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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant ascites is often refractory to therapy and rapidly deteriorating the nutritional and physical state of the cancer patient. Nevertheless, ascites does not always implicate preterminal state of the cancer process (e.g. ovarian carcinoma). A short review is made of the pathophysiology of ascites in cirrhosis and in malignancy, and different modes of treatment are discussed. The results of medical therapy of malignant ascites (salt and water restriction, diuretics, intraperitoneal cytostatics or radiocolloids) are not convincing. The immunotherapy with OK-432, as worked out by Katano (16-46) has to prove its value. The best and most hopeful results in cases of massive previously resistant ascites, are obtained with a peritoneojugular shunt, improving immediately the nutritional status and life condition, providing excellent palliation. The superiority of the Denver shunt versus the Le Veen shunt has been assessed recently, especially for malignant ascites. Some technical and perioperative details merit more attention, to limit the high risk ratio. Control of the intrathoracic position of the catheter tip, the maintenance of the bloodflow in the jugular vein, the intramuscular tunnelisation of the peritoneal catheter, the discard of 3 or 5 liters ascitic fluid and the substitution of part of it by physiological fluid, perioperative prophylactic antibiotics and heparinisation, flow-rate control in the postoperative period by changing patients position, respiratory exercises, daily flushing, all those measures limit the risk of fibrinolysis (DIC), shunt occlusion, fluid overload and infection. The fear of metastasis by shunt is unfounded, since the survival of the primary tumor is mostly too short (41). The postoperative follow up in an intensive care unit is necessary during 24-72 hours.
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PMID:[The Denver shunt in malignant ascites]. 258 Apr 8

The intestinal carcinoid tumors of 26 patients were stained for the presence of serotonin, gastrin, somatostatin, motilin, secretin, glucagon, pancreatic polypeptide, ACTH, and neurotensin. Argentaffin and argyrophil stains were also performed in all cases. Thirty-five separate tumors (counting metastases and multiple primaries) from the 26 patients were studied. Serotonin was present in 30 of the 35 tumors. Nineteen tumors contained serotonin only. Fourteen tumors contained multiple neuroendocrine products. One tumor contained gastrin only. One tumor did not stain immunohistochemically, but was argyrophilic. Metastatic deposits were studied in nine patients. Some metastases produced the identical neuroendocrine products as the primary tumor, whereas others produced either additional or fewer hormones than the primary tumor. Moreover, different metastases from the same primary tumor were observed to produce different hormones. Argyrophilic cells were present in all cases and were much more numerous than cells staining by immunohistochemistry. Argyrophilic cells probably contain monoamines and polypeptide hormones in addition to those studied in this series. The argyrophil stain was the best general stain in this study for the demonstration of neuroendocrine cells. Argentaffin staining was negative in ten cases that were serotonin positive and two argentaffin positive cases were serotonin negative. The carcinoid syndrome, as clinically defined by the presence of flushing and diarrhea, was noted in five patients, all of whom had serotonin-containing small bowel carcinoids. Endocrine-related symptoms were not clinically appreciated in the remaining patients.
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PMID:The neuroendocrine products of intestinal carcinoids. An immunoperoxidase study of 35 carcinoid tumors stained for serotonin and eight polypeptide hormones. 618 28

