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Biomedical subjects

M Meybehm

Publications and source records attributed to M Meybehm.

15 recordsLinked to original sources
PubMed2001

Littoral cell angioma as a rare cause of splenomegaly.

A 58-year-old, otherwise healthy man presented with a sudden onset of watery diarrhea. A pseudomembranous colitis due to antibiotics was identified as the cause of the diarrhea. Enlargement of the spleen was detected during the evaluation. The enlarged, plump spleen (20 cm long, 7.1 cm wide) had multiple nodules that differed in size from 1 to 8 cm. Neither clinical nor other symptoms of an underlying malignant disease could be detected. Because the signs were of little diagnostic value we arranged a splenectomy, which showed a littoral cell angioma (LCA) to be the cause of splenomegaly. In addition to the case report, we have reviewed the literature, clinical manifestations, differential diagnosis, special gross and microscopic pathological findings, and the location of this benign vessel tumor in the pathology of the spleen.

Hemangioma↗
PubMed1998

[Splenic echinococcosis--a rare differential diagnosis in a cystic lesion of the spleen].

Cystic tumours of the spleen are generally rare and a parasitic origin is relatively improbable. Our case report, however, shows that in case of a splenic cyst, differential diagnosis must always consider the possibility of echinococcosis. We report on a patient suffering from a cystic lesion of the spleen where radiology yielded the final pointer to diagnosing an echinococcosis of the spleen.

Adult↗
PubMed1997

[Littoral cell angiosarcoma of the spleen. Morphologic, immunohistochemical findings and consideration of histogenesis of a rare splenic tumor].

A case of primary splenic angiosarcoma with involvement of two accessory spleens is presented. The tumor cells are immunoreactive for endothelial markers (CD 31, CD 34, factor VIII associated antigen) and express also histiocytic antigens (CD 68, lysozyme, Cat-hepsin D, alpha-1-antitrypsin, alpha-1-anti-chymotrypsin) as well as CD 8. This marker profile suggests that the presented angio-sarcoma originates from sinus cells with histiocytic and endothelial differentiation and may be regarded as the malignant variant of littoral cells angioma.

Aged↗
PubMed1997

Cholestasis associated with mesalazine therapy in a patient with Crohn's disease.

BACKGROUND/AIMS: Mesalazine is a widely prescribed medication, developed as an alternative to sulfasalazine in the treatment of inflammatory bowel disease. In contrast to sulfasalazine, there are only a few case reports on its causing hepatic injury. We here report on a patient with cholestasis after mesalazine therapy for Crohn's disease of the ileum. METHODS/RESULTS: The patient, a 30-year-old man, developed clinical signs of severe hepatic injury 4 months after treatment with mesalazine (4 g/day) including biopsy-proven hepatocellular cholestasis with minimal focal mononuclear inflammatory infiltration. Contrary to previous reports, no symptoms of generalized hypersensitivity were seen. The patient's illness was resolved by discontinuing the mesalazine treatment and he recovered completely in 40 days. CONCLUSIONS: This case reinforces the possibility of a causal relationship between mesalazine treatment and toxic hepatic injury without systemic hypersensitivity.

Adult↗
PubMed1997

Spiradenoma and dermal cylindroma: comparative immunohistochemical analysis and histogenetic considerations.

We carried out an immunohistochemical analysis of nine spiradenomas and seven cylindromas. Our findings underscore the histomorphological similarities of the two adnexal neoplasms-namely, the expression of S-100 protein ascribed to eccrine differentiation within the tubular and large, pale-staining cells of both entities. Human milk fat globulin (HMFG) and lysozyme, two markers associated with apocrine differentiation, are expressed by tubular cells in spiradenomas and cylindromas. Lysozyme is also expressed in cylindromas by large, pale-staining cells. In addition, antibodies to alpha-smooth muscle actin strongly characterized the small basaloid cells of both types of neoplasm. Both spiradenomas and cylindromas expressed identical cytokeratin patterns. As with the various regions of eccrine and apocrine units, the expression by spiradenomas and cylindromas of keratins 7, 8, and 18 indicates differentiation toward the secretory tissue, whereas the expression of keratin 14 in some of the neoplastic cells points toward ductal differentiation. Malformed ductal and glandular structures in continuity with evolving spiradenomas and cylindromas in two of our cases also suggest that these tumors might arise from abortive adenxal anlagen.

Actins↗
PubMed1996

[Libyan patient with chronic diarrhea].

A 22-year-old Libyan patient suffering from chronic diarrhea presented with an alpha-heavy chain paraprotein and a lympho-plasmacellular lymphoma infiltration of the duodenal mucosa. These findings supported the diagnosis of "immunoproliferative small intestinal disease" (IPSID). In this disease, that occurs almost solely in countries with low socioeconomic status, a diffuse infiltration of small intestinal mucosa by neoplastic lymphoid cells causes chronic malabsorption. About 65% of patients exhibit a paraprotein in serum, urine or jejunal juice that consists of the heavy chain of immunoglobulin A (alpha-heavy chain). In advanced stages, IPSID resembles histologically and clinically high grade lymphoma: some patients develop masses in the gut wall, an abdominal lymphadenopathy and involvement of other organs including bone marrow. The disease is believed to be triggered by a chronic infectious antigenic stimulus. Thus, in early stages in some patients cure may be achieved by antibiotic therapy alone. In advanced disease, chemotherapy including anthracyclins is necessary.

Adult↗
PubMed1995

[Hepatic neoductules].

