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F Smithline

Publications and source records attributed to F Smithline.

7 recordsLinked to original sources
PubMed1978

Neuroleptic-induced prolactin level elevation and breast cancer: an emerging clinical issue.

This article reviews the evidence that neuroleptics may increase the risk of breast cancer via their effects on prolactin secretion. All available neuroleptics, including reserpine, raise serum prolactin levels. Elevated serum prolactin level increases the incidence of spontaneously occurring mammary tumors in mice, and increases the growth of established carcinogen-induced mammary tumors in rats. Caution is necessary in extrapolating this relationship to human mammary tumors because human and rodent tumors differ in some important characteristics, including hormone responsiveness. Serum prolactin levels in women with, or at risk for, breast cancer have generally been normal, and only a minority of human mammary tumors respond to changes in serum prolactin levels. Epidemiologic studies have failed to demonstrate an increased risk of breast cancer associated with the use of neuroleptics or reserpine. Thus, although some human mammary tumors are prolactin dependent, the available evidence does not demonstrate an increased risk of breast cancer in women receiving neuroleptics. We conclude that (1) additional epidemiologic studies of the incidence of mammary tumors in women treated with neuroleptics are desirable; (2) it is premature to mandate warning patients of an unknown and undemonstrated increase in the risk of developing breast cancer associated with neuroleptic treatment; (3) detection of existing mammary tumors by breast examination prior to administration of neuroleptics is desirable; and (4) development of antipsychotic drugs that do not increase serum prolactin level may be indicated.

Animals↗
PubMed1975

Failure of the omnicardiogram to predict coronary artery disease in patients with normal resting electrocardiograms.

Seventy-two male patients over the age of 35 had normal resting twelve lead eletrocardiograms (ECG's). All patients were studied by invasive techniques including complete right and left sided cardiac catheterization, selective coronary arteriography, and left ventricular angiography. All patients had been referred because of chest pain with a presumed diagnosis of coronary artery obstruction and myocardial ischemia. Omnicardiograms were generated from the twelve lead ECG's and diagnosed as "abnormal" or "normal" by observers having no knowledge of the cardiac catheterization findings. Of 72 patients studied, 21 were free of coronary artery disease. Of these, 14 (66%) had "abnormal" omnicardiographic reports. Seven (33%) had "normal" omnicardiograms, indicating an incidence of false positive "abnormal" omnicardiographic reports as 66%. Fifty-one patients had hemodynamically significant coronary artery disease. In this group, 19 (38%) were reported as "normal" by omnicardiogram, an incidence of false negative diagnosis of 38%. When the patients with coronary artery disease were classified as to single, double, or triple coronary obstruction, it was evident that the omnicardiogram had failed to separate patients with more extensive disease. Of the 32 patients with "abnormal" omnicardiograms, 56% had double or triple vessel disease, while of the 19 patients with "normal" omnicardiograph reports, 78% had double or triple vessel disease. Similarly, the omnicardiograms failed to identify the patients with abnormal left ventricular angiography. Of 19 patients with coronary artery disease and "normal" omnicardiograms, only 8 (42%) had normal ventricular angiography. However, of the 32 patients with coronary disease and "abnormal" omnicardiograms, only 11 (34%) had abnormal ventriculogram. The omnicardiogram cannot be considered a useful technique for predicting the presence or severity of coronary artery disease or for the identification of abnormal left ventricular function in patients with known coronary artery disease.

Adult↗