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)

The case report of a 10-year-old boy, admitted to the hospital after he had experienced 4 days of periumbilical abdominal pain, intermittent vomiting, and diarrhea, is presented. He had proctoscopic and radiologic findings resembling ulcerative colitis. However, further analysis of laboratory data suggested hemolytic-uremic syndrome. Since the patient in the pediatric age group presents with a clinical picture mimicking ulcerative colitis, this hemolytic-uremic syndrome should be included in the differential diagnosis. Examination of a peripheral smear revealing typical findings of microangiogpathic, hemolytic anemia, thrombocytopenia, and a rising blood urea nitrogen value will lead to the diagnosis of hemolytic-uremic syndrome and early appropriate therapy.
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PMID:Acute colitis resembling ulcerative colitis in the hemolytic-uremic syndrome. 125 52

Tropiestron is a potent and selective antagonist of 5-hydroxytryptamine receptors. Tropisetron was developed for the indication of cancer chemotherapy-induced emesis. The pharmacokinetic and metabolic dispositions of tropisetron were studied in 12 healthy male volunteers receiving a single oral dose of 62 or 312 mumol (20 or 100 mg) of [14C]tropisetron. Serial plasma samples and complete urine and feces were collected for 120 hr postdose. Whereas the absorption of oral doses of 62-312 mumol tropisetron was rapid and complete, bioavailability was estimated to be only 66% for the 312 mumol dose and 52% for the 62 mumol dose, apparently because of saturable first-pass metabolism. Maximal concentrations of tropisetron averaged 87 and 608 nM after doses of 62 and 312 mumol, respectively, and the parent drug accounted for 21 and 36% of the radioactivity in AUC0-24 hr pools. Approximately 90% of the drug was metabolized before excretion, and approximately 70% of the dose was recovered in the urine. Following both the 62 and 312 mumol doses, the terminal half-life of tropisetron averaged 6-7 hr and that of total radioactivity was 10-11 hr. Tropisetron and its metabolites in plasma and urine were separated by gradient elution reversed-phase HPLC. Structures of eight metabolites were assigned on the bases of NMR and MS data. Tropisetron was metabolized by oxidative hydroxylation of the indole ring at positions 5, 6, and 7. The hydroxylated derivatives are further conjugated with glucuronic acid and sulfate. N-Oxygenation and oxidative N-demethylation at the tropinyl nitrogen also occur in trace amounts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and metabolism of the 5-hydroxytryptamine antagonist tropisetron after single oral doses in humans. 135 42

This is the first report from Ethiopia of a case of cryptococcal meningitis in a patient with AIDS. A 20-year-old woman was admitted to Tikur Anbessa Hospital in January 1990 with complaints of generalized pruritic skin lesions of six months, and headache, fever, and poor appetite of three months duration. The headache and low-grade intermittent fever were accompanied by nausea, vomiting, anorexia, and progressive weight loss, without diarrhea. She had had multiple sex partners. Upon admission, after being bedridden for two weeks, she appeared acutely ill and restless. Her temperature was 39.5 degrees Celsius, and she had oral thrush. There was no lymphadenopathy. Widespread, irregular erythematous and whitish macular patches (3 x 5 to 8 x 10 sq. cm in size) with peripheral scaling and tiny vesicles were found on the skin, pubic and perineal regions. She had neck stiffness, but was conscious and well-oriented. Hemoglobin (Hb) was 10.5 g%; the white cell count (WBC) was 3400/cu. mm; the erythrocyte sedimentation rate (ESR) was 92 mm/hr; the platelet count was 175,000/mm; and blood films were negative for hemoparasites. Urinalysis showed 3+ albumin and many pus cells and red cells/HPF. Urine culture was negative, and the VDRL test was nonreactive. Lumbar puncture, which was performed upon arrival, showed clear cerebrospinal fluid (CSF), with normal protein and glucose levels and no cells. CSF culture showed yeast cells, and an India ink preparation was positive for Cryptococcus neoformans. Blood taken for bacterial culture grew yeast cells. Renal and liver function tests, and chest x-rays were normal. A potassium hydroxide (KOH) preparation from a skin snip showed rounded yeast cells. ELISA and Western blot tests were both positive. The patient was given supportive treatment and amphotericin B (0.6 mg/kg daily). Although the fever decreased, the patient's general condition did not improve. She complained of headache, photophobia, nausea, and vomiting. Lumbar puncture was repeated eight days after the start of treatment; CSF culture and India ink preparations were negative. Urea nitrogen (BUN) repeated two weeks later was normal. Four weeks after admission, the patient suddenly vomited massive amounts of fresh blood and died before transfusion could be given. A discussion follows regarding the clinical manifestations, diagnosis, and treatment of this disease, particularly in AIDS patients, with a review of the literature.
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PMID:Cryptococcal meningitis in a young Ethiopian woman with AIDS. 139 20

