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)

Twenty-eight patients with malignant esophageal obstruction had palliative treatment using the Fell endoesophageal tube. The usual plan for these patients, irradiation followed by resection, was not followed because of the presence of tracheoesophageal fistula, celiac or hepatic metastases, or marked debilitation which precluded major operation. Palliation was obtained in ten patients who were discharged in a mean of 16.5 days with the ability to swallow liquids or pureed or ground foods and had a mean survival of 116 days. There was a high incidence of tube-related symptoms in all patients, and increased dysphagia, tube regurgitation, and difficulties in initiating swallowing were noted in patients with lesions above 24 cm from the incisors. The high incidence of postoperative ocmplications was responsible for the poor palliation and low survival in the remaining 18 patients who had a mean survival of 41 days. It was concluded that orthograde dilatation or forced seating of the prosthesis through a malignant esophageal obstruction carries a significant risk of perforation of the esophagus which, if it occurs, negates the palliative aspects of the procedure, increases hospitalization, and decreases survival. It is recommended that this procedure be used selectively in patients not otherwise amenable to resectional therapy with lesions beyond 24 cm from the incisors.
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PMID:Fell tube insertion after orthograde dilatation of malignant esophageal obstruction: palliation and morbidity. 6 53

Esophageal carcinomas in two cats are described. The main clinical sign was regurgitation of food and fluids. Radiographic examination revealed severe esophageal abnormalities in both cats. In the second cat, the radiographic appearance of the esophagus together with the esophagoscopic findings provided a presumptive diagnosis of neoplasia. Histologic examination in both cats revealed squamous cell carcinoma with metastases.
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PMID:Esophageal squamous cell carcinoma in two cats. 70 48

A 62-yr-old woman was evaluated for a 2-wk history of regurgitation and weight loss. Radiologic studies demonstrated a stenotic region in the distal third of the esophagus. Multiple endoscopic biopsies were nondiagnostic. Esophagectomy and esophagogastrostomy revealed a diffusely infiltrating adenocarcinoma ("linitis plastica") of the distal esophagus, sparing the gastroesophageal junction and stomach. Despite the absence of metastatic disease at laparotomy, the patient developed metastases unresponsive to chemotherapy. The pathologic, radiographic, and endoscopic findings are consistent with primary linitis plastica of the esophagus.
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PMID:Linitis plastica of the esophagus. 284 10

The most common initial symptom of esophageal neoplasm is dysphagia. When metastasis occurs, it is most frequent to neighboring lymph nodes, mediastinum, or viscera, eg, the lungs and liver, and only infrequently to bones. Even less frequently do these metastases occur with hypercalcemia. A 59-year-old woman was initially seen with hypercalcemia and bone pain in the hip and leg, which subsequently proved to be the site of metastatic spread secondary to squamous cell carcinoma of the esophagus. Until her death, approximately four months after the diagnosis, she never experienced dysphagia, epigastric or substernal pain, or regurgitation.
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PMID:Femoral and skull metastasis with hypercalcemia: occurrence with esophageal carcinoma without dysphagia. 713 70

Drug-induced cholestasis may be due to impairment of hepatocellular bile secretion (pure cholestasis or cholestatic hepatitis), obstruction of ductules (cholangiolitis) or interlobular ducts (cholangitis), or extrahepatic obstruction (sclerosing cholangitis). Mechanisms of hepatocellular cholestasis are multiple and include inhibition of various transport systems, cytoskeleton poisoning, disturbed intracellular calcium homeostasis and increased permeability with regurgitation of bile constituents into plasma. Pure hepatocellular cholestasis is mostly observed with sex steroid hormones and anabolic steroids. Ductular or ductal cholestasis (drug-induced cholangiopathy) may be acute and self-limited, or prolonged with ductopenia, occasionally leading to biliary cirrhosis. An immune mechanism has been proposed. Sclerosing cholangitis with strictures near the confluent of hepatic ducts is observed after intraarterial administration of floxuridine for chemotherapy of hepatic metastases. Some drugs may induce the formation of cholesterol gallstones, or precipitate in bile and form biliary sludge or stones in the gallbladder or common bile duct.
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PMID:Drug-induced cholestasis. 913 22

