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)

Suramin sodium is a reverse transcriptase inhibitor with in vitro activity against the human immunodeficiency virus (HIV), the causative agent of acquired immunodeficiency syndrome (AIDS). Ninety-eight patients with AIDS manifest as opportunistic infections (n = 38), AIDS with Kaposi's sarcoma (n = 38), AIDS-related complex (n = 20), or AIDS-associated non-Hodgkin's lymphoma (NHL) (n = 2) were treated with suramin sodium at 0.5, 1.0, or 1.5 g/wk for six weeks followed by maintenance therapy with 0.5 or 1.0 g/wk. Of 72 patients who were HIV culture positive before therapy and were assessable for subsequent HIV culture 40% became culture negative during treatment, with no apparent correlation between virus recovery and serum suramin concentration. No immunologic improvement was noted. One complete clinical remission was noted in a patient with Kaposi's sarcoma and stage IV NHL. Seven minor clinical responses were also noted. Toxic reactions were generally reversible, and included fever (78%), rash (48%), malaise (43%), nausea (34%), neurologic symptoms (33%), and vomiting (20%). Suramin-induced neutropenia was noted in 26%, thrombocytopenia in 12%, a serum creatinine level of 180 mumol/L or higher (greater than or equal to 2.1 mg/dL) in 12%, liver dysfunction in 14%, and clinical and/or laboratory evidence of adrenal insufficiency in 23%. Sixteen patients died while receiving suramin or within three weeks of discontinuation of drug therapy due to infection (n = 6), hepatic failure (n = 3), pulmonary Kaposi's sarcoma (n = 2), AIDS encephalitis (n = 2), AIDS-associated NHL (n = 1), iatrogenic hemo-pneumothorax (n = 1), or pulmonary disease of uncertain etiology. Suramin as currently administered cannot be recommended as effective therapy for AIDS.
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PMID:Suramin therapy in AIDS and related disorders. Report of the US Suramin Working Group. 365 Mar 39

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

Non-steroidal, anti-inflammatory agents (NSAIDs), wellknown inhibitors of prostaglandins, have been used in the treatment of biliary and ureteral pain since the end of the 1970s. The efficacy and tolerance of a new injectable formulation of naproxen sodium in ureteral and biliary pain was investigated in 77 out-patients, observed in an emergency ward, and affected by acute lithiasic symptomatology. Forty-four patients received one 275 mg vial of naproxen sodium intramuscularly, while 33 patients were given one vial at the same dosage intravenously. In 56% of the cases complete relief of pain was achieved within 30 minutes of injection, while in 86% pain was completely relieved or greatly decreased within one hour. Side-effects (nausea, vomiting) occurred in three patients, but were linked to a simultaneous aggravation of the ureteral colic.
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PMID:Treatment of acute pain of ureteral and biliary colic with naproxen sodium administered by the parenteral route. 380 21

Gold compounds, often used in the treatment of rheumatoid arthritis, have been associated with gastrointestinal disturbances in some patients. Use of auranofin, an oral gold preparation, in a 50-year-old woman with rheumatoid arthritis resulted in diarrhea, abdominal tenderness, nausea, and vomiting, which persisted despite discontinuation of auranofin therapy. The presumptive diagnosis was gold-induced colitis and eosinophilia. Administration of cromolyn sodium provided relief. Although this complication may be rare, evolving bowel symptoms in patients receiving auranofin demand prompt attention.
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PMID:Auranofin-associated colitis and eosinophilia. 380 38

We administered cisplatin and etoposide by peritoneal dialysis to 39 patients with i.p. malignancies in order to investigate the toxicity, pharmacokinetics, and clinical activity of this 2-drug combination. All patients received i.v. sodium thiosulfate concurrently with the i.p. chemotherapy. Myelosuppression, nausea, vomiting, and malaise were the primary toxicities encountered. The maximum tolerated dose of etoposide was 350 mg/m2, when administered with a fixed dose of cisplatin, 200 mg/m2. Although the total (free and protein-bound) etoposide exposure for the peritoneal cavity was only 1.5-fold greater than that for the plasma, the free (non-protein bound) etoposide peritoneal exposure was 65-fold greater than the plasma. Tumor regressions were noted in patients with ovarian and pancreatic carcinomas. This study is the first demonstration of the large pharmacokinetic advantage that exists for the i.p. administration of highly protein-bound drugs, and it also documents the clinical activity of i.p. cisplatin and etoposide.
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PMID:Phase I/pharmacokinetic study of intraperitoneal cisplatin and etoposide. 381 69

In order to examine the influence of carotid baroreceptor stimulation on arginine vasopressin secretion, 8 normal healthy males were subjected to static neck suction of -3.3 kPa for 20 min in the upright sitting position after overnight food and fluid restriction. The plasma concentration of arginine vasopressin did not change significantly during neck suction. However, in 3 subjects the termination of neck suction induced large increases in plasma arginine vasopressin from 1.8 to 63.7 ng/l, from 0.7 to 34.3 ng/l and from 2.1 to 19.0 ng/l, respectively. Two subjects experienced symptoms such as nausea and paleness during neck suction. Systolic arterial pressure increased slightly but significantly during neck suction from 15.3 +/- 0.3 to 15.7 +/- 0.4 kPa (N = 7, P less than 0.05), whereas mean arterial pressure, diastolic arterial pressure, central venous pressure, heart rate, plasma osmolality, plasma sodium and potassium were unchanged. Haemoglobin concentration in blood and haematocrit increased significantly during and after neck suction, whereas plasma volume decreased. We conclude that neck suction with a negative pressure of 3.3 kPa in upright sitting man does not significantly affect plasma arginine vasopressin. However, termination of the stimulation induces large increases in some subjects. This may be explained by a direct effect on the vagus nerve or by a selective deloading of carotid baroreceptors.
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PMID:Plasma arginine vasopressin during neck suction in upright sitting man. 382 42

