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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluvoxamine facilitates serotoninergic neurotransmission via potent and selective inhibition of serotonin (5-hydroxytryptamine; 5-HT) reuptake into presynaptic neurones. The overall antidepressant efficacy of fluvoxamine 100 to 300 mg/day for 4 to 6 weeks in once daily or divided dosage regimens appears to be at least comparable to that of imipramine and similar to that of clomipramine, dothiepin, desipramine, amitriptyline, lofepramine, maprotiline, mianserin and moclobemide. The efficacy of fluvoxamine has been maintained for up to 1 year, but long term data are limited, and there are no comparative studies of fluvoxamine with other selective serotonin reuptake inhibitors. In some studies, fluvoxamine appeared to have an earlier beneficial effect on suicidal ideation and/or anxiety or somatic complaints compared with imipramine, dothiepin and maprotiline. Gastrointestinal adverse effects, especially nausea, are commonly reported with fluvoxamine but are generally mild to moderate in severity. The tolerability profile of fluvoxamine appears to be more favourable than that of tricyclic antidepressants in terms of cardiotoxic and anticholinergic adverse effects, sedation, weight gain and death from overdosage. Thus, fluvoxamine is an effective and well tolerated antidepressant agent that is becoming established as an alternative to older agents in patients with mild, moderate or severe depression. Fluvoxamine may be particularly beneficial in potentially suicidal patients with severe depression, in those with an underlying compulsive personality or cardiovascular disorder, in patients with coexistent anxiety or agitation, and in the elderly.
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PMID:Fluvoxamine. An updated review of its pharmacology, and therapeutic use in depressive illness. 750 38

Over an eight year period (1985-1993), we treated 424 patients with various forms of cardiovascular disease by adding coenzyme Q10 (CoQ10) to their medical regimens. Doses of CoQ10 ranged from 75 to 600 mg/day by mouth (average 242 mg). Treatment was primarily guided by the patient's clinical response. In many instances, CoQ10 levels were employed with the aim of producing a whole blood level greater than or equal to 2.10 micrograms/ml (average 2.92 micrograms/ml, n = 297). Patients were followed for an average of 17.8 months, with a total accumulation of 632 patient years. Eleven patients were omitted from this study: 10 due to non-compliance and one who experienced nausea. Eighteen deaths occurred during the study period with 10 attributable to cardiac causes. Patients were divided into six diagnostic categories: ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), primary diastolic dysfunction (PDD), hypertension (HTN), mitral valve prolapse (MVP) and valvular heart disease (VHD). For the entire group and for each diagnostic category, we evaluated clinical response according to the New York Heart Association (NYHA) functional scale, and found significant improvement. Of 424 patients, 58 per cent improved by one NYHA class, 28% by two classes and 1.2% by three classes. A statistically significant improvement in myocardial function was documented using the following echocardiographic parameters: left ventricular wall thickness, mitral valve inflow slope and fractional shortening. Before treatment with CoQ10, most patients were taking from one to five cardiac medications. During this study, overall medication requirements dropped considerably: 43% stopped between one and three drugs. Only 6% of the patients required the addition of one drug. No apparent side effects from CoQ10 treatment were noted other than a single case of transient nausea. In conclusion, CoQ10 is a safe and effective adjunctive treatment for a broad range of cardiovascular diseases, producing gratifying clinical responses while easing the medical and financial burden of multidrug therapy.
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PMID:Usefulness of coenzyme Q10 in clinical cardiology: a long-term study. 775 28

