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)

Desferrioxamine (DFX) remains the most effective and safe iron chelator for treatment of patients with transfusional iron overload. It is usually given by intermittent subcutaneous infusions for 8-12 h on 4-6 days weekly using a battery-driven pump. Disposable balloon infusers provide a suitable method of giving continuous subcutaneous infusions with improved patient compliance. For patients with cardiac abnormalities due to iron overload, continuous intravenous desferrioxamine is essential to eliminate toxic plasma non-transferrin bound iron and to reduce body iron stores. Deferiprone (L1, l-2 dimethyl-3hydroxy-pyrid-4-one) is a less effective iron chelator but has the advantage of being orally active. Long-term trials in which patients have taken 75 mg/kg/day have shown that deferiprone is capable of maintaining body iron stores at safe levels in a proportion of thalassaemia major patients but body iron stores, assessed by liver biopsy remain at high levels (> 15.0 mg/g dry weight) in a substantial number of patients. These concentrations have been associated with tissue damage. Trials of increased doses of deferiprone (up to 100 mg/kg/day) or of combined therapy with daily deferiprone and DFX or 1 or 2 days each week are being carried out in an attempt to achieve lower body iron burden in these patients. Preliminary results show that the drugs can be given safely together and urine iron excretion produced is additive, implying that the drugs chelate different body iron pools. Patients previously well chelated with serum ferritin levels less than 2500 micrograms/L have the fewest side-effects from deferiprone and usually may be kept at the same level of body iron for periods of at least 4 years, assessed by serum ferritin and urine iron excretion. The side-effects of deferiprone result in some patients discontinuing therapy. These side-effects, especially arthropathy, mainly occur in previously poorly chelated and so the most heavily iron-loaded patients. Nausea and other gastrointestinal symptoms, agranulocytosis or milder degrees of neutropenia account with arthropathy for nearly all the withdrawals from deferiprone therapy. Patients with cardiomyopathy due to iron overload should be given intravenous DFX rather than deferiprone. Deferiprone, licensed for pharmaceutical use in India, awaits official approval for widespread clinical use in Western Europe and North America. Meanwhile, attempts to find new orally active iron chelators and improved methods of administration of desferrioxamine are in progress.
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PMID:Iron chelation therapy. 935 Jan 80

The prevalence of Noonan syndrome has been estimated at between 1 out of 1000 and 1 out of 2500 live births; it is often confused with Turner syndrome because the two conditions display a common phenotype. Even if Noonan syndrome is typically associated with congenital heart diseases, prognosis is generally good. We describe the case of a female patient, deaf from infancy, in whom the presence of obstructive cardiomyopathy had been previously demonstrated angiographically at 29 years of age. A diagnosis of Turner syndrome had been made on the basis of her physical features. One year later she began to complain of accessional headache with nausea; seizures occurred at 48 years of age. The patient suddenly died during a hospital stay for investigation of these symptoms. Autopsy evidenced multiple cerebral hemorrhages due to vascular anomalies. She had normal female genitalia. This case demonstrates that Noonan syndrome is still misdiagnosed, and that it may have various clinical symptoms. In particular, it underscores the opportunity of carrying out systematic research on cerebrovascular abnormalities in these patients because they are potentially fatal.
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PMID:[Noonan's syndrome associated with cerebral hemorrhage. Report of a case]. 1168 53

Due to concerns about toxicity, many elderly patients with aggressive non-Hodgkin's lymphoma (NHL) are not considered candidates for standard chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP). The cytoprotective agent amifostine has the potential to reduce toxicity when added to chemotherapy. The purpose of the current study was to examine the toxicity of CHOP combined with amifostine in elderly patients with aggressive NHL. A prospective phase II study was performed in patients aged 60 years and older. Patients with stage I/II disease received 4 cycles of CHOP followed by involved-field irradiation. Patients with stage III/IV received 6-8 cycles of CHOP. Amifostine (740 mg/m(2)) was administered as a 15-min i.v. infusion immediately before chemotherapy. Forty-one (median age 69.5 years, range 60-87) of 49 consecutive previously untreated patients, aged 60 years and older, with aggressive NHL seen in our center were included in the study. Twenty-one patients had stage I/II disease and 20 had stage III/IV disease. The patients received a total of 207 cycles of amifostine-CHOP. Infusion of amifostine caused mild to moderate transient side effects, including a drop of systolic blood pressure >20 mmHg in 54 cycles and nausea/vomiting in 36 cycles. Hematotoxicity of CHOP consisted of leukopenia grade 4 in only 15.4% of cycles. There were two cases of grade 3 anemia. No thrombocytopenia higher than grade 2 occurred. Febrile neutropenia was rare, occurring in 4.3% of cycles. One patient died after the first CHOP administration because of anthracycline-related acute cardiomyopathy (corresponding to a toxic death rate of 2.4%). The complete response rates were 85 and 75% in stage I/II and stage III/IV patients, respectively. After median follow-up of 33 months (range 17-50 months) the median overall survival was not reached in patients with stage I/II and was found to be 32 months in patients with stage III/IV. At 2 years, 76% of patients with stage I/II and 70% with stage III/IV were alive. Twelve of the 15 patients who died were aged older than 70. Amifostine pre-treatment was associated with a low toxicity of CHOP in elderly patients with aggressive NHL treated with curative intent. Treatment outcomes appeared not to be impaired by the addition of amifostine to CHOP. This schedule merits further testing in a randomized trial.
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PMID:Influence of amifostine on toxicity of CHOP in elderly patients with aggressive non-Hodgkin's lymphoma--a phase II study. 1198 85

