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)

The purpose of this study was to compare the toxicity, immunomodulatory changes, and antitumor efficacy of interleukin 2 (IL-2) and lymphokine activated killer (LAK) cell therapy with two durations of IL-2 infusion. Patients with progressive melanoma, non-Hodgkin's lymphoma, renal carcinoma, or colon carcinoma received IL-2 at 3 X 10(6) units/m2/day on days 1-5 and 13-17, either by bolus injection every 8 h (q8h) or by continuous i.v. (CIV) administration. Peripheral blood mononuclear cells were harvested by leukapheresis on days 8, 9, and 10, were incubated in vitro for 5 days for generation of LAK cells, and were infused on days 13, 14, and 15. The first 11 patients were treated with IL-2 q8h, and the subsequent 13 patients were treated by CIV infusion. Toxicity consisted primarily of fever, chills, emesis, diarrhea, weight gain, and edema but did not require intensive care unit support and did not differ significantly between treatment groups. IL-2-induced lymphocytosis on day 8 was higher with CIV than with q8h administration with a mean lymphocyte count/microliter of 5610 +/- 700 (SE) versus 3300 +/- 500. Immunomodulatory changes observed on days 8 and 20 were also greater with CIV IL-2 and included an increase in peripheral blood mononuclear cell IL-2 receptor expression as well as a marked rise in the number of Leu-11+ and Leu-19+ peripheral blood mononuclear cells. The total leukapheresis yield per patient and total number of LAK cells infused per patient were higher with CIV than q8h administration, with 49.8 +/- 4.9 X 10(9) versus 39.4 +/- 5.4 X 10(9) and 42.6 +/- 5.0 X 10(9) versus 34.0 +/- 5.4 X 10(9), respectively. The cells infused displayed phenotypic evidence of activation and exhibited marked lytic reactivity to Daudi, Raji, and HT-144 targets. One complete and one minimal response were observed in 2 of 8 patients with metastatic renal cell carcinoma who received CIV IL-2 and LAK cells. The results show that IL-2 is more biologically active by CIV than q8h administration, as demonstrated by greater rebound lymphocytosis, LAK cell yield, and in vivo immunostimulation.
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PMID:Influence of schedule of interleukin 2 administration on therapy with interleukin 2 and lymphokine activated killer cells. 278 43

A murine anti-idiotypic monoclonal antibody (mAb), F1, (IgG2a) was produced against the variable part of the T-cell receptor for antigen (Ti, alpha/beta) on the tumor cells of a patient with T-cell chronic lymphatic leukemia (CD3+,8+,4-). The molecular weight of the protein reactive with mAb F1, comodulation and coprecipitation with anti-CD3 antibody, and the restricted tumor-cell reactivity strongly support the anti-idiotypic nature of mAb F1. MAb F1 also stained less than or equal to 4% of peripheral blood lymphocytes of healthy donors. MAb F1 did not stimulate the tumor cells to DNA synthesis, but stimulated a fraction of the normal peripheral blood lymphocytes, mAb F1 did not mediate antibody-dependent cellular cytotoxicity or complement lysis to any significant degree in vitro. Three infusion of 1-10 mg anti-idiotypic mAb were given over a period of 4 weeks. The plasma half-life for mAb F1 was 3 h in the first 2 h after infusion and 44 h from 2 h to 120 h after infusion. After each treatment a rapid decrease of circulating tumor cells was seen. During the observation period an 80% reduction of the total circulating tumor cells was noted. After the second infusion, IgM and IgG antimouse antibodies were detected. Side-effects from therapy were fever, chills, nausea, vomiting, diarrhea, tachycardia, increase in systolic blood pressure and shortness of breath. Thus, in T-cell malignancies a major reduction of circulating tumor cells can be accomplished by low doses of anti-idiotypic mAb. Anti-idiotypic mAb might be a therapeutic agent of significant importance.
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PMID:Anti-idiotypic monoclonal antibody to a T-cell chronic lymphatic leukemia. Characterization of the antibody, in vitro effector functions and results of therapy. 278 57

Based on a phase I study in 1986, 22 patients have been entered in a phase II study of high-dose human tumor necrosis factor (rH-TNF) since May 1987. Of these patients, 18 are evaluable at present, 2 are still under investigation, and 2 have dropped out. All had advanced stages of cancer (9 soft-tissue sarcomas, 3 melanomas, 5 hypernephromas) and inclusion in the study was ethically acceptable (informed consent). The daily dose of rH-TNF was 15 x 10(5) units/m2, escalated to 21 x 10(5) units/m2 (683-956 micrograms/m2 every week; range 1-6 cycles). Additional prophylactic ketoprofen administration was carried out. Of the 18 evaluable patients, 4 responded with no change (2/4, clinical improvement) and 14 showed progressive disease. The main toxicities observed were hypotension (decrease in systolic blood pressure, 21-60 Torr), leukocytosis, increases in ALAT/ASAT (WHO grade 0-4), fever (WHO grade 1-2), chills (mild to moderate), neurotoxicity (WHO grade 0-2), and nausea/vomiting (WHO grade 0-3).
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PMID:Phase II clinical trial of high-dose recombinant human tumor necrosis factor. 279 Nov 93

