Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Marrow is cryopreserved for use in autologous bone marrow transplants, but little is known of the incidence of reactions in patients transfused with these cryopreserved marrows. Reactions in patients transfused during a 4-year period with 134 autologous marrows cryopreserved in dimethyl sulfoxide (DMSO) were compared with those in patients transfused with marrow that had been collected from HLA-compatible donors and that had not been cryopreserved. Patients transfused with cryopreserved marrow had significantly more nausea (44.8 vs. 14.1%; p less than 0.0005), vomiting (23.9 vs. 8.5%; p less than 0.01), chills (31.3 vs. 1.4%; p less than 0.0005), and fever (17.9 vs. 0%; p less than 0.005) than patients transfused with fresh allogeneic marrow. The incidence of emesis correlated with the dose of DMSO received, but that of nausea did not. All cryopreserved marrows were cultured for bacteria at the time of transfusion and 17 (12.7%) were found to be positive. Only 1 of the 17 patients transfused with culture-positive marrow developed sepsis during the transplant course with the same organism that was present in the transfused marrow. Although the reactions in donors transfused with cryopreserved marrow were readily treated, this study suggests that the incidence of some reactions might be decreased by reducing the dose of DMSO transfused. Bacterial contamination of transfused marrow was a worrisome complication, and efforts should be made to improve marrow collection and processing techniques to minimize that risk.
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PMID:Adverse reactions in patients transfused with cryopreserved marrow. 185 47

A phase I trial of natural human beta-interferon (nHuIFN-beta) was initiated to evaluate its biological activity, maximum tolerated dose, and toxicity in patients with refractory malignancies. nHuIFN-beta was administered to successive groups of 4-6 patients as an i.v. bolus on days 1 and 4, for 4 consecutive weeks. Dose levels were 0.1, 1.0, 10, 30, 60, 100, and 200 x 10(6) units/m2. Thirty-five patients were entered, and 34 patients were evaluable for toxicity, immunomodulatory, and antitumor effects. Toxicity was mild to moderate and included fever and chills, fatigue, arthralgias, nausea, transient renal and hepatic dysfunction, and leukopenia. No dose-limiting toxicity was observed, and no responses were seen. Significant immunological changes included the following: an increase in natural killer activity on day 5 when compared to pretreatment values (P less than 0.01) and an increase in activated T-cells (CD3+/HLA-DR+) with increasing doses of nHuIFN-beta (P less than 0.01). Pharmacokinetic data demonstrated a short alpha half-life of 12.1 +/- 2.5 (SE) min and a beta half-life of 129.7 +/- 14.7 min. Neutralizing serum antibodies were detected in 2 of 27 patients receiving nHuIFN-beta. In conclusion, toxicity of nHuIFN-beta given twice weekly was moderate, and further dose escalation is possible. The immunological changes and pharmacokinetic behavior of nHuIFN-beta resemble those reported with rHuIFN-beta ser.
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PMID:Phase I trial of natural human interferon beta in metastatic malignancy. 198 23

A 55-year-old woman with common variable immunodeficiency and mild chronic obstructive lung disease received 3 units of plasma as immunoglobulin replacement therapy. During the administration of the final unit, her temperature rose 1 degree C, with no other observable symptoms. Fifteen minutes later she developed shortness of breath without nausea, vomiting, rash, or pruritus. In 30 min she lost consciousness, was breathless, and cyanotic. Resuscitative efforts failed. Autopsy failed to pinpoint a cause of death. There was no evidence of ABO or Rh incompatibility, bacterial contamination, or hemolysis. There were no neutrophil, platelet or IgA antibodies detectable in the patient or the 3 plasma donors. There were no lymphocytotoxic HLA antibodies in the patient or two of the plasma donors. The third donor had HLA-B35 lymphocytotoxic antibodies that did not agglutinate or aggregate neutrophils. The patient's HLA type was A2, A3; B35, B40. Lymphocytotoxic crossmatches using lymphocytes of the patient were positive with plasma from the third donor but negative with the other two. An eluate prepared from post-mortem lung parenchymal tissue was cytotoxic to 7 of 8 panel lymphocytes positive for the HLA-B35 antigen but not with cells lacking B35. The implicated plasma donor was healthy with a history of 6 pregnancies. This case report illustrates the potential hazard of transfusion of plasma containing HLA antibodies.
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PMID:Fatal pulmonary transfusion reaction to plasma containing donor HLA antibody. 280 Apr 69

