Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mean fasting levels of pancreatic polypeptide (PP) in 24 patients with Zollinger-Ellison syndrome (ZES) and in 12 patients with hyperparathyroidism originating from families with multiple endocrine adenomatosis type I (MEAI-HPT) were significantly higher than in 72 normal controls. The overlap between the 3 groups, however, was large. In patients with ZES, increased PP levels were not related to the presence of MEAI or metastases; nor was there a correlation between serum PP and gastrin concentrations. The post-prandial PP release in 10 ZES patients and in 10 patients with MEAI-HPT was lower than in 9 normal controls. The physiological significance of the present findings is unclear.
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PMID:Serum levels of pancreatic polypeptide in Zollinger-Ellison syndrome, and hyperparthyroidism from families with multiple endocrine adenomatosis type I. 3 34

The importance of scintigrpahy in the diagnosis of liver and spleen tumors is well known. There is, however, up to this time only poor information regarding the use of scintigraphy in follow up studies in patients with liver and spleen metastases undergoing cytostatic therapy. We had the opportunity to investigate 30 patients in whom Hodgkin's disease, Zollinger-Ellison syndrome, ovarian, breast or bronchial and GI malignancy was confirmed by histology. The scintigraphic examinations were performed by means of a scintillation camera using 99mTc sulfur colloid as radiotracer. In each case, three views of the organ were recorded firstly prior to therapy and (at least) once again during or after therapy respectively. The results of liver and spleen scintigraphy were compared with clinical findings, laboratory tests, laparoscopy and histopathology. In 13 of our patients, diminution of metastases was detected. In one patient an increase of the size of the tumors was seen after temporary improvement. In 8 patients, there was no change of the metastatic pattern after cytostatic therapy. 6 patients showed an increase of liver metastases under therapy. Two patients with normal liver scintigraphy in whom clinical and laboratory findings indicated liver involvement yielded no evidence of metastasis at autopsy. In 13 cases, the diagnosis of liver metastasis was detected earlier by scintigraphy than by laboratory tests.
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PMID:[Scintigraphic follow-up of patients with liver and spleen metastases undergoing cytotoxic therapy (author's transl)]. 9 40

Twelve patients with Zollinger-Ellison syndrome and one patient with WDHA syndrome are reviewed. Three of the Z-E patients exhibited MEA, two having hyperinsulinism and one hyperparathyroidism. Ages ranged from nine to 71 years. Diagnosis of Z-E syndrome was established from history, gastric acid secretion, radiologic studies, serum gastrin measurements and from actual tissue biopsy in 10 of the 12 patients. Total gastrectomy was performed in 8 of the 12 Z-E patients, with abolition of the ulcer diathesis in all. However, in none of our patients was there objective evidence of subsequent tumor regression. Three patients remain alive. Four died of tumor, one from post-total gastrectomy complications, one from post-subtotal gastrectomy in another hospital, two from ulcer hemorrhage, and one from electrolyte imbalance with autopsy diagnosis of Z-E tumor. A patient is recorded in detail who exhibited both hyperinsulinemia and hypergastrinemia from a malignant islet cell tumor, had the tumor "debulked" four times over a 14 year period and whose hepatic metastases were temporarily abolished by streptozotocin infusion. The question is raised regarding relationships between chronic organic hyperinsulinism and subsequent hypergastrinemia.
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PMID:Zollinger-Ellison syndrome: special considerations. 14 Jun 31

The article discusses the y-ray diagnosis of the Zollinger-Ellison syndrome, including 13 with multiple endocrine adenomatosis, Type I. This syndrome is governed by complex pathophysiological processes determining the x-ray symptoms. Besides the predisposition to ulcers, which will persist despite partial gastrectomy, changes at the duodenum (hypertrophy of Brunner's glands) and proximal jejunum (bulging of folds) are relatively typical. However, the final diagnosis of the Zollinger-Ellison syndrome is a clinical one. The syndrome is caused by non-beta islet cell tumors of the pancreas, associated with hypergastrinemia. Since these tumors are often multiple and small, angiography is not very rewarding. It is frequently impossible to distinguish the benign from the malignant tumors on the grounds of histological findings, the only criterion being their biological behaviour, if the exclusion or identification of metastases.
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PMID:[The radiological diagnosis of the Zollinger-Ellison syndrome (author's transl)]. 15 Oct 8

According to the authors' findings malignant forms of ulcerogenic tumors of the pancreas in the Zollinger-Ellison syndrome clinically show a relatively favourable course in oncological aspect. As a rule, patients die from complications of peptic ulcer before a progressive tumor growth or its metastases result in mortality. Therefore, in cases when the routine radical operators prove to be unfeasible, it is recommended to perform surgery for the purpose of liquidating ulcer and conditions for its recurrence.
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PMID:[Surgical tactics in malignant forms of ulcerogenic tumors of the pancreas]. 17 19

