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Biomedical subjects

E J Feuer

Publications and source records attributed to E J Feuer.

64 records · Page 4Linked to original sources

Predicting the outcome of corticoid therapy for acute ulcerative colitis. Results of a prospective, randomized, double-blind clinical trial.

We looked for factors predicting the therapeutic outcome in 66 patients with severe ulcerative colitis treated with intravenous hydrocortisone or corticotropin (ACTH) for 10 days. Patients were randomized before therapy within strata defined by whether they had received oral corticosteroids continuously before the study (group A, 35 patients) or not (group B, 31 patients). Comparisons were made between groups receiving what we considered optimal corticoid therapy, hydrocortisone for group A and ACTH for group B. Overall, therapeutic success was achieved in 28 (42%), with a median time of 7.5 days. Favorable factors measured on admission to the study were those suggesting less severe colitis activity: absence of fulminant disease, limited disease extent, a shorter duration of the present attack, fewer stools, a lower erythrocyte sedimentation rate (ESR), and a higher hemoglobin. Factors compatible with more severe colitis including fulminant activity, more extensive disease, a shorter total disease duration, bloody stools, and fewer bowel movements, favored an early response among those patients who were to achieve a remission. Prolonging therapy beyond 10 days by switching to the alternate corticoid drug did not improve the remission rate. Achieving remission during the initial therapy period, especially when it occurred early, was the most important predictive factor for a favorable clinical course during the following year. Prolonging therapy did not improve the 1-year remission rate. In fact, a higher proportion of patients who continued to require therapy underwent colectomy than those who received one treatment course.

Acute Disease↗

Prognostic factors in breast cancer--a pathological and immunological study of patients with stage 1 breast cancer.

In order to analyze which features determine a poorer prognosis we undertook a study of 91 consecutive patients with pathological Stage I breast cancer operated on at Beth Israel Medical Center (1968-71). Tumor tissue slides were reviewed and features such as: tumor size, histologic type, nuclear grade, lymphocytic and perivenular lymphocytic infiltration, as well as sinus histiocytosis in the lymph nodes removed. Records were reviewed and classified according to age and ethnic background. Survival and recurrence data were recorded up to 14 years post-mastectomy. Also determined was the presence of an antigen, previously detected in certain human breast cancer tumor tissues, which has been found to cross-react immunologically with the 52,000 dalton major envelope protein of the mouse mammary tumor virus (MMTV--gp52). Ten-year cumulative disease-free survival was 0.65. Univariate analysis of survival within various factors revealed that the only statistically significant influencing factor was the presence or absence of the antigen. Factors such as perivenous lymphocytic infiltration, diffuse lymphoid infiltration and sinus histiocytosis in regional lymph nodes also showed trends in favor of improved survival but the sample may be too small for statistical significance. The presence or absence of the antigen was independent of the host immunological reaction. There was no relationship between localization of tumor, whether medial or lateral and survival, nor with presence or absence of antigen.

Antigens, Neoplasm↗

The protective effect of experimental subarachnoid haemorrhage on sodium dehydrocholate-induced blood-brain barrier disruption.

The potential interactive effects between subarachnoid hemorrhage (SAH) and blood brain barrier (BBB) disruption were studied in a rat model. Experimental subarachnoid hemorrhage was produced in twenty rats (experimental group) by the intracisternal injection of blood. In ten additional rats (control group), saline was administered in place of blood. Analysis of mean blood pressure (MBP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) demonstrated an increase in ICP and MBP and a drop in CPP in all animals following intracisternal injection. Subsequent infusion of the left internal carotid artery with sodium dehydrocholate resulted in blood-brain barrier (BBB) disruption in both groups as evidenced by Evans blue staining of the infused cortex. The extent of BBB disruption was significantly greater in the control group than the experimental group. Analysis of the experimental group demonstrated that animals with the lowest pre-SAH MBP and the lowest CPP during the maximum blood pressure response to SAH demonstrated the greatest resistance to experimental BBB disruption. The possibility of ischemia as a contributing factor in BBB protection subsequent to SAH is discussed.

