Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported that flushing associated with a gastric carcinoid tumor can be provoked by pentagastrin and inhibited by either somatostatin or combined histamine H1- and H2-receptor blockade. In this report, the effects of pentagastrin and somatostatin on histamine release in a patient with a metastatic gastric carcinoid tumor were examined. Small doses of intravenous pentagastrin (0.1-0.4 micrograms) produced a dose-dependent increase in the level of circulating plasma histamine. Graded infusions of somatostatin suppressed both basal and pentagastrin-stimulated plasma histamine levels in a dose-dependent fashion. A close correlation was found between circulating plasma histamine levels and attendant changes in blood pressure and pulse rate. This study documents that pentagastrin directly evokes the release of histamine from this patient's gastric carcinoid tumor and that the release of histamine is inhibited by somatostatin. In addition, this study provides additional evidence that the primary mediator of the flushing in this patient with foregut carcinoid syndrome is histamine.
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PMID:Histamine release from a gastric carcinoid: provocation by pentagastrin and inhibition by somatostatin. 618 58

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

A 55-year-old woman with an ovarian carcinoid presented with intermittent facial and cervical flushing for 10 years, watery diarrhea for 4 years, and abdominal pain without hepatomegaly. Markedly elevated systemic venous and arterial serotonin levels (830 ng/ml; nl = 50-200 ng/ml) were found. The highest serotonin levels were observed in the superior vena caval system, but serotonin as a marker for tumor localization was inaccurate and led to an unproductive neck exploration. The histological pattern of this tumor contained purely insular elements. No hepatic or nodal metastases were identified and the lesion was unilateral. Substance P levels were elevated in the venous drainage of the left ovary and in retrospect correctly localized the ovarian tumor. This peptide may prove to be another carcinoid tumor marker in addition to serotonin and 5-hydroxyindoleacetic acid. Substance P may also be an important mediator of symptoms in patients with carcinoid syndrome.
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PMID:Substance P in the localization of a carcinoid tumor. 620 86

Previous reports of endocrine activity of glomus jugulare tumors have been of pheochromocytomas but not carcinoid apudomas. This paper is to alert the otolaryngologist to the presence of carcinoid apudomas in glomus jugulare tumors. A patient with a long history of explosive diarrhea, facial flushing, and violent headaches, the symptom of carcinoid syndrome, was cured after removal of his large glomus jugulare tumor. The diagnosis of carcinoid syndrome is made with a good history and confirmed with a 24 hour urine collection for 5 Hydroxy indole acetic acid (5 Hiaa). a series of patients treated at the Johns Hopkins Hospital for glomus jugulare tumors is reviewed for the presence of endocrine activity and the literature on endocrine active glomus jugulare tumors is presented. Preoperative evaluation for the presence of both pheochromocytoma and carcinoid apudoma is recommended for all patients with glomus jugulare tumors.
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PMID:Carcinoid apudoma arising in a glomus jugulare tumor: review of endocrine activity in glomus jugulare tumors. 624 85

Eighteen patients with severe symptoms of the carcinoid syndrome were assessed for hepatic embolisation. Four were too ill, and one had mild symptoms; thus 13 received a periembolisation regimen of cyproheptadine, fenclonine, aprotinin, methylprednisolone, tobramycin, flucloxacillin, and metronidazole. Embolisation was not performed in one patient with an occluded portal vein and was unsatisfactory in two others, in one because she was moribund and in the other because the hepatic artery had been ligated. Dramatic improvement in symptoms occurred in the nine patients in whom embolisation was successfully carried out, with abolition of flushing, severe abdominal pain, and wheeze and reduction in diarrhoea from 10.5 (SD 7.6) to 1.6 (0.9) stools/day. Urinary excretion of 5-hydroxyindole acetic acid fell from 1048 (716) to 289 (184) mumol/24 h (200 (137) to 55 (35) mg/24 h). Complications included one death from septicaemia, a hepatic abscess requiring surgical drainage, abdominal pain in three patients, pleural effusion in two, and transient encephalopathy in one. Relief of symptoms lasted for one to 24 months, and second embolisation in two patients produced further remissions of four to six months. Five patients died, one to 40 months after embolisation, in four cases because of metastases or heart failure. Hepatic embolisation is the treatment of choice for symptoms of the carcinoid syndrome resistant to medical treatment.
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PMID:Role of hepatic arterial embolisation in the carcinoid syndrome. 641 93