The anthracycline glycoside antibiotics represent a group of potent anticancer agents with a wide spectrum of activity against solid tumours and haematological malignancies, and are the mainstay of a large number of clinical protocols for the treatment of adult and childhood neoplastic diseases. Their clinical activity is limited, however, by acute and chronic adverse effects. Myelosuppression, predominantly neutropenia and leucopenia, is the dose-limiting toxicity; in addition to this, mucositis, nausea, vomiting and alopecia are frequent, whereas hepatopathy, characterised by elevated bilirubin concentrations, occurs less frequently. Cardiotoxicity is a major adverse effect of the anthracycline antibiotics and can be acute or chronic; in the acute setting, electrocardiographic abnormalities may be seen, including ST-T elevations and arrhythmias, but chronic cardiotoxicity represents a serious adverse effect that may be lethal due to the development of irreversible, cumulative dose-dependent, congestive cardiomyopathy. The occurrence of toxicity displays a marked interindividual variation, and for this reason the pharmacokinetics and pharmacodynamics of anthracyclines have been extensively investigated in order to identify integrated models that can be used in the clinical setting to prevent the development of serious toxicity, mainly leucopenia, and maximise tumour exposure. Pharmacokinetics has been recognised to influence both the toxicity and the activity of anthracyclines; in particular, there is increasing evidence that the mode of administration plays an important role for cumulative cardiotoxicity and data indicate that bolus administration, rather than continuous infusion, appears to be an important risk factor for anthracycline-induced cardiomyopathy, thus implying that this type of toxicity is maximum concentration-dependent. On the contrary, exposure to the drug, as measured by area under the curve, seems best related to the occurrence of leucopenia. Finally, the development of pharmacokinetic-pharmacodynamic models allows the simulation of drug effects and ultimately dose optimisation in order to anticipate important toxicities and prevent their occurrence by the administration of prophylactic treatments.
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PMID:Pharmacokinetic-pharmacodynamic relationships of the anthracycline anticancer drugs. 1207 91

Treatment of patients with mitoxantrone for worsening multiple sclerosis (MS) requires careful monitoring for possible adverse events. Common side effects that are minor and easily managed include transient leukopenia and elevated liver enzymes, nausea, alopecia, bluish discoloration of urine, and urinary tract infections. Amenorrhea, severe infection, cardiac toxicity, and toxic leukemias are more serious adverse events associated with mitoxantrone treatment but occur infrequently. The potential for clinically significant heart failure is low and is dose-related. Subclinical reductions in left ventricular ejection fraction may occur with serial doses, underscoring the importance of careful monitoring before initiating and during treatment. The risk for chronic cardiomyopathy limits the approved cumulative dose of mitoxantrone for treatment of MS to 140 mg/m2. Dexrazoxane has a cardioprotective effect when used with anthracycline in the treatment of patients with neoplasms. Studies under way address whether concomitant administration of dexrazoxane with mitoxantrone might decrease the risk for cardiac toxicity in MS patients and perhaps increase the allowable cumulative dose of mitoxantrone. A phase IV clinical study of mitoxantrone (RENEW) is in progress to assess the long-term safety and tolerability of treatment. Careful laboratory and cardiac monitoring can reduce the possibility of adverse events and enhance patient safety.
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PMID:Mitoxantrone treatment of multiple sclerosis: safety considerations. 1638 Jun 36

