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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The small intestine is a well documented target organ in mouse and human GVHD, and diarrhea is a prominent part of the clinical GVHD syndrome. Although a plethora of systemic immune deficits has been documented in GVHD, the integrity of the small intestinal immune system has not been investigated. A correlation has not been demonstrated between systemic immune dysfuction and the incidence of lymphomas in mouse GVHD survivors. If gastrointestinal immune deficiency exists in mouse GVHD, its possible relationship to GVHD lymphomas, frequently abdominal. should be investigated. GVHD was produced in newborn BLA (C57 BL/Ka females x BALB-C males) mice house in a specific pathogen-free environment by the i.p. inoculation of 10(7) male BALB-C spleen cells. Control mice received syngeneic spleen cells. Twenty GVHD and 16 control mice were sacrificed at 3 weeks and specimens of duodenum were removed for routine histologic and immunofluorescent examination. All but one GVHD mouse (95%) had virtually absent duodenal IgA and IgM. Duodenal cellular fluorescence was demonstrated in all controls. A significant duodenal immunoglobulin deficit has been demonstrated in 3-week-old GVHD mice. The relationship of this finding to GVHD diarrhea, wasting, and neoplasia remains to be determined.
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PMID:Duodenal immunoglobulin deficiency in graft versus host disease (GVHD) mice. 0 29

The nutritional status of a cancer patient may be affected by the tumor, the chemotherapy and/or radiation therapy directed against the tumor, and by complications associated with that therapy. Chemotherapy-radiotherapy is not confined exclusively to malignant cell populations; thus, normal tissues may also be affected by the therapy and may contribute to specific nutritional problems. Impaired nutrition due to anorexia, mucositis, nausea, vomiting, and diarrhea may be dependent upon the specific chemotherapeutic agent, dose, or schedule utilized. Similar side effects from radiation therapy depend upon the dose, fractionation, and volume irradiated. When combined modality treatment is given the nutritional consequences may be magnified. Prospective, randomized clinical trials are underway to investigate the efficacy of nutritional support during chemotherapy-radiotherapy on tolerance to treatment, complications from treatment, and response rates to treatment. Preliminary results demonstrate that the administration of total parenteral nutrition is successful in maintaining weight during radiation therapy and chemotherapy, but that weight loss occurs after discontinuation of nutritional support. Thus, long-term evaluation is mandatory to learn the impact of nutritional support on survival, disease-free survival, and complication rates, as well as on the possible prevention of morbidity associated with aggressive chemotherapy-radiation therapy.
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PMID:Alterations of nutritional status: impact of chemotherapy and radiation therapy. 10 84

A sensitive and specific radioimmunoassay for the detection of vasoactive intestinal peptide has been used to study patients with the watery diarrhea syndrome. In eleven patients the syndrome was associated with tumors, and plasma levels of vasoactive intestinal peptide were elevated. VIP levels returned towards normal in five treated patients coincident with amelioration of symptoms. Normal values were obtained in patinets with chronic pancreatitis, sprue, medullary carcinoma, Zollinger-Ellison Syndrome and laxative abuse. In six other patients with indistinguishable syndrome and no findings of tumor at laparotomy and autopsy, vasoactive intestinal peptide levels were normal. The results suggest that VIP may be the causative agent in patients with the watery diarrhea syndrome and tumors, but that an indistinguishable syndrome exists for which VIP is not the cause.
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PMID:Vasoative intestinal peptide and the watery diarrhea syndrome. 14 46

Functioning tumors of the pancreatic islets are now recognized as the source of clinical syndromes affecting the gastrointestinal tract which have a wide variety of catastrophic symptoms. Experiences with thirty-six cases suggest at least four separate diagnostic categories in the ulcerogenic tumor syndrome. These include: a typical history, gastric analysis, and roentgenographic findings with boderline fasting serum gastrin levels; ulcerogenic tumor with evidence of hyperparathyroidism; iatrogenic ulcerogenic syndrome associated with failure of a previous operation for duodenal ulcer; and the classic ulcerogenic syndrome associated with a fulminating ulcer diathesis or diarrhea and high serum gastrin levels. The problems presented at operation include: decisions to be make in the presence of a negative exploration; the finding of a solitary tumor in the wall of the duodenum; solitary pancreatic tumors particularly in the body and tail; ulcerogenic tumors in the very young; liver metastases in the elderly; and the wisdom of removing gross metastases in combination with total gastrectomy. The long-term survival in the ulcerogenic tumor syndrome approximated 50 per cent, with 40 per cent of those having proved malignancy living five years. Evidence of hyperparathyroidism is relatively common in association with both the ulcerogenic and the diarrheogenic tumor syndromes. The association may by a result of a congenital abnormality, metabolic alkalosis, or a direct effect of the islet cell tumor. Parathyroidectomy may be indicated when both the serum calcium and parathormone levels are elevated in the presence of borderline fasting gastrin levels. The latter may return to normal after parathyroidectomy. The evidence of hyperparathyroidism closely parallels the episodes of diarrhea in the diarrheogenic syndrome, and hyperparathyroidism may regress spontaneously after total removal of the pancreatic tumor. Just as routine calcium determinations made the diagnosis of hyperparathyroidism more commonplace, it is suggested that the gastrointestinal syndromes associated with islet cell tumor would receive wider recognition if radioimmunoassays for gastrin as well as secretin, and the other secretin-like polypeptides, were carried out routinely.
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PMID:Islet cell tumors of the pancreas and the alimentary tract. 16 36