Although patients with bronchial and ovarian carcinoid tumors can develop the carcinoid syndrome (diarrhea and/or flushing) in the absence of hepatic metastasis, it is believed that development of the carcinoid syndrome in patients with carcinoid tumors of gastrointestinal origin occurs only after the patient has hepatic metastasis. This is explained by hepatic inactivation of most of the serotonin in the portal circulation or by the fact that hepatic metastases are larger than the primary tumor in the gastrointestinal tract. Three patients with ileal and jejunal carcinoid tumors who developed the carcinoid syndrome without obvious hepatic metastasis are described. Two of the patients had intra-abdominal, but extrahepatic, metastasis that probably drained directly into the systemic circulation. The third patient had an ileal carcinoid with clinical involvement limited to adjacent mesenteric lymph nodes. Following resection of her tumor, her urinary 5-HIAA excretion and platelet serotonin level returned to normal, and her attacks of carcinoid flushing virtually ceased. She has occasional spells of "blushing" that are thought to be benign; however, further close follow-up study will be needed to be certain that she is free of disease. It is suggested that each patient with the carcinoid syndrome be evaluated with CT and technetium-99 pertechnetate liver scans. If there is no liver involvement detected with these studies, one should consider hepatic arteriogram or laparotomy to determine if the patient's tumor might be totally resectable.
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PMID:Carcinoid syndrome from gastrointestinal carcinoids without liver metastasis. 709 50

The prognosis and the quality of life of patients with carcinoid tumors is related either to symptoms from the substances secreted or to progressive tumor growth. Medical treatment with cytotoxic agents is of marginal value for increasing life expectancy and reducing clinical symptoms. Recent studies with interferon have shown interesting results. In the present investigation, 22 patients with carcinoid tumors and syndrome were treated with recombinant interferon alpha-2a (r-IFN alpha-2a) at the dose of 6 x 10(6) IU intramuscularly daily for 8 weeks and three times weekly thereafter. The primary tumor was localized in the foregut (n = 11), midgut (n = 7), hindgut (n = 1), and unknown site (n = 3). Most cases had liver metastasis. Seventeen patients had elevated 5-hydroxyindoloacetic acid (5-HIAA) excretion and 5 had flushing and/or diarrhea as the only clinical manifestation. Six cases presented a complete syndrome (flushing, diarrhea and 5-HIAA excretion). Control of symptoms was obtained in 80% and a 5-HIAA level reduction in 58% of the patients. The interferon treatment was more effective for control of the carcinoid syndrome than for control of tumor growth. The treatment was well tolerated and fever, myalgia, anorexia and fatigue were the most frequent side-effects.
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PMID:Treatment of carcinoid syndrome with recombinant interferon alpha-2a. 768 66

Carcinoids, tumors arising from enterochromaffin cells, represent the most common type of gastrointestinal endocrine neoplasm; they are often multiple and may appear anywhere in the gut. Carcinoid tumors may also occur in bronchi and ovaries. Classic symptomatology includes secretory diarrhea, flushing, edema, bronchospasm and cutaneous teleangectasias; however, over 30% of patients with demonstrably elevated serotonin levels may not exhibit any symptoms at all. The diagnosis of carcinoid tumor is typically made by measurement of 24-hour urinary excretion of 5-hydroxyindoloacetic acid. Commonly, tumor localisation is established with CT, US, NMR and arteriography. MIBG scintigraphy is also used to visualize tumors deriving from neuroendocrine cells as carcinoid. These tumors may express somatostatin receptors located on the cell surface. Therefore 111In Octreotide (Octreoscan), a somatostatin analogue, can be employed for tumor localisation. A 32-years-old man with liver metastases secondary to a carcinoid tumor of unknown origin is presented. Classic carcinoid symptoms were absent. Diagnosis was supported by elevated values of urinary 5-hydroxyindolocetic acid and liver fine-needle aspiration. Abdominal US and CT scan detected only liver masses but not the primary tumor. Arteriography was not performed. 131I MIBG and 111I octreotide scans both failed in locating the primary cancer too; only the second tracer showed marked uptake in liver metastases. Beside localization, these two tracers give also informations about the following therapy especially in malignant tumors where local resection isn't an adequate treatment.
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PMID:131I MIBG/111In octreotide mismatch in a patient with liver metastases secondary to a carcinoid of unknown origin. 853 97