This study explored the prevalence and burden of symptoms in a community-based sample of patients aged >60 with symptomatic heart failure. Five hundred forty-two patients were recruited from UK general practices. Participants completed the Kansas City Cardiomyopathy Questionnaire every 3 months for 2 years. Data are presented at baseline alongside findings from in-depth interviews with patients and focus groups with primary care professionals. Over half the participants experienced breathlessness and/or fatigue daily. Factors identified as predictive of symptom prevalence and burden were as follows: being female; being staged at New York Heart Association Class III or IV; having symptoms of depression; and having two or more comorbidities. Interviews identified other symptoms, including chest pain, nausea, sleep disruption, and confusion. Participants felt that symptoms restricted activities of daily living. Health professionals reported symptom control as being a concern of patients and identified their own educational needs in this area. Findings suggest that symptom prevalence and burden for this population is high. Primary care professionals should offer comprehensive assessment and treatment of symptoms.
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PMID:Prevalence of symptoms in a community-based sample of heart failure patients. 1693 45

Metastatic cancers are associated with cellular oxidative stress, and during cancer chemotherapy excess drug-induced oxidative stress can limit therapeutic effectiveness and cause a number of side effects, including fatigue, nausea, vomiting, diarrhea and more serious adverse effects, such as cardiomyopathy, peripheral neuropathy, hepatotoxicity and pulmonary fibrosis. We review here the hypothesis that the acute and chronic adverse effects of cancer chemotherapy can be reduced by molecular replacement of membrane lipids and enzymatic cofactors, such as coenzyme Q(10). By administering nutritional supplements with replacement molecules and antioxidants, oxidative membrane damage and reductions of cofactors in normal tissues can be reversed, protecting and restoring mitochondrial and other cellular functions and reducing chemotherapy adverse effects. Recent clinical trials using cancer and non-cancer patients with chronic fatigue have shown the benefit of molecular replacement plus antioxidants in reducing the damage to mitochondrial membranes, restoring mitochondrial electron transport function, reducing fatigue and protecting cellular structures and enzymes from oxidative damage. Molecular replacement and antioxidant administration mitigates the damage to normal tissues, such as cardiac tissue, and reduces the adverse effects of cancer therapy without reduction in therapeutic results.
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PMID:Reversing mitochondrial dysfunction, fatigue and the adverse effects of chemotherapy of metastatic disease by molecular replacement therapy. 1805 28

Takotsubo cardiomyopathy (TC), or "broken heart syndrome", is an increasingly recognized condition that mimics acute myocardial infarction with morphologically characteristic left ventricular dysfunction in the absence of coronary artery disease. TC is seen almost exclusively in postmenopausal women following extreme emotional or physiologic stress. Although most patients present with chest pain, limited data suggest that African American patients with TC tend to present with atypical symptoms such as dyspnea or nausea. We present a 57 year-old African American female with TC who presented with severe dyspnea following the shooting death of her son. Added to existing data, our case alerts clinicians to consider Takotsubo syndrome in African American patients with atypical presentation.
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PMID:Takotsubo cardiomyopathy presenting with dyspnea. 1930 82

Takotsubo cardiomyopathy (TC) is an uncommon entity. It is known to occur in the setting of extreme catecholamine release and results in left ventricular dysfunction without evidence of angiographically definable coronary artery disease. There have been no published reports of TC occurring with visual stimuli, specifically 3-dimensional (3D) entertainment. We present a 55-year-old woman who presented to her primary care physician's office with extreme palpitations, nausea, vomiting, and malaise <48 hours after watching a 3D action movie at her local theater. Her electrocardiogram demonstrated ST elevations in aVL and V1, prolonged QTc interval, and T-wave inversions in leads I, II, aVL, and V2-V6. Coronary angiography revealed angiographically normal vessels, elevated left ventricular filling pressures, and decreased ejection fraction with a pattern of apical ballooning. The presumed final diagnosis was TC, likely due to visual-auditory-triggered catecholamine release causing impaired coronary microcirculation.
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PMID:Three-dimensional entertainment as a novel cause of takotsubo cardiomyopathy. 2188 91

A 49-year-old white man was admitted to the emergency department with nausea and diarrhea of 11 hours duration. He had experienced crampy abdominal pain as well. He reported that his stools had been dark and malodorous. He had no prior history of gastrointestinal disorders, nor travel, unusual oral or liquid intake. There was a remote history of alcohol abuse, but no hepatitis or cirrhosis. Recent alcohol intake was denied by the patient. He had no medical allergies. His past medical history was pertinent for a history of hypertension, congestive heart failure, and a dual chamber pacemaker insertion. There was no history of diabetes mellitus, smoking, or myocardial infarction. Medications included lisinopril, a small dose of aspirin daily, and thyroid supplement. Family history was negative for cardiomyopathy, sudden cardiac death, gastric or duodenal ulcers, colon cancer, or any congenital abnormalities.
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PMID:Pacemaker limitation of tachycardia in hypovolemic shock. 2222 62


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