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)

A combination of the antigestagen mifepristone (RU 486) and a synthetic prostaglandin analogue, gemeprost, was used to induce therapeutic abortion in 100 women in early pregnancy. Local family planning services and general practitioners in Edinburgh referred women of less than 56 days' amenorrhea who had requested abortion. Pregnancy was confirmed by measurement of the serum level of human chorionic gonadotropin. Group I (n=20) received 150 mg mifepristone orally each day for 4 days. Groups II (n=30), III (n=30), and IV (n=20) received a single oral dose of mifepristone, 400 mg, 500 mg, or 600 mg, respectively. Samples of peripheral blood were collected at recruitment for measurement of the concentration of hemoglobin, urea, electrolytes, cortisol, and HCG and for liver function tests. Blood also was taken for estradiol and progesterone essay from women in Groups II, III, and IV. Each woman recorded symptoms in a diary from the day prior to the start of treatment. Study participants were reviewed 1, 2, and 4 weeks after treatment and discharged from followup after the onset of the next menstrual period. The effectiveness of the 4 treatment regimens was similar. Only 10 (14%) of the 74 women who received half a gemeprost pessary required the 2nd half. 95 of the women aborted completely; 5 women needed surgical intervention. Data were pooled for analysis because there was no significant difference between the 4 groups in the onset of bleeding and pain, requirement for analgesia, side effects, duration of bleeding, measured blood loss, and the time until the next menstrual period. The 94 women who experienced pain became aware of pelvic discomfort 46.6 hours after the initiation of treatment. No patient needed analgesia during the first 48 hours of treatment. After insertion of the pessary, 44 women received an oral analgesic drug and 9 an intramuscular opioid. 47 women did not need an analgesia. There was no significant difference in the frequency of nausea before and during treatment, but there was a significant increase in the incidence of vomiting and of diarrhea. 30 women vomited after the pessary was inserted compared with 13 the day before treatment; 10 women had diarrhea compared with 3 before treatment. No women had clinical evidence of pelvic infection. Liver function tests and cortisol levels were similar prior to and following treatment. Levels of HCG, and estradiol and progesterone decreased significantly after treatment. There were no significant differences in the results between those who needed evacuation and those who did not.
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PMID:Induction of therapeutic abortion in early pregnancy with mifepristone in combination with prostaglandin pessary. 289 91

Two methods of administration of amphotericin B were compared for their ability to produce nephrotoxicity in 12 dogs. Six dogs received six alternate day doses of amphotericin B: 1 mg/kg administered as a rapid bolus in 25 mL 5% dextrose in water. Another six dogs received alternate day treatments of the same dose of amphotericin B in 1 L 5% dextrose in water over 5 h. Both treatment groups experienced significant reductions in glomerular filtration rate, as measured by inulin clearance, 24 h endogenous creatinine clearance, serum creatinine and serum urea. This reduction in glomerular filtration rate was most marked in the group receiving the drug as a rapid bolus. The inulin clearances decreased from 3.54 +/- 0.30 mL/min/kg (means +/- SEM) on day 0 to 1.15 +/- 0.25 mL/min/kg on day 12 in the slow infusion group and from 3.24 +/- 0.25 mL/min/kg on day 0 to 0.46 +/- 0.11 mL/min/kg on day 12 in the rapid bolus group. Renal lesions characteristic of amphotericin B administration were observed in all dogs tested. The dogs which received amphotericin B as a rapid bolus had a significantly greater number of tubular lesions than the slow infusion group. Systemic side effects, such as vomiting, diarrhea and weight loss, were observed in both treatment groups but were most severe in the rapid bolus group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotoxicity of amphotericin B in dogs: a comparison of two methods of administration. 291 23

Acute and 1-month toxicity studies with SCH 31846, a nonsulfhydryl anti-hypertensive agent which acts by inhibiting angiotensin-converting enzyme, were initiated to evaluate its toxicity. The oral LD50s in mice and rats were approximately 1.8 and 2.5 g/kg, respectively, while the iv LD50 was approximately 450 mg/kg in mice and 150 mg/kg in rats. Signs of acute toxicity in rats and mice included salivation, hypoactivity, ataxia, prostration, and convulsions. In a 1-month dog study at oral doses of 25, 75, or 150 mg/kg, there was a dose-related increase in emesis between 1 and 2 hr after dosing. Absorption studies showed peak blood concentrations occurring in dogs between 0.3 and 1 hr after dosing. No other noteworthy antemortem changes were observed. In a 1-month rat study at oral doses of 30, 180, or 600 mg/kg, the hematocrit and hemoglobin values of the 600 mg/kg-dosed female rats were slightly but significantly (p less than 0.05) decreased and the blood urea nitrogen was slightly but significantly (p less than 0.05) increased in all SCH 31846-dosed male rats and the 600 mg/kg-dosed female rats. Absorption studies in male rats at doses of 30, 180, and 600 mg/kg indicate that SCH 31846 is well absorbed in rats. The 150 mg/kg-dosed dogs and the 180- and 600 mg/kg-dosed rats had a slight increase in the number of renin-containing granules in the renal juxtaglomerular cells. No other compound-related microscopic changes were observed. These data are similar to data reported for Captopril and suggest that in the dog and rat the toxicity of ACE inhibitors is not dependent upon the presence or absence of a sulfhydryl group.
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PMID:Acute and subchronic toxicity of a nonsulfhydryl angiotensin-converting enzyme inhibitor. 300 64

