Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tonsillectomy in adults and older children is typically accompanied by 7 to 14 days of pain. On the basis of clinical observations of patients treated perioperatively with dantrolene sodium for malignant hyperthermia, we hypothesized that pharyngeal muscle spasms are a major factor in tonsillectomy pain. We entered 113 patients, 11 years of age and older, into a double-blind, placebo-controlled study to evaluate the effectiveness of dantrolene sodium in reduction of tonsillectomy pain. Patients were randomly assigned either dantrolene (1.5 mg/kg per day) or placebo orally four times a day for 5 days postoperatively. On a standardized questionnaire, the patient recorded pain, diet, activity level, analgesics, and side effects, daily for 2 weeks. Also, alkaline phosphatase (alk phos) and serum aspartate aminotransferase (SGOT) levels were determined before the operation and 2 weeks after. Patients who received dantrolene had no significant differences in subjective pain, diet, or activity level scores from those of patients who received placebo. Dantrolene patients did, however, require significantly less analgesic use than placebo patients (p = 0.034, 0.015, and 0.005 for postoperative days 2, 3, and 4, respectively). There was no significant difference in side effects or changes in liver enzyme between the dantrolene and placebo groups. We conclude that dantrolene sodium, given in the dosage noted, is effective in reduction of analgesic requirements after tonsillectomy.
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PMID:Oral dantrolene sodium for tonsillectomy pain: a double-blind study. 312 47

Experimental and clinical experience with compounds containing antimony have shown that the trivalent compounds are generally more toxic than the pentavalent ones. APT can cause severe pain and tissue necrosis and is therefore not given by intramuscular or subcutaneous injection. APT has the actions and uses of AST, but it is less soluble and more irritating than the sodium salt which is therefore more suitable for intravenous use. Trivalent antimony compounds are toxic when used topically. Adverse effects are similar for all trivalent compounds, and include nausea, vomiting, weakness and myalgia, abdominal colic, diarrhoea, and skin rashes, including pustular eruptions. Hypersensitivity reactions also occur. Respiratory symptoms include cough, dyspnoea, and chronic lung changes. Cardiotoxicity is the most important and may produce arrhythmias, myocardial depression and damage, Stokes-Adams attacks, heart failure, and cardiac arrest. Hepatic damage and necrosis, as well as blood dyscrasias, may occur. Toxic effects on the kidney may follow chronic use. Continuous treatment with small doses of antimony may give rise to symptoms of subacute poisoning, similar to those of chronic arsenic poisoning, due to accumulation of antimony in the body, especially if trivalent compounds are used, because of their long biological half-lives. Reproductive disorders and chromosome damage have been reported; antimony compounds are, therefore, potentially toxic to reproduction and have mutagenic, and oncogenic potential. Antimony compounds should, therefore, not be used during pregnancy or in the presence of hepatic, renal, or heart disease. Pentavalent antimony preparations especially the organic compounds, together with non-metallic synthetic preparations, such as the diamidines, have now replaced APT for use in leishmaniasis. Because of the toxicity of antimony compounds, investigations have been undertaken to reduce their adverse effects by combining them with chelating agents. These preparations appear to have reduced the toxic effects of antimony without affecting the efficacy of the preparations. Liposome-encapsulated antimony products have, more recently, been shown to be much less toxic because of the reduced dose of the antimony compound required for effective therapy. The historical uses of antimony were based on the belief that the topical and systemic adverse effects, for example, skin eruptions and diarrhoea and vomiting, were signs that the condition being treated was responding by being brought to the surface to relieve congestion at the diseased area. There is no evidence in topical use, but there is evidence that such use can cause severe reactions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxicity of antimony and its compounds. 330 36

2'-Fluoro-5-iodoarabinosylcytosine (FIAC) has potent antiviral activity in vivo against herpes simplex virus types 1 and 2 and cytomegalovirus. For examination of the clinical efficacy of FIAC, a randomized, double-blind study of FIAC versus adenine arabinoside (ara-A) was conducted in 34 immunosuppressed individuals with varicella-zoster virus infections. The median time to the appearance of the last new lesion was shorter in patients who received FIAC relative to those who received ara-A (two versus five days, respectively; P less than .001) FIAC also reduced pain and accelerated initial crusting within 72 hr in a significantly greater proportion of patients when compared with ara-A (P = .004 and P = .0009, respectively). FIAC caused few toxic reactions (mild nausea and transient elevation in activity of serum aspartate aminotransferase). Thus FIAC is therapeutically superior to ara-A for the treatment of varicella-zoster virus infections in immunosuppressed subjects.
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PMID:2'-Fluoro-5-iodoarabinosylcytosine, a new potent antiviral agent: efficacy in immunosuppressed individuals with herpes zoster. 352 94

