Selected immunohistochemical markers in stromal neoplasms of the gastrointestinal tract.

We studied immunohistochemical reactions to vimentin, desmin and protein S-100 in 43 cases of stromal tumors of the gastrointestinal tract. The material studied included: 1 esophageal tumor, 18 gastric tumors, 19 small intestinal tumors and 5 colonic tumors, classified in 13 cases as benign and in 30 cases as malignant neoplasms of various degree of malignancy. Mean age of the patients was 58.9 years. A positive reaction to vimentin was found in 37 cases, a negative reaction concerned an esophageal tumor, two benign tumors (gastric and small intestinal) and three malignant tumors (gastric and two small intestinal). A positive reaction to desmin was detected in an esophageal tumor and in nine gastric tumors. Only one benign small intestinal tumor and three benign colonic tumors showed a positive reaction to desmin. Protein S-100 was found in an esophageal tumor and in 7 out of 18 gastric tumors and in 12 out of 24 intestinal tumors. Coexpression of vimentin and desmin was found in 8 gastric tumors, only in one small intestinal tumor and in three colonic tumors. Three gastric tumors showing both these reactions were all benign. Coexpression of desmin and protein S-100 was found in 7 out of 43 tumors of the alimentary tract. In six cases these tumors were benign. Basing on the results we may say that the presence of these antigens reflects the degree of differentiation of gastrointestinal stromal tumors of the gastrointestinal tract, though it does not allow to choose unequivocally conclusions as to their histogenesis.

Coexpression of vimentin and desmin in gastric leiomyomas. An immunohistochemical study in paraffin sections.

The aim of the study was to evaluate the incidence of the reactions for vimentin and desmin in gastric leiomyomas routinely processed in formalin and embedded i paraffin. The material studied included four benign leiomyomas, seven malignant leiomyomas and three malignant epithelioid leiomyomas. A positive reaction to vimentin was found in 13 out 14 leiomyomas under study. The number of neoplastic cells showing vimentin expression was larger in malignant, especially epithelioid leiomyomas than in non-malignant leiomyomas. A positive reaction for desmin in neoplastic cells was found in 9 leiomyomas 64%. One non-malignant leiomyoma showed a moderate reaction. In the remaining eight cases the reaction was weak and occurred in single neoplastic cells. Coexpression of vimentin and desmin in neoplastic cells occurred in 8 out of 9 leiomyomas with a positive reaction for desmin. Coexpression of vimentin and desmin occurred also in the smooth muscle cells of blood vessels in all 14 cases. A weak reaction for desmin or its lack in the tumour cells of leiomyomas with its marked expression in the smooth muscle cells of the blood vessels and gastric wall outside the tumor points rather to a small number of desmin filaments in the neoplastic cells than to their destruction by fixation in formalin. The occurrence of the reaction to desmin only in a limited number of neoplastic cells questions the reliability of its use in the oligopiopsy material.

Morphometry of normal, regenerating and cancerous hepatocytes.

During the morphometric analysis of liver cell carcinomas arising in cirrhotic livers, the sizes and shapes of 2200 cancerous and 1800 regenerative hepatocytes were measured and compared to normal hepatocytes. The neoplastic population showed significantly higher polymorphism, nucleocytoplasmic ratio and the percentage of multinucleated cells, whereas the sizes of cancerous cells were the smallest. Values for regenerative cells were mainly between those of neoplastic and normal cells. The exception was constituted by the group of very large regenerative cells which met the criteria of large liver cell dysplasia (LLCD). Low nucleocytoplasmic ratio achieved by these cells is consistent with the hypothesis of regenerative character of LLCD.

Prostaglandin protection of carbon tetrachloride-induced liver cell necrosis in the rat.

