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At least 757 records · Page 42Linked to original sources
PubMed1995

[Homozygote deficiency of thiopurine methyltransferase. A contraindication to the use of azathioprine in kidney transplantation].

Azathioprine-induced myelosuppression is the most important side effect observed in kidney transplantation. We report a case of severe neutropenia after kidney transplantation due to a thiopurine methyltransferase deficiency. This cause of azathioprine-induced myelotoxicity is rare, but its infectious consequences may be severe. Thiopurine methyltransferase deficiency must therefore be suspected when early and severe leukopenia occurs during azathioprine therapy. Erythrocyte thiopurine methyltransferase activity measurement confirms the diagnosis. Azathioprine and 6-mercaptopurine must afterwards be definitively avoided.

Azathioprine↗
PubMed1995

[Atenolol i.v. in the acute phase of AMI: the indications, contraindications and interactions with thrombolytic drugs in the GISSI-2 study. The GISSI-2 Researchers. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico].

BACKGROUND: In the pre-thrombolytic era, several studies showed the effectiveness of beta-blocker administration in the treatment of patients (pts) with acute Myocardial Infarction (MI). Results from the ISIS-1 and GISSI trials suggested that the combined administration of beta-blocker and of thrombolytic drugs in the acute phase of infarction could lead to a better prognosis. The possibility of synergic effects from the associated administration of these drugs was confirmed by small clinical trials. In GISSI-2 study a large number of patients treated with thrombolytic drugs were given i.v. atenolol (10 mg) as recommended therapy, not following a randomized study design. AIM: We reviewed the data of the GISSI-2 study population in order to evaluate: 1) the number of pts treated with i.v. atenolol; 2) the anamnestic and clinical characteristics of treated und untreated pts; 3) the causes of exclusion from the beta-blocker therapy; 4) the causes of scheduled dose withdrawal and the incidence of side effects related to atenolol administration; 5) the interaction between atenolol and streptokinase (SK) and rtPA; 6) the incidence of relevant clinical events and the causes of death during the in-hospital period. RESULTS: Among 12377 evaluated pts, 5616 (45.4%) were given atenolol i.v., 2772 received SK (49.5%) and 2844 (50.5%) rtPA. Mean age was 59.5 +/- 11.3 yrs in atenolol treated pts vs 63.4 +/- 10.9 yrs in untreated pts (p < 0.001); 34.1% of pts aged > 70 yrs vs 48.6% of younger pts (p < 0.00001) and 42.1% of females vs 46.2% of males (p < 0.003) received atenolol. Pts with previous MI received less frequently atenolol than those without MI (17.5% vs 13.5%, p < 0.00001). 88.5% of the treated pts was in Killip class I at entry (untreated 69.5%, p < 0.00001); anterior and lateral site, non-Q type and > or = 5 electrocardiographic leads with ST segment elevation were more frequently found in atenolol treated pts, inferior and unknown site in untreated pts. Among 6761 untreated pts, 32% did not receive atenolol for the occurrence of bradycardia, 15.2% for hypotension, 14.1% for heart failure, 7.2% for bronchospasm or history of asthma, 6.2% for bradycardia and hypotension, 0.3% for death; in 25% of the untreated pts, none of the above-mentioned causes was detectable. 1064 pts (18.9%) did not complete the scheduled dose of atenolol for the occurrence of bradycardia or atrioventricular block > or = II degree (7.3%), hypotension (7%), bradycardia and hypotension (1.8%), heart failure (0.7%), death (0.03%), other causes (1.9%). Transient hypotension was found more frequently in pts treated with SK than in those receiving rtPA (9.3% vs 4.8%, p < 0.0001), but the rate of persistent hypotension was not different in both groups (4.6%). During the hospital phase a higher incidence of advanced atrioventricular block (12.3% vs 4.3%), need of temporary or permanent pacing (5.6% vs 1.9%), sustained ventricular tachycardia (4.5% vs 2.8%), heart failure (12% vs 7.1%), ventricular fibrillation (8% vs 4.9%) and death (11.9% vs 5.1%) were shown in pts that were not given i.v. atenolol. Heart failure was the main cause of death in both groups (untreated 2.3% vs 2.2%); ventricular fibrillation (0.2% vs 0.48%), cardiac rupture (0.5% vs 1.4%), and electromechanical dissociation (0.9% vs 1.9%) were less frequent in treated pts. CONCLUSIONS: The absence of randomized design of atenolol administration limits the value of the differences found in the clinical outcome of the two groups of pts. In spite of that, the low incidence of death and side effects in treated pts, and the high percentage of pts who completed the scheduled dose of atenolol, confirm that the iv. administration of beta-blockers in the acute phase of the myocardial infarction is safe, well tolerated and suitable in almost an half of the patients submitted to thrombolytic therapy with SK or rtPA.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1995

Thrombolytic therapy for venous thromboembolism. Complications and contraindications.

There is renewed interest in the treatment of acute deep vein thrombosis and acute pulmonary embolism with thromboembolytic therapy because of the demonstrated mortality reduction in patients with acute myocardial of the demonstrated mortality reduction in patients with acute myocardial infarction and because of the development of newer, fibrin-specific drugs. Bleeding is the major complication of thrombolytic therapy. This article addresses the benefits and risks of using thrombolytic therapy in patients with acute deep vein thrombosis or acute pulmonary embolism.

Clinical Trials as Topic↗
PubMed1994

Ketamine's psychological effects do not contraindicate its use based on a patient's occupation.

Since ketamine was approved for clinical use, there has been debate over whether the psychological effects of ketamine warrant avoiding use of the drug in patients based on their occupation. This article reviews the literature to determine if such concerns are valid. After 25 years of clinical experience with ketamine, fewer than 10 cases document the occurrence of delayed psychological effects potentially attributable to that drug. In most cases, the delayed effects were temporary, resolving within 3 weeks. Further, there were no long-term psychological effects clearly attributable to ketamine. Children who manifested delayed effects had several other factors present placing them at risk for long-term psychological changes independent of their receiving ketamine. Several controlled studies investigating the risk of long-term psychological effects due to ketamine fail to document that the risk of permanent psychological changes from ketamine is any greater than that from any other anesthetic. In conclusion, there is no evidence in the literature that ketamine presents a higher risk compared to other anesthetics for causing long-term psychological effects that result in a patient not being able to return to his or her occupation. The decision of whether to use ketamine should be a clinical decision weighing relative risks versus benefits, and not a decision based on the patient's career.

Anesthesia↗