[Subarachnoid hemorrhage, cerebral ischemia and endothelin-1]. / Hemorragia subaracnoidea, isquemia cerebral y endotelina-1.

INTRODUCTION: Cerebral vasospasm is involved in the development of delayed ischemic lesions in patients with subarachnoid hemorrhage. We developed an integral theoretical model to explain the pathophysiology of cerebral vasospasm, in which endothelin-1 has a pivotal role in the development of both cerebral vasospasm and delayed ischemic neurological deficits (DIND). OBJECTIVE: The objective of this study is to analyze the relationship between temporal profile of plasma endothelin-1 levels and the development of cerebral vasospasm and DIND. PATIENTS AND METHODS: We analyzed sequentially plasma endothelin-1 levels in 17 patients with aneurysmatic subarachnoid hemorrhage. All the patients had complete clinical and neuroradiological studies. Patients were classified according to Fisher's score. RESULTS: Patients (4 males and 13 females, aged 48.1 +/- 20.3 years) had a good clinical condition (Hunt-Hess < 4, GCS > 10). Two weeks after bleeding, patients had higher plasma endothelin-1 levels than healthy volunteers (p = 0.024). Patients who developed DIND had higher plasma endothelin-1 levels (p = 0.034) and a different evolution (p = 0.0146) than patients without DIND. There is a significant correlation (p = 0.02) between basal plasma endothelin-1 levels and GOS score. Multiple regression analysis shows a significant dependence between plasma endothelin-1 levels and Fisher's score (p = 0.0195), development of DIND (p = 0.0095), and GOS score (p = 0.0319). Logistic regression analysis finds a predictive relation between Fisher's score and plasma endothelin-1 levels for the development of DIND (overall predicted = 74.24%; p = 0.0148). CONCLUSIONS: Plasma endothelin-1 levels are increased in patients after subarachnoid hemorrhage and are associated with the development of cerebral vasospasm and DIND.

Correlation between plasma estradiol and estrone-3-glucuronide in urine during the monitoring of ovarian induction therapy.

An improved radioimmunoassay was developed to determine estrone-3-glucuronide in daily urine. Resulting levels were compared with those of estradiol in plasma of 10 healthy women and 14 undergoing ovulation induction therapy with human menopausal gonadotropin and human chorionic gonadotropin. A highly significant correlation between plasma estradiol and urinary estrone-3-glucuronide in normal (r = .9209; P less than .01) and stimulated (r = .9229; P less than .01) women was demonstrated. These results proved that the pattern of excretion of estrone-3-glucuronide perfectly reflected the changes in plasmatic estradiol levels when monitoring ovarian induction and that estrone-3-glucuronide determinations can provide clinically useful information in human induction therapy.

Chronic administration of amiodarone and thyroid function: a follow-up study.

In order to evaluate the effects of amiodarone on thyroid function in chronically treated patients, 43 consecutive patients, who had been taking a mean weekly dose of 1420 +/- 488 mg for more than 9 months (mean 16.5 months), were studied. In a first evaluation, three patients with hypothyroidism and two with hyperthyroidism were discovered. In the remaining 38 patients, mean T4 (131 +/- 38 nmol/L) and rT3 (0.85 +/- 0.3 nmol/L) levels were significantly higher than reference values (p less than 0.05 and p less than 0.001, respectively), and mean T3 levels (1.89 +/- 0.73 nmol/L) were significantly lower (p less than 0.001). Thirteen patients showed hyperresponsiveness to thyrotropin-releasing hormone (TRH) stimulation testing. In a second evaluation, performed 12 to 18 months later, two new cases of hypothyroidism were discovered. T3 levels showed significantly lower values (p less than 0.02) than in the first evaluation, whereas basal thyroid-stimulating hormone levels and levels 30 and 60 minutes after TRH stimulation were significantly higher than those in the first evaluation (p less than 0.001). Five new hyperresponders to TRH were found. In the present series, the progressive appearance of clinical thyroid dysfunction with an elevated total incidence (16%) is demonstrated. Moreover, a progressively high prevalence of hyperresponsiveness to TRH stimulation is shown. These findings indicate that chronic amiodarone administration may carry a high risk of thyroid dysfunction.