Animals↗

Physiological and electrophysiological consequences of etoposide-induced blood-brain barrier disruption.

The present study investigates the effects of etoposide-induced blood-brain barrier (BBB) disruption on systemic blood pressure (SBP), intracranial pressure (ICP), and electroencephalographic (EEG) activity. A total of 29 rats were divided into two groups. In Group 1, 8 control animals received intracarotid normal saline; in Group 2, 21 animals received intracarotid etoposide. SBP, ICP, and EEG were monitored continuously under general anesthesia and controlled ventilation after tracheostomy. Intravenous Evans blue dye was used for determination of BBB disruption. Although none of the Group 1 animals showed BBB disruption, 57% of the animals in Group 2 showed marked BBB disruption (3+). A slight but statistically significant increase in ICP was noted in the Group 2 animals with 3+ BBB disruption, although lesser degrees of barrier disruption (1+ or 2+) resulted in no significant alteration in ICP. The amplitude and frequency of the EEG decreased significantly ipsilateral to the side of intracarotid infusion in all animals with 3+ barrier disruption with a tendency to return toward normal within 2 hours. The degree of transient EEG change observed correlates well with the degree of barrier disruption, potentially allowing clinical determination of BBB disruption by this method.

Animals↗

Etoposide induced blood-brain barrier disruption in rats: duration of opening and histological sequelae.

The intracarotid infusion of the antineoplastic compound etoposide enhances blood-brain barrier (BBB) permeability. In a rat model system, the functional reversibility and anatomic sequelae of etoposide induced BBB disruption were investigated. Etoposide, in a dose range from 3.0 to 22.5 mg/kg, was infused into the left internal carotid artery of Sprague-Dawley rats. BBB disruption was evaluated by the appearance in the infused hemisphere of systemically administered Evans blue dye and quantitatively by the ratio of counts of the technetium labeled chelate of diethylenetriaminepentaacetic acid in the infused to the noninfused hemisphere. Functional reversibility of altered BBB permeability was investigated at three dose levels of etoposide (3.0, 15.0, and 22.5 mg/kg) by the administration of Evans blue dye at the time of etoposide infusion and the administration of the technetium labeled chelate of diethylenetriamine-pentaacetic acid at varying time intervals after etoposide infusion. Fourteen groups of 12 rats each were studied to define the time course of altered BBB permeability at these three doses. The anatomic sequelae of etoposide induced BBB disruption were investigated at varying time intervals (up to 3 weeks) after intracarotid etoposide infusion. Nineteen rats were examined after sacrifice by intracardiac fixation perfusion with 10% formalin. Each brain was sectioned coronally and examined under light microscopy after hematoxylin and eosin staining. Evidence of BBB disruption was seen at all dose levels of etoposide. The degree of BBB disruption increased with increasing doses of etoposide. The duration of altered BBB permeability increased from less than 1 day at 3.0 mg/kg to between 3 and 4 days at 22.5 mg/kg. Histological studies revealed no evidence of parenchymal damage, although at 4 days postdisruption, a mild perivascular lymphocytic infiltration was noted in the infused hemisphere. Etoposide infusion and subsequent BBB disruption were well tolerated by all test animals. In a rat model system the intracarotid infusion of etoposide is capable of producing prolonged reversible BBB disruption.

Animals↗

Fecal alpha 1-antitrypsin measurement: an indicator of Crohn's disease activity.