The effect of two conventional high-osmolality and two new low-osmolality contrast media on plasma histamine levels has been examined. The study population included 25 patients undergoing intravenous urography with Urovison 58% (sodium and meglumine diatrizoate), 24 patients receiving intravenous Hexabrix 320 (sodium and meglumine ioxaglate) for urography, 16 patients receiving intravenous Iopamiro 370 (iopamidol) for urography and 12 patients receiving Urografin 76% (sodium and meglumine diatrizoate) for coronary angiography. Seventy-four percent of the 77 patients studied suffered adverse reactions ranging from a feeling of warmth and nausea to laryngeal oedema and bronchospasm. Hexabrix 320 and Iopamiro 370 were associated with the least patient discomfort. All contrast agents usually produced a rise in plasma histamine following injection (Iopamiro 370 causing the least change) and the histamine levels then fell towards preinjection values over a space of about 10 minutes. No relationship was observed between the magnitude of the increase in histamine and the severity of the reaction that occurred. However, a relationship was suggested between the mean peak plasma histamine level achieved and the occurrence of a Grade II reaction (i.e., dry retching/vomiting, mild urticaria or rash). These findings raise the probability that histamine contributes to the more severe grades of reaction to radiographic contrast media.
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PMID:Plasma histamine levels following administration of radiographic contrast media. 384 11

Intravenous bolus injection of an 80- to 120-mg/m2 dose of cisplatin followed by "rescue" with sodium thiosulfate (STS) was tried in the treatment of 7 patients with advanced tumor. STS was given continuously i.v. six hours after cisplatin injection, combined with methylprednisolone and metoclopramide as antiemetics. Four patients were evaluable, consisting of one CR, one PR and two NC. Severe nausea and emesis occurred in two patients and irreversible renal dysfunction occurred in one. The clinical use of the STS rescue regimen was discussed in conjunction with our basic investigation of "STS-rescue" in an animal model.
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PMID:[Systemic chemotherapy with high-dose cisplatin and sodium thiosulfate rescue]. 386 35

In nonanesthetized young pigs, the influence of prednisolone sodium succinate therapy on a 65% lethal dose of Escherichia coli endotoxin was studied by evaluating clinical signs, several hemodynamic variables, survival rate, and changes seen at necropsy. Endotoxin infusion induced reproducible clinical signs characterized by nausea, vomiting, dyspnea, cyanosis, and moderate excitement followed by severe CNS depression. Among the hemodynamic variables, there were decreases in arterial blood pressure and cardiac output and increases in pulmonary arterial pressure, heart rate, and total peripheral and pulmonary vascular resistances. Core temperature and arterial pH did not change significantly. Survival rate at 30 hours after the start of the endotoxin infusion was 35%. According to the necropsy, marked edema and hemorrhages were in several organs. Treating the experimental animals with prednisolone sodium succinate (3 injections of 10 mg/kg of body weight after the start of the endotoxin infusion) did not influence any of the monitored hemodynamic variables, except for arterial blood pressure, which was higher at the end of the hemodynamic recording period (270 minutes after the start of the endotoxin infusion). Clinical signs, survival rate, and changes at necropsy were similar in both treated and nontreated pigs. This lack of effect can be due to an inappropriate dosage of the steroid or failure of steroid treatment to alleviate endotoxin-mediated effects.
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PMID:Endotoxic shock in the awake young pig: absence of beneficial effect of prednisolone sodium succinate treatment. 389 34

The efficacy of safety of naproxen sodium and ergotamine tartrate were compared for the treatment of acute migraine attack in a randomized, parallel trial with 114 participating patients. At the start of symptoms, patients took either three tablets of naproxen sodium (275 mg each) or one of an ergotamine combination (containing 2 mg ergotamine tartrate, 91.5 mg caffeine, and 50 mg cyclizine chlorhydrate). Patients were followed for three months or until six attacks were monitored, whichever came first. Both medications substantially shortened the duration of migraine attacks and reduced the severity of symptoms. When the test medications were taken within 2 h of onset of attack, naproxen sodium was statistically significantly more effective than the ergotamine combination in reducing the severity of headache pain, nausea, and lightheadedness. The ergotamine combination was associated with significantly more vomiting, need for rescue medication, and side effects than was naproxen sodium. Four patients required discontinuation of the ergotamine combination and one of naproxen sodium. Both patients and investigators rated tolerance for naproxen sodium as superior to tolerance for the ergotamine combination. Naproxen sodium seems to be an effective and safe treatment for migraine attacks.
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PMID:Acute migraine attack therapy: comparison of naproxen sodium and an ergotamine tartrate compound. 392 22


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