The patient was a 63-year-old female, who was admitted to the National Nagoya Hospital with complaints of left cervical and bilateral axillary lymphadenopathy on 12 May, 1987. Since May 1985, with the diagnosis of non-Hodgkin lymphoma, she had been successfully treated with combination chemotherapy (VEPA) and radiotherapy at another hospital. Left axillary lymphode biopsy revealed a diagnosis of non-Hodgkin lymphoma, diffuse large cell type. Then, she was given intravenous administration of carboplatin (400 mg/body) on 26 May, 1987. After a single course of this regimen, the lymphnode swelling subsided, and she achieved complete remission on 6 June. Thereafter, she was placed on the maintenance chemotherapy of carboplatin (400 mg/body) every 5 weeks. Through the whole course of this patient, the serum levels of blood urea nitrogen and creatinine were normal, and she did not notice nausea, vomiting and peripheral neuropathy. To our knowledge, this is the first report of complete response by the administration of carboplatin for non-Hodgkin lymphoma.
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PMID:[A case of non-Hodgkin lymphoma with complete remission achieved by carboplatin]. 304 95

Benzoate and phenylacetate improve prognosis in inherited urea cycle enzyme deficiencies by increasing waste nitrogen excretion as amino acid acylation products. We studied metabolic changes caused by these substances and their pharmacokinetics in a biochemically different urea cycle disorder, lysinuric protein intolerance (LPI), under strictly standardized induction of hyperammonemia. Five patients with LPI received an intravenous infusion of 6.6 mmol/kg L-alanine alone and separately with 2.0 mmol/kg of benzoate or phenylacetate in 90 min. Blood for ammonia, serum urea and creatinine, plasma benzoate, hippurate, phenylacetate, phenylacetylglutamine, and amino acids was obtained at 0, 120, 180, and 270 min. Urine was collected in four consecutive 6-h periods. Alanine caused hyperammonemia: maximum increase 107, 28-411 microM (geometric mean, 95% confidence interval); ammonia increments were nearly identical after alanine + benzoate (60, 17-213 microM) and alanine + phenylacetate (79, 13-467 microM) (NS). Mean plasma benzoate was 6.0 mM when extrapolated to the end of alanine + benzoate infusions; phenylacetate was 4.9 mM at the end of alanine + phenylacetate. Transient toxicity (dizziness, nausea, vomiting) occurred in four patients at the end of combined infusions, and we suggest upper therapeutic plasma concentrations of 4.5 mM for benzoate and 3.5 mM for phenylacetate. Benzoate and phenylacetate then decreased following first-order kinetics with t1/2S of 273 and 254 min, respectively. Maximal plasma hippurate (0.24, 0.14-0.40 mM) was lower than maximal phenylacetylglutamine (0.48, 0.22-1.06 mM, p = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Waste nitrogen excretion via amino acid acylation: benzoate and phenylacetate in lysinuric protein intolerance. 309 49