In this report we present the history of a patient with symptomatic carcinoid syndrome. During flushing he suffered from variant angina. The observation of coronary spasm due to excess 5-hydroxytryptamine (5-HT) is discussed with regard to the discharge of 5-HT from clotting platelets in the coronary arteries.
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PMID:Evidence for coronary spasm during flushing in the carcinoid syndrome. 646 96

Nine patients with mid-gut carcinoid tumours received leucocyte interferon (IFN) i.m. daily for 90 days. Six patients clearly ameliorated in symptoms typical of the carcinoid syndrome (flushing, diarrhoea, asthma) which correlated with reduced serum levels of tumour related polypeptides and urinary output of 5-hydroxyindole acetic acid (5-HIAA). Before IFN treatment, peripheral blood mononuclear leucocytes (PBLs) from carcinoid patients showed markedly deficient production of pH 2 labile IFN-alpha in response to Staphylococcus aureus Cowan I (SACoI) in vitro. In contrast, IFN-alpha responses to the inducers Sendai virus and beta-haemolytic streptococcus group G and IFN-gamma responses to Lens culinaris lectin and concanavalin A were normal. Also, basal and in vitro IFN enhanced natural killer (NK) cell activity and T cell mitogen-induced cell proliferation were similar in patients and controls. During 90 days of IFN therapy, SACoI-induced IFN responses became entirely undetectable. There were transient declines at 1 and 30 days in IFN responses to the other IFN inducers, of mitogen-induced lymphocyte proliferation and of basal NK activities. The increments of NK cell activities after in vitro IFN exposure were clearly decreased in IFN treated patients, suggesting in vivo activation of these cells. Thus, the results demonstrate one remarkable abnormality in carcinoid patients: a deficient IFN response to SACoI and a clear influence of IFN therapy on several parameters of the IFN-NK system.
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PMID:Evaluation of the natural killer cell-interferon system in patients with mid-gut carcinoid tumours treated with leucocyte interferon. 661 63

Carcinoid heart disease is a rare entity and has always been hallmarked by its late appearance in the malignant carcinoid syndrome. Most cases are discovered when patients complain of typical symptoms, including flushing and diarrhea, with subsequent heart failure and valvulopathy developing years later. Only a few case reports of successful valve replacements have appeared in the literature, and the cause of the valvulopathy in those patients was known at surgery. I discuss herein a unique case of carcinoid heart disease that was diagnosed postoperatively.
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PMID:Carcinoid heart disease. A unique case of postvalvotomy diagnosis. 687 Apr 45

The carcinoid syndrome is a rare clinical entity, the unique manifestations of which continue to excite the interest of physicians. Despite a common origin from neural crest tissue, the tumors are partially differentiated, as evidence by the different secretory products of foregut, midgut, and hindgut carcinoids. They also differ in their ability to metastasize, thus presenting an even more varied clinical picture. The prognosis of patients with carcinoid syndrome varies with the origin of the tumor and extent of metastases. The management of patients with carcinoid syndrome is difficult. Despite an understanding of the neurohormones that carcinoid tumors secrete, their various antagonists and inhibitors have been only partially successful in providing symptomatic relief. Carcinoid heart disease represents the most intriguing aspect of this syndrome. Although valvular dysfunction most often coexists with flushing and diarrhea, the findings of tricuspid regurgitation or stenosis occasionally provide the first clue to the presence of the disease. Despite intensive research, the definite etiology of these valvular lesions has not been established. A small group of patients has been managed by valve replacement. While surgical treatment has been successful in improving hemodynamics in most of these patients, it is expected to prolong life only in those without extensive liver metastases. In patients with extensive metastatic disease, one must carefully consider whether the risks and trauma of cardiac surgery for palliation are justified.
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PMID:Carcinoid heart disease: a clinical pathologic, and therapeutic update. 704 96

A patient with the carcinoid syndrome had flushes provoked by the ingestion of water at 60 degrees C, red wine, and milk chocolate. The patient was given sequential courses of clonidine hydrochloride, chlorpheniramine maleate, cimetidine, and a combination of chlorpheniramine and cimetidine. No flushes followed ingestion of red wine or milk chocolate during treatment courses with cimetidine (alone or in combination with chlorpheniramine) or clonidine. Chlorpheniramine alone did not affect flushing. None of the pharmacologic agents altered the flushing response to the ingestion of water at 60 degrees C.
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PMID:Blockade of carcinoid flush with cimetidine and clonidine. 705 11


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