Random fecal alpha 1-antitrypsin levels were determined in 34 patients, 24 with Crohn's disease, and 10 "controls" having diarrheal illnesses not associated with intestinal protein loss, in an effort to evaluate its usefulness as a measure of Crohn's disease intestinal activity. In the control group, all alpha 1-antitrypsin levels were less than 2 mg/g dry wt of stool. The mean fecal level among those with Crohn's disease was 52.9 mg/g (range less than 2 to greater than or equal to 200). There was a strong correlation between disease activity, as measured by a clinical score, and the alpha 1-antitrypsin levels (Spearman r = 0.65, p = 0.001). This correlation was similarly strong among those with colitis or ileitis. A fecal value greater than 20 mg/g may provide a rough guideline to separate patients with clinically active disease from those with inactive Crohn's disease, despite a considerable range of fecal levels among patients with a particular clinical score. Fecal alpha 1-antitrypsin levels correlated with several other laboratory measures that have been proposed as indicators of Crohn's disease activity. The serum orosomucoid, C-reactive protein, and albumin correlated with the clinical activity score among some of our patient groups. Both clinical scores and laboratory parameters, however, may have limited usefulness in a variety of circumstances. Random fecal alpha 1-antitrypsin determinations seem to provide a reliable, although not directly quantitative, measure of the intestinal activity among patients with Crohn's disease, especially when other methods may be inconclusive.

Adolescent↗

Platelet monoamine oxidase activity and the classification of depression.

An attempt was made to compare platelet monoamine oxidase (MAO) activity in descriptively based types of nonbipolar depression. Platelet MAO activity was significantly higher in depression secondary to chronic anxiety, compared with primary unipolar depression and depression secondary to borderline personality, and in women compared with men. No significant differences were observed between endogenous-nonendogenous, delusional-nondelusional, psychomotor states, or different age groups.

Adult↗

Catechol-O-methyltransferase activity and classification of depression.

Red blood cell catechol-O-methyltransferase (COMT) activity was compared across different depressive diagnoses. In a sample of 88 depressed inpatients, using defined criteria, no difference was found in respect of enzyme activity and the following categories: primary, secondary, delusional, nondelusional, endogenous, nonendogenous (neurotic), characterological depressions. COMT did not vary with age or sex. A significant increase in COMT activity was noted in agitated, depressed males, as compared to other groups.

Adult↗

Recent incidence trends for breast cancer in women and the relevance of early detection: an update.

The incidence of breast cancer in women has been rising dramatically in the United States since 1982, based on data collected by the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute. An additional three years of incidence and mortality data are included in this update of the earlier analyses; however, the focus of this report remains on examining the steeply increasing incidence trend between 1982 and 1986. Over this period, incidence rates for in situ and localized invasive tumors increased among women age 50 and older, while rates for regional and distant tumors remained stable. The incidence of localized tumors less than 1.0, 1.0 to 1.9, and 2.0 to 2.9 cm in size increased more rapidly than that of tumors 3.0 cm and greater among women over age 50. Survival rates also improved among cases diagnosed over this time period. These descriptive data suggest that early detection may be playing a role in the recent increase in the incidence of breast cancer in women, although other factors cannot be ruled out. Conclusions regarding improved cancer control await confirmation by reduced breast cancer mortality.

Age Factors↗

The effect of Medicare reimbursement for screening mammography on utilization and payment. National Cancer Institute Breast Cancer Screening Consortium.

OBJECTIVE: In January 1991, Medicare extended its mammography benefit to reimburse for breast cancer screening mammograms. In 1991 and again in 1993, the National Cancer Institute Breast Cancer Screening Consortium (BCSC) conducted a survey to test the hypothesis that this benefit would increase mammography use among women over the age of 65. METHODS: The authors analyzed data on non-Hispanic white women ages 65 to 74 living in 11 geographic areas targeted by the BCSC for an earlier study--six that had received cancer screening educational interventions and five control subsites--to measure the impact of the newly adopted Medicare benefit on the use of mammography and use of Medicare to reimburse mammography costs. RESULTS: The data show little overall increase between 1991 and 1993 in reported mammography use among respondents to the survey. However, in six intervention and five control subsites there was an increase in the percentage of women who reported using public payment sources to at least partially reimburse the cost of mammograms. In three intervention subsites, the increase from 1991 to 1993 in the percentage of women using public sources of payment was greater than in the corresponding control subsites. CONCLUSIONS: These findings suggest that public health interventions are more likely to succeed when educational promotion accompanies a financial benefit.

Aged↗