Biomedical subjects
Publications and source records attributed to B Stamm.
The first two cases reported in the literature of patients with immune-mediated type A gastritis with microcarcinoids (as part of a polyglandular syndrome type II in one) in combination with chronic glomerulonephritis are presented. Immune-mediated type A gastritis appears to be another immunologic disorder that can be associated with chronic glomerulonephritis.
The solid and cystic tumor of the pancreas (also called pancreatic cystic tumor of the pancreas) is a very rare tumor of the pancreas, which we meet mainly in younger women. The tumor was described for the first time in 1981 and since that time there were published more than 150 cases. It is a matter of a potentially malign tumor with low malign characteristics. By radical exstirpation most of the patients can be healed definitely. Long-term controls are yet necessary although recidives are rare (4-7%), but are described up to 10 years after the first treatment. Also singular cases with synchronous metastasis of the liver are mentioned. Except of abdominal volume increase the tumor gives little trouble. The diagnosis is placed with ultrasonography resp. with a computer-tomogram and ensured by needle cytology. The therapy consists in the radical exstirpation with resection of the left pancreas in case of location on the left side, with Whipple operation in case of localisation in the head of the pancreas.
In a series of 22 pancreatic acinar cell carcinomas, including two acinar cystadenocarcinomas, cellular differentiation was analyzed by immunocytochemistry and electron microscopy. In addition, overexpression of p53 protein and Ki-ras codon 12 mutation was studied. Four of the 20 noncystic acinar cell carcinomas showed a pure acinar pattern, nine an acinar-solid, and seven a solid pattern. All tumors stained for at least one of the following pancreatic acinar markers: trypsin (21 of 22), lipase (19 of 22), chymotrypsin (13 of 22), phospholipase A2 (nine of 22), and pancreatic stone protein (19 of 22). One-third of the tumors expressed neuroendocrine markers (synaptophysin, eight of 22; chromogranin A, six of 21) and duct cell markers (CA19.9, nine of 21; B72.3, six of 21). Cellular coexpression of trypsin and synaptophysin was demonstrated in one tumor. Electron microscopy revealed zymogen granules (nine of nine). In only one of 16 tumors a Ki-ras mutation at codon 12 was found, whereas in none of 19 tumors could overexpression of p53 protein be demonstrated. The results suggest that acinar cell carcinomas show obvious capacity to differentiate into several directions, but nevertheless constitute an entity different from ductal adenocarcinomas or endocrine tumors.
A case of a 67-year old woman with adenosarcoma of the uterus is reported. Adenosarcoma is a mixed mesodermal tumour with a low malignant potential. It is characterised by a benign glandular and a malignant stromal component. Adenosarcomas are usually treated by hysterectomy with bilateral salpingo-oophorectomy. Patients with myometrial invasion have an increased risk of recurrence. It may be appropriate, to consider adjuvant chemotherapy or radiation treatment for these patients.
The lectin Amaranthin has been shown to be highly specific for the galactose beta 1,3 N-acetylgalactosamine-alpha and sialic acid alpha 2,3 galactose beta 1,3 N-acetylgalactosamine-alpha sequence which represents the Thomsen-Friedenreich (T) antigen and its cryptic form, respectively. Previously, we demonstrated the usefulness of gold-labeled Amaranthin for the histochemical detection of the T antigen and its cryptic form. Application of the galactose oxidase (GO)-Schiff sequence abolished lectin binding to the T antigen but not its cryptic form, and therefore permitted their differentiation. In the present study we have analyzed by light and electron microscopy the distribution and subcellular localization of Amaranthin binding sites in normal, dysplastic and neoplastic colonic epithelium. Furthermore, a monoclonal antibody raised against synthetic galactose bera 1,3 N-acetylgalactosamine-alpha-bovine serum albumin was applied as a reagent for the T antigen. In normal colonic mucosa, two different Amaranthin staining patterns existed: (a) reactivity restricted to the lower portion of the crypts which was principally observed in the left colon, and (b) reactivity along the entire length of the crypts and in the surface epithelium with goblet cell staining in the upper portion of the crypts which was principally observed in the right colon. This Amaranthin staining was resistant to GO-Schiff treatment. No immunostaining with the monoclonal anti-T antigen was observed. Investigation of transitional mucosa, adenocarcinomas of different degrees of differentiation and mucinous carcinomas as well as adenomas with different degrees of dysplasia all revealed positive Amaranthin staining. The lectin staining was resistant to GO-Schiff treatment, and immunolabeling with the monoclonal antibody against the T antigen was absent. These results indicate that only the cryptic form of the T antigen is expressed in normal, dysplastic and neoplastic human colonic epithelium.
