[Factors determining hyperhomocysteinemia in the chronic phase of strokes]. / Factores determinantes de la hiperhomocisteinemia en la fase crónica del ictus.

INTRODUCTION: Several prospective and case-control studies have pointed to an association between hyperhomocysteinemia and ischaemic stroke. AIM: To analyse the main factors determining hyperhomocysteinemia in the chronic phase of strokes. PATIENTS AND METHODS: We studied 280 patients with ischaemic stroke (130 subjects < 45 years old; 150 > 45 years old; 50.7% males) who were admitted to the Neurology Service consecutively over the years 2002 and 2003. Both plasma levels of homocysteine (Hc) and the mutation of the gene for 5, 10-methylenetetrahydrofolate reductase (MTHFR) were determined. An analysis was conducted to determine the distribution of the mean levels of Hc according to the aetiological subtype of stroke (TOAST classification) and the presence of vascular risk factors. RESULTS: Hc levels were found to be above normal (> 13 micromol/L) in 44.3% of cases. Hyperhomocysteinemia was more frequent in those above the age of 45 (55.3 versus 31.5%; p < 0.01). The mean Hc value was 16.3 micromol/L and was high both in young patients (15.1 +/- 14.9 micromol/L) and in adults (17.4 +/- 9.1 micromol/L). Results showed that 42.5% were carriers of the C677T mutation (7.1% in homozygosis and 35.4% in heterozygosis). There were more young patients carrying the homozygotic mutation than adults (9.2 versus 5.3%; p = 0.05). Hc levels in plasma were significantly higher (p < 0.01) in patients who were carriers of the homozygotic mutation (29.4 versus 14.2 micromol/L). The main factors determining hyperhomocysteinemia in the multiple linear regression analysis were: age, mutation of the gene for MTHFR, smoking and being male (R = 0.386). CONCLUSION: Genetic and environmental factors determine the levels of Hc in the chronic phase of strokes.

Plasma catecholamines during an ultrarapid heroin detoxification.

The adrenergic system has long been known to be activated in a situation of stress and thus during opiate withdrawal. A method for detoxification that decreases the stimulation of the sympathetic nervous system will prevent changes of catecholamine levels. Some of such methods have been developed. One of them uses direct transition from heroin to oral naltrexone after deep sedation with midazolam in conjunction with naloxone, droperidol, ondansetron, and clonidine treatment for 24 hours. Can such method prevent adrenergic changes? Moreover, 5-HT has been related to mood disorders. This study aims to determine plasma catecholamines and 5-HT before heroin withdrawal, during the day of the withdrawal, and at the ends of the first day, the first week, and the first 6 months. Forty-three patients with more than 6 years of drug abuse volunteered to seek help to detoxify. After clinical evaluation, blood samples were taken. Plasma catecholamines were isolated by standard alumina procedures and measured by high-performance liquid chromatography with electrochemical detection. Only for NE was there a significant decrease in the day of heroin withdrawal with deep sedation, followed the next day by an increase. During the following days, NE plasma concentrations returned slowly to basal levels. Epinephrine and dopamine plasma levels did not significantly change. Platelet 5-HT levels progressively decreased from the day before detoxification until the last period of observation. We also found that there were no abrupt changes in cardiovascular functions. In conclusion, our results suggest that this type of ultrarapid opiate detoxification prevents the dramatic activation of the autonomic nervous system.

[Severe Raynaud's phenomenon associated with interferon-beta therapy for multiple sclerosis: case report]. / Fênomeno de Raynaud grave associado a terapia com interferon-beta para esclerose múltipla: relato de caso.

Interferon-beta (IFN-beta) is administered for treatment of multiple sclerosis (MS). We report on a woman with MS who presented with severe Raynaud's phenomenon, livedo-reticularis and digital necrosis two weeks after beginning therapy with IFN-beta. Symptoms improved after the IFN-beta was discontinued and anticoagulation associated with cyclophosphamide and corticoid were introduced. Raynaud's phenomenon is probably a side effect of IFN-beta therapy for multiple sclerosis.