Embolization of carotid cavernous fistulas via the superior ophthalmic vein

Background: Carotid cavernous fistulae are treatable by various means, one of which is embolization via the superior ophthalmic vein (SOV). The use of this technique over the past 12 years at the Royal Melbourne Hospital, Victoria, Australia, is reviewed.
Methods: Five patients with carotid cavernous fistulas were treated with embolization of the fistula via the surgically isolated SOV.
Results: Each patient had successful endovascular closure of the fistula using embolization via the SOV approach.
Conclusions: Treatment of certain types of carotid cavernous fistulas that cannot be closed by the conventional endovascular (arterial and venous) approaches can be successfully closed by using a transvenous approach through the SOV     

Computed tomographic angiography of the body

Large and medium-sized blood vessels can be identified on extracranial computed tomographic (CT) scans when a combination of infusion and bolus injection of conventional contrast material is administered. The cases illustrated in this report show that CT angiography can sometimes offer clinically useful information not present on CT scans obtained without contrast injection.     

A case of metoclopramide-induced oculogyric crisis in a 16-year-old girl with cystic fibrosis

Oculogyric crisis is a neurologic reaction characterized by bilateral dystonic elevation of visual gaze as well as hyperextension of the neck. This reaction is most commonly explained as an adverse effect of numerous medications, such as dopamine receptor blocking agents or neuroleptic medications and traditional antipsychotic or antiemetic drugs, such as prochlorperazine or metoclopramide. A case of oculogyric crisis induced by metoclopramide is described in this paper.     

Sex hormone associations with breast cancer risk and the mediation of randomized trial postmenopausal hormone therapy effects

Introduction

Paradoxically, a breast cancer risk reduction with conjugated equine estrogens (CEE) and a risk elevation with CEE plus medroxyprogesterone acetate (CEE + MPA) were observed in the Women’s Health Initiative (WHI) randomized controlled trials. The effects of hormone therapy on serum sex hormone levels, and on the association between baseline sex hormones and disease risk, may help explain these divergent breast cancer findings.

Methods

Serum sex hormone concentrations were measured for 348 breast cancer cases in the CEE + MPA trial and for 235 cases in the CEE trial along with corresponding pair-matched controls, nested within the WHI trials of healthy postmenopausal women. Association and mediation analyses, to examine the extent to which sex hormone levels and changes can explain the breast cancer findings, were conducted using logistic regression.

Results

Following CEE treatment, breast cancer risk was associated with higher concentrations of baseline serum estrogens, and with lower concentrations of sex hormone binding globulin. However, following CEE + MPA, there was no association of breast cancer risk with baseline sex hormone levels. The sex hormone changes from baseline to year 1 provided an explanation for much of the reduced breast cancer risk with CEE. Specifically, the treatment odds ratio (95% confidence interval) increased from 0.71 (0.43, 1.15) to 0.92 (0.41, 2.09) when the year 1 measures were included in the logistic regression analysis. In comparison, the CEE + MPA odds ratio was essentially unchanged when these year 1 measures were included.

Conclusions

Breast cancer risk remains low following CEE use among women having favorable baseline sex hormone profiles, but CEE + MPA evidently produces a breast cancer risk for all women similar to that for women having an unfavorable baseline sex hormone profile. These patterns could reflect breast ductal epithelial cell stimulation by CEE + MPA that is substantially avoided with CEE, in conjunction with relatively more favorable effects of either regimen following a sustained period of estrogen deprivation. These findings may have implications for other hormone therapy formulations and routes of delivery.

Trial registration

clinicaltrials.gov identifier: {"type":"clinical-trial","attrs":{"text":"NCT00000611","term_id":"NCT00000611"}}NCT00000611.