Nineteen patients with advanced cancer for which there was no effective standard therapy or whose disease was refractory to standard therapy were treated with recombinant tumor necrosis factor (rTNF). The rTNF was administered subcutaneously for 5 consecutive days every other week for 3 treatment weeks. The doses administered ranged from 5 micrograms/m2/day to 150 micrograms/m2/day. There was no intrapatient dose escalation. Systemic side effects of chills, fever, hypotension, nausea, vomiting, and headache were mild and self-limiting. At the maximum tolerated dose of 150 micrograms/m2/day, five of seven patients experienced moderate to severe thrombocytopenia. Mild rapid declines in total leukocyte count occurred within 60-90 min of administration of the drug, followed by a rise in the total leukocyte count by 120 min. When the total daily dose was administered in a single subcutaneous site, skin ulceration and necrosis occurred at the 100 micrograms/m2/day dose. By giving the total daily dose in two subcutaneous sites, the maximum tolerated dose increased to 150 micrograms/m2/day, and there was no further skin ulceration or necrosis. Skin necrosis occurred in the abdomen and thigh but not on the upper extremity at the 100 micrograms/m2/day dose given in a single site. There was no other significant organ toxicity. No rTNF was detectable in the serum even at the highest doses. No antibodies to TNF developed in any of the patients. The recommended dose of rTNF for Phase II trials given for 5 days subcutaneously is 150 micrograms/m2/day divided into two or more sites.
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PMID:A phase I trial of subcutaneously administered recombination tumor necrosis factor to patients with advanced malignancy. 279 95

Twenty-seven patients with metastatic cancer were treated with a daily continuous intravenous (IV) infusion of recombinant human interleukin-2 (rhIL-2) along with daily intramuscular recombinant interferon-alpha-2a (rIFN-alpha-2a) 4 days per week for 4 weeks with repeated treatment after 2 to 4 weeks of rest. The maximum-tolerated dose (MTD) was 3 million U/m2/d of rhIL-2 with 5 to 10 million U/m2/d of rIFN-alpha-2a. The dose-limiting toxicities are moderate hypotension requiring low doses of pressors and chronic fatigue associated with decreased performance status. Other common side effects included fever, chills, fluid retention, nausea/vomiting, erythrodermia, weight loss, elevated liver transminase levels, anemia, thrombocytopenia, and CNS toxic effects. There were seven objective responses among 25 evaluable patients. Four major responses (one complete response and three partial responses) were observed among 10 patients with melanoma treated with the MTD level. These data suggest that for cancer patients, concomitant rhIL-2 and rIFN-alpha-2a therapy is tolerable and has manageable side effects. Further phase II studies will be needed to define the antitumor activity of this combination.
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PMID:Concomitant administration of recombinant human interleukin-2 and recombinant interferon alpha-2A in cancer patients: a phase I study. 280 85

2 cases of thromboembolism in young women with no risk factors except use of triphasic oral contraceptives are reported. A 21-year old White woman, Gravida I Para I, presented to the emergency room with a painful, blue, mottled right lower leg after pain in the hip and buttock for 1 week. She had taken a triphasic oral contraceptive containing 35 mcg ethinyl estradiol and 0.5, 0.75, 1 mg norethindrone for 1 month, and had no other related history. Doppler and venogram tests showed thrombosis of the ileal, femoral, popliteal and infrapopliteal veins. She was treated with heparin, streptokinase, and urokinase without success and recovered after ileal, femoral and popliteal thrombectomy. The 2nd case was a 30-year-old Gravida III Para I Black woman who had taken a pill containing 50 mcg ethinyl estradiol and 500 mcg norgestrel for 13 years and had recently switched to the triphasic pill described above. She had dull midepigastric pain, nausea, vomiting, diarrhea and chills, for 1 week. Physical exam was negative except for abdominal tenderness and a heart murmur. Abdominal ultrasound revealed portal venous thrombosis extending to the splenic and superior mesenteric veins. She was treated with transhepatic urokinase without effect and celiotomy was performed. She was discharged with an occluded right branch of the portal vein. These cases point out the fact that the estrogen dose in triphasic pills is not lower than that in low dose combined oral contraceptives.
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PMID:Idiopathic thromboembolism associated with triphasic oral contraceptives. 281 53