A 35-year-old man with the Zollinger-Ellison syndrome who is alive and well 20 years following diagnosis at age 15, is represented. At the initial operation for a bleeding duodenal ulcer a ZE tumor of the pancreas also was excised. After two additional ineffective ulcer operations, total gastrectomy was performed. At that time, retroperitoneal and peripancreatic metastases were noted, and several were removed. Three years later at laparotomy, extensive hepatic metastases were biopsied as well. Spontaneous remission occurred and when re-explored at age 34, after 14 years, no metastases were identifiable in any area. The serum gastrin level has remained elevated, casting doubt upon its value as a criterion for evaluation of tumor recurrence or activity. Other additional interesting aspects are discussed. The importance of elimination of the acid-secreting cells by total gastrectomy is emphasized. The patient remains well.
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PMID:Zollinger-Ellison syndrome. Spontaneous regression of advanced intra-abdominal metastases with 20 year survival. 44 14

Gastrinomas were localized by concurrent blood sampling in the hepatic vein and portal vein tributaries in 10 of 12 Zollinger-Ellison patients. In one patient, the portal vein could not be catheterized; in the other, a gastrin gradient could not be picked up in either of two examinations. Six of the patients were subsequently operated upon: 5 had pancreatoduodenal resection and 1 had laparotomy at which metastases were found. Four of the resections were probably curative as the patients have done well without treatment since with concentrations of gastrin in serum near zero. The observation period ranges from 17 to 20 mo. It is concluded that transhepatic catheterization of the hepatic vein and portal vein tributaries with blood sampling for gastrin determination permit the verification of the Zollinger-Ellison diagnosis and the localization of the gastrinomas. The latter may lead to the selection of a curative operative treatment in some of the patients.
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PMID:Localization of gastrinomas by transhepatic portal catheterization and gastrin assay. 45 40

With better methods of diagnosis, patients will be identified earlier in the course of their disease and will often have atypical and borderline manifestations of the syndrome. Serum gastrin measurements with calcium and especially with secretin challenge will be the most important method of diagnosis. Any patient with acid hypersecretion who has a high serum gastrin level that does higher on secretin infusion should be considered to have the Zollinger-Ellison syndrome. A firm diagnosis of the Zollinger-Ellison syndrome should be made, if at all possible, prior to operation. At operation, a thorough search of the pancreas, duodenum, stomach, greater and lesser omentum and liver should be made for primary and secondary gastrinomas. If the preoperative data firmly establish the diagnosis of the Zollinger-Ellison syndrome, a total gastrectomy should be carried out even if no primary tumor is found. Similarly, a total gastrectomy should be done even if there are massive hepatic metastases. If total gastrectomy is not performed, the patient is apt to die of complications of acid hypersecretion. The only possible exceptions to the rule of always performing a total gastrectomy are in asymptomatic patients with easily excisable tumors or patients with tumors of the duodenum that are easily excisable, providing that in both instances after the excision of the tumor the output of gastric acid as measured at operation is immediately halted. All possible metastatic tumor tissue should be removed. The more tumor tissue removed, the longer the patient will survive. Metastases should be treated aggressively. They do not disappear after total gastrectomy in our experience, and they may kill patients. Patients should be followed after operation with serial measurements of serum gastrin concentrations and by hepatic scintillation scans and hepatic angiography. If hepatic metastases develop, intrahepatic artery infusions of 5-fluorouracil may slow tumor growth.
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PMID:Natural history and experience with diagnosis and treatment of the Zollinger-Ellison syndrome. 114 7

The authors describe a case of osteoblastic metastasis in a patient with Zollinger-Ellison syndrome resulting from the presence of a pancreatic tumor, which they believe is the first such case documented. Following a total gastectomy for hyperacidity in a 53-year-old woman, a gradually enlarging liver was treated with steptozotocin. Radiation therapy to the areas of bony metastases resulted in complete alleviation of pain.
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PMID:Osteoblastic bone metastasis in Zollinger-Ellison syndrome. 124 75

Gastrinomas from 25 patients were examined by immunohistochemistry (IHC) and in situ hybridization histochemistry (ISH). Most patients (84%) presented with the Zollinger-Ellison syndrome. Six had multiple endocrine neoplasia type I (MEN-I). Twelve patients (48%) had duodenal primaries and 11 of 12 of these had metastases to regional lymph nodes and/or liver in spite of the small sizes of the primary tumors (mean size of 0.9 cm). Five patients had pancreatic gastrinomas and eight patients had metastatic tumor in regional lymph nodes or liver at surgery but a primary was not found. IHC and ISH analyses showed that all cases were positive for gastrin protein and 24 of 25 (96%) expressed gastrin mRNA that was easily detected in formalin-fixed, paraffin-embedded tissue sections. Both benign and malignant tumors expressed alpha subunit of human chorionic gonadotropin protein (alpha-HCG). However, only malignant gastrinomas (29%) expressed adrenocorticotropic hormone protein or proopiomelanocortin (POMC) mRNA. ISH and Northern hybridization analysis revealed that chromogranin A mRNA was the most common member of the chromogranin/secretogranin (Cg/Sg) family which was expressed in both benign and malignant gastrinomas. These results indicate that duodenal gastrinomas are common in both sporadic and MEN-1-associated cases, and small duodenal primaries may be associated with extensive regional lymph node and liver metastases. Expression of ACTH/POMC protein and mRNA was consistently associated only with malignant gastrinomas while gastrin protein, gastrin mRNA and Cgs/Sgs mRNAs were readily detected in both benign and malignant gastrinomas.
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PMID:Analysis of gastrinomas by immunohistochemistry and in situ hybridization histochemistry. 128 76


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