The aim of this investigation was to study central haemodynamics in initially uncomplicated acute myocardial infarction (AMI) with respect to natural history, relation to enzyme estimated infarct size, mortality and effects of metoprolol. A total of 212 patients with AMI but without clinical signs of serious heart failure or hypotension and with a mean delay from onset of pain to study entry of about 7 hours were studied. They were randomised to placebo or metoprolol (15 mg i.v. + 50 mg orally q.i.d.) treatment. Central pressures and cardiac output were evaluated by repeated measurements over 24 hours by means of pulmonary artery catheters. The pharmacokinetics of metoprolol were studied in further 20 patients with AMI. The natural history, as reflected by the placebo group, was observed to be a gradual significant fall in systemic artery pressures, pulmonary capillary wedge pressure (PCWP; 13.6-10.5 mmHg) and stroke volume, while heart rate increased, leaving cardiac output unchanged. The decrease in PCWP was confined to the group with baseline pressure above the median of 13 mmHg and was of equal magnitude in the group given concomitant medication to that of those who required no such therapy. Significant but weak correlations between the peak serum aspartate aminotransferase level and the baseline PCWP (r = 0.28) and stroke volume (r = 0.22) were found. Non-survivors had a significant baseline depression of cardiac output and stroke volume, while PCWP was increased. However, the overlap with survivors was large. The dosage of metoprolol used resulted in mean plasma levels of about 200 nmol/l, which should induce a rapid and sustained degree of beta-blockade. The patients randomised to placebo or metoprolol were assessed according to initial heart rate. The haemodynamic changes induced by metoprolol were similar but were more pronounced in patients with high heart rate compared to those with low rate. In patients with heart rate greater than 65 beats/min, the metoprolol treated group, in comparison to the placebo group, was characterised by a decrease of 10-20% in systolic artery pressure and heart rate, suggesting a decreased myocardial oxygen consumption. Cardiac index (2.9-2.2 l/min/m2) and stroke volume index (36-32 ml/beat/m2) decreased to a minimum after 30 minutes and gradually rose thereafter. The PCWP increased from 13.7 to 15.4 mmHg, 30 minutes after the injection of metoprolol. This increase was confined to the group with baseline low pressure and the difference compared to the placebo group disappeared after 8 hours.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central haemodynamics in acute myocardial infarction. Natural history, relation to enzyme release and effects of metoprolol. 353 97

Nineteen patients with isolated meniscus lesions were randomly assigned to operation with or without tourniquet. All patients underwent arthroscopic meniscectomy. Measurements of CK (creatinin-kinase), CK-B (isoenzymes MB of creatinin-kinase), LD (lactate dehydrogenase), ASAT (aspartate aminotransferase), and ALAT (alanine aminotransferase) were performed preoperatively and postoperatively over 6 days. The muscle torque was measured on a Cybex II isokinetic dynamometer preoperatively, 1 week and 4 weeks postoperatively. The mean CK level rose significantly in both groups, but did not pass the upper normal serum level. There was no effect on the other muscle enzymes. Quadriceps torque was significantly lowered in both groups 1 week after operation. Four weeks postoperatively, it was still lowered in the nontourniquet group, which also had a slower increase in torque between weeks 1 and 4 than the tourniquet groups. There was no effect from the operation on isometric or hamstrings torque. The slight rise in CK was similar to that seen after hard physical exercise. The decrease in muscle torque was, therefore, mostly due to pain inhibition. The slightly slower rehabilitation in the nontourniquet group may be caused by the technique of raising saline flow and pressure during the arthroscopy to control bleeding. This causes extravasation of fluid which may increase postoperative pain and stiffness.
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PMID:Muscle rehabilitation after arthroscopic meniscectomy with or without tourniquet control. A preliminary randomized study. 952 58

Lyme disease, caused by a tick-transmitted spirochete, typically begins with a unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin lesion, almost half developed multiple annular secondary lesions; some patients had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis, periorbital edema, or diffuse erythema. Skin manifestations were often accompanied by malaise and fatigue, headache, fever and chills, generalized achiness, and regional lymphadenopathy. In addition, patients sometimes had evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat, nonproductive cough, or testicular swelling. These signs and symptoms were typically intermittent and changing during a period of several weeks. The commonest nonspecific laboratory abnormalities were a high sedimentation rate, an elevated serum IgM level, or an increased aspartate transaminase level. Early Lyme disease can be diagnosed by its dermatologic manifestations, rapidly changing system involvement, and if necessary, by serologic testing.
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PMID:The early clinical manifestations of Lyme disease. 685 26

The use of serum myoglobin determinations in the diagnosis and quantitation of acute myocardial infarction was studied in 53 patients. Serial blood samples collected for the first 72 h after pain were analysed for serum myoglobin using a radioimmunoassay procedure. Samples were also assayed for serum creatine kinase (CK) and its myocardial isoenzyme CK-MB, aspartate aminotransferase (AST) and alpha-hydroxybutyrate dehydrogenase (alpha HBDH). Analysis of first and second samples obtained at mean times of 7.6 and 10.7 h respectively after pain produced the following detection rate: serum myoglobin 85% and 98%; serum CK 71% and 85%; serum AST 58% and 81%; serum CK-MB 29% and 60%; serum alpha HBDH 23% and 33% respectively. Total CK-MB and myoglobin release from damaged myocardium were calculated using the method of Norris et al. [16]. A significant correlation was obtained between infarct size calculated from CK-MB and myoglobin in the whole group (n = 29, r = 0.71, p < 0.001). The correlation was even more significant for smaller infarcts with CK-MB release < 220 U/l (n = 13, r = 0.92, p < 0.001).
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PMID:The role of serum myoglobin in the detection and measurement of myocardial infarction. 740 5

