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)

Dopamine receptor stimulation causes vascular and neurohumoral responses that may be beneficial in patients with heart failure. Oral inactivity, emesis and adrenergic-induced arrhythmias have limited the use of currently available compounds. Fenoldopam (SKF-82526-J) is a new, orally available, selective, dopamine-receptor agonist with potent renal vasodilating properties (six times that of dopamine) without positive inotropic or adrenergic activity. Drug efficacy was clinically evaluated in 10 patients with heart failure after single oral doses of placebo and 50, 100 and 200 mg of medication. Placebo produced no changes. Peak efficacy was noted 30 minutes to 1 hour after the 200 mg dose with mean blood pressure decreasing from 96 +/- 15 (mean +/- SD) to 83 +/- 8 mm Hg (p less than 0.05), pulmonary capillary wedge pressure decreasing from 23 +/- 6 to 20 +/- 8 mm Hg (p less than 0.05) and mean pulmonary artery pressure decreasing from 32 +/- 9 to 29 +/- 8 mm Hg (p less than 0.05). Systemic vascular resistance decreased from 1,987 +/- 887 to 1,191 +/- 559 dynes.s.cm-5 (p less than 0.05) with a subsequent 55% increase in cardiac index from 2.2 +/- 1.1 to 3.1 +/- 1.3 liters/min per m2 (p less than 0.05). Heart rate and right atrial pressure did not change (p greater than 0.05). No emesis or new tachycardia was noted at any dose. Baseline hemodynamics generally returned within 3 to 4 hours. Fenoldopam, therefore, is a short-acting, orally effective drug that decreases systemic vascular resistance and increases cardiac index in patients with heart failure and represents a new class of oral compounds that may be useful in treating such patients.
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PMID:Hemodynamic effects of an oral dopamine receptor agonist (fenoldopam) in patients with congestive heart failure. 286 95

Ten sheep were inoculated with bluetongue virus (BTV) serotype 17. Six of the sheep had been vaccinated before challenge exposure, 4 sheep served as nonvaccinated challenge-exposed controls, and 2 additional sheep served as nonvaccinated, nonchallenge-exposed, contact controls. Biopsy specimens (oral labial mucosa and skin) were obtained periodically after challenge exposure. Sheep were killed 8 to 13 days after challenge exposure, and necropsy was done. Vaccination did not seem to affect the nature or severity of the lesions observed. The changes in the mucosa of the cranial portion of the digestive tract included hyperemia, edema, inflammation, petechiae, erosions, ulcers, and surface encrustations. Lesions of skeletal, cardiac, and smooth muscles included hemorrhage, edema, myofiber degeneration, and necrosis. Lesions in cardiac muscles were sometimes widespread, indicating that cardiac failure may have been the major contributor to pulmonary congestion, edema, and eventual death during acute BTV infection. Damage to esophageal musculature resulted in vomiting. Hemorrhage was observed within the base of the pulmonary artery of all challenge-exposed sheep. Using immunofluorescence, bluetongue viral antigens were detected in small blood vessels of the skin, oral labial mucosa, tongue, esophagus, rumen, reticulum, urinary bladder, and pulmonary artery and in skeletal and cardiac muscles. Viral antigens were present in tissues obtained 3 to 11 days after inoculation. Ultrastructurally, changes in small-caliber blood vessels included congestion, hemorrhage, swollen degenerated endothelial cells, and occasional fibrin-platelet thrombi. Tubular structures and virus-like particles were observed within some of these endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental bluetongue virus infection of sheep; effect of vaccination: pathologic, immunofluorescent, and ultrastructural studies. 301 27