The arterial infusion of lipiodol (LPD) containing SMANCS (SMANCS/LPD) has been considered to be a tumor-targeting therapy for hepatocellular carcinoma (HCC). It is important to establish a role of this new therapy in systematic strategies for HCC. LPD has no embolic effect, and the lipophilic anti-cancer agent, SMANCS, suspended in LPD and delivered selectively in tumors, shows therapeutic effect. Accordingly, it is essential for therapeutic efficacy that HCC cells have a chemosensitivity to SMANCS. The maximum dose of SMANCS/LPD is 6 ml at one time, which is not sufficient for voluminous tumors. These are the disadvantages of SMANCS/LPD therapy. Furthermore, HCC tissues, in which lipiodol is retained, is limited to moderately differentiated, with large blood spaces. SMANCS/LPD is not effective for well- and poorly -differentiated HCCs, because blood spaces in these histological types are too small for SMANCS/LPD to be deposited. On the other hand, transcatheter arterial embolization therapy (TAE) is effective by occluding feeding artery with small pieces of gelatin sponge, and a much tumor necrosis is obtained by TAE at one time. However, HCC cells beneath and within the capsule, and invading outside the capsule, are viable, possibly due to backflow of blood via drainage vein. Tumor thrombi and tiny intrahepatic metastases also escape the TAE effect. Previously we reported the new therapy at the first time: the combination of arterial infusion of SMANCS/LPD and TAE (LpTAE). LpTAE has some therapeutic benefits of both therapies; SMANCS/LPD fills up a whole tumor, and part of the LPD flows out from the tumor, is trapped in the capsular invasion and microscopic metastatic foci with the necrotic change. LPD prevents regurgitation of blood flow in drainage vein, and promotes necrotic change. After LpTAE, Lipiodol CT shows 4 kinds of LPD-deposition pattern in HCC; the therapeutic effects of LpTAE are exactly evaluated by these patterns. For total necrosis, HCC nodule shows a complete type, in which the whole tumor shows a metallic density by lipiodol deposition. In other patterns, the LPD-deposited area in tumors generally shows necrosis, and non-LPD-deposited areas are viable. The second line of the therapies. PEIT or resection, can be selected by the LPD-deposition pattern. We consider that the intraarterial infusion of SMANCS/LPD reinforces TAE, and LpTAE is one of the most effective therapies.
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PMID:[Significance of arterial infusion of SMANCS-dissolved Lipiodol in therapeutic strategies for hepatocellular carcinoma]. 951 95

Since its description in the 1950s, the definition of Barrett's esophagus has evolved from the macroscopic visualization of gastric-appearing mucosa in the esophagus to the histologic identification of goblet cells confirming the presence of intestinal metaplasia within the esophagus. The length of intestinal metaplasia necessary to be classified as Barrett's, and the relationship between intestinal metaplasia of the esophagus and that limited to the cardia are all areas currently being evaluated. However, any segment of intestinal metaplasia is capable of undergoing dysplastic change and ultimately of becoming a focus of adenocarcinoma. It is logical to expect the degree of risk for developing cancer to be proportional to the amount of intestinal metaplasia present; however, within a population, the low risk to any individual is balanced by the relative frequency of the process. Thus, given the large numbers of people in America with CIM, even a small risk of progression to cancer will result in a large number of patients with adenocarcinoma of the cardia. This is exactly what is occurring today, with the incidence of adenocarcinoma of the cardia and esophagus currently rising faster than any other cancer in the United States. A major risk factor for adenocarcinoma of the esophagus is intestinal metaplasia, which occurs as a consequence of GERD. Patients with Barrett's esophagus usually have more severe reflux disease with significant impairment of LES function and esophageal body motility compared with patients without Barrett's. Furthermore, in patients with Barrett's, the composition of the refluxed juice is different. Patients who reflux both gastric and duodenal juice have a higher prevalence of Barrett's than do those who reflux gastric juice alone. Among patients with Barrett's, a significantly greater esophageal bilirubin exposure has been demonstrated in those with dysplasia. The mechanically defective sphincter and impaired esophageal body function in many patients with Barrett's makes their disease difficult to control medically. In addition, symptoms are unreliable as a guide to successful control of reflux. The hardest symptom to control is regurgitation, and there is concern that this and continued reflux of pharmacologically altered gastric contents, particularly bile acids in their nonpolar form, may contribute to progression of Barrett's. Both medical therapy and failed antireflux surgery are associated with progression of Barrett's to dysplasia and adenocarcinoma. On the other hand, a functioning fundoplication seems to be associated with protection from progression of Barrett's. Intestinal metaplasia of the esophagus is unlikely to regress after antireflux surgery; however, intestinal metaplasia limited to the cardia is perhaps more dynamic and able to regress. Furthermore, low-grade dysplasia frequently regresses after an antireflux procedure. Antireflux surgery is safe, effective, and durable, and often can be performed using minimally invasive techniques. Thus, antireflux surgery should be strongly considered in any patient with intestinal metaplasia of the esophagus or cardia. The possibility of mucosal ablation after an antireflux repair should be considered in patients with low-grade dysplasia. Patients with Barrett's and high-grade dysplasia are at high risk for having a focus of adenocarcinoma present. Even with multiple biopsies, a degree of sampling error exists. Also, adenocarcinoma can develop within the space of several months; and if the cancer is allowed to invade into the submucosa, 50% of these patients will have lymphatic metastases, thereby negating the purpose of surveillance. Although patients with high-grade dysplasia and intramucosal adenocarcinoma on biopsy who do not have an endoscopically visible lesion are unlikely to have lymphatic metastases, 7% do have submucosal invasion. Thus, even in these very early tumors, treatment directed only at the mucosa may be inadequate. (ABSTRACT
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PMID:The diagnosis and management of Barrett's esophagus. 1057 61

