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)

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

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

Chlorpropamide alcohol flushing (CPAF) in non-insulin-dependent diabetics (NIDDs) has been reported to be associated with a lower tendency to develop late complications. The flush was thought to be mediated by enkephalins and prostaglandins. Early studies could not correlate CPAF to increased levels of acetaldehyde in blood and the flush was not regarded as an antabuse-like reaction. In this study, the increase of plasma acetaldehyde during the flush in 13 CPAF positive diabetics was significantly (P less than 0.005) higher than in the 13 CPAF negative diabetics during a CPAF challenge test. The increase of plasma acetaldehyde was reduced to the level of CPAF negative diabetics in three CPAF positive diabetics when they were exposed to alcohol without premedication with chlorpropamide and they did not flush. The normal breakdown of ethanol to acetic acid via acetaldehyde appears to be inhibited by chlorpropamide in the flushers. Acetaldehyde measurement is an objective method to study the chlorpropamide alcohol flush and it appears superior to the measurement of skin temperature.
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PMID:Increase of plasma acetaldehyde. An objective indicator of the chlorpropamide alcohol flush. 726 73

Capsaicin-sensitive afferent neurons are involved in maintaining the integrity of the gastrointestinal mucosa. These neurons are closely apposed to mast cells and could, therefore, lead to their activation. In the present study, the role of capsaicin-sensitive neurons in the pathogenesis of experimental colitis and the possible involvement of mast cells and nitric oxide were evaluated. Rats were treated with capsaicin subcutaneously, 20, 30, and 50 mg/kg, on three consecutive days, a regimen shown to ablate primary afferent neurons. Colitis was induced two weeks later by flushing 2 ml 5% acetic acid into the proximal colon. Control rats received saline, acetic acid, or capsaicin alone. Another group of rats received ketotifen (100 micrograms/100 g body wt x 2/day) intragastrically 48 hr prior to damage induction and thereafter. Rats were sacrificed 24 hr after damage induction, the colon isolated, damage assessed, explants were organ-cultured for 24 hr for determination of nitric oxide generation, and mucosa extracted for determination of leukotriene B4 generation and nitric oxide synthase activity. Significant increases in colonic weight, nitric oxide synthase activity, and nitric oxide and leukotriene B4 generation accompanied the near tripling of acetic acid-induced damage in capsaicin-pretreated rats. Ketotifen pretreatment significantly decreased the macroscopic damage and the increase in colonic weight. The protection provided by ketotifen was accompanied by a significant decrease in leukotriene B4 generation and nitric oxide synthase activity (80%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ketotifen ameliorates capsaicin-augmented acetic acid-induced colitis. 753 78

Enhanced nitric oxide (NO) generation by stimulated NO synthase (NOS) activity may, through its oxidative metabolism contribute to tissue injury in experimental colitis. In this study the possible amelioration of experimental colitis by NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS activity, was evaluated. Colitis was induced in rats by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB) dissolved in 0.25 ml 50% ethanol or by flushing the colon of capsaicin pretreated rats with 2 ml of 5% acetic acid. In several experiments, L-NAME 0.1 mg/ml was added to the drinking water at the time of colitis induction with TNB or seven days before acetic acid treatment. Rats were killed at various time intervals after induction of colitis. A 10 cm distal colonic segment was isolated, weighed, lesion area measured, and explants organ cultured for 24 hours for determination of NO generation by the Greiss reaction. The rest of the mucosa was scraped for determination of myeloperoxidase and NOS activities and leukotriene generation. In TNB treated rats mean arterial pressure was also determined up to 72 hours after damage induction, with or without cotreatment with nitroprusside. L-NAME significantly decreased the extent of tissue injury in TNB treated rats. Seven days after TNB treatment lesion area was reduced by 55%, colonic weight by 37%, and myeloperoxidase and NOS activity by 59% and 42%, respectively. Acetic acid induced colitis in capsaicin pretreated rats was also significantly decreased by L-NAME. Twenty four hours after acetic acid treatment lesion area was reduced by 61%, colonic weight by 21% and NOS activity by 39%. Mean (SEM) arterial blood pressure in TNB+L-NAME treated rats was 37.6 (8.1) mm Hg higher than in TNB treated rats, an effect that was only partially abolished by nitroprusside. These results show that inhibition of NO synthesis by an L-arginine analogue significantly ameliorates the extent of tissue injury in two models of experimental colitis, an effect that is not due only to its vasoconstrictor properties. Modulation of NO generation may be a novel therapeutic approach in inflammatory bowel disease.
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PMID:Experimental colitis is ameliorated by inhibition of nitric oxide synthase activity. 867 8