Carcinoid tumors are very rare and originate mainly in the gastrointestinal tract. The tumor histology is ambiguous and malignancy is determined by metastases. Carcinoid tumors affect both sexes equally and have been found in all age groups. Many carcinoid tumors are found incidentally or from symptoms related to the hormones that the tumor produces. Carcinoid syndrome occurs when vast quantities of hormones are produced from GI carcinoid metastases or a non-GI primary tumor. The classic "carcinoid triad" associated with the syndrome includes flushing, diarrhea, and cardiac involvement. The hormone largely responsible for most of these symptoms is serotonin. Treatment consists of a wide-resection for local primaries and usually palliative, medical support for patients with metastases. The tumors are very slow-growing and patients have lived for up to 30 years after metastasis is diagnosed. Somatostatin analogue (lanreotide and octreotide) administration controls many of the carcinoid symptoms. Somatostatin is a naturally occurring gastrointestinal peptide (hormone) which can augment or counteract a wide variety of other peptides. This article provides an overview of carcinoid tumor and carcinoid syndrome including diagnosis and treatment. Aspects important to patient care will also be addressed.
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PMID:Carcinoid tumors and syndrome. 1205 78

Patients with clinically evident medullary thyroid cancer should have a total extracapsular thyroidectomy with bilateral central neck dissection and an ipsilateral prophylactic or therapeutic modified (functional) radical neck dissection when the primary tumor is greater than 1 cm and when the central neck nodes are positive. A prophylactic contralateral neck dissection should be done when the primary tumor is bilateral and when there is extensive lymphadenopathy on the side of the primary tumor. Patients who have gross, unresectable residual medullary thyroid cancer should receive postoperative external radiotherapy. Patients who are carriers of germ-line RET proto-oncogene point mutations or have an elevated (basal or stimulated) calcitonin levels on screening should have a prophylactic total thyroidectomy before age 6 years. In patients with an elevated basal or stimulated plasma calcitonin level and an intrathyroidal nodule on ultrasound, a total thyroidectomy and central neck lymph node dissection should be done. Patients with persistent or recurrent medullary thyroid cancer should have a complete thyroidectomy (if not done initially) and bilateral central and modified radical neck dissection, including upper mediastinal lymphadenectomy. Patients who are symptomatic from distant medullary thyroid cancer metastases (diarrhea, flushing, weight loss, or bone pain) should be treated with somatostatin analogs. Bone metastases should be resected if possible, and symptomatic lesions that are unresectable should be treated with external radiotherapy. Cytoreductive procedures such as radiofrequency ablation or cryoablation for liver metastases should be considered in symptomatic patients to reduce tumor burden. Localized pulmonary metastases should be resected. Chemotherapy or radioactive immunotherapy (iodine 131 labeled carcinoembryonic antigen monoclonal antibody) protocols should be considered in patients with nonoperative widely metastatic progressing medullary thyroid cancer.
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PMID:Medullary thyroid cancer. 1205 61