Four hundred and fifty-three adults in 25 British hospitals entered a prospective study of community-acquired pneumonia. A microbiological diagnosis was established in 67 per cent; Streptococcus pneumoniae (34 per cent). Mycoplasma pneumoniae (18 per cent) and Influenza A virus (7 per cent) were the commonest microorganisms. Our observations support the view that most of those in the microbiologically negative group (33 per cent) had S. pneumoniae infection. In addition to cultures of blood and sputum the most useful initial tests were for sputum pneumococcal antigen and serum mycoplasma specific IgM. Twenty-six patients (5.7 per cent) died, seven within 48 h of admission. Multivariate analyses showed age, absence of chest pain, absence of vomiting, previous treatment with digoxin, tachypnoea, diastolic hypotension, confusion, leucopenia, leucocytosis, and raised blood urea levels were significantly correlated with death. Patients had a 21-fold increased risk of death if they had two of the following: admission respiratory rate greater than or equal to 30/min, admission diastolic BP less than or equal to 60 mmHg, urea greater than 7 mmol/l during admission. Mortality was not related to aetiology except that all three patients with combined Influenza A virus and Staphylococcus aureus infection died. Nine patients had legionella pneumonia; none died. No patients who died from pneumococcal pneumonia, mycoplasma pneumonia or staphylococcal pneumonia had received an appropriate antibiotic before admission. Such deaths are possibly preventable. Assisted ventilation was used in 22 patients of whom 14 survived. Hospital stay in survivors averaged 10.8 days; after six weeks 79 per cent were fit for normal activities, and 55 per cent showed resolution of radiographic signs of pneumonia. We recommend that antibiotics should be given as early as possible and chosen always to cover S. pneumoniae, and in addition M. pneumoniae during outbreaks, and S. aureus during influenza epidemics.
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PMID:Community-acquired pneumonia in adults in British hospitals in 1982-1983: a survey of aetiology, mortality, prognostic factors and outcome. The British Thoracic Society and the Public Health Laboratory Service. 311 95

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA. Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3-4 units protamine-zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11.4 pmol/l compared with 1.6 pmol/l; P less than 0.05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, beta-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P less than 0.05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = + 0.75; P less than 0.01), and plasma ketone bodies and plasma AVP (r = +0.60; P less than 0.05) were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible mechanisms responsible for the rise in plasma vasopressin associated with diabetic ketoacidosis in the rat. 312 19

Acute toxicity of cefodizime sodium (THR-221) was examined in mice of both sexes, rats of both sexes (including 5-day-old young), and male dogs. The LD50 values of THR-221 (mg/kg) were as follows: (1) mice: intravenous, 7200 for males and 5000 for females; intraperitoneal, 10500 for males and 11000 for females; subcutaneous, 17500 for males and 16500 for females; and oral, 28000 for males and 29000 for females. (2) rats (adult): intravenous, 7000 for males and 8200 for females; intraperitoneal, 9500 for males and 8800 for females; subcutaneous, 17000 for males and 15500 for females; oral, more than 20000 for both sexes; and intramuscular, more than 3200 for both sexes. (3) 5-day-old rats: subcutaneous, 5278 for males and 5314 for females. (4) male dogs: intravenous, more than 5000. Major changes in general conditions observed in mice and rats were decreased spontaneous activity, lying prone, respiratory changes, staggering gait, clonic or clonic-tonic convulsions, and cyanosis, and in the animals dosed orally, diarrhea or salivation was also noted. The changes in 5-day-old rats were respiratory changes, agony, loss of reflex to an external stimulus, and congestion at the injection site, and those in dogs were vomiting, dryness of the nose, and soft or mucous stools. Autopsies on the mice and rats which died revealed hemorrhage on the brain surface. In addition, the following were seen: intraperitoneal retention of fluid and dark red spots on the abdominal wall (i.p.), subcutaneous retention of fluid or jellylike material and hemorrhage at the injection site (s.c.), and retention of fluid and dark red spots on the mucosa in the digestive tract (mice p.o.). In 5-day-old rats which died, the subcutaneous tissue at the injection site showed hemorrhage macroscopically and inflammatory changes microscopically. Hematological and blood chemical tests performed in dogs showed an increase in white blood cells and changes suggesting anemia, increases in GOT, LDH and ALP activities, and slight changes in urea nitrogen and inorganic phosphorus. In one animal given a low dose of 2500 mg/kg, an increase in GPT activity was also seen. However, these changes were all transient. Microscopic findings in dogs were slight inflammatory changes in the subcutaneous tissue around the injection site.
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PMID:[Acute toxicity study of cefodizime sodium]. 317 86

A seventy-two-year-old man with hypertensive cerebral hemorrhage acutely developed severe headache, nausea, vomiting, agitation, and disorientation with abrupt rise in blood pressure on the sixth day after the onset. At that time, there were no remarkable changes in focal neurologic deficits, and repeated brain CT scans revealed a small hematoma located in the right basal ganglia without further enlargement or herniation. Blood chemistry and arterial gas analysis were within the normal ranges except for a slight rise in blood urea nitrogen. Similar episodes occurred three times within two days, and each time the cerebral symptoms disappeared in accordance with lowering of blood pressure by antihypertensive therapy. Complication of hypertensive encephalopathy was strongly suggested. The authors discuss the pathophysiology of this encephalopathy in relation to cerebral hemorrhage.
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PMID:Transient encephalopathy related to rapidly and markedly elevated blood pressure in acute stage of hypertensive cerebral hemorrhage--relationship to hypertensive encephalopathy--a case report. 317 64


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