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PubMed1976

Blastic phase of agnogenic myeloid metaplasia simulating malignant lymphoma.

A patient with angogenic myeloid metaplasia in blastic transformation with unusually prominent lymphadenopathy simulating lymphoma is described. Interestingly, the initial evidence of myeloblastic transformation was present in the lymph nodes but not in the marrow. Serial bone marrow biopsies showed fibrosis throughout the course of the disease, in spite of a gradual increase in the percentage of peripheral blood myeloblasts. Aneuploidy with a marker chromosome and a Philadelphia-like chromosome was present in the lymph node, bone marrow, and peripheral blood cells. The literature is reviewed regarding the incidence of prominent lymphadenopathy and chromosome abnormalities in agnogenic myeloid metaplasia and other myeloproliferative disorders.

Aneuploidy↗
PubMed1983

Red cell aplasia in myelofibrosis with myeloid metaplasia. A distinct functional and clinical entity.

Three patients with myelofibrosis with myeloid metaplasia are described. All three presented with grave anemia and red cell aplasia. Erythroid failure was the functional characteristic of erythropoiesis as resulted from erythrokinetic studies. Bone marrow was hypercellular or normocellular with hyperplasia of granuloblasts and megakaryocytes. Despite absent or mild splenomegaly at diagnosis, massive splenomegaly associated with a leukoerythroblastic blood film developed during the course of the disease. A relative young age (42-47 years), a subacute course of the disease and terminal blast crisis in two of them were the prominent clinical features of the patients. The differentiation from acute or malignant myelofibrosis is discussed. The patients appear to be a distinct subset within myelofibrosis with myeloid metaplasia.

Adult↗
PubMed2007

Clearance of the Janus kinase 2 (JAK2) V617F mutation after allogeneic stem cell transplantation in a patient with myelofibrosis with myeloid metaplasia.

A patient with myelofibrosis with myeloid metaplasia displaying the V617F mutation of the JAK2 gene was given an allogeneic stem cell transplantation using a reduced-intensity conditioning regimen. The patient engrafted, and as he became a chimera, the expression of the V617F mutation of the JAK2 gene decreased progressively until its disappearance. Accordingly, the concept of "molecular remission" of the myelofibrosis with myeloid metaplasia could be entertained and added to the categories of response to treatment which have been recently described.

Biomarkers↗
PubMed1983

Pericardial tamponade associated with myeloid metaplasia.

A 32-year-old white male with agnogenic myeloid metaplasia developed pericardial tamponade shortly after elective splenectomy. Tamponade was relieved by pericardiocentesis but recurred, necessitating partial pericardiectomy. Following surgery and a course of radiation therapy to the heart, there was no further significant reaccumulation of fluid. Pathologic evaluation demonstrated foci of extramedullary hematopoiesis in the pericardium. To our knowledge, pericardial tamponade has not previously been reported as a biopsy-proven complication of myeloid metaplasia.

Adult↗
PubMed2006

Palliative goals, patient selection, and perioperative platelet management: outcomes and lessons from 3 decades of splenectomy for myelofibrosis with myeloid metaplasia at the Mayo Clinic.

BACKGROUND: Although splenectomy may palliate massive splenomegaly in patients with myelofibrosis with myeloid metaplasia, this procedure carries significant risks. The authors retrospectively analyzed their experience with splenectomy over the course of 30 years to analyze the impact of improved techniques, antimicrobials, and aggressive postoperative control of platelet counts on outcome. METHODS: A total of 314 patients underwent splenectomy between 1976 and 2004 for mechanical symptoms (= 156 patients [49%]), anemia (= 78 patients [25%]), portal hypertension (= 47 patients [15%]), or thrombocytopenia (= 33 patients [11%]). Of a total of 91 patients studied during the last decade, 69 patients (76%) experienced a palliative benefit for their primary surgical indication for a median of 12 months (range, 1-91 months). RESULTS: Perioperative complications occurred in 87 patients (27.7%) including infection (= 31 patients [9.9%]), thrombosis (= 31 patients [9.9%]), or bleeding (= 44 patients [14%]), 21 of which (6.7% of all patients) were fatal. Perioperative thrombohemorrhagic complications decreased in the last decade through the use of platelet apheresis and the prompt use of cytoreductive agents to counteract postsplenectomy thrombocytosis. Survival after splenectomy was found to be decreased in patients with preoperative thrombocytopenia (<100 x 10(9)/L [P = 0.006]) but not by indication, myelofibrosis with myeloid metaplasia (MMM) prognostic score, or the decade in which splenectomy was performed. CONCLUSIONS: The lack of improvement in overall postsplenectomy survival over time may be a reflection on the failure of medical therapy to improve survival in patients with MMM.