The patient is a woman who was born in 1936. Her father died of a valvular heart disease and her mother died of apoplexy. She was healthy until 1976 when she noticed stiffness of extremities and so she came to our hospital. At this time, her symptoms disappeared without any specific therapy. In 1979, she entered this hospital because of generalized edema. She was diagnosed as heart failure and treated effectively with frusemide. In 1982, stiffness and gait disturbance aggravated and entered the hospital. At this hospitalization, she was diagnosed as Kearns-Sayre syndrome. After the discharge, she was followed periodically. In May 1983, it was found that she could not abduct and spinate her thumbs. This abnormal hand posture was seen constantly thereafter although the severity of it varied. In April 1985, she was admitted to this hospital because of vomiting and the aggravation of the stiffness. EMG study disclosed spontaneous continuous motor unit discharges. F wave was exaggerated in both frequency and amplitude. The spontaneous activity of the thenar muscle was reduced by blocking the median nerve at the wrist. The patient was administered 250 mg of carbamazepine. Abnormalities of hand posture and EMG were markedly ameliorated by the regimen. We considered that the patient was a rare case of Kearns-Sayre syndrome which was complicated by a syndrome of continuous muscle fiber activity (Isaacs-Mertens syndrome). We speculated that disorders of energy metabolism of motor neurons and inter neurons in the spinal cord might causally relate to spontaneous neuronal discharges.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Report of a case of Kearns-Sayre syndrome associating with Isaacs-Mertens syndrome]. 317 91

Experimental and clinical experience with compounds containing antimony have shown that the trivalent compounds are generally more toxic than the pentavalent ones. APT can cause severe pain and tissue necrosis and is therefore not given by intramuscular or subcutaneous injection. APT has the actions and uses of AST, but it is less soluble and more irritating than the sodium salt which is therefore more suitable for intravenous use. Trivalent antimony compounds are toxic when used topically. Adverse effects are similar for all trivalent compounds, and include nausea, vomiting, weakness and myalgia, abdominal colic, diarrhoea, and skin rashes, including pustular eruptions. Hypersensitivity reactions also occur. Respiratory symptoms include cough, dyspnoea, and chronic lung changes. Cardiotoxicity is the most important and may produce arrhythmias, myocardial depression and damage, Stokes-Adams attacks, heart failure, and cardiac arrest. Hepatic damage and necrosis, as well as blood dyscrasias, may occur. Toxic effects on the kidney may follow chronic use. Continuous treatment with small doses of antimony may give rise to symptoms of subacute poisoning, similar to those of chronic arsenic poisoning, due to accumulation of antimony in the body, especially if trivalent compounds are used, because of their long biological half-lives. Reproductive disorders and chromosome damage have been reported; antimony compounds are, therefore, potentially toxic to reproduction and have mutagenic, and oncogenic potential. Antimony compounds should, therefore, not be used during pregnancy or in the presence of hepatic, renal, or heart disease. Pentavalent antimony preparations especially the organic compounds, together with non-metallic synthetic preparations, such as the diamidines, have now replaced APT for use in leishmaniasis. Because of the toxicity of antimony compounds, investigations have been undertaken to reduce their adverse effects by combining them with chelating agents. These preparations appear to have reduced the toxic effects of antimony without affecting the efficacy of the preparations. Liposome-encapsulated antimony products have, more recently, been shown to be much less toxic because of the reduced dose of the antimony compound required for effective therapy. The historical uses of antimony were based on the belief that the topical and systemic adverse effects, for example, skin eruptions and diarrhoea and vomiting, were signs that the condition being treated was responding by being brought to the surface to relieve congestion at the diseased area. There is no evidence in topical use, but there is evidence that such use can cause severe reactions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxicity of antimony and its compounds. 330 36

In a review of pediatric autopsies from 1951 to 1985, we identified 40 cases in which pancreatitis was diagnosed pathologically. Twenty-six of these patients were under 4 years of age, and the male-to-female ratio was 1.5. Six groups of patients were identified: 10 with hepatobiliary disease, including 9 with biliary atresia; 7 with immunosuppressive therapy for tumors (n = 2), leukemia (n = 4) and aplastic anemia (n = 1); 6 with viral infections; 8 with congenital anomalies, including congenital heart disease (n = 3); and 9 with miscellaneous problems. Several patients had surgery and various intercurrent complications. Clinical features attributable to the pancreatitis included vomiting or excessive nasogastric drainage (60%), pleural effusions (40%), and abdominal pain (25%). However, the diagnosis was suspected clinically in only 5 of 40 patients. Our findings suggest several pathogenic mechanisms exist for childhood pancreatitis: biliary obstruction, infections, drug toxicity, immunosuppression (acting in synergy with drug toxicity, trauma, and low-flow states resulting from shock, heart failure, and vasculopathy.
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PMID:Clinicopathologic studies in childhood pancreatitis. 334 10

