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)

To define a maximum tolerable dose, chloroquinoxaline sulfonamide (CQS) was given as a 1-h infusion every 28 days to cancer patients for whom no effective standard therapy was available. Doses were escalated in cohorts of at least three patients each. Plasma for characterization of the pharmacokinetics of free and total CQS was obtained during and after the initial infusion and, when possible, during and after subsequent infusions of CQS if the dose had been reduced. A total of 101 courses of CQS in 55 patients were evaluated. Dose levels ranged from 18 to 3,700 mg/m2. The dose-limiting toxicity was hypoglycemia, first recognized at the 3,700-mg/m2 dose. When dose-limiting hypoglycemia was recognized, patients were entered at successively lower doses, with close monitoring of plasma glucose and insulin concentrations being done in 26 patients. Grade 1-3 hypoglycemia occurred within 4 h of the termination of CQS infusion and cleared by 24 h. Symptomatic hypoglycemia was more frequent at doses of CQS above 1,000 mg/m2. Concomitant administration of 5% glucose did not ameliorate the hypoglycemia associated with CQS doses of > 1,000 mg/m2. The total calorie intake, percentage of ideal body weight, or percentage of weight lost did not explain the incidence or severity of hypoglycemia in 12 patients in whom these data were obtained. Cardiac tachyarrhythmias occurred in 7 patients who received CQS at doses of > or = 1,000 mg/m2, and tachyarrhythmia was associated with hypoglycemia in 3 patients. Other toxicities were sporadic, but the frequency of toxicity was higher at CQS doses of > or = 1,000 mg/m2. These toxicities included fever, rash, lightheadedness, leukopenia, thrombocytopenia, alopecia, diarrhea, nausea, and vomiting. All toxicities were reversible. Mean peak plasma [CQS] and AUC increased with dose, with a suggestion that peak plasma [CQS] plateaued at higher doses. The decline in plasma [CQS] was fitted to a three-compartment, open linear model. The terminal half-life ranged from 28 to 206 h. Total body clearance ranged from 44 to 881 ml/h with no evidence of saturation. Urinary excretion of the parent compound in 24 h averaged < 5%. CQS not bound to plasma protein (free CQS) comprised 1%-17% of total plasma CQS and was not related to dose. A relationship was defined between the magnitude of hypoglycemia and CQS pharmacokinetic parameters. The percentage of decrease in plasma [glucose], i.e., (predose [glucose]-nadir [glucose]/predose [glucose]) x 100, correlated with both free and total peak plasma [CQS].(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Phase I trial of chloroguinoxaline sulfonamide, with correlation of its pharmacokinetics and pharmacodynamics. 749 83

Intraduodenal lipid infusion induces symptoms and increases sensitivity to gastric distension in patients with functional dyspepsia. To test whether these effects are specific for lipid, we compared the effects of intraduodenal infusions of either lipid or glucose on symptoms and gastric sensory and motor responses to gastric distension. Eighteen dyspeptic patients and nine controls were studied. The stomach was distended with a flaccid bag during isocaloric infusions (1 kcal/ml) of saline and either 10% Intralipid (nine patients) or 26.7% glucose (nine patients) into the duodenum. Dyspeptic symptoms and sensory thresholds for epigastric fullness and discomfort were assessed. Gastric pressure profiles during distensions were similar during lipid and glucose infusions in patients and controls, but both were significantly lower than during saline infusion. Lower volumes were required to induce fullness and discomfort in the patients compared with the controls. In the controls, the threshold volumes required to induce fullness and discomfort were greater during infusion of lipid and glucose than during saline infusion, but in the patients, the threshold volumes were increased during glucose infusion but further reduced during lipid infusion. Moreover, in the patients, nausea was more common during lipid than glucose infusion and did not occur during saline. The controls did not experience any symptoms during any infusion. In conclusion, intraduodenal lipid but not glucose sensitizes the stomach to distension in patients with functional dyspepsia but not in controls.
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PMID:Nutrient-specific modulation of gastric mechanosensitivity in patients with functional dyspepsia. 764 62