Proliferation of preexisting bile ducts, ductular metaplasia of hepatocytes and proliferation and differentiation of liver stem cells are discussed in the pathogenesis of neoductular structures in the liver. Under the condition of experimental bile duct obstruction and in extrahepatic bile duct stenosis neoductular structures are first the result of proliferation and sprouting of preexisting ducts and cholangioles. Especially in later stages of cholestasis but also in other chronic progredient liver diseases such as chronic alcoholic liver disease and chronic active hepatitis periportal hepatocytes may show a phenotypic shift towards ductular epithelia. In postnatal liver diseases hepatocytes first express keratin 7 and later keratin 19 during ductular transdifferentiation. This is in contrast to embryonal cholangiogenesis. In alpha-1-antitrypsin-deficiency, hemochromatosis, Wilson's disease, and chronic active hepatitis B cellular deposites typically located in hepatocytes such as alpha-1-AT, siderin, copper, HBs-Ag, and HBc-Ag can also be found in neoductular cells close to hepatocytes. These deposites seem to be retained during the ductular transdifferentiation of hepatocytes. Expression of bile duct-type integrin subtypes and TGF beta 1 in neoductular cells are involved in the changing parenchymal/mesenchymal interplay during neoductogenesis, resulting in periductular basal membrane and periductular fibrosis. In FNH the ductular transdifferentiation of hepatocytes is integrated in the histogenesis of micronodules and portal tract equivalents of these tumor-like lesions. Ductular structures in hepatoblastomas and especially in combined hepatocellular and cholangiocarcinomas (CHCC) may reflect the common embryologic derivation of hepatocytes and biliary epithelia. Non-neoplastic liver tissue in resection specimens of our CHCC showed a lower rate of cirrhosis, and a significantly higher Ki 67-LI of neoductular cells compared to liver tissue in resection specimens of HCC and liver metastases. 3 of 10 CHCC had developed in alpha-1-AT-deficiency, in which this protease-inhibitor was predominantly retained in periportal hepatocytes. These findings in non-neoplastic tumor-bearing liver tissue suggest that CHCC include a special histogenic type of primary liver carcinoma which in analogy to some experimental liver tumors might develop from periportal parenchymal cells.

Animals↗
PubMed1993

Expression of HBs- and HBc-antigen in neoductular epithelium in chronic active hepatitis B. A further support for hepato-ductular metaplasia.

Biopsy specimens (n = 61) from patients with chronic active hepatitis B and progressive fibrosis (n = 61) were studied immunohistochemically to obtain information about the histogenesis of neoductules. All the biopsies contained clusters of oval-shaped cells often arranged in the form of neoductular aggregates. These expressed cytokeratins 7 and 19 which in the normal liver are found only in bile duct and ductular epithelium but not in hepatocytes. Using monoclonal and polyclonal antibodies both hepatocytes and these oval neoductular cells were found to express HBs- and HBc-antigen in 15% and 20% of the biopsies, respectively. Taking into consideration the strong hepatocytotropism of the hepatitis B virus, the expression of HBV-antigens in neoductular cells suggest their development from HBV-infected hepatocytes. Using proliferating cell nuclear antigen (PCNA) as a marker of cell proliferation positive staining was detected only in hepatocytes but not in neoductular cells. Taken together findings further support the concept of hepatoductular metaplasia in the histogenesis of so-called "proliferating" ductules. In general the data show that hepatitis B virus infection does not prevent hepatocytes from undergoing ductular metaplasia.

Bile Ducts, Intrahepatic↗
PubMed1992

[Cytomegalovirus infections of the gastrointestinal tract].

Histopathological findings in 8 cases of CMV infections of the gastrointestinal tract including 5 cases with AIDS are presented. The cytomegalic cells were irregularly distributed and were predominantly found in esophagus, small bowel and colon. Viral inclusions were detected in "stromal" cells and in endothelial cells, sometimes associated with lesions of the vascular wall. Cytomegalic smooth muscle cells and glandular epithelia were also observed. No correlation was found between the number of cytomegalic cells per mm2 of tissue and the inflammatory response. Monoclonal CMV antibodies reacted immunohistologically not only with cytomegalic cells but also with a few normally appearing cells. The in-situ-hybridization detected CMV-DNA also in cells which were negative for CMV antigens. Notwithstanding the new immunohistological techniques the searching for cytomegalic cells and their recognition still belong to the most important steps required for the diagnosis of CMV infection.

AIDS-Related Opportunistic Infections↗
PubMed1989

[Granulomatous colitis with pseudopolyp in schistosomiasis].

A 26-year-old Arab had epigastric pain and bloody mucous stools. At coloscopy distal proctitis and a polyp at the rectosigmoid junction were discovered. The polyp had granulomatous inflammatory changes and eggs of Schistosoma mansoni with a characteristic egg shell, central miracidium and lateral spine. Bilharziasis should be considered in the differential diagnosis of chronic inflammatory disease of the intestines.

Adult↗
PubMed1988

[Angiofollicular lymphatic hyperplasia with plasmacytoma and polyneuropathy: a case report with immunohistochemical study].

A rare case of a 43-year-old man with polyneuropathy, monoclonal gammopathy, myeloma and Castleman's disease of plasma cell type was diagnosed. Immunohistological examination of the lymph node with Castleman's disease showed polyclonal binding while the myeloma was monoclonal containing IgA with lambda-light chains. At the immunoelectrophoresis IgA/IgA paraprotein was demonstrated. The possible pathogenetical relationship between polyneuropathy and plasmacytoma as well as Castleman's disease will be discussed.

Adult↗