A 49-year-old woman had a right adrenalectomy for pheochromocytoma in April 1989. In May 1990 she underwent an operation to remove paraaortic lymph nodes, and the lymph nodes showed pheochromocytoma. Twenty-two months after the first operation, metastases to the left cervical nodes, lung, and liver occurred. Her blood pressure was 172/104 mmHg; fasting plasma glucose (FPG), 342 mg/dl; urinary noradrenaline (NA), more than 2000 micrograms/day; and plasma NA, 17.28 ng/ml. Treatment with the CVD regimen (cyclophosphamide, 750 mg/m2 on day 1; vincristine, 1.4 mg/m2 on day 1; dacarbazine, 600 mg/m2 on days 1 and 2, every 21 days) was begun on February 14, 1991. After 3 cycles of the CVD regimen her blood pressure was 140/82 mmHg; FPG, 157 mg/dl; urinary NA, 917 micrograms/day 1; and plasma NA, 4.54 ng/ml. The size of the metastatic lesions in the liver had decreased. Treatment with the CVD regimen was continued until May 1992. After that she did not go to the hospital for about 2 months. Metastatic lesions progressed gradually and treatment with the CVD regimen was repeated again. She was admitted to the hospital on February 17, 1993 because of appetite loss and nausea. Her blood pressure was 188/94 mmHg; FPG, 197 mg/dl; HbA1c, 9.5%; urinary NA, 18265.3 micrograms/day; and plasma NA, 47.20 ng/ml. She was treated with the CVD regimen in 2 repeated cycles (28th cycle of treatment with the CVD regimen) but there was no effect. She died following hemoptysis on March 15, 1993.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of malignant pheochromocytoma treated with a combination of cyclophosphamide, vincristine, and dacarbazine (CVD). A review of the Japanese literature of malignant pheochromocytoma treated with a combination of CVD]. 785 22

Despite advances in the delivery of hemodialysis, significant dialytic morbidity persists. Sodium modeling in older adults has been shown to decrease some dialytic symptoms, but clear benefits in young patients without coexisting diabetes or advanced cardiovascular disease have not been shown. The effects of sodium modeling were evaluated in 16 adolescent and young adult hemodialysis patients (16 to 32 yr of age) treated with conventional hemodialysis for a median of 11.5 months. The 8-wk study was divided into four 2-wk blocks. During each block, one of three sodium programs or a constant (control) dialysate sodium of 138 mEq/L was used. During each sodium program, the initial dialysate sodium of 148 mEq/L was decreased by an exponential, linear, or step program to 138 mEq/L. Treatments with sodium modeling were significantly better than those with constant sodium dialysate. When all sodium programs were grouped and compared with constant dialysate sodium, the odds of improvement in dialytic cramps, headaches, and nausea were 1.8, 2.1, and 3.9, respectively (P < 0.05). Sodium modeling also significantly decreased the frequency of postdialysis hypotension and interdialytic fatigue, dizziness, and muscle cramping (P < 0.05). No differences were seen among the sodium protocols in the incidence of symptomatic hypotension, the amount of normal saline administered, the degree of hemo-concentration during treatments, or the decrease in serum osmolality. There was no increase in pretreatment or posttreatment serum sodium concentrations, interdialytic thirst, weight gain, or hypertension. Sodium modeling dramatically decreases both intradialytic and interdialytic morbidity in young hemodialysis patients. There was no increase in adverse events associated with sodium modeling.
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PMID:Sodium modeling ameliorates intradialytic and interdialytic symptoms in young hemodialysis patients. 830 46