To understand whether disease caused by the human immunodeficiency virus (HIV) affects zidovudine disposition, we compared the drug's pharmacokinetics in six healthy volunteers; six persons with the acquired immunodeficiency syndrome (AIDS) and no evidence of gastrointestinal (nausea, vomiting, diarrhea), renal (elevated blood urea nitrogen, serum creatinine), or hepatic (elevated liver function tests) disease; and three patients with AIDS and hepatic disease. After a single oral dose of zidovudine, serial blood samples were analyzed for drug concentration by radioimmunoassay. A one-compartment oral absorption model was fit to the concentration-time data. The absorption rate constant (4.05 vs 2.11 hr-1) and time to maximum concentration (0.61 vs 1.03 hr) were significantly different in healthy volunteers versus patients with AIDS without hepatic disease. Differences in half-life, oral clearance, and area under the curve were not statistically significant. In the three patients with AIDS plus hepatic disease, clearance was reduced an average of 63%, and area under the curve was increased by a factor of 2.3. These comparative pharmacokinetic data do not support profound differences between zidovudine's disposition in healthy volunteers and individuals with AIDS; however, the differences and trends that were observed may represent an effect of HIV disease. Although the presence of hepatic disease clearly indicates a need to modify individual dosages, these pharmacokinetic data may have more generalized implications for zidovudine dosing as the relationships between drug concentration and therapeutic or toxic effects are clarified.
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PMID:Comparative pharmacokinetics of zidovudine in healthy volunteers and in patients with AIDS with and without hepatic disease. 149 5

Synthesis and pharmacological evaluation of a series of 1,2-dihydro-1-[(5-methyl-1-imidazol-4-yl)methyl]-2-oxopyridine 5-HT3 antagonists are described. The key pharmacophoric elements were defined as a basic nitrogen, a linking group capable of hydrogen bonding interactions, and an aromatic moiety. 1,2-Dihydro-2-oxopyridine moiety could be a good linking group because of its nicely planar structure. The steric limitations of the aromatic moiety were investigated by X-ray analysis and computer analysis and shown to be optimal when the aromatic moiety was constrained within an arched planar system, which could be successfully replaced by 3-(2-thienyl)-2-oxopyridine function or 6-amino-7-chloro-1-isoquinolinone function without any loss of the activity. Among the synthesized compounds, 42 showed the most potent activity in the inhibition of Bezold-Jarisch reflex in rats. Compounds 44a and 64 were orally active in the protection against cisplatin-induced emesis in dogs or ferrets. Structure-activity relationships are discussed.
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PMID:Novel 5-HT3 antagonists. Isoquinolinones and 3-aryl-2-pyridones. 152 80

Beagle dogs were allocated to 4 groups, each consisting of 3 males and 3 females, which received 0.055, 0.165 or 0.495 mg paraquat (PQ)/kg/day sc for 4 w to investigate subacute toxicity. Recovery 4 and 8 w postadministration was studied. In the early stage there was vomiting, decreased activity and undernourishment. Induration and ulcers at the injection sites were seen. The group receiving 0.495 mg PQ/kg had reduced food ingestion and occasional decreases in water consumption until the end of the 4-w injection period. Three animals in the 0.495 mg PQ/kg group were sacrificed in the moribund stage with marked decreases in body weight. Ophthalmologic examination at 4 w of recovery detected hemorrhage around the nasalis vein of the left fundus in 1 animal that received 0.495 mg PQ/kg. No abnormal changes in electrocardiography (ECG) were noted throughout the experimental period. Slightly increased urinary protein, reticulocyte counts, and fibrinogen were observed in a few animals in each group. A few animals that received 0.165 or 0.495 mg PQ/kg had increased phospholipid, blood urea nitrogen, and creatine phosphokinase. The lungs of the moribundly sacrificed animals had moderate atelectasis, localized atelectasis, moderate thickening of alveolar wall and pleura, proliferation of fibroblast-like cells, and abundant fibers in interstitium and alveoli. In the liver there was slight hemorrhage along the gallbladder. On electron microscopy of the lung, proliferation of fibroblasts, myofibroblasts and type II alveolar cells, and some mast cells were observed in thickened alveolar walls. Abundant collagen fibers, destroyed cell debris and mitotic figures of spindle-shaped fibroblasts were also observed in the dilated interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subacute toxicity of paraquat in beagle dogs: clinicopathology and pathologic examinations. 162 56