Thirty-seven evaluable patients with progressive disseminated breast carcinoma were treated with a combination of mitoxantrone 14 mg/m2 i.v. every 3 weeks plus prednisone 20 mg/m2 p.o. daily with a reducing dose over several weeks. Thirteen of 37 patients (35%) achieved an objective response with two complete regressions. The median duration of response was 7 months and the median duration of survival 14 months. The cardiac function of all patients was monitored by serial left ventricular ejection fraction, at rest and after stress, and 3-monthly thereafter. Ten patients showed a deterioration in the ejection fraction after a minimum cumulative dose of 86 mg/m2 (six cycles), but only four developed clinical cardiac failure which was easily reversible after stopping mitoxantrone. Leucopenia was the dose-limiting toxicity. Nausea and/or vomiting were generally mild and transient. Alopecia was minimal. These results confirmed that this combination is effective and well tolerated in the treatment of disseminated breast carcinoma, and cardiotoxicity can be avoided with adequate monitoring of the left ventricular ejection fraction after six cycles of therapy (86 mg/m2).
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PMID:Primary chemotherapy with mitoxantrone and prednisone in advanced breast carcinoma. A phase II study. 338 49

Ninety patients with breast cancer refractory to cyclophosphamide/fluorouracil/methotrexate (CMF) have been randomized in their treatment, receiving either doxorubicin or mitoxantrone. Seventy-nine have received two full courses of therapy. Twelve of the 40 (30%) who initially received doxorubicin responded, whereas eight of the 47 (17%) who received mitoxantrone responded. These rates are not statistically different. The degree of myelosuppression was equivalent. Patients who received mitoxantrone had less nausea, vomiting, alopecia, and fatigue. Controllable clinical congestive heart failure developed in seven patients, and four others had a deterioration of noninvasive measures of cardiac function without clinical failure. One patient with clinical heart failure developing received only doxorubicin and one, only mitoxantrone, whereas the others received both agents. The duration of remission and time lapsed before disease progression were almost identical for the two regimens. This study included a crossover design. Two of 22 (10%) patients receiving doxorubicin and five of 24 (21%) receiving mitoxantrone as secondary therapy responded. This suggests that there is not absolute cross-resistance between these agents. We conclude that the efficacy of these two drugs is comparable in patients refractory to CMF, though the nonhematologic side effects of mitoxantrone are less.
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PMID:A comparison of mitoxantrone and doxorubicin in breast cancer. 351 41

Sixteen patients with advanced evaluable urothelial cancer were treated with a chemotherapy regimen of cyclophosphamide, adriamycin and cisplatin (CAP). Cisplatin 50 mg/m2 and adriamycin 30 mg/m2 were given on the first day and cyclophosphamide 200 mg/m2 was given from the second to the fifth day. This course was repeated every 3 weeks. The objective response rate was 25% (4 of 16 patients), with 1 patient achieving complete remission. The survival time of responders was longer than that of nonresponders, although the difference was not significant (generalized Wilcoxon method). As side effects, nausea with vomiting (43.8%), renal dysfunction (6.3%), anemia (12.5%), leucopenia (12.5%), thrombocytopenia (25.0%), alopecia (68.8%), heart failure (6.3%) and peripheral neuropathy (6.3%) were noticed. One patient died of sepsis due to agranulocytosis and another died suddenly of heart failure.
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PMID:[Combination chemotherapy of cyclophosphamide, adriamycin and cisplatin in advanced urothelial cancer]. 367 92

Results of first-line mitoxantrone chemotherapy for advanced breast cancer are presented. Full dose (14 mg/m2 iv every 3 weeks) was given to 22 patients who had received no previous adjuvant chemotherapy; five (23%) partial responses were seen. No responses were seen in eight patients who had failed adjuvant chemotherapy, of whom seven received full dose. No responses were seen in nine patients receiving lower doses (mean, 10 mg/m2). The overall response rate was 13%. Treatment was well tolerated. Moderate or severe nausea/vomiting and alopecia were infrequent. One patient developed heart failure without predisposing risk factors.
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PMID:First-line mitoxantrone chemotherapy for advanced breast cancer. 373 Nov 48

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.
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PMID:[Candidiasis of the esophagus. Prospective study of incidence, type of complaints and predisposing factors]. 373 73


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