The side effects of oral contraceptives (OCs) can be minimized by appropriate OC selection. Side effects or perceived side effects that manifest themselves physically--e.g., weight gain, breakthrough bleeding (BTB), nausea, headache, breast tenderness, mood swings, acne, and hirsutism--are the most common causes of premature discontinuation of oral contraception. The relative androgenicity of the progestin component of combination OCs has become an important differential in selecting OC formulations. Several studies have indicated that preparations with less androgenic potential can minimize some of the "physical" side effects and adverse metabolic effects traditionally associated with oral contraception. Acne and hirsutism, common pre-existing conditions that are clearly related to the androgenicity of the progestin component, can be eliminated or improved by use of OCs with low androgenic activity. Many women perceive that OCs cause weight gain; although weight gain is to some extent androgen related, most studies comparing low-androgenic OCs with medium- or high-androgenic preparations have found little or no change in weight regardless of formulation. BTB, which usually subsides within a few months, is related to the dose, potency, and ratio of the estrogen and progestin in the OC formulation. Low-estrogen-dose OCs (< or = 35 micrograms ethinyl estradiol [EE]) containing less androgenic progestins are associated with bleeding patterns as acceptable as older low-estrogen-dose formulations. The same analysis found that smoking cigarettes promotes BTB in women who use OCs. There is no convincing evidence that the use of one progestin or another is less likely to cause or exacerbate headache; however, changing preparations sometimes reduces the incidence. Women with persistent headaches during the pill-free interval may benefit from a longer cycle of OC treatment. Nausea and breast tenderness are primarily estrogen-related effects; if a women experiences persistent nausea, switching to an OC formulation containing 20 micrograms EE may be appropriate as long as the patient is cautioned that BTB is more likely. Mood changes are a common, highly subjective complaint whose relationship to OC use is hard to assess. Concerns about the potentially deleterious effects of combination OCs on lipid/lipoprotein and carbohydrate metabolism have been substantially diminished by new epidemiologic findings relative to cardiovascular disease as well as by the development of low-androgenic progestins. Formulations containing these progestins lower LDL cholesterol and increase HDL cholesterol; they do not affect carbohydrate metabolism as much as older, more androgenic formulations.
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PMID:OC practice guidelines: minimizing side effects. 916 75

An 81-year-old woman reported with chest pain occurring shortly after initiating treatment with sertraline. She had no prior history of cardiovascular disease. She developed nausea and malaise 4 h after her first dose, which resulted in avoidance of further treatment. After voluntarily reinitiating sertraline 10 days later, she again developed nausea and malaise but persisted with treatment. On the second day, her gastrointestinal symptoms were accompanied by crushing retrosternal chest pain radiating to both arms and resolving spontaneously after 10 mins. Following the third dose of sertraline, the patient experienced severe and persistent crushing retrosternal chest pain radiating to both arms. She was hospitalized with a diagnosis of unstable angina and treated with acetylsalicylic acid, intravenous heparin and nitroglycerin. The temporal relationship of chest pain onset following ingestion of sertraline is strongly suggestive of an adverse medication effect.
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PMID:Unstable angina associated with sertraline. 934 35

This paper summarizes all postmarketing safety surveillance data collected by Solvay Pharmaceuticals, Inc. (Marietta, Georgia), between 1989 and 1996 for Estratest and Estratest HS (half-strength). These oral esterified estrogens--methyltestosterone combination products have been marketed in the United States since 1964 for the treatment of moderate-to-severe vasomotor symptoms associated with menopause in patients whose symptoms have not been relieved by estrogens alone. Between 1989 and 1996, more than 1 million woman-years of exposure occurred. The safety profile contained in this paper is based on a cumulative total of 568 individual cases comprising 863 adverse events (AEs). The proportions of AEs associated with the use of Estratest (575 events; 66.6%) and Estratest HS (288 events; 33.4%) were commensurate with the proportions of individual reports of adverse experiences for the two formulations (369 reports [65.0%] and 199 reports [35.0%], respectively). The rank order and percentage of types of AEs reported were also similar. The cumulative volume of reports was relatively low given the extent of exposure. Despite the limitations inherent in spontaneous postmarketing surveillance, the safety profile derived from this assessment does not indicate a significant safety concern with Estratest or Estratest HS. No deaths were reported, and no adverse findings indicative of the need for more comprehensive surveillance or concern on the part of the medical community or consumers were observed. Reports of cancer, cardiovascular disease, thromboembolic phenomena, and hepatic dysfunction were few and were assessed as not related to treatment with Estratest or Estratest HS; reports of drug overdose, drug-drug interaction, and birth defects were rare (4 of 863 events; 0.5%). The most commonly reported AEs were those known to be associated with estrogen therapy (weight gain, headache, nausea, and vasodilatation) and androgen treatment (alopecia, acne, and hirsutism). Twenty-three (4.0%) of the 568 cases reported had at least one event that was regarded as serious, and 53 (6.1%) of the total 863 AEs were regarded as serious. The findings indicate that Estratest and Estratest HS are safe when used as directed and that the marginal increase in risk associated with androgen coadministration can be managed with appropriate patient selection and monitoring, as stated in the package insert for these compounds.
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PMID:Safety surveillance of esterified estrogens-methyltestosterone (Estratest and Estratest HS) replacement therapy in the United States. 938 94