Adolescent↗
PubMed1990

Hepatic vascular disease and portal hypertension in polycythemia vera and agnogenic myeloid metaplasia: a clinicopathological study of 145 patients examined at autopsy.

The pathogenesis of portal hypertension arising in patients with myeloproliferative disorders has been difficult to understand because liver biopsy findings often show minimal changes. It has been suggested that increased splenic blood flow, hepatic infiltration with hematopoietic cells or sinusoidal fibrosis may be important. We have reviewed the autopsy findings and clinical histories of 97 patients with polycythemia vera and 48 patients with agnogenic myeloid metaplasia collected from three institutions and from the Polycythemia Vera Study Group. Cirrhosis was present in seven patients, one of whom had bleeding varices. Esophageal varices were present clinically in 10 patients without cirrhosis (seven polycythemia and three agnogenic myeloid metaplasia). All of these patients had lesions in small or medium-sized portal veins and four had stenosis of the extrahepatic portal vein with histology compatible with organized thrombi. Nodular regenerative hyperplasia occurred in 14.6% and correlated closely with the presence of portal vein lesions. Thirty patients had greater than 500 ml of ascites, seven of these patients also had varices and six of them had hepatic vein thrombosis. Ascites also correlated with hepatic vein disease confined to small intrahepatic branches. No correlation was seen between hepatic hematopoietic infiltration and signs of portal hypertension. We conclude that esophageal varices are common and are almost always associated with portal vein lesions visible by light microscopy. These portal vein lesions, and the secondary effects of nodular regenerative hyperplasia and portal hypertension, are most likely a result of portal vein thrombosis in patients with myeloproliferative disorders.

Adult↗
PubMed2001

Risks and benefits of splenectomy in myelofibrosis with myeloid metaplasia: a retrospective analysis of 26 cases.

BACKGROUND AND OBJECTIVES: To evaluate the outcomes of splenectomy in myelofibrosis and myeloid metaplasia (MMM). METHODS: We retrospectively reviewed our records of 26 patients with MMM who underwent an open splenectomy at Boston University Medical Center between 1979 and 1995. Fourteen patients had agnogenic myeloid metaplasia (AMM) and 12 had myelofibrosis with antecedent myeloproliferative disorders (MF). The main indications for splenectomy were progressive transfusion-dependent anemia, painful splenomegaly, and hypercatabolic symptoms associated with cytopenia. RESULTS: Median time to splenectomy after the diagnosis of MMM was 29 months ranging from 1 to 96 months. Three patients (11%) died within 1 month after the surgery because of sepsis. The most common peri- and postoperative complications were pneumonia and other bacterial infections (42%), cardiac events (19%), acute bleeding (15%), ileus (15%), and venous thrombosis (12%). Of the eight surviving patients who underwent splenectomy for transfusion dependent anemia, six (75%) had improvement in their hematocrit levels with abolishment of blood transfusions. A durable symptomatic palliation was achieved in all patients. Liver enlargement was noted in seven patients at 1-year evaluation. None of these patients developed hepatic failure. Leukemic transformation occurred in 8 of 18 patients (44%) postsplenectomy. The median overall survival for the entire group was 58.5 and 28 months from the diagnosis of MMM and the time of splenectomy, respectively. There was no difference in survival rates between patients with AMM and MF. CONCLUSIONS: Splenectomy is an effective palliative procedure with an acceptable morbidity in selected patients with MMM. Progressive transfusion-dependent anemia should also be considered an indication for splenectomy in the absence of leukemic evolution.

Adult↗
PubMed1989

Squamous metaplasia with Hashimoto's thyroiditis presenting as a thyroid nodule.

A 59-year-old Japanese female presented a well-limited and movable thyroid nodule. Histologically, the nodule consisted of clusters of squamous cells surrounded by dense connective tissue in Hashimoto's thyroiditis. The squamous cells were well arranged and showed no mitotic figures. We therefore interpreted this nodule as being squamous metaplasia with Hashimoto's thyroiditis rather than squamous carcinoma of the thyroid. There are no previous reports in the literature of nodular formation of squamous metaplasia in the thyroid.

Carcinoma, Squamous Cell↗
PubMed1994

Expression of the trefoil peptides pS2 and human spasmolytic polypeptide (hSP) in Barrett's metaplasia and the native oesophageal epithelium: delineation of epithelial phenotype.