Many chemotherapeutic agents have been evaluated during the last 40 years and some have now an established place in the management of malignant disease. However these agents have a level of toxicity well above any other group of drugs. Chemotherapeutic agents do not discriminate between normal and neoplastic tissue. Chemotherapeutic regimens that are toxic to rapidly dividing malignant cells, are liable to be particularly harmful to lymphoid tissues, bone marrow and the epithelium of the gastrointestinal tract. The side effects due to chemotherapy are classified as immediate, early, delayed and late. Immediate side effects are those that may occur within the first 24 hours of treatment. The most common immediate side effect is nausea and vomiting, due to direct central effect on the vomiting center of the brain. Cisplatin and nitrogen mustard are particularly prone to this complication. The antiemetics usually used are metoclopramide, domperidone and steroid. The efficacies of these drugs are not so good for nausea and vomiting due to cisplatin administration, however several blockades against serotonin M-receptor recently developed are quite effective to nausea and vomiting of chemotherapeutic regimens including cisplatin. Early side effects commence within about one month of therapy. The most common is bone marrow toxicity and can occur after therapy with the vast majority of anticancer drugs. The relative importance of leukopenia and thrombocytopenia vary between the drugs and their route of administration. Recently, hematopoietic cytokines, such as granulocyte-colony stimulating factor (G-CSF) and granulocyte-macrophage-colony stimulating factor (GM-CSP) have been introduced to granulocytopenia developed by cancer chemotherapy. In the phase II study of G-CSF, a rapid recovery of granulocytes after chemotherapy and marked efficacy on infection in granulocytopenic patients were observed. In addition to this, autologous bone marrow transplantation after chemotherapy has been described in patients with solid tumors.
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PMID:[Palliative therapy in cancer. 5. Side effects by anticancer drugs and their treatments]. 169 55

Fifteen patients with advanced, measurable renal cell carcinoma entered a Phase II clinical trial of interleukin-2 (IL-2) (Teceleukin, Hoffmann-La Roche Inc., Nutley, NJ) and interferon (IFN) (Roferon A, Hoffmann-La Roche Inc.). IL-2 was administered by continuous infusion daily for 4 days and IFN was administered by intramuscular injection daily for 4 days; therapy continued for 4 weeks. Eight men and seven women were treated in this trial (median age, 61 years). Toxicity was moderate to severe with fatigue, nausea, vomiting, hypotension, and elevated blood urea nitrogen bunion and creatinine levels seen in all patients. Two patients achieved a complete remission and two patients achieved a partial remission. The median duration of response was 18 months. IL-2 and IFN is an active combination in the treatment of renal cell carcinoma and warrants further investigation.
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PMID:A phase II trial of interleukin-2 by continuous infusion and interferon by intramuscular injection in patients with renal cell carcinoma. 171 25

After at least 6 months on conventional hemodialysis (cellulosic dialyzers, acetate dialysate, and a 3- to 4-hour treatment time), 56 patients were changed to short-time hemodialysis (less than 180 minutes) using polysulfone dialyzers and bicarbonate-containing dialysate. Treatment time decreased (191 +/- 5 v 147 +/- 5 min; P = 0.001), while Kt/V (1.22 +/- 0.04 v 1.29 +/- 0.06; P = NS) and normalized protein catabolic rate (pcr) (1.10 +/- 0.05 v 1.10 +/- 0.07 g/kg/d; P = NS) remained constant. When compared with the conventional period, 30 months of short-time hemodialysis resulted in no changes in predialysis blood pressure (BP) (151 +/- 2/84 +/- 1 v 151 +/- 2/86 +/- 1 mm Hg), postdialysis BP (144 +/- 2/81 +/- 1 v 143 +/- 3/84 +/- 1 mm Hg), interdialytic weight gain (2.4 +/- 0.1 v 2.7 +/- 0.2 kg), or blood urea nitrogen (BUN) (26.1 +/- 0.71 v 25.3 +/- 1.07 mmol/L [73 +/- 2 v 71 +/- 3 mg/dL]). Shorter treatment times were not associated with an increase in intradialytic complications. Actually, the frequency (%) of dialysis treatments associated with nausea (5.94 +/- 1.33 v 2.21 +/- 0.52), vomiting (3.12 +/- 0.87 v 0.54 +/- 0.14; P less than 0.05), headaches (5.60 +/- 1.13 v 2.03 +/- 0.52; P less than 0.05), and back pain (0.91 +/- 0.25 v 0.05 +/- 0.05; P less than 0.05) was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience with short-time hemodialysis. 173 82

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
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PMID:Management of severe hypercalcemia. 200 13


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