Cardiovascular disease is the leading cause of mortality in patients whose lives depend on hemodialysis. We developed a method for measuring cardiac output (CO) and central blood volume (CBV) in hemodialyzed patients that may help to elucidate the mechanisms and consequences of cardiac disease in this population. This report describes the technique, focusing on the main sources of error and how they can be prevented. Three principal sources of error were identified: (1) access recirculation (existing or induced during injection); (2) the second pass of the indicator through the cardiopulmonary system, exacerbated by prolonging the duration of intravenous injection; and (3) the transit time of the indicator through the dialysis blood lines. After the algorithms were adjusted to prevent the above errors, the reproducibility of CO and CBV, expressed as the absolute percent deviation from the average of duplicates (3,488 values duplicated within 5 minutes), was 4.3 +/- 3.8% for CO and 4.1 +/- 3.8% for CBV. To determine the clinical value of routine CO and CBV measurements, morbid events (nausea, vomiting, and/or muscle cramps) were prospectively recorded in 73 randomly selected hemodialysis patients. CO and CBV were measured near the beginning and near the end of 98 dialysis sessions during which 28 morbid events were identified. In 10 of these sessions, where morbid events took place within 30 minutes of the measurements, CBV appeared to be a more sensitive indicator of morbid events than CO. We conclude that CO and CBV can be routinely and reliably measured during hemodialysis if precautions are taken to avoid specifically identified sources of error. Preliminary studies suggest that these measurements may have significant prognostic value.
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PMID:Cardiac output and central blood volume during hemodialysis: methodology. 1045 5

Peripheral blood progenitor cell reinfusion (PBPC) in patients undergoing high-dose chemotherapy (HDC) for poor prognosis malignancies, has been described as causing possible acute gastrointestinal (nausea, vomiting), allergic (oedema, bronchospasm, anaphyl- axis), renal (proteinuria, haematuria) and/or cardiovascular (hypotension, arrhythmia, conduction disturbances, transient ischaemic phenomena) toxicities. To establish the clinical relevance of these observations and the possible relationship with different HDC regimens used, we performed a clinical and instrumental evaluation on 33 patients with advanced breast cancer, non-Hodgkin's lymphoma, Hodgkin's disease, relapsed ovarian cancer, Ewing's sarcoma, extragonadal germinal tumour and small cell lung cancer. They underwent at least one reinfusion each for a total of 51 studied procedures. No patient had a previous history of cardiovascular disease or significant intercurrent illness such as diabetes or liver, renal or neurologic impairment. All patients had totally implanted central venous catheters, through which the transplants had been collected and reinfused without technical consequences. To evaluate cardiovascular function, we continuously monitored 12-lead ECGs, with arterial pressure (AP) measurements every 5 min from the beginning of the procedure to 15 min after the reinfusion ended. We did not observe any significant differences between basal and subsequent steps in AP, heart rate, PQ and QTc time, P wave and QRS complex duration or P wave and QRS electrical axes. No patient showed any ST-T tract pathological abnormality, but one patient developed a transient ectopic atrial rhythm, without any haemodynamic disfunction and with spontaneous reversion to sinus rhythm. No patient complained of symptoms of haemodynamic failure. Gastrointestinal side-effects appeared to be strictly related to speed of reinfusion and to the number of packs reinfused, probably reflecting on the amount of dimethylsulphoxide infused. In one patient a tonic-clonic seizure occurred during a vomiting episode, but no patient developed allergic or renal toxicities. We conclude that PBPC reinfusion, if managed according to the procedure we propose in patients without organic impairment, is a safe procedure not associated either with increased risk of acute arrhythmias or ischaemic or significant systemic acute toxicities. Bone Marrow Transplantation (2000) 25, 173-177.
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PMID:Evaluation of acute toxicities associated with autologous peripheral blood progenitor cell reinfusion in patients undergoing high-dose chemotherapy. 1196 Feb 81

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8


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