A formalin-inactivated aluminium hydroxide adsorbed hepatitis A vaccine was evaluated in a dose-response study on 195 healthy male adults (age range: 18-31 years) in two French hospitals (Lyon, Rouen). Four doses (20, 40, 80, 160 RIA antigen units) were administered intramuscularly (i.m.) in two injections over a 6-month period. At the time of the first vaccine injection, 32 subjects (16.4%) were found positive (> 20 mIU ml-1) for HAV antibody (total Ig RIA HAVAB assay, Abbott Laboratories) and were excluded from the analysis of immunogenicity criteria. Fourteen days after the first vaccine injection, 78.1% (95% confidence interval (CI): 62-90) of seronegative subjects who received the 160 RIA antigen unit dose seroconverted with a geometric mean titre (GMT) of 43 mIU ml-1 (95% CI: 33-56). Seroconversion was 100% (95% CI: 91-100) at 1 month with a GMT of 95 mIU ml-1 (95% CI: 79-112). Statistical analysis revealed a significant dose-related effect (p < 0.0001) on GMT by multivariate regression analysis of the results after the first injection. Biological safety was evaluated and alanine aminotransferase and aspartate aminotransferase levels were similar prior to and 14 days after the first injection in the four groups. Reactions after injection were similar in the four dosage groups: 6.2% of subjects reported immediate reactions after first vaccination (feeling sick, spontaneous pain, headache), 8.9% reported local reactions at the site of injection (spontaneous pain, haematoma, local adenopathy) and 13.5% reported general reactions ('flu-like' syndrome, gastrointestinal tract disorders, fatigue, headache).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Good immunogenicity of GBM strain inactivated hepatitis A vaccine in healthy male adults. 762 20

Attempts have long been made to use the prostigmine-morphine provocation test for the selection of postcholecystectomy patients suffering from sphincter of Oddi (SO) dyskinesia. Since the whole procedure is based upon the evaluation of subjective complaints, this test has frequently been criticized. To improve the diagnostic value of this method, we have visualized SO spasms during prostigmine-morphine provocation by means of quantitative hepatobiliary scintigraphy (QHBS). Twenty-two cholecystectomized patients with typical postprandial biliary pain were included in this study. In the first series of studies, QHBS with technetium-99m 2,6-diethylphenylcarbamoylmethyl-diacetic acid was performed in each patient 2 days before prostigmine-morphine provocation. The time to peak activity (Tmax) and the half-time of excretion (T1/2) over the liver parenchyma (LP), hepatic hilum (HH) and common bile duct (CBD), and the duodenum appearance time (DAT), were determined and served as control values. In the second series of experiments, sphincter spasms were evoked by prostigmine-morphine administration and visualized by means of QHBS. The same parameters were evaluated and serum levels of aspartate aminotransferase (AST) were determined simultaneously at regular intervals. In 12 patients who responded to prostigmine-morphine provocation with typical biliary pain and a significant AST elevation (Nardi positive group) the hepatobiliary scintigram demonstrated a marked biliary obstruction. Tmax and T1/2 over the LP, HH and CBD were significantly increased, while DAT was significantly longer relative to the corresponding data obtained without provocation. Four of the remaining ten patients indicated atypical abdominal pain during prostigmine-morphine provocation, but the AST level remained unchanged in all ten (Nardi negative group).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of results of the prostigmine-morphine test with quantitative hepatobiliary scintigraphy: a new method for the diagnosis of sphincter of Oddi dyskinesia. 778 95

Anomalous responses to morphine are common in patients with unexplained pain in the upper abdomen after cholecystectomy and may be linked to activation of the sympathetic nervous system. The hypothesis that sympathetic suppression would attenuate anomalous responses to morphine was tested by a randomized, cross-over trial using a standard challenge with morphine, with and without pretreatment with clonidine (300 micrograms orally, 1 h prior to the administration of morphine). In 13 of the 15 patients who completed the study, pre-treatment with clonidine decreased plasma concentrations of noradrenaline, dopamine and adrenaline by 56, 15 and 25% respectively. This was associated with a significant reduction in morphine-induced pain (p = 0.02) and nausea (p = 0.04) and attenuated increases in plasma aspartate aminotransferase (AST) activity (p = 0.03). Clonidine attenuates anomalous responses to morphine, perhaps through effects on sympathetic nervous activity or plasma concentrations of catecholamines.
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PMID:Sympathetic suppression attenuates anomalous responses to morphine in unexplained pain after cholecystectomy. 784 98


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