smears from 2 of these patients showed clusters of small-to-medium-sized cells with nuclei containing coarse, granular chromatin and prominent nucleoli. Cytoplasmic vacuoles and engulfment of neutrophils were present, findings suggestive of endometrial adenocarcinoma. The third patient's smear showed clusters of large cells with ample, vacuolated cytoplasm and vesicular nuclei containing prominent nucleoli, findings suggestive of endocervical adenocarcinoma. In 3 cases evaluated by cervical conization, histologic slides showed tubal metaplasia. The cervical smears showed clusters and sheets of cells with round-to-oval-shaped nuclei containing evenly distributed, finely granular chromatin and inconspicuous nucleoli. Pseudoglandular formation was present in 2 cases, a finding suggestive of AIS. Since the cytologic features of microglandular endocervical hyperplasia and tubal metaplasia overlap those of adenocarcinoma, a differential diagnosis is prudent on cytologic smears of AGUS.

Adenocarcinoma↗

PubMed1998

Transitional cell metaplasia of the cervix: a newly described entity in cervicovaginal smears.

Transitional cell metaplasia (TCM) of the cervix is rarely reported in the pathology literature. To our knowledge, no case reports describing TCM in cervicovaginal smears exist. We report the cytologic features of TCM and compare them with squamous-cell carcinoma in situ (CIS), tubal metaplasia (TM), and atrophy. One hundred twenty-seven cervicovaginal smears from 31 patients with histologically proven cervical TCM were reviewed: seven smears (five patients) showed TCM. Five smears each of CIS, TM, and atrophy were evaluated as to architecture, nuclear features, nuclear to cytoplasmic ratios, and cytoplasmic haloes for comparison to TCM. The features that characterize TCM and allow its distinction from CIS, TM, and atrophy include cohesive groups of streaming spindled nuclei with haloes, grooves, tapered ends, and wrinkled contours.

Aged↗

PubMed2007

Osseous metaplasia in diffuse large B-cell lymphoma of the kidney.

A 57-year-old female with a history of diffuse large B-cell lymphoma (DLBCL) presented with a renal mass. Microscopic analysis of the nephrectomy specimen revealed DLBCL, confirmed by immunohistochemical analysis (CD45, CD20, CD3, pan-keratin) and polymerase chain reaction (PCR). Multiple spicules of metaplastic bone were identified within the tumor mass, but not within the uninvolved kidney parenchyma. No evidence of bone or dystrophic calcification was detected on the pre-nephrectomy computerized tomography (CT) scan. To our knowledge, this is the first incidence of osseous metaplasia occurring within DLBCL. The pathogenesis of osseous metaplasia is briefly discussed.

Antigens, CD20↗

PubMed1993

Localized primary amyloid tumor associated with osseous metaplasia presenting as bilateral breast masses: cytologic and radiologic features.

This report details the cytologic features of primary localized amyloid tumor of the breast presenting as bilateral breast masses in a 72-yr-old woman. Clinically and radiographically, the masses simulated metastatic or multifocal carcinoma. Fine-needle aspiration revealed irregular globules of acellular amorphous material and numerous multinucleated giant cells resembling granulomatous inflammation. Histology confirmed amyloid tumors with a foreign-body giant cell reaction in response to amyloid and foci of osseous metaplasia. Subsequent clinical workup included a serum electrophoresis and immunofixation which showed a small IgG kappa monoclonal protein. Urine immunofixation was negative for Bence Jones protein. Bone marrow examination revealed no evidence of a plasma cell dyscrasia. To date the patient has not developed clinical or laboratory evidence of systemic amyloidosis or multiple myeloma. Amyloidosis involving the breast and specifically localized primary amyloid tumors of the breast are rare and infrequently reported entities. To our knowledge, osseous metaplasia within isolated primary amyloid tumors of the breast has not been reported. We present this unusual case to illustrate the intratumoral calcification patterns mimicking carcinoma and to characterize the cytologic features. Emphasis is placed on the inclusion of amyloidosis in the differential diagnosis of breast masses.

Aged↗

PubMed1985

Squamous metaplasia in colonic adenomata: report of two cases.

Two cases of squamous metaplasia in colonic adenomata are reported. Since squamous metaplasia is known to occur rarely in the colon it is surprising that its occurrence in colonic adenomata has not been emphasized; this is more remarkable as its presence may have clinical significance as a precursor of rare forms of carcinoma of the colon.

Aged↗

PubMed2002

Expression of trefoil peptides (TFF1, TFF2, and TFF3) in gastric carcinomas, intestinal metaplasia, and non-neoplastic gastric tissues.

Trefoil factor family (TFF) domain peptides consist of three members that play a role in intestinal mucosal defence and repair, and in tumourigenesis. The role of the three TFF members in the gastric carcinogenesis cascade remains poorly defined. This study examined seven gastric cell lines, 50 gastric cancers and their adjacent non-cancer tissues, and tissues from 40 non-cancer patients, in order to elucidate the chronology of TFF expression in various stages of gastric carcinogenesis. TFF expression was determined by RT-PCR, immunohistochemistry, and western blot. Aberrant expression of TFF1, TFF2, and TFF3 was frequently detected in gastric cell lines. Specifically, TFF1 was detected in all non-cancer patients, but was detected in only 50% of gastric cancer and 66% of adjacent normal tissues. TFF2 expression was demonstrated in 87.5% of non-cancer patients, 34% of gastric carcinomas, and 58% of adjacent non-cancer tissues. There was a significant correlation between TFF1 and TFF2 expression in gastric cancer and adjacent non-cancer tissues (p<0.001). By contrast, TFF3 was detected in 25% of non-cancer patients and showed a predilection for areas with intestinal metaplasia (p=0.005). Sixty-two per cent of gastric cancers and 24% of neighbouring non-cancer tissues showed TFF3 expression. Immunoreactivity against TFF3 was demonstrated in goblet cells of intestinal metaplasia and within the cytoplasm and nuclei of tumour cells. Progressive loss of TFF1 and TFF2, together with the induction of TFF3, is likely to be involved in the early stage of the multi-step gastric carcinogenesis pathway.

Adult↗

PubMed1993

Ulcer-associated cell lineage ('pyloric metaplasia') in Crohn's disease: a lectin histochemical study.

Chronic intestinal ulceration in Crohn's disease is associated with the development of an epidermal growth factor-secreting cell lineage, or 'ulcer-associated cell lineage' (UACL). Expression of oligosaccharides by UACL was studied using a panel of 25 biotinylated lectins with an avidin peroxidase revealing system and compared with that of adult and fetal Brunner's glands, gastric antral mucosa, and 'gastric metaplasia' within the duodenum, in order to clarify further the interrelationships of these lineages. UACL was obtained from ileal resections performed for Crohn's disease. Lectin binding of the glandular component of UACL closely resembled that of antral mucosal glands and also that of fetal and adult Brunner's glands. Lectin binding of the ductal component of immature UACL, in which a surface component had not developed, resembled that of the gland. The surface and ductal components of mature UACL showed a distinct lectin-binding profile, which was very different from that of the gland, but closely resembled that of antral foveolar epithelium and 'gastric metaplasia' within the duodenum. It is concluded that there is differentiation of UACL from the glandular to surface components and that oligosaccharide expression of the lineage reflects that of normal Brunner's gland and gastric antral mucosa.

Brunner Glands↗