We identified two siblings with exercise-induced anaphylaxis who share the HLA haplotype A3-B8-DR3 with their atopic father. The index case, a 16-year-old female, noted initial episodes at age 13. Intense pruritus, urticaria, facial edema, choking sensation, nausea, hypothermia, and collapse followed vigorous running but not swimming, cycling, racquetball, solar exposure, or cold exposure. Neither antihistamine, antiserotonin, anticholinergic nor epinephrine therapy was entirely effective or protective; only modification of running prevented episodes. Three similar episodes were noted at age 15 years by a brother who, now age 25, relates a 4-year history of seasonal rhinitis and exercise-related urticaria without anaphylactoid reaction. The remainder of the family (father, 47; mother, 46; brother, 22 years) does not have exercise intolerance. The father has allergic rhinitis; his nephew suffers exercise-induced urticaria without collapse. HLA typing revealed the father to be A1-B8-DR3, A3-B8-DR3; the symptomatic daughter to be A3-B8-DR3, A30-B5-DR8; and the symptomatic son to be A3-B8-DR3, A30-B5-DR8. The asymptomatic mother was A30-B5-DR8, A2-B7-DR5 and the asymptomatic son A1-B8-DR3, A30-B5-DR8. We describe exercise-induced anaphylaxis in a unique familial setting, perhaps linked to the HLA haplotype A3-B8-DR3.
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PMID:Familial exercise-induced anaphylaxis. 347 Oct 98

Twenty-eight patients with refractory rheumatoid arthritis completed a randomized 24-week double-blind crossover trial comparing oral methotrexate (2.5 to 5 mg every 12 hours for three doses weekly) with placebo. The methotrexate group had significant reductions (P less than 0.01 as compared with the placebo group) in the number of tender or painful joints, the duration of morning stiffness, and disease activity according to physician and patient assessments at the 12-week crossover visit; reductions in the number of swollen joints (P less than 0.05) and 15-m walking time (P less than 0.03) also occurred. These variables, as well as the grip strength and erythrocyte sedimentation rate, showed significant (P less than 0.01) improvement at 24 weeks in the population crossed over to methotrexate. A significantly increased frequency (P less than 0.03) of the HLA-DR2 haplotype occurred in the eight patients with the most substantial response to methotrexate. Adverse reactions during methotrexate therapy included transaminase elevation (21 per cent), nausea (18 per cent), and diarrhea (12 per cent); one patient was withdrawn from the trial because of diarrhea. One patient died while receiving the placebo. Methotrexate did not affect measures of humoral or cellular immunity. We conclude that this trial provides evidence of the short-term efficacy of methotrexate in rheumatoid arthritis, but the mechanism of action is unknown. Longer trials will be required to determine the ultimate safety and effectiveness of this drug.
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PMID:Efficacy of low-dose methotrexate in rheumatoid arthritis. 388 72

11 courses of EACA were given to 9 acutely ill, severely thrombocytopenic patients (platelet count less than 20 X 10(9)/l). 6 patients were being treated for acute leukaemia while 1 each had cyclical amegakaryocytic thrombocytopenia, dysmyelopoietic syndrome and advanced chronic lymphocytic leukaemia. 8 were refractory to HLA-matched platelets and 1 refused blood product transfusion. All had simultaneous major medical complications such as infection and granulocytopenia. The highest dose of EACA used was 24 mg/d. Improvement in haemostasis was noted in all patients with successful control of epistaxis in 1, control of gastrointestinal bleeding in 3 and lack of significant bleeding for 4-29 d in the remaining 5 patients. The only toxicity was dose-related nausea. Since this patient group was at extremely high risk for haemorrhage, we conclude that EACA is safe and useful in the management of thrombocytopenia including that occurring during leukaemic induction.
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PMID:Anti-fibrinolytic therapy with aminocaproic acid for the control of bleeding in thrombocytopenic patients. 408 29