We studied whether 16,16--dimethyl prostaglandin E2 (dmPGE2) may prevent acute liver damage induced by carbon tetrachloride (CCl4) in the rat. One hundred thirty male rats were divided into the following groups: (1) controls, (2) rats given CCl4 6670 mg/kg body wt subcutaneously, (3) rats pretreated with 5 micrograms/kg dmPGE2 given subcutaneously 30 min before, and 8 and 24 h after CCl4 administration, and (4) animals given dmPGE2 only as in group 3. Liver damage was assessed by biochemical studies (SGPT, serum alkaline phosphatase, and bilirubin) and by histology. In rats receiving CCl4 alone, SGPT activities were significantly elevated to 1024 +/- 82 U/L, 1270 +/- 120 U/L, 386 +/- 48 U/L and 208 +/- 20 U/L at 24, 48, 96, and 120 h after CCl4 respectively. In animals pretreated with dmPGE2 before CCl4, SGPT activities were 201 +/- 24 U/L, 55 +/- 4.6 U/L, 28 +/- 4 U/L, and 24 +/- 4 U/L at 24, 48, 96, and 120 h after CCl4, respectively (p less than 0.01, versus animals receiving CCl4 only). Histologically, livers of rats treated with CCl4 alone showed severe centrilobular necrosis at 24 and 48 h. Livers of animals pretreated with dmPGE2 before CCl4 did not show necrosis. It is concluded that dmPGE2 protects the liver against cell necrosis induced by CCl4 in the rat.

Cytoprotective effect of 16, 16' dimethyl prostaglandin E2 and some drugs on an acute galactosamine induced liver damage in rat.

Present experiment was aimed to study whether 16, 16' dimethylprostaglandin E2 (dmPGE2), Hepatofalk (HF), or Orotofalk (OF) may prevent an acute liver damage induced in rats with D-galactosamine (GalN). Fifty male rats were divided into 5 groups: 1. controls, 2. rats receiving GalN 750 mg/kg b. w. intraperitoneally, 3. animals pretreated with 5 microgram/kg dmPGE2 given subcutaneously 24 hours prior to, 30 min prior to and 6 hours after GalN. Rats of group 4 received HF 0,8 ml/kg intramuscularly and group 5 OF 0,3 caps/kg intragastrically 24 hours prior to, 30 min prior to and 6 hours after GalN. Animals were sacrificed 24 hours after GalN injection. Histological, histochemical and ultrastructural studies of the liver were performed. In rats receiving GalN alone (group 2) typical severe liver damage consisting of acidophilic necrosis of hepatocytes, periportal and intralobular inflammatory infiltration, hypertrophy and hyperplasia of Browicz-Kupffer cells has been observed. Histochemical investigations showed in this group fatty degeneration and a decrease in glycogen content in hepatocytes, irregular distribution of lysosomes, numerous cytolysosomes and uneven decrease in lysosomal enzymes activity (acid phosphatase and beta-glucuronidase). Ultrastructural studies revealed depletion in glycogen, fat droplets, hypertrophy of smooth endoplasmic reticulum and numerous autophagic vacuoles. Some of these vacuoles or residual bodies were dropping out into intercellular space. Focal accumulation of lamellar cytomembranes as well as condensation of heterochromatin in nuclei were also observed. Pretreatment of animals with dmPGE2 (group 3), HF (group 4) or OF (group 5) prior to GalN prevented liver cell necrosis. Histological, histochemical and ultrastructural picture of the liver was in these groups close to normal. Only very slight hypertrophy and hyperplasia of Browicz-Kupffer cells, was seen as well as depletion of glycogen and hypertrophy of smooth endoplasmic reticulum in hepatocytes. We conclude dmPGE2, HF and OF offered impressive cytoprotection against GalN induced liver damage in rat.

Obstruction of a ureter by isolated primary focal amyloidosis.

A rare case of obstruction of the pelvic segment of the ureter by an isolated focus of primary amyloidosis is described. The operation consisted of resection of the constricted segment of the ureter and end-to-end anastomosis, with very good early and late results. The differential diagnosis and therapy of this type of ureteral obstruction are discussed.