The distribution of the two trefoil peptides pS2 and human spasmolytic polypeptide (hSP) and their mRNAs was investigated in 90 selected oesophageal biopsies, 23 of which contained epithelium with wholly gastric cardiac-type morphology, 52 specialized (intestinal)-type metaplasia, and 15 non-metaplastic oesophageal epithelium. No fundic-type epithelium was represented. The cardiac-type epithelium resembled true gastric antral epithelium, with hSP and pS2 mRNA localization to the superficial/foveolar compartment and hSP mRNA alone in deeper glands. The pattern of peptide distribution was broadly in line with the mRNA, but hSP peptide was generally not demonstrable in the surface epithelium. pS2 immunostaining was diffusely cytoplasmic, whereas in specialized-type mucosa it was aggregated and cytoplasmic. hSP mRNA was demonstrable in surface epithelium of incomplete- but not complete-type intestinal (specialized) metaplasia. Deep glands with morphological features of pyloric glands/ulcer-associated cell lineage (UACL) typically contained only hSP peptide and its mRNA. In three biopsies containing specialized epithelium, small foci morphologically identical to true small intestinal surface epithelium were seen in which only pS2 mRNA and peptide were found and then only in rare goblet cells. Neither squamous epithelium nor oesophageal glands contained demonstrable pS2/hSP mRNA or peptide. The function of these proteins in the metaplastic mucosa of Barrett's oesophagus is unknown but they may reflect an epithelium responding to repeated insult. Their localization facilitates definition of the disparate epithelium types seen in this portion of the gut, with both native gastric and intestinal epithelia, and may help to pinpoint high-risk epithelium in Barrett's oesophagus, a potentially preneoplastic condition.

Barrett Esophagus↗
PubMedDate not supplied

Expression of p185erbB2 and p21ras in carcinoma, dysplasia, and intestinal metaplasia of the stomach: an immunohistochemical and in situ hybridization study.

The expression of p185erbB2 and p21ras was determined immunohistochemically in normal mucosa, intestinal metaplasia, dysplasia and in intestinal and diffuse type carcinoma of the stomach. The positive rates of p185erbB2 and p21ras in intestinal type were significantly higher than those of diffuse-type carcinoma. The results indicate that there are differences not only in clinical and biologic features, but also in molecular abnormalities between the two types of stomach cancer. Positive staining of cell membrane for p185erbB2 was observed specifically in intestinal type cancer, but not in the other lesions. Positive expression of p185erbB2 on the cell membrane appears to be a useful marker in identification of malignant change of gastric mucosa, as well as a late event of gastrocarcinogenesis. The results of in situ hybridization analysis in cancer tissues were consistent with those obtained by immunohistochemistry and demonstrated amplification of erbB2 gene at the mRNA level. No significant difference of p21ras expression was found among intestinal metaplasia, dysplasia, and intestinal type carcinoma; therefore, it might not be a specific marker of malignancy in gastric mucosa. Expression of p21ras may be an early event in the development of lesions predisposing to carcinoma.

Animals↗
PubMed1981

Falx myeloid metaplasia in myelofibrosis. A CT demonstration.

Myelofibrosis, known also as myelosclerosis, tends to form myeloid metaplasia in all organs of the body. The nervous system and intracranial structures are rarely involved. A case of myeloid metaplasia in the falx, which caused headache and papilledema, was observed gaining in size on repeated CT scans.

Adult↗
PubMed1981

The mucin profiles of normal gastric mucosa, intestinal metaplasia and its variants and gastric carcinoma.

Human gastrectomy specimens, including 48 carcinomas and 25 selected benign cases showing extensive intestinal metaplasia (IM), were examined in detail histologically and histochemically. IM was classified into complete (type I), incomplete without sulphomucins (type IIA) and incomplete with sulphomucins (type IIB). Type IIB was associated with 'intestinal' but not 'diffuse' cancers (P less than 0.01) or benign lesions (P less than 0.01). The mucin profiles of IIB IM were similar to 'intestinal' cancers with sulphomucins predominating over N-acetylsialomucins. O-acetylsialomucins were not seen in IIB IM or tumours but were observed in complete or type I IM. These findings suggest a histogenic link between incomplete IM secreting sulphomucins (or 'colonic' metaplasia) and 'intestinal' cancers of the human stomach.

Epithelial Cells↗
PubMed2002

Gastric-type adenocarcinoma of the duodenal second portion histogenetically associated with hyperplasia and gastric-foveolar metaplasia of Brunner's glands.

