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)

Anorexia is a common problem in terminally ill patients. The loss of appetite brings with it physical, psychological, and social problems. Effective treatment, therefore, should be multidimensional. The pharmacist is well-positioned to evaluate the appropriate use of medications for their effects on appetite, weight gain, mood, nausea, and anorexia. Studies have demonstrated that megestrol acetate has the most positive results in patients with advanced cancer and human immunodeficiency virus. Other medications studied have a less significant impact. Total parenteral nutrition can also sustain meaningful life for many terminally ill patients, but it is rarely successful in alleviating the anorexia associated with terminal illness.
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PMID:Appetite stimulants in terminal care: treatment of anorexia. 780 82

Valaciclovir, the L-valyl ester of acyclovir, is rapidly and extensively converted in humans to acyclovir after oral administration by first-pass metabolism. A phase I study was conducted in two cohorts of volunteers with advanced human immunodeficiency virus (HIV) disease (absolute CD4 lymphocyte count of < 150 cells per microliters) who received oral valaciclovir at dosages of 1,000 or 2,000 mg four times daily for 30 days. All patients were clinically stable without any changes in underlying HIV-related medications for > or = 6 weeks prior to entry in study; these medications were continued throughout the study. Multiple-dose administration of valaciclovir showed a generally favorable safety profile. Nausea, vomiting, diarrhea, and abdominal pain each were reported in < or = 31% of the patients; of these symptoms, only one episode of diarrhea was considered causally related to valaciclovir exposure. Four patients developed neutropenia (two at each dose level) which was not clinically significant. There were no renal or neurologic adverse events. Valaciclovir was rapidly absorbed and converted to acyclovir, with plasma valaciclovir levels generally undetectable or levels of < or = 0.4 microgram/ml. After 3 h postdosing, valaciclovir was not detectable in plasma. Acyclovir was measurable in plasma as early as 15 min following valaciclovir dosing, and plasma concentrations of acyclovir greatly exceeded those of valaciclovir. The mean values for the maximum concentration of drug in plasma, time to maximum concentration of drug in plasma, area under the concentration-time curve from 0 h to infinity, and apparent half-life of acyclovir obtained after single- and multiple-dose valaciclovir administration in HIV-infected patients were similar to those reported in normal healthy volunteers. The time to maximum concentration in serum and half-life of acyclovir after valaciclovir administration were approximately 2 and 3 h, respectively, which were similar to those reported after oral administration of acyclovir itself. The mean trough and peak acyclovir concentrations and the daily area under the concentration-time curve acyclovir values at steady state were 2.5 and 8.4 micrograms/ml and 120 h micrograms/ml, respectively, after a dosage of 2,000 mg of valaciclovir four times daily. These values were approximately fivefold greater than those achieved with high dosages of oral acyclovir (800 mg, five times daily) and were not affected by continued use of medications necessary for management of advanced HIV disease. Thus, 2,000 mg of valaciclovir given orally four times daily should be evaluated for its potential efficacy in suppressing cytomegalovirus and other herpes group virus infections not optimally managed with current oral acyclovir therapy.
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PMID:Phase I trial of valaciclovir, the L-valyl ester of acyclovir, in patients with advanced human immunodeficiency virus disease. 797 85

Infections of the esophagus are unusual in the general population and strongly imply immunodeficiency, although immunocompetent individuals are not exempt. HIV infection is predominant among risk factors for infectious esophagitis. For all immunocompromised patients, the most frequently identified esophageal pathogens are Candida, CMV, and HSV. Peculiar to HIV-infected patients are idiopathic esophageal ulcers as well as unusual bacteria and parasites. Patterns of presentation differ with each infecting organism, and clinical features should be used as a guide in achieving a correct diagnosis. For example, a patient with AIDS presenting with esophageal symptoms and thrush, along with abdominal pain, nausea, vomiting, and fever, is unlikely to resolve all symptoms with empiric antifungal therapy alone. Parsimony of diagnosis does not hold among immunodeficient patients in whom concurrent infections are common. Accurate and timely diagnoses are essential as effective treatments are available for particular etiologies. Finally, among immunocompromised patients, all esophageal symptoms are not necessarily due to an infection, and possible diagnoses of pill esophagitis, acid-peptic injury, or structural and functional abnormalities should not be overlooked.
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PMID:Esophageal infections: risk factors, presentation, diagnosis, and treatment. 752 21