Specimens from the pancreas and duodenum of 26 patients with sporadic Zollinger-Ellison syndrome (ZES) and 18 patients with multiple endocrine neoplasia type 1 (MEN-1) and hypergastrinemia (17 with ZES) were screened immunocytochemically for gastrinomas. Location, size, multicentricity, and malignancy of the gastrinomas were evaluated. The MEN-1 patients had gastrinomas in the duodenum (nine of 18), pancreas (one of 18), and periduodenal lymph nodes (two of 18). No gastrinoma was identified in six patients. Most duodenal gastrinomas were multiple (five of nine) and smaller than 0.6 cm (six of nine). Lymph node metastases were present in eight of 12 patients. All 26 patients with sporadic ZES had a solitary gastrinoma; 14 were found in the pancreas and had a diameter greater than 2 cm. Ten patients had a duodenal gastrinoma, two with a diameter less than 0.6 cm. In two patients, only periduodenal "lymph node gastrinomas" were detected. Eighteen of the sporadic gastrinomas were malignant. These results suggest that duodenal location and multicentricity of gastrinomas are associated with the MEN-1 syndrome, and solitary gastrinomas, either in the pancreas or the duodenum, are predominantly seen in sporadic ZES.
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Increased sialylation of cell surface glycoconjugates has been demonstrated in malignant tumors and shown to be correlated with the invasive and metastatic growth of colon carcinoma cells. The authors have applied the Maackia amurensis lectin, which interacts with alpha 2,3-linked sialic acid, and the Sambucus nigra I lectin specific for alpha 2,6-linked sialic acid. In human colon, alpha 2,3-linked sialic acid was detectable in normal and transitional mucosa as well as in adenomas with different degrees of dysplasia and in carcinoma. In contrast, alpha 2,6-linked sialic acid as visualized with Sambucus nigra I lectin was found only in severe dysplasia and carcinoma. Thus expression of binding sites for Sambucus nigra I lectin was associated with the occurrence of histologic features of malignancy. It is concluded that malignant transformation in human colonic epithelium is accompanied by the de novo expression of an alpha 2,6 sialyl-transferase. These findings provide the basis for more detailed studies of the possible role of cell surface glycoconjugates bearing alpha 2,6-linked sialic acid in growth behavior of human colonic epithelial cells.
We describe a patient with an aneurysmatic dilatation of the hepatic artery feeding a giant cavernous hemangioma. The 51-years-old man presented with massive gastrointestinal hemorrhage due to chronic rupture of the aneurysm into the pancreatic duct. The patient died 25 days after resection of the aneurysm in liver failure and septic shock. We think that this cavernous hemangioma was responsible for a high blood flow within the hepatic artery for many years. This high blood flow caused the degenerative alterations in the wall of the artery, resulting in aneurysm formation and rupture. This is the first case mentioned in literature with rupture of a hepatic aneurysm generated by high blood flow.
The effects of extracorporeal spark-gap shockwave lithotripsy (ESWL) on human gallbladder-morphology are barely known. We studied the gallbladders of nine patients cholecystectomized 5 to 166 days after ESWL. Patients were treated one to three times receiving a mean of 1928 +/- 693 shockwaves per treatment, with a total of 3375 +/- 1307 per patient. Control gallbladders were of randomly selected patients after plain cholecystectomy (age and sex-matched). There was no difference in pathomorphology of the two groups. No signs of trauma related damage (hemorrhage, necrosis, ulceration, scar, or hemosiderin deposits) other than from surgical manipulation were found. Predominant pathomorphological changes were signs of chronic cholecystitis due to gallstone disease. In conclusion, spark-gap ESWL did not induce deleterious morphological damage to the gallbladder, although large numbers of shock waves were applied.
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The Gastrointestinal Pathology Study Group of the German Pathological Society has drawn up a proposal for a unifying nomenclature for the graduation and classification of gastritis. The severity of chronic gastritis is divided into 4 grades (minimal, light, moderate and severe) and the activity of the process is characterized by 3 grades (grade 1, 2 and 3 activity). In addition, the presence or absence of Helicobacter pylori (formerly Campylobacter pylori), the extent and type of intestinal metaplasia, and the degree of glandular atrophy are recorded. To the two already well established types of gastritis (type A and type B) a third type is added, type C gastritis due to biliary reflux or other chemical, mechanical or toxic influences.
The pathology of insulinoma and gastrinoma was studied in 81 patients (31 men, 50 women, mean age 48.4 years) suffering from persistent hyperinsulinaemic hypoglycaemia, and in 44 patients (28 men, 16 women, mean age 48.5 years) with Zollinger-Ellison syndrome. Insulinomas were seen in the pancreas of all patients with persistent hyperinsulinaemic hypoglycaemia. In 70 of the 81 patients the insulinoma was solitary, whereas six patients had multiple insulinomas. In five patients with multiple endocrine neoplasia type I, multiple endocrine tumours of the pancreas were visible, only one of them in each case being an insulinoma. 75% of all insulinomas were less than 2 cm in size and 15% were malignant. 18 of the 44 Zollinger-Ellison syndrome patients also had multiple endocrine neoplasia type I. Nine of these patients presented with duodenal gastrinomas which were often multiple and smaller than 0.5 cm. The gastrinoma was located in the pancreas of one of the patients with multiple endocrine neoplasia, in two patients in lymph nodes, and no gastrinoma was identified in the specimens from six patients. 33% of the duodenal gastrinomas had metastasised. Solitary gastrinomas were found in all 26 patients with sporadic Zollinger-Ellison syndrome, 14 being located in the pancreas (diameter over 2 cm in eight cases) and ten in the duodenum (diameter less than 1 cm in seven cases). 16 of these gastrinomas were malignant.