A 57-year-old man was admitted because of headache, nausea, and fever up (38 degrees C). He showed nuchal rigidity slightly. CSF analysis showed 833 white blood cells (WBC) (80% monocyte), protein value of 68 mg/dl, glucose level of 36 mg/dl and ADA level of 11.8 IU/l. Brain pre-contrast CT indicated high density area in right parietal lobe, and it showed slightly homogeneously enhancement with contrast medium. MRI on T2 WI demonstrated hypointense lesion with bright central core in right parietal lobe. The lesion showed isointense on T1WI, and indicated homogeneous enhancement with Gd-DTPA. He was sent to our hospital after one week. With only antibiotics the symptoms were relieved and the CSF findings improved during the previous hospital. However, Mycobacterium tuberculosis (M. tuberculosis) DNA was detected in CSF by PCR amplification, and he recovered completely with anti-tuberculous treatment. This case was interesting to reveal atypical features of spontaneous recovery. Since Shankar's study using polymerase chain reaction (PCR) for detection of M. tuberculosis in cerebrospinal fluid (CSF), the PCR assay have been recognized to be a rapid method for diagnosis of tuberculous meningitis (TBM). But there are problems of PCR sensitivity when dealing with CSF samples containing small amount of M. tuberculosis DNA. Comparing direct PCR with nested PCR, we studied on the evaluation of PCR for diagnosis of TBM. In this study the nested PCR was positive in all CSF specimens from 4 patients with TBM, but we could not detect M. tuberculosis DNA by only the direct PCR. Nested PCR amplification improved the sensitivity and specificity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intracranial tuberculoma with spontaneous recovery]. 766 22

Some diabetic patients--particularly those with nausea and vomiting--frequently have evidence of delayed gastric emptying while other diabetic patients may in fact exhibit accelerated gastric emptying. Whether the presence or absence of symptoms of upper gastrointestinal dysfunction correlated with objective measures of gastric emptying in insulin dependent diabetic subjects was investigated. Twenty one insulin dependent diabetic patients underwent a solid phase gastric emptying scintiscan using in vivo labelled chicken liver. Thirteen patients had symptoms suggestive of gastrointestinal dysfunction (nausea, vomiting, early satiety, or constipation), while eight patients had no gastrointestinal symptoms. Eleven patients had orthostatic hypotension. All patients had been diabetic since childhood or adolescence. As a group, the diabetic patients showed a half time (T50) of gastric emptying (mean (SD) 150.0 min (163.7) that was not significantly different from that of 12 healthy control subjects (148.1 min (62.4)). Those diabetic patients without gastrointestinal symptoms and without orthostatic hypotension, however, showed a gastric emptying half time (70.1 min (41.6)) that was significantly faster than that of the control subjects. Conversely, those diabetic patients with nausea, vomiting, and early satiety (or early satiety alone) showed T50 values that were significantly greater than those of the diabetic patients without these symptoms. No correlation was found between the T50 value and the duration of diabetes, the fasting blood glucose at the time of study, or the respiratory variation in heart rate (E:I ratio). These observations indicate that highly variable rates of gastric emptying occur in insulin dependent diabetic patients, and that accelerated gastric emptying may occur in diabetic patients who have no symptoms of gastrointestinal dysfunction.
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PMID:Highly variable gastric emptying in patients with insulin dependent diabetes mellitus. 856 52

The clinical experience with a combined oral contraceptive (COC) containing 150 micrograms desogestrel and 30 micrograms ethinylestradiol is reviewed. Fourteen clinical trials have been reported involving over 44,000 women for more than 190,000 cycles. None of the 17 pregnancies which occurred (overall Pearl Index 0.12) were due to method failure. The incidences of breakthrough bleeding and spotting after 6 treatment cycles varied from 0.1-6.0% and 2.8-11% of subjects, respectively, and at this time they were not significantly different from pretreatment in most trials. About 90% of subjects maintained regular cycles. The incidence of subjective side effects (approximately 5% for headache, 4% for breast tenderness, 2% for nausea) was low. No significant changes occurred in body weight or blood pressure. In all trials, the COC was well accepted and the rates of discontinuation were similar to those in other COC trials. Pharmacodynamic effects have been widely investigated. There were no significant changes in glucose metabolism or in haematological factors except for possibly minor increases in factors VII and X, fibrinogen and plasminogen. Over thirty studies of the effect of the COC on lipid metabolism have been published; significant increases occur in serum triglycerides, HDL-C and apoprotein A1. SHBG concentrations increase 2-3 fold with a consequent decrease in the levels of free testosterone. This effect can be particularly important therapeutically in women with hyperandrogenic skin disorders and 14 trials in women with these disorders have demonstrated significant clinical improvement with the COC. The findings from the various trials show the COC to be effective and acceptable with no adverse metabolic effects.
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PMID:Twelve years of clinical experience with an oral contraceptive containing 30 micrograms ethinyloestradiol and 150 micrograms desogestrel. 775 Feb 81