We report a case of a pedunculated polyp with a focus of gastric-type adenocarcinoma arising in the opposite side of the papilla Vater of the duodenal second portion. The carcinoma was surrounded by lobules of hyperplastic Brunner's glands. Immunohistochemically the carcinoma tissue showed both gastric foveolar-type mucin ( MUC5AC) and pyloric/Brunner's gland-type mucin ( MUC6), in which proliferating cells positive for MIB-1 (Ki-67) were scattered diffusely. Most of the hyperplastic Brunner's glands were positive for MUC6, while cells toward the lumen in the superficial layer were positive for MUC5AC and MIB-1. This directional pattern of differentiation of Brunner's glands has recently been demonstrated by our group in the histogenetic course of gastric metaplasia originating directly from Brunner's glands. Therefore the present carcinoma is thought to have developed under induction of gastric-foveolar differentiation in a manner very similar to that of gastric metaplasia in hyperplastic Brunner's glands.

Adenocarcinoma↗
PubMed2003

Metastatic papillary thyroid carcinoma of the submandibular lymph nodes with extensive squamous metaplasia: report of a case.

We report a unique case of metastatic papillary thyroid carcinoma of the submandibular lymph nodes with extensive squamous metaplasia. A 48-year-old man was referred to our hospital for treatment of a thyroid tumor and right submandibular masses. A tumor, 2 cm in its largest dimension, was palpated in the right lobe of the thyroid gland. The masses in the submandibular region measured up to 3 cm in diameter. Each submandibular tumor had a cystic cavity containing slightly opaque fluid. Aspiration cytology of the thyroid established a diagnosis of papillary carcinoma. Aspirated material from the cystic cavity of one of the submandibular masses contained only keratinized material with a thyroglobulin level of 175 ng/ml. The patient underwent a total thyroidectomy with modified radical neck dissection. Microscopic examination of the resected specimen confirmed a diagnosis of papillary carcinoma of the thyroid, as well as well-differentiated squamous cell carcinoma with cystic changes in the submandibular lymph nodes. Focal immunoreactivity for thyroglobulin, combined with the absence of any other possible primary lesions in the head and neck region, suggested metastatic papillary thyroid carcinoma of the submandibular lymph nodes with extensive squamous metaplasia.

Carcinoma, Papillary↗
PubMed1987

Massive hepatomegaly following splenectomy for myeloid metaplasia. Case report and review of the literature.

Massive compensatory hepatic myeloid metaplasia occurs infrequently after splenectomy for myeloid metaplasia, and it usually develops gradually over several years if it does occur. In this report, a patient is described in whom massive hepatomegaly and evidence of portal hypertension developed within three months of splenectomy. Early evidence for rapid hepatic growth was present at a second laparotomy three weeks after the first surgery, and probably should have triggered initiation of chemotherapy. Indications for splenectomy in these patients, surgical morbidity, and response to splenectomy are discussed.

Hepatomegaly↗
PubMed1987

Agnogenic myeloid metaplasia, portal hypertension, and sinusoidal abnormalities.

A patient with agnogenic myeloid metaplasia suffered from gastrointestinal bleeding due to ruptured esophageal varices. The portal vein and its intrahepatic branches were patent. Except for the presence of myeloid cells, mainly megakaryocytes, in the sinusoids, liver histology was more or less normal. However, on Sirius red staining there was marked perisinusoidal fibrosis. In addition to numerous collagen bundles in the Disse space, electron microscopy also revealed the presence of hemopoietic cells, the transformation of perisinusoidal cells into fibroblasticlike or myofibroblasticlike cells, or both, and fragmentary deposits of basement membrane-like material. In the pathogenesis of sinusoidal hypertension as it occurs in agnogenic myeloid metaplasia, all the factors mentioned above should probably be taken into consideration.

Biopsy, Needle↗
PubMed1987

Isochromosome 17q in a case of myelofibrosis with myeloid metaplasia terminating in blastic transformation.

A case of myelofibrosis with myeloid metaplasia in a 61-year-old female patient is reported. Cytogenetic studies were performed using short-term culture without phytohemagglutinin. A chromosomal aberration of an isochromosome 17q, [i(17q)], was revealed in 88% of the metaphases of peripheral blood cells in the blastic phase. However, all metaphases of bone marrow cells in the chronic phase showed a normal karyotype. Furthermore, i(17q) was also observed in 10% of the metaphases of spleen cells examined 8 months before blastic transformation. In this case, therefore, the cells with i(17q) were associated with an abnormal clone of blastic transformation, with the abnormal clone originating in the spleen with myeloid metaplasia.

Aged↗