In patients with multiple endocrine neoplasia type 1 (MEN-1), gastrinomas are common and thought to occur predominantly in the pancreas. We describe eight patients with MEN-1 and hypergastrinemia (seven with the Zollinger-Ellison syndrome) in whom we searched for neuroendocrine tumors in the pancreas and duodenum. Tumors were found in the proximal duodenum in all eight patients: solitary tumors (diameter, 6 to 20 mm) in three patients and multiple microtumors (diameter, 2 to 6 mm) in the other five. Paraduodenal lymph-node metastases were detected in four patients. Immunocytochemical analysis revealed the presence of gastrin in all the duodenal tumors and in their lymph-node metastases. In contrast, no immunoreactivity for gastrin was present in the endocrine tumors found in the seven pancreatic specimens available for study, except for one tumor with scattered gastrin-positive cells. In four of the six patients whose duodenal gastrinomas were removed, serum gastrin levels returned to normal; in the other two patients gastrin concentrations decreased toward normal. We conclude that in patients with MEN-1 and the Zollinger-Ellison syndrome, gastrinomas occur in the duodenum, but the tumors may be so small that they escape detection.
Data are reported to demonstrate the usefulness of a monoclonal anti-polysialic acid antibody for (i) the visualization of immature and mature neural elements in human teratomas, and (ii) the distinction of small cell lung carcinoma from bronchial carcinoids as well as squamous cell and adenocarcinomas of the lung. Lectins which discriminate between the various types of sialylated sequences, such as the Sambucus nigra L. I lectin specific for Neu5Ac alpha 2,6 Gal/GalNAc and the leukoagglutinin from Maackia amurensis (MAL) specific for Neu5Ac alpha 2,3 Gal beta 1,4 GlcNAc have been applied to the study of human colonic mucosa. The Neu5Ac alpha 2,3 Gal beta 1,4 GlcNAc sequence was detectable in normal and transitional mucosa and carcinomas, whereas the Neu5Ac alpha 2,6 Gal/GalNAc sequence was found in carcinomas. The lectin Amaranthin reacts with Gal beta 1,3 GalNAc-alpha (the T antigen) and NeuAc alpha 2,3 Gal beta 1,3 GalNAc-alpha (the cryptic T antigen). It stained normal and transitional colonic mucosa as well as carcinoma. The reactivity was solely due to the cryptic T antigen and indicates that the T antigen may not represent a general carcinoma autoantigen.
Campylobacter pylori (C.p.) infection is often found in patients with antral gastritis and peptic ulcer disease. Pathophysiological links are still unclear, and we therefore tested the hypothesis whether C.p. affects the gastrointestinal peptides and thus influences gastric acid secretion and protective factors. 94 patients were examined by upper GI endoscopy and blood analyzed for gastrin, somatostatin, pancreatic polypeptide and neurotensin. Biopsies of antral mucosa were investigated for C.p. in urease testing, culture and microscopy. C.p. was found in 42 patients (45%). In microscopy all of these patients had chronic gastritis (100%). A significant increase in gastrin uninfluenced by C.p. was found in patients with antral gastritis (normal: 6.4 +/- 0.7, [n = 27]; gastritis without C.p.: 18.4 +/- 5.9 [p less than 0.02], [n = 7]; gastritis with C.p.: 10.7 +/- 2.2, [n = 22]). Somatostatin, pancreatic polypeptide and neurotensin showed no difference.
Eight patients with stomach cancer are described who had also a striking glandular hyperplasia of the fundic mucosa adjacent and remote from the tumor. Five of the eight patients were young women (30 to 37 years of age). The tumors were poorly differentiated carcinomas and six of the eight patients have died of their disease. None of the patients had clinical evidence of endocrine dysfunction including the Zollinger-Ellison syndrome. Immunohistochemistry revealed cells with endocrine differentiation in five of eight tumors, and in two tumors gastrin producing cells were found. Five of seven patients showed increased numbers of antral G-cells. In two patients numerous endocrine (chromogranin-positive) cells were present in the fundic mucosa, specific products of which could not be identified with the antigens tested. No satisfactory explanation exists for this coincidence and its apparent predominance in young female patients. It may be that endocrine substances are responsible for this fundic hyperplasia and that they may also act as promotors of tumor growth.
A 43 year old man is presented who suffered from the association of a toxic adenoma of the thyroid gland and a Zollinger-Ellison syndrome (ZES) due to a metastasizing duodenal gastrinoma. There were no other signs of a multiple endocrine neoplasia syndrome, type I (MEN-I). The patient presented here shows that the association of ZES and thyroid disease may also occur in patients with sporadic ZES.