Adult identical twins with Moyamoya disease are reported. Laboratory examinations such as blood types, AB, Rh(+), HLA (human leucocytic antigen) analysis [AW26(9), A26(10), BW62(15), BW61(40), CW3], and finger prints, and hairs confirmed that two patients were identical twins. Both had normal serum immunoglobulin levels and no anti-DNA antibodies. Patient No. 1, a 39-year-old female, was admitted to our service with chief complaints of nausea, vomiting and left hemiparesis with sudden onset on Oct 31, 1981. The patient had an episode of tetraplegia that occurred suddenly at 4 years of her age and lasted about a week. Motor weakness had completely disappeared but moderate mental retardation remained. She had been employed just prior to this attack. CT and angiographic examinations revealed ventricular hemorrhage with Moyamoya disease, which had miliary aneurysm in the branch of the right posterior choroidal artery. The operation of encephalomyosynangiosis was performed on her left hemisphere. The postoperative course was uneventful. Patient No. 2, the twin sister of patient No. 1, was in good health and mental state until 19 years of her age, when she suddenly lost consciousness and developed hemiparesis. After this attack, her motor function had recovered well. However, mental ability gradually deteriorated and she was admitted to a psychiatric ward. CT examination and angiographic studies were performed on Oct 12, 1982, and she was diagnosed as having Moyamoya disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adult identical twins with moyamoya disease]. 654 69

A 60-year-old woman was admitted to our hospital complaining of nausea, thirst, and dyspnea on exertion. She had skin eruptions on her back and right knee. Her serum calcium level was 12.6 mg/dl. The chest roentgenogram showed diffuse nodular shadows in both lung fields. The level of angiotensin-converting enzyme in serum was markedly high, and epithelioid cell granulomas were found in the specimens obtained by skin biopsy and by transbronchial lung biopsy. Sarcoidosis was diagnosed. After administration of prednisolone, the serum calcium level decreased to within the normal range and the shadows on the chest roentgenogram resolved. Hypercalcemia complicated with sarcoidosis is caused by overproduction of 1 alpha,25-dihydroxyvitamin D in granulomas. The content of 1 alpha, 25-dihydroxyvitamin D in the transbronchial lung biopsy specimen from this patient was higher than that from a sarcoidosis patient whose serum calcium level was normal. A few case reports of sarcoidosis with hypercalcemia have been published in Japan. The association with HLA type and the possibility of overintake of dietary vitamin D are discussed in reference to hypercalcemia in this patient.
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PMID:[Sarcoidosis with hypercalcemia and increased 1 alpha, 25-dihydroxyvitamin D in lung tissue]. 747 74

This study evaluated the acute toxicity of trimetrexate (TMTX) used in combination with cyclosporine (CsA) for prevention of acute graft-versus-host disease (GVHD) in patients undergoing allogeneic marrow transplantation from HLA-mismatched, related donors. TMTX has a mechanism of action similar to that of methotrexate (MTX); however, unlike MTX, TMTX is not primarily dependent on renal excretion. Patients were conditioned for transplant with cyclophosphamide, anti-thymocyte globulin, and total body irradiation. TMTX, 10 mg/m2 i.v., was administered on days 1, 3, 6, 11, 18, 25, 32, and 39 after transplant. CsA, 1.5 mg/kg i.v., was administered every 12 hr beginning on day-1. Eleven patients with hematologic malignancies or aplastic anemia (median age = 34 yr) received TMTX. Toxicity assessed included nausea, vomiting, fever, rash, time to myeloid and platelet engraftment, mucositis, and hepatic and renal dysfunction. Toxicity of TMTX was not different from that observed with MTX in a similar patient population. One patient died on day 16 before engraftment. The other 10 patients all engrafted and all developed acute GVHD at a median time of 11 days after transplant. The major manifestation of acute GVHD was in the skin, and all but one patient responded to primary therapy with corticosteroids. Seven patients have survived a median of 447 days after transplant. No significant toxicity from TMTX was observed. Further trials are warranted to define the role of TMTX in marrow transplantation.
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PMID:A toxicity study of trimetrexate used in combination with cyclosporine as acute graft-versus-host disease prophylaxis in HLA-mismatched, related donor bone marrow transplants. 762 43

Cataplexy is a cardinal manifestation of the narcolepsy syndrome. Although symptomatic narcolepsy is well described, isolated cataplexy is extremely rare. We reviewed clinical and radiologic data in two patients with isolated symptomatic cataplexy and associated CNS disease. In an HLA-DR2-positive patient with chronic progressive MS, we confirmed cataplexy by observation of reported spells. MRI revealed diffuse white-matter lesions involving the medial medulla, pons, and subcortical white matter; protriptyline provided symptomatic relief. A second patient with a pontomedullary pilocytic astrocytoma developed infrequent but recurrent cataplectic attacks in association with sleep fragmentation due to nocturnal cough and nausea. MRI revealed an enhancing lesion involving the dorsal pons and medulla. Genetic predisposition and sleep fragmentation may precipitate symptomatic cataplexy in patients with structural pontomedullary lesions.
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PMID:Symptomatic cataplexy in pontomedullary lesions. 796 83


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