A number of reports over the last several years have linked a previously unidentified acid-fast organism with prolonged diarrhea in humans. Initially thought to be a cyanobacterium, the organism has been identified as a coccidian protozoan of the genus Cyclospora, and the name Cyclospora cayetanensis has been proposed. Organisms that resemble Cyclospora protozoa have been discovered in human stool samples around the world and have been isolated from children, immunocompetent adults, and human immunodeficiency virus (HIV)-seropositive individuals. The apparently waterborne organisms cause disease predominantly in summer months. In wet mounts of fresh stool specimens, the organisms are wrinkled spheres of 8-9 microns in diameter, with well-defined nonrefractile external walls and internal granular material, and resemble large oocysts of Cryptosporidium species. Organisms fluoresce under ultraviolet illumination. Formalin-preserved oocysts are variably acid-fast, and the results of staining with the modified carbolfuchsin technique (which is used to stain Cryptosporidium species) range from no staining to deep-red staining. The clinical syndrome is characterized by watery diarrhea (approximately 6 stools/day), nausea, anorexia, abdominal cramping, fatigue, and weight loss. Diarrhea appears to be self-limiting in the immunocompetent host but may be prolonged in patients with advanced HIV infection. Symptoms have abated in a handful of people treated with trimethoprim-sulfamethoxazole. Many questions remain to be answered about this newly identified pathogen.
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PMID:Cyclospora: a newly identified intestinal pathogen of humans. 803 19

Zidovudine delays the progression of infection and prolongs the survival of human immunodeficiency virus (HIV)-infected patients, but these benefits are limited by dose-related toxicity and the cost of the drug. Dipyridamole, in micromolar concentrations, acts synergistically with zidovudine, reducing the anti-HIV 95% inhibitory concentration of zidovudine 5- to 10-fold in vitro. We sought to establish a well-tolerated dose of dipyridamole for use in combination with zidovudine and to detect clinically significant pharmacokinetic interactions. Both objectives are essential for planning studies of the efficacy of the zidovudine-dipyridamole combination. Eleven asymptomatic HIV-infected subjects (median CD4+ cell count, 311 cells per mm3), 10 of whom had been on zidovudine at 500 mg/day for at least 6 months, were admitted to the study. Zidovudine pharmacokinetics were measured on day 1. Dipyridamole was then begun at 600 mg/day (subjects 1 to 3) or 450 mg/day (subjects 4 to 11), and zidovudine and dipyridamole pharmacokinetics were measured on day 5. All subjects given 600 mg of dipyridamole per day developed headache or nausea, or both. Six of eight subjects given dipyridamole at 450 mg/day developed headache or mild nausea that resolved after a median of 2 days. The area under the zidovudine concentration-time curve was not significantly different on day 1 in comparison with that on day 5 (P = 0.11). Symptoms were significantly correlated with the maximum zidovudine concentrations, which were achieved when dipyridamole was dosed concomitantly (p = 0.03). Total (free and protein-bound) dipyridamole trough concentrations were near those demonstrating synergy with zidovudine against HIV in vitro. Dipyridamole was highly protein bound, with a median free/total dipyridamole ratio of 0.7%; the percent free/total dipyridamole ratio was inversely correlated with alpha 1 acid glycoprotein concentrations (r2 =0.66). Results of the study indicate that adjustment of the zidovudine dose was not required to achieve equivalent zidovudine concentrations when zidovudine was administered in combination with dipyridamole at the doses studied. In the short study described here, the zidovudine-dipyridamole combinations was well tolerated in asymptomatic HIV-infected subjects after the occurrence of mild transient symptoms.
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PMID:Effect of dipyridamole on zidovudine pharmacokinetics and short-term tolerance in asymptomatic human immunodeficiency virus-infected subjects. 806 34

Valaciclovir (BW256U87) is an L-valyl ester of acyclovir, which is extensively and almost completely converted to acyclovir. In healthy human volunteers, single valaciclovir doses of 100-1000 mg resulted in dose-proportional increases in acyclovir area under the curve (AUC). The 1,000 mg dose produced an acyclovir peak plasma concentration (Cmax) of 5-6 micrograms/ml, AUC6 of 19 hr. micrograms/ml, time to maximum plasma concentration (Tmax) of 1-2 hr, and half-life (T1/2) of 2.8 hr. Plasma valaciclovir peak levels were < 0.3 micrograms/ml, and the prodrug was undetectable after 3 hr. Multiple valaciclovir doses of 250-2,000 mg given four times daily for 10 days resulted in dose-proportional increases in acyclovir Cmax. There were less than proportional increases in the AUCs. No serious or unexpected adverse events or laboratory abnormalities were reported. In volunteers with advanced human immunodeficiency virus (HIV) disease (absolute CD4 lymphocyte count < 150 cells/microliters), acyclovir and valaciclovir pharmacokinetic results were nearly identical to those in healthy volunteers. At the 2 g dose administered four times daily, steady-state acyclovir Cmax = 8.4 micrograms/ml, Tmax = 2.0 hr, AUC6 = 30.5 hr. micrograms/ml, and T1/2 = 3.3 hr. Nausea, vomiting, diarrhoea, and abdominal pain were commonly reported; however, only one adverse event (diarrhoea) was causally linked to valaciclovir exposure. There were no renal or neurologic adverse events. Valaciclovir is well absorbed and is rapidly converted to acyclovir, resulting in three- to fourfold higher acyclovir levels than can be achieved with oral acyclovir, even in patients with advanced HIV disease. The safety profile is generally favourable, with no evidence of nephrotoxicity or neurotoxicity.
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PMID:Valaciclovir (BW256U87): the L-valyl ester of acyclovir. 824 83