A 68-year old woman was hospitalised because of isolated right heart failure. Doppler echocardiography revealed severe tricuspid regurgitation with thickened, shortened, hypomobile leaflets. Pulmonary valve was thickened with mild pulmonary regurgitation. Mitral and aortic valves were normal. The patient was finally diagnosed with carcinoid heart disease from an isolated ovarian carcinoid cancer without hepatic metastases. Ovarectomy was performed and the patient was considered cured of her cancer. Because of refractory right heart failure, she underwent tricuspid valve replacement with a bioprosthesis. Such cardiovascular manifestations are rarely the presenting symptoms of carcinoid disease. Carcinoid heart disease from ovarian primary cancer is exceptional. In this circumstance, carcinoid cardiac lesions may develop in the absence of hepatic metastases because the venous blood from the ovaries drains into the inferior vena cava without hepatic first past effect. Surgical resection of primary ovarian carcinoid tumor is often curative and the prognosis depends mainly on the cardiac condition. The diagnosis of carcinoid syndrome should be discussed in patients with organic tricuspid regurgitation without left valvular disease.
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PMID:[Isolated carcinoid tumor of the ovary disclosed by tricuspid insufficiency]. 1462 39

Nasopharyngeal carcinoma (NPC) is a tumor arising from the epithelial cells that cover the surface and line the nasopharynx. The annual incidence of NPC in the UK is 0.3 per million at age 0-14 years, and 1 to 2 per million at age 15-19 years. Incidence is higher in the Chinese and Tunisian populations. Although rare, NPC accounts for about one third of childhood nasopharyngeal neoplasms. Three subtypes of NPC are recognized in the World Health Organization (WHO) classification: 1) squamous cell carcinoma, typically found in the older adult population; 2) non-keratinizing carcinoma; 3) undifferentiated carcinoma. The tumor can extend within or out of the nasopharynx to the other lateral wall and/or posterosuperiorly to the base of the skull or the palate, nasal cavity or oropharynx. It then typically metastases to cervical lymph nodes. Cervical lymphadenopathy is the initial presentation in many patients, and the diagnosis of NPC is often made by lymph node biopsy. Symptoms related to the primary tumor include trismus, pain, otitis media, nasal regurgitation due to paresis of the soft palate, hearing loss and cranial nerve palsies. Larger growths may produce nasal obstruction or bleeding and a "nasal twang". Etiological factors include Epstein-Barr virus (EBV), genetic susceptibility and consumption of food with possible carcinogens--volatile nitrosamines. The recommended treatment schedule consists of three courses of neoadjuvant chemotherapy, irradiation, and adjuvant interferon (IFN)-beta therapy.
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PMID:Nasopharyngeal carcinoma. 1680 Aug 83

The carcinoid syndrome is usually evident when enterochromaffin (EC) cell-derived neuroendocrine tumors (carcinoids) metastasize to the liver. In addition to carcinoid symptomatology, about 40% of patients exhibit carcinoid heart disease (CHD) with fibrotic endocardial plaques and associated heart valve dysfunction. The mechanism behind CHD development is not fully understood, but serotonin (5-HT) is considered to be a major initiator of the fibrotic process. Most patients present with right-sided heart valve dysfunction since pulmonary and tricuspid valves lesions are the most common (>95%) cardiac pathology. Left-sided valvular involvement, and angina associated with coronary vasospasm occur in ~10% of subjects with CHD. Pathognomonic echocardiograpic features include immobility of valve leaflets and thickening and retraction of the cusps most commonly resulting in tricuspid valve regurgitation and pulmonary stenosis. Therapeutic options include cardioactive pharmacotherapy for heart failure and, in selected individuals, cardiac valve replacement. Previously valve replacement was reserved for advanced disease due to a perioperative mortality of >20% however in the last decade, technical advances as well as an earlier diagnosis have decreased surgical mortality to <10% and valve replacements are undertaken more frequently. A recent analysis of 200 cases demonstrated an increase in median survival from 1.5 years to 4.4 years in the last two decades. Although the improved prognosis might also reflect the increased use of surgical cytoreduction, hepatic metastatic ablative therapies and somatostatin analogs a robust correlation between diminution of circulating tumor products and an increased long-term survival in CHD has not been rigorously demonstrated.
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PMID:Carcinoid heart disease. 1857 Dec 50


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