Thirteen patients with bile duct cancer (excluding gallbladder) and associated chronic ulcerative colitis (CUC) were seen at the Mayo Clinic from 1935 through 1973. Most patients had initial symptoms of severe diarrhea and bleeding, followed by a pattern of mild-to-moderate disease with exacerbations and remissions. Three patients had especially severe symptoms and underwent total colectomy (1 patient) or proctocolectomy (2 patients) an average of 15.7 years from onset of CUC symptoms. Anorexia, followed rapidly by the development of progressive jaundice (or a sudden deterioration when liver disease was already present), marked the onset of symptoms of bile duct cancer in the 13 patients. The overall mean duration from onset of CUC to development of symptoms of bile duct cancer was 19 years. The patients in whom colitis was managed by proctocolectomy or total abdominal colectomy developed symptoms of bile duct cancer an average of 9.4 years after colectomy. When cancer was diagnosed, the tumor had spread beyond the bile ducts in 10 patients. The tumors were difficult to identify and often infiltrated the hepatic hilus. The present series and review of the literature suggest that the relationship between CUC and bile duct cancer is more than a chance occurrence. The carcinoma has an onset approximately 3 decades earlier than does carcinoma of the bile ducts without CUC. Surgical removal of the diseased colon and mode of medical management of the unresected colon have no relationship to the subsequent development of carcinoma of the bile ducts; neither does the extent or severity of the colonic disease. The prognosis of carcinoma of the bile ducts unfortunately continues to be dismal.
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PMID:Cancer of the bile ducts associated with ulcerative colitis. 16 91

Three patients with profuse diarrhea, hypokalemia, metastatic nonbeta islet cell carcinoma, and the absence of gastric hypersecretion were found to have elevated levels of vasoactive intestinal peptide. One patient also had elevated serum gastrin levels. Two patients experienced prolonged remissions of diarrhea after operations in which only tumor biopsies were done. These cases further implicate vasoactive intestinal peptide as the agent mediating the diarrhea in the syndrome of pancreatic cholera.
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PMID:Islet cell carcinoma, pancreatic cholera, and vasoactive intestinal peptide. 17 21

A case of watery diarrhea, hypokalemia and hypercalcemia associated with an islet cell tumor was described. A 62-year old man exhibited frequent watery diarrhea and hypokalemia for two years. He had no peptic ulcer and serum gastrin level was normal. His serum calcium was abnormally high and serum phosphate was lowered. He had secretin-like activity in his plasma. Autopsy revealed a small islet cell tumor in the pancreas and several metastatic masses in the liver. Microscopic examination revealed the tumor cell was not beta, alpha nor D cells. By electron microscopy the secretion granules of the tumor cell resembled those of S, M and T cells. It was not possible to decide which of the tree cell types was responsible for the pancreatic cholera.
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PMID:A case of watery diarrhea, hypokalemia and hypercalcemia associated with nonulcerogenic islet cell tumor of the pancreas. 17 23

The combination of diarrhea with an islet cell tumor (Verner-Morrison Syndrome) is a clinical picture presenting many diagnostic problems. It is probable that larger numbers of cases will be encountered with more widespread knowledge of this disease. The clinical features and the pathologic-anatomical findings of two characteristic cases are reported and discussed.
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PMID:[Diarrhea and islet cell tumor. Clinical and morphological report on 2 observations]. 17 10

The Verner-Morrison Syndrome is a clinically defined entity caused by an islet cell tumor of the pancreas. More than 60 cases have been described so long. The syndrome is characterized by diarrhea, hypokalemia and hypochlorhydria. In addition to a diabetic disposition, raised calcium levels and skin alterations may be present. The diagnosis is a clinical one. A pancreatic tumor should be searched for and removed. Morphologically a benign and a maligne islet cell tumor or a diffuse hyperplasia of the islets of Langerhans can be found. Until now identification of the tumor cells has not been possible. There seems no doubt that the tumor cells produce a peptide hormone. Secretin, gastric inhibitory polypeptide, vasoactive intestinal polypeptide and combinations of hormones are discussed. The results are contradictory. Theories concerning the formal and causal pathogenesis are only incomplete and unproved up to now.
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PMID:[The Verner-Morrison syndrome. The clinical picture and pathologic anatomy]. 17 9

A case of a non-beta islet cell tumor of the pancreas that produced the WDHA (watery diarrhea, hypokalemia, and achlorhydria) syndrome is presented. An enlarged body-tail region of the pancreas is demonstrated on transaxial views; multiple fluid-filled loops of small and large bowel are also noted. The angiography of the tumor is similar to other non-beta islet cell lesions consisting of a large hypervascular mass with hypertrophied feeding vessels and a persistent, dense capillary stain. The demonstration of elevated levels of vasoactive intestinal polypeptide in both tumor and plasma and the ultrastructural description of endocrine granules may help to explain the pathophysiology in this case.
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PMID:Radiologic and pathologic characteristics of the WDHA syndrome. 18 23


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