We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
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PMID:Temporal lobe epilepsy caused by domoic acid intoxication: evidence for glutamate receptor-mediated excitotoxicity in humans. 781 46

We reported a case of opsoclonus-myoclonus syndrome. A 63-year-old man was admitted to Kenwakai Hospital with rapidly progressing symptoms, including lumbago, whole body pain, vertigo, nausea, and anorexia. He became bed-ridden because of severe vertigo and truncal ataxia. Five days after admission, he developed opsoclonus followed by myoclonus and mild disturbance of consciousness, but he showed no appendicular ataxia or pyramidal tract sign. He was treated with prednisolone, 40 mg/day, which was effective for disturbance of consciousness, but opsoclonus and myoclonus persisted. He died of liver dysfunction and ventricular fibrillation 3 weeks after onset. Blood examination revealed high LDH (1,106 IU/l), Al-P, and gamma-GTP titers. Tumor markers were normal except for increase NSE activity (129 ng/ml). The cerebrospinal fluid showed normal cell count, 63.9 mg/dl of protein, 7.3 mg/dl of IgG, and normal glucose. A cranial CT scan showed an old lacune only. Chest rentgenogram and CT scan revealed mediastinal and hilar lymph node enlargement. An abdominal CT scan showed multiple low density masses in the liver. Small cell lung cancer associated with opsoclonus-myoclonus syndrome was suspected. Western blot analysis revealed that his serum reacted with protein in the cerebellum, cerebrum, and dorsal root ganglion with a molecular weight of 77 kDa. This is the first time such an antibody was ever been detected in patients with opsoclonus-myoclonus syndrome. The molecular weights of the antigens previously found by the serum of patients with this syndrome, were 55 kDa and 80 kDa in patients with breast cancer, and 210 kDa in patients with neuroblastoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of opsoclonus-myoclonus syndrome associated with anti-central nervous system antibody]. 782 Sep 64

We describe a case of keto- and lactic acidosis in a 22 year old, healthy woman hospitalized for preterm labor at week 32 of gestation. One former pregnancy was normal. Blood glucose level at admission was 115 mg/dl after 8 mg of betamethasone. Continuous salbutamol infusion was used for management of preterm labour. 18 hours later, the patient complained about nausea and dyspnoea followed by tachypnoea and hyperventilation. Blood gas analysis showed severe metabolic acidosis (ph 7.25, BE-17.5, pO2 114 mm Hg, pCO2 15.5 mm Hg). At this moment blood glucose level was 178 mg/dl. Ketone bodies in urine were positive, serum lactate level was also elevated at 8.6 mmol/l. Cesarean section was performed because of prolonged fetal bradycardia. 6 months post partum type-I-diabetes could be excluded. We conclude that this case of acidosis was due to both, beta-2-adrenergic treatment and beginning gestational diabetes.
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PMID:[Metabolic acidosis in the 32nd week of pregnancy--uncontrolled diabetes in pregnancy, dehydration or sequela of tocolysis?]. 784 85

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

We report a case of carcinomatous meningitis from transitional cell carcinoma of the urinary bladder. A 70-year-old man with invasive bladder cancer and multiple pulmonary metastases received 3 courses of systemic M-VAC (methotrexate, vinblastine, doxorubicin, and cisplatin) chemotherapy, after which the primary tumor and pulmonary metastases diminished in size and number. During the 4th course of chemotherapy, he complained of nausea, headache, diplopia, and neck stiffness. Computer tomographic (CT) scan of the brain showed no evidence of parenchymal metastases, cerebral hemorrhage, or infarction. Cerebrospinal fluid examination revealed an increase in cells along with elevated protein and depressed glucose concentrations, but no malignant cells were identified. He died two weeks after the onset of neurological symptoms. Autopsy revealed numerous tiny metastatic lesions in the leptomeninx, so called carcinomatous meningitis, without parenchymal metastases in the brain. Although metastases to the central nervous system from transitional cell carcinoma of the bladder, especially carcinomatous meningitis rarely have been reported, this unusual complication will be seen more frequently with the development of more effective systemic chemotherapy such as M-VAC.
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PMID:[A case of carcinomatous meningitis from transitional cell carcinoma of the urinary bladder]. 786 65


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