The range of diseases in which intravenous immunoglobulin (IVIG) is effective has expanded significantly since its initial use in primary antibody deficiency. There are at present at least 17 preparations of IVIG in use worldwide with similar profiles of adverse effects. Infusion-related effects range in severity. Mild adverse reactions (headache, flushing, low backache, nausea, wheezing) are often associated with a fast infusion rate, and respond rapidly on slowing the infusion. Very rare episodes of life-threatening anaphylaxis may occur, particularly in those IgA-deficient patients with anti-IgA antibodies; such patients should receive an IgA-depleted preparation of IVIG. There are concerns with any blood product about safety in regard to viral transmission. The 4 outbreaks of non-A non-B hepatitis (probably hepatitis C) in the 1980s were associated with the use of particular batches of IVIG. The more recent exclusion of all anti-hepatitis C virus positive individuals from the donor pool, and the introduction of specific antiviral steps in the manufacture of IVIGs, should prevent further outbreaks. The human immunodeficiency virus (HIV) is effectively inactivated during the manufacturing process itself and HIV transmission has not been reported with IVIG. Rarely, haematological (Coombs' test positive haemolysis), neurological (aseptic meningitis) or renal (transient rises in serum creatinine) adverse effects may be seen when high doses of IVIG are used for immunomodulatory purposes. Haemolysis, due to passive transmission of blood group antibodies (anti-A, anti-D), may be prevented by selecting IVIG batches that give a negative cross-match between the recipient's red cells and IVIG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effects of intravenous immunoglobulin. 826 Jan 19

A pilot study was initiated to explore a sequential combination antiretroviral regimen in 21 patients with AIDS or advanced human immunodeficiency virus (HIV) infection, who had received little or no prior anti-HIV therapy. The mean entry CD4 cell count was 184/mm3. Patients received 3-week cycles consisting of zidovudine plus acyclovir, dideoxyinosine, and dideoxycytidine for 1 week each. Overall, the regimen was well tolerated for up to 3 years. The principal toxicities were anemia, nausea, and vomiting; 1 patient developed retinal lesions. The mean CD4 cell count reached a peak of 64 cells/mm3 above baseline at week 8 (P = .005 compared to baseline) and remained above baseline for > 40 weeks. Patients also gained weight and had decreases in serum HIV p24 antigen. Eight patients developed opportunistic infections or tumors. Only 4 patients died during 3 years of follow-up. This regimen appears to be generally tolerable and to have anti-HIV activity. Additional studies will be needed, however, to learn how to best combine the available agents in patients with HIV infection.
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PMID:A pilot study of sequential therapy with zidovudine plus acyclovir, dideoxyinosine, and dideoxycytidine in patients with severe human immunodeficiency virus infection. 839 67

Neurotologic manifestations are apparent in human immunodeficiency virus (HIV) infection, but are poorly understood. Symptoms related to the vestibular system include episodes of vertigo, imbalance, ataxia, and nausea. Although patients present more often with hearing impairment, vestibular complaints are described and electrophysiologic studies indicate vestibular dysfunction in HIV-infected patients. Whether the disease involvement includes the central, or the peripheral nervous system has not been established. Ultrastructural analysis of vestibular end-organs obtained from HIV autopsy cases revealed pathologic changes in the labyrinth wall, the epithelial lining, and the receptor maculae and cristae. Cytologic changes in hair cells included inclusion bodies, viral-like particles, and hair bundle malformations. Epithelial lining cells, supporting cells, and connective tissue cells had inclusions and viral-like particles. These findings are consistent with those of a previous cochlear study demonstrating intracellular viral-like particles with the morphologic characteristics of HIV. Further cytologic evaluation of decalcified temporal bones and immunohistochemical analysis of freshly harvested HIV-infected temporal bones may provide further insight into the pathogenesis of viral-induced hearing loss and vestibular impairment.
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PMID:Ultrastructural findings in the vestibular end-organs of AIDS cases. 857 11

Massive steatosis has recently been described among a few human immunodeficiency virus-seropositive patients who were receiving antiretroviral therapy. Although clinical and light-microscopic pathological findings were carefully described, no ultrastructural studies of the liver were performed in these cases. We report the light-microscopic and ultrastructural findings at autopsy of a 35-year-old woman with AIDS who developed severe lactic acidosis and hepatic failure. The patient had been receiving standard doses of zidovudine for 5 months when she was hospitalized because of the rapid onset of abdominal pain, nausea, and vomiting. The most significant findings at autopsy were massive hepatomegaly and steatosis. Ultrastructural examination of the liver and skeletal muscle showed slightly enlarged mitochondria in the liver but no mitochondrial changes in the skeletal muscle. The pathogenesis of mitochondrial toxicity associated with antiviral therapies is briefly discussed.
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PMID:Massive hepatic steatosis and lactic acidosis in a patient with AIDS who was receiving zidovudine. 864 49


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