Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used an antihuman tumor necrosis factor monoclonal antibody, CB006 (murine IgG1), to prevent the OKT3-induced acute clinical syndrome. This syndrome is due to the massive, although transient release in the circulation of various cytokines (TNF, interferon gamma, interleukin 2, interleukin 6) and represents one important side effect linked to in vivo use of OKT3. Fourteen kidney allograft recipients undergoing prophylactic OKT3 therapy were treated with CB006 in a single i.v. injection of either 0.4 mg/kg (group I, 7 patients) or 2 mg/kg (group II, 7 patients), 1 hr before the first OKT3 administration. Nineteen consecutive patients formed a historical control group. None of the CB006-pretreated patients showed any of the common, severe OKT3-associated symptoms (hypotension, respiratory distress, or neurotoxicity), which were observed in 10% of the historical controls. In addition, CB006-treated patients showed a lower frequency of pyrexia (> or = 39 degrees C) and gastrointestinal symptoms. None of the CB006-treated patients presented severe vomiting or diarrhea, defined as repeated episodes inducing significant fluid and electrolyte loss. Two out of the 7 patients in group I and group II had mild transitory diarrhea. Mild single vomiting episodes occurred in 2 group I patients and 3 group II patients. At variance in all controls, gastrointestinal symptoms were long lasting and associated with major prostration due to electrolyte and fluid loss. Importantly, CB006-treated patients who presented mild symptoms had detectable bioactive circulating TNF, showing incomplete inactivation of OKT3-induced TNF by CB006. CB006 was perfectly well tolerated, did not induce xenosensitization, and did not affect the biological or clinical effectiveness of OKT3.
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PMID:Evidence that antihuman tumor necrosis factor monoclonal antibody prevents OKT3-induced acute syndrome. 146 94

Staphylococcal enterotoxin A (SEA), the most common cause of food poisoning, is capable of stimulating human T lymphocyte proliferation at concentrations as low as 10(-13) to 10(-16) M. SEA also induces the lymphokines interleukin 2 (IL 2) and interferon gamma (IFN gamma) at similarly low concentrations. HPL cultures were stimulated with SEA in the presence of antibodies to IL2 to determine the possible role of this lymphokine in its potent mitogenic effects. Polyclonal and monoclonal antibodies to human IL 2 blocked SEA-induced mitogenesis. Treatment of cultures with higher concentrations of SEA overcame the anti-IL 2 blockage, corresponding to induction of higher concentrations of IL 2. Blockage of HPL mitogenesis by anti-IL 2 antibodies also resulted in inhibition of IFN gamma production, which is dependent on IL 2. Neutralizing monoclonal antibody to IFN gamma failed to block SEA-induced proliferation. The data indicate that the induction of IL 2, but not IFN gamma, is a requirement for SEA induced lymphocyte proliferation. SEA food poisoning and IL 2 therapy for cancer result in similar toxic symptoms, characterized by malaise, fever, nausea or vomiting, and diarrhea. The similarity between SEA and IL2 toxic effects, the fact that SEA is a potent inducer of lymphokines such as IL 2, and the fact that IL 2 induction is a prerequisite for the mitogenic effects of SEA raises the intriguing question of the role of lymphokines such as IL 2 in SEA-induced food poisoning.
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PMID:Potent mitogenic activity of staphylococcal enterotoxin A requires induction of interleukin 2. 313 70

The toxicity of recombinant Interleukin-2 (IL-2) was studied in patients with acquired immunodeficiency syndrome (AIDS) or persistent lymphadenopathy syndrome (LAS). Increasing doses of the drug from 10(3) Units/m2 to 10(6) U/m2 were given as an intravenous bolus injection. At the high-dose levels some minor effects, such as fever up to 39.5 degrees C, chills, malaise or vomiting, were observed. The administration of 10(6) U/m2 as a 4-hour infusion showed identical results. No particular alterations of laboratory parameters were found. At the high-dose level the serum concentration of neopterin, which is released from macrophages after interferon gamma stimulation, was significantly (p less than 0.001) elevated above pretreatment levels. The clinical observation of daily infusions of 10(6)/m2 for 14 days revealed the same side effects. All patients developed lymphocytosis and eosinophilia. Two patients had suffered from severe diarrhoea for several weeks presumably due to cryptosporidiosis. In both cases diarrhoea ceased under the treatment with IL-2 and did not occur in the following two months.
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PMID:Preliminary clinical observations with recombinant interleukin-2 in patients with AIDS or LAS. 387 44