Ingestion of ethyl alcohol may be associated with a number of adverse reactions. Apart from toxicological effects, intolerance syndromes occur, which are caused by genetic or acquired defects in alcohol metabolism and are manifest clinically as flushing. In addition to these abnormalities, rare cases of generalized urticaria and anaphylactoid reactions after ingestion of ethyl alcohol have been reported, the pathogenesis of which is still a matter of debate. We describe three patients who presented with recurrent generalized urticaria, which developed within minutes of consumption of small amounts of ethyl alcohol. Common causes of chronic recurrent urticaria were excluded by case history, physical examination and laboratory investigations, and by comprehensive allergy testing. All patients produce positive prick tests with acetic acid, and developed urticaria after oral challenge with small amounts of highly purified ethyl alcohol. The symptoms are most probably caused by an intolerance to ethyl alcohol or its metabolites, whereas an allergy sensu strictu seems unlikely.
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PMID:Urticarial and anaphylactoid reactions following ethanol intake. 771 68

Right-sided valvular heart disease is a common complication of metastatic carcinoid tumors. On the contrary, left valve involvement is a rare finding. In our report we describe a patient in whom the subsequent involvement of right and left heart valves was documented by 2D and Doppler echocardiography. The patient was a 46-year-old woman who, in the last three years, complained of face flushing, postprandial diarrhea and shooting epigastric pain lasting for hours. She came at our observation for increasing dyspnoea, peripheral edemas and asthenia. 2D-echocardiography and Color Doppler revealed a severe tricuspid regurgitation and a turbulent blood flow across the pulmonary valve. An Angiographic examination confirmed the severe tricuspidal regurgitation and disclosed a mild pulmonary stenosis. These findings were associated with high 5 hydroxyndole acetic acid (5-HIAA) urinary excretion and the presence of a liver metastasizing ileal carcinoid tumor. Some months later, a new 2D echo-Doppler examination showed thickening and reduced motion of the posterior mitral leaflet, associated with regurgitation and an aortic insufficiency without evident structural valvular abnormalities. Even if carefully investigated no right-to-left shunt was found.
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PMID:[Left valvular involvement in carcinoid: description of a case]. 805 18

Reinfusion of autologous hematopoietic peripheral blood stem cells (PBSC) or bone marrow is often accompanied by flushing, dyspnea, abdominal cramping, nausea and diarrhea. These symptoms and the observation that they can be prevented by ondansetron, a selective 5-HT3 receptor antagonist, led to the assumption that these side-effects are due to infusion of free serotonin during the reinfusion of PBSC or bone marrow. Twenty-five patients with solid tumors received, after myeloblative chemotherapy, a total of 30 reinfusions of PBSC and/or bone marrow. In 17 patients, serotonin levels in the bags containing the PBSC were measured. In all patients, platelet serotonin levels were determined before and 1 h post-reinfusion. In addition, before and 24 h after reinfusion urine was collected for determination of 5-hydroxyindole acetic acid (5-HIAA) and serotonin concentrations. Mean (+/- s.d.) total serotonin concentration in the bags was 2404 +/- 1555 nmol/l. Mean total volume reinfused was 471 +/- 185 ml. After reinfusion, the mean (+/- s.d.) levels of serotonin in platelets in patients increased from 3.2 +/- 1.4 nm/10(9) at baseline to 3.8 +/- 2.0 nm/10(9) (P = 0.02). Neither 24 h urinary 5-HIAA nor serotonin levels were affected. These results indicate that reinfusion of PBSC or bone marrow is accompanied by substantial infusion of free serotonin, which might explain the observed side-effects and justify the use of 5-HT3 receptor antagonists as pre- medication for this procedure.
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PMID:Effects of peripheral stem cell or bone marrow reinfusion on peripheral serotonin metabolism. 1055 62

Otitis externa is most commonly caused by infection (usually bacterial, although occasionally fungal), but it may also be associated with a variety of noninfectious systemic or local dermatologic processes. The most characteristic symptom is discomfort that is limited to the external auditory canal, while the most characteristic signs are erythema and swelling of the canal with variable discharge. Excessive moisture and trauma, both of which impair the canal's natural defenses, are the two most common precipitants of otitis externa, and avoidance of these precipitants is the cornerstone of prevention. Thorough cleansing of the canal is essential for diagnosis and treatment, but flushing should be avoided. Acidification with a topical solution of 2 percent acetic acid combined with hydrocortisone for inflammation is effective treatment in most cases and, when used after exposure to moisture, is an excellent prophylactic. Other prophylactic measures such as drying the ears with a hair dryer and avoiding manipulation of the external auditory canal may help prevent recurrence.
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PMID:Otitis externa: a practical guide to treatment and prevention. 1126 68


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