A phase I trial of intramuscularly administered recombinant human tumor necrosis factor (rTNF) was conducted in 19 adult patients with advanced solid tumors. The agent was administered daily for up to five consecutive days every other week for two to four courses. Doses of rTNF ranged from 5 to 200 micrograms/m2/d. Dose-limiting toxicities were encountered at doses greater than 100 micrograms/m2/d. Toxicities included tenderness, erythema and induration at the site of injection, fatigue, fever, chills, headache, anorexia, nausea, vomiting, and diarrhea. Moderate to marked reductions in WBC and platelet counts were observed regularly at the highest dose levels, but none were clinically significant. Hepatic enzyme elevation was seen frequently, and two patients developed hyperbilirubinemia. Only one of seven patients treated with doses greater than 100 micrograms/m2/d completed the planned course of therapy. Even at the highest dose levels, serum concentrations of rTNF could only rarely be detected in the serum. No therapeutic responses were observed. The maximal tolerated dose (MTD) of rTNF in this trial was 150 micrograms/m2/d, administered for two courses.
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PMID:Phase I trial of intramuscularly administered tumor necrosis factor in patients with advanced cancer. 291 29

An explosive outbreak of gastrointestinal illness occurred among students and employees at a small college in Florida in November 1980. Common symptoms were diarrhea, nausea, weakness, abdominal cramps, chills, vomiting, and low-grade fever. Cases of illness were identified in 40% of 628 students and 15% of 162 employees who responded to a survey. Among students, there was a sevenfold excess risk associated with eating one or more meals at the campus cafeteria November 3-5 (p much less than 0.001). Tossed salad from one meal was strongly associated with illness (p less than 0.0001). Fecal contamination of the salad was documented, although the source of contamination was not identified. Person-to-person spread could not be demonstrated. Seroconversion to Norwalk antigen occurred in significantly more cases (5/6) than noncases (1/6) (p = 0.04).
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PMID:Norwalk virus gastroenteritis. An outbreak associated with a cafeteria at a college. 299 Jan 97

A Phase I study of rHu-TNF (PT-050) was conducted in patients with various malignant tumors refractory to conventional therapy. rHu-TNF was administered by 30-min intravenous (i.v.) infusion or intratumor (i.t.) injection. The starting dose of 1 X 10(5) U/body was increased to 5 X 10(6) U/body in the i.v. group and to 2 X 10(6) U/body in the i.t. group. rHu-TNF was evaluated in 41 patients among the enrolled 43 patients of the i.v. group, and in 9 out of 10 in the i.t. group. In the i.v. group, fever (68.3%), chills (75.6%), hypotension (46.3%), general fatigue (34.1%), nausea/vomiting (22.0%/22.0%), pain in the extremities (17.1%), etc. were observed as adverse reactions (ADRs), and elevation of GOT/GPT (46.3%/43.9%), elevation of ALP(26.8%)and decrease in platelets (12.2%), etc. were observed as abnormal laboratory findings. Among these, hypotension was recognized as the dose-limiting factor and the maximum tolerated dose was considered to be 1 X 10(6) U/body. Plasma levels of rHu-TNF after 30-min i.v. administration were dose-related, and decreased with half-lives of 0.5-2.4 hours. In the i.t. group, ADRs occurred with a lower incidence than in the i.v. group except for fever, chills and general fatigue. Plasma levels after i.t. administration were all within the assay limit. Evident tissue necrosis was observed in the region where rHu-TNF was administered in the i.t. group.
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PMID:[A phase I study of recombinant human tumor necrosis factor (rHu-TNF: PT-050). The PT-050 Study Group]. 302 81

A study was conducted at the Ndola Central Hospital, Zambia, in 1987 to determine whether human immunodeficiency virus (HIV) infection increases the risk or severity of infection with falciparum malaria in patients aged 12 years and over. The 170 patients examined all presented with symptoms suggestive of malaria, including fever, chills, rigors, headaches, joint pains, myalgia, acute diarrhea, and vomiting. 67 (39%) were diagnosed as having falciparum malaria and 28 (17%) were positive for the HIV antibody. The prevalence of malarial parasitemia in patients with HIV antibodies was lower than that in patients without such antibodies (29% versus 42%, respectively), and differences in densities of parasites also failed to provide evidence of increased susceptibility to malaria in patients infected in HIV. There were no significant differences in antibody titers to P falciparum in patients who were positive for HIV antibody and in those who were negative, whether or not they had parasitemia. The earlier finding of a significant association between malaria and HIV infection is now believed attributable to false positive results with the 1st enzyme linked immunosorbent assays and to interpretation difficulties with the Western blot test. Of interest is the fact that 20 patients in this study had symptoms suggestive of malaria, but had negative results for parasites and positive results for HIV antibody. This indicates that many patients with HIV infection may be presenting with an illness clinically similar to malaria before acquired immunodeficiency syndrome (AIDS)-related complex or AIDS is recognizable.
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PMID:Relation between falciparum malaria and HIV seropositivity in Ndola, Zambia. 304 86


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