Endocrine tumors (ET) of the digestive tract (formerly called neuroendocrine tumors) are rare. They are classified into two principal types: gastrointestinal ET's (formerly called carcinoid tumors) which are the most common, and pancreaticoduodenal ET's. Functioning ET's secrete polypeptide hormones which cause characteristic hormonal syndromes. The management of ET is multidisciplinary. Poorly-differentiated ET's have a poor prognosis and are treated by chemotherapy. Surgical excision is the only curative treatment of well-differentiated ET's. The surgical goals are to: 1. prolong survival by resecting the primary tumor and any nodal or hepatic metastases, 2. control the symptoms related to hormonal secretion, 3. prevent or treat local complications. The most common sites of gastrointestinal ET's ( carcinoids) are the appendix and the rectum; these are often small (<1 cm), benign, and discovered fortuitously at the time of appendectomy or colonoscopic removal. Ileal ET's, even if small, are malignant, frequently multiple, and complicated in 30-50% of cases by bowel obstruction, mesenteric invasion, or bleeding. The carcinoid syndrome (consisting of abdominal pain, flushing, diarrhea, hypertension, bronchospasm, and right sided cardiac vegetations) is caused by the hypersecretion of serotonin into the systemic circulation; it occurs in 10% of cases and is usually associated with hepatic metastases. More than half of the cases of pancreatic ET are non-functional. They are usually malignant and of advanced stage at diagnosis presenting as a palpable or obstructing mass or as liver metastases. Insulinoma and gastrinoma (cause of the Zollinger-Ellison syndrome) are the most common functional ET's. 80% are sporadic; in these cases, tumor size, location, and malignant potential determine the type of resection which may vary from a simple enucleation to a formal pancreatectomy. In 10-20% of cases, pancreaticoduodenal ET presents in the setting of multiple endocrine neoplasia (NEM type I), an autosomal-dominant genetic disease with multifocal endocrine involvement of the pituitary, parathyroid, pancreas, and adrenal glands. For insulinoma with NEM-I, enucleation of lesions in the pancreatic head plus a caudal pancreatectomy is the most appropriate procedure. For gastrinoma with NEM-I, the benefit of surgical resection for tumors less than 2-3 cm in size is not clear. The lesions are frequently small, multiple, and widespread and recurrence is frequent after excision. The long-term prognosis is nevertheless fairly good. But the eventual development of liver metastases which are the most common cause of mortality still argues for an aggressive surgical approach in the early stages of the disease.
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PMID:[Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors]. 1614 76

Carcinoid tumors are part of a heterogeneous group of gastrointestinal and pancreatic endocrine tumors that are characterized by their capacity to produce and secrete hormones, 5-hydroxytryptamine, tachykinins and other mediators. These substances are thought to be responsible for the collection of symptoms, which include diarrhea, flushing and wheezing, that is known as carcinoid syndrome. Fibrosis that occurs either local to or distant from the primary tumor is one of the hallmarks of carcinoid tumors that originate from the midgut. The fibrotic process can occur in the mesentery as a desmoplastic response and may lead to obstruction of the small bowel, but it can also occur in the lungs, skin or retroperitoneum. Importantly, up to one-third of patients develop cardiac valvulopathy. One or more products that are secreted by the tumor and enter into the circulation are likely to have a role in this process. This Review discusses the incidence and prevalence of fibrosis in carcinoid syndrome and explores evidence to date for causative agents, in particular the roles of 5-hydroxytryptamine and elements of the downstream signaling pathway. Improved understanding of the etiology of carcinoid-tumor-related fibrosis may lead to better treatments for this condition than those we currently have.
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PMID:Fibrosis and carcinoid syndrome: from causation to future therapy. 1944 61

Midgut neuroendocrine tumors (MNETs) are rare, and the primary tumor is usually small and difficult to visualize at imaging. Patients often present late with extensive liver and nodal metastases and may experience symptoms secondary to the release of active substances by the primary tumor, such as serotonin and its metabolites, which have local and systemic effects. Locally, this causes desmoplasia and vascular encasement and may lead to small bowel obstruction and ischemia, with significant morbidity and mortality. Systemically, the release of active substances into the circulation can cause flushing, diarrhea, and abdominal pain (carcinoid syndrome); these substances can be detected in urine and blood serum and used as markers for diagnosis and treatment follow-up. MNETs retain expression of specific peptide receptors such as somatostatin receptors, which will bind to synthetic somatostatin analogs such as octreotide. This feature is useful for functional imaging of patients with MNETs and for peptide receptor radionuclide therapy using somatostatin analogs. Resection of the primary tumor is advocated, even in patients with extensive metastases, because it may prevent development of local complications, can help control systemic symptoms, and has been shown to confer some survival advantage. Computed tomography and functional imaging are used to identify the primary tumor and assess its resectability. The main factors governing resectability are patient comorbidities (eg, carcinoid heart disease), vascular involvement, and desmoplasia.
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PMID:Midgut neuroendocrine tumors: imaging assessment for surgical resection. 2461 88


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