Chronic granulomatous disease (CGD), an inherited disorder of phagocytic leukocyte function, is characterized by recurrent infections with catalase-positive organisms. Gastrointestinal (GI) tract involvement, present in the majority of affected individuals, may be present initially and recurrently, mimics other entities such as inflammatory bowel disease, and causes substantive morbidity and mortality. Disorders of motility, ulceration, obstruction, and infection (e.g., abscesses) occur from the mouth to the anus and stereotypically manifest with vomiting, diarrhea, abdominal pain, weight loss, and fever. Careful physical examination, in concert with appropriate diagnostic studies, is necessary to delineate intraabdominal pathologic processes. Abdominal radiographs, ultrasonography, computerized tomography, and endoscopy are useful ancillary diagnostic procedures. Drainage of accessible abscesses, antimicrobial therapy based on organisms cultured from blood and tissue, and interferon gamma may lead to suppression or eradication of infections and resolution of symptoms. Corticosteroids are useful for gastric outlet obstruction and sulfasalazine and cyclosporine for large bowel disease. Gallbladder dysfunction may be ameliorated, as in our patient, with administration of cholestyramine.
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PMID:Gastrointestinal complications of chronic granulomatous disease: case report and literature review. 956 72

Natural killer (NK) cells may be expanded in vivo with a prolonged course of daily subcutaneous interleukin-2 (IL-2). However, cellular activation requires higher concentrations of IL-2 than are achieved with low-dose therapy. The objective of the current trial was to determine the toxicity and immunological effects of periodic subcutaneous intermediate-dose IL-2 pulses in patients receiving daily low-dose therapy. A group of 19 patients were treated with daily subcutaneous low-dose IL-2 at 1.25 x 10(6) International Units (1.25 MIU) m(-2) day(-1). After 4-6 weeks, patients received escalating 3-day intermediate-dose IL-2 pulses administered as single daily subcutaneous injections, repeated at 2-week intervals. The maximum tolerated pulse dose was 15 MIU m(-2) day(-1), with transient hypotension, fatigue, and nausea/vomiting dose-limiting. Subcutaneous IL-2 resulted in in vivo expansion of CD56+ NK cells (796+/-210%) and CD56bright natural killer (NK) cells (3247+/-1382%). Expanded NK cells coexpressed CD16, and showed lymphokine-activated killer activity and antibody-dependent cellular cytotoxicity in vitro. Intermediate-dose pulsing resulted in serum IL-2 concentrations above 100 pM. Cellular activation was suggested by rapid margination of NK cells following pulsing, coincident with peak IL-2 levels, with return to baseline by 24 h. In.addition, interferon gamma production in response to lipopolysaccharide was augmented. Subcutaneous daily low-dose IL-2 with intermediate-dose pulsing is a well-tolerated outpatient regimen that results in in vivo expansion and potential activation of NK cells, with possible application in the treatment of malignancy and immunodeficiency.
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PMID:Evaluation of natural killer cell expansion and activation in vivo with daily subcutaneous low-dose interleukin-2 plus periodic intermediate-dose pulsing. 975 16

We investigated associations between markers of damage of vascular endothelial cells (MDVECs) and plasma cytokine levels, hemoglobin level and temperature in individuals with acute uncomplicated malaria, as well as healthy controls, using enzyme linked immunosorbent assay (ELISA) for the presence of soluble endothelial cell adhesion molecule-1 (sE-selectin), circulating granule membrane protein-140 (sP-selectin), circulating thrombomodulin (TM), circulating von Willebrand factor (VWf), interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha). Significant differences were observed between falciparum malaria patients and the healthy people in term of levels of both sE-selectin and TM. The serum levels of sP-selectin and VWf were comparable between the two groups. The levels of both sE-Selectin and TM correlated positively with temperature, levels of IFN-gamma and levels of TNF-alpha; and negatively with hemoglobin levels. Trends of positive correlations were observed between level of sP-selectin or VWf and temperature. Furthermore, sE-selectin levels correlated with vomiting. These data suggest that sE-selectin and TM might be useful markers of endothelium activation in in vivo studies. Moreover, our results highlight the use of both sE-selctin and TM as markers of anemia.
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PMID:Markers of vascular endothelial cell damage and P. falciparum malaria: association between levels of both sE-selectin and thrombomodulin, and cytokines, hemoglobin and clinical presentation. 1877 3

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food allergy characterized by severe vomiting, diarrhea, and often failure to thrive in infants. Symptoms typically resolve after the triggering food-derived protein is removed from the diet and recur within few hours after the re-exposure to the causal protein. The diagnosis is based on clinical symptoms and a positive food challenge. In this study, we report a case of FPIES to rice in an 8-month-old boy. We performed a double-blind placebo-controlled food challenge (DBPCFC) to rice and we measured the intracellular T cell expression of interleukin-4 (IL-4); IL-10, and interferon gamma (IFN-gamma) pre-and post-challenge during an acute FPIES reaction and when tolerance to rice had been achieved. For the first time we describe an increase in T cell IL-4 and decrease in IFN-gamma expression after a positive challenge with rice (i.e. rice triggered a FPIES attack) and an increase in T cell IL-10 expression after rice challenge 6 months later after a negative challenge (i.e., the child had acquired tolerance to rice) in an 8 month old with documented FPIES to rice. A Th2 activation associated with high IL-4 levels may contribute to the pathophysiology of the disease. On the other hand, T cell-derived IL-10 may play a role in the acquisition of immunotolerance by regulating the Th1 and Th2 responses.
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PMID:Cytokine expression in CD3+ cells in an infant with food protein-induced enterocolitis syndrome (FPIES): case report. 2001 55