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Biomedical subjects

J Fishman

Publications and source records attributed to J Fishman.

At least 235 records · Page 13Linked to original sources
PubMedDate not supplied

Systemic lupus erythematosus associated with klinefelter's syndrome.

Studies in estrogen metabolism were carried out in 2 males with systemic lupus erythematosus (SLE) who also had Klinefelter's syndrome. Although these studies revealed elevated levels of urinary estrogens in 1 patient, abnormalities of estradiol metabolism suggesting persistent estrogen stimulation were detected in both. This report notes an association between SLE and Klinefelter's syndrome and suggests that chronic estrogenic stimulation may be significant in the development of SLE in these 2 patients.

Adult↗
PubMedDate not supplied

Multiple vessel coronary angioplasty: classification, results, and patterns of restenosis in 494 consecutive patients.

We report the immediate results and 6 month follow-up data of 494 consecutive patients who underwent coronary angioplasty in two or more major epicardial arteries. Clinical success was achieved in 95% of the 494 patients. The technical success rate of the 1,117 vessels dilated was 89%, defined as at least a 35% reduction (mean = 53%) of the initial percent diameter stenosis and a decrease in the transstenotic gradient to less than or equal to 15 mmHg (mean = 9 mmHg). Complications of the procedure included emergency bypass surgery (2.8%), myocardial infarction (3.0%), and hospital death (0.4%) inclusive. At least one of these complications (major cardiac event) occurred in 3.8% of patients. Prior to angioplasty, 46% of patients were in Canadian Cardiovascular Society Class II, 42% in Class III, and 12% in Class IV. Follow-up clinical evaluation (mean follow-up period of 16.9 months) showed 83% of patients in Class I, 14% in Class II, and 3% in Class III. Of the 286 successful patients who have reached 6 month follow-up plateau (mean follow-up period of 20.5 months), 164 (57%) have so far had repeat coronary angiography and exhibited three different patterns: all lesions patent (N = 54), some lesions restenosed (N = 60), and all lesions restenosed (N = 32). There were 18 patients with new vessel lesions (not previously dilated). Logistic regression analyses demonstrated that clinical factors including diabetes (P less than .05), hypercholesterolemia, (P less than .01), new onset angina (P less than .05), current smoking (P less than .01), and morphologic and technical factors such as preangioplasty diameter stenosis greater than 95% (P less than .05) and higher balloon inflation pressure (P less than .05) were predictive of increased risk of recurrence. Patients were classified into two groups based on the anatomy of the target lesions. In Group A (N = 217), patients had a single lesion in each of the vessels to be dilated; Group B (N = 277) patients had a complex lesion in at least one of the vessels dilated. Group B patients were more likely to develop recurrence (P less than .05). Of the original 494 patients, 488 (99%) are alive. Coronary angioplasty (either initially or with repeat PTCA) has been the definitive treatment in 453 of the 494 patients for an overall success of 92%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMedDate not supplied

Recurrence after coronary angioplasty.

Recurrence (restenosis) after coronary angioplasty has undermined the initial success of the procedure and has compromised, to some extent, the attractiveness of the technique in the treatment of ischemic heart disease. Assessment of recurrence predictors has been problematic due to lack of coordination of angioplasty recurrence research and includes: incomplete angiographic documentation, variations in definitions of restenosis anatomically and the results of restenosis physiologically (ie, myocardial ischemia), the dirth of morphologic specifications of subsets under investigation and late outcome pathology, limitations in statistical analyses used, and minimal efforts to classify the available data on recurrence. A review of the literature suggests that all findings regarding recurrence after angioplasty can be organized in four categories: clinical, morphologic, technical (or procedural), and pharmacologic. The reported findings with high concordance as risk factors for recurrence after angioplasty include the clinical factors of diabetes mellitus, hyperlipidemia, and angina of short duration or unstable presentation. Morphologic factors which have been corroborated vis-à-vis recurrence include stenoses with diameter reduction of greater than 90% before and greater than 30% after angioplasty, residual trans-stenotic pressure gradients of greater than 20 mmHg after angioplasty, and lesions that are diffuse, long, eccentric, or calcified. Technical factors associated with recurrence include lower balloon/vessel (or graft) ratios and the absence of (uncomplicated) "intimal dissection." The category most deficient in research regarding recurrence after angioplasty is pharmacologic. Since there are statistically documented and reproducible factors predictive of restenosis, to ignore or minimize these findings or resist further evaluation (because of the ease and safety of performing repeat angioplasty) is to deny the opportunity to understand the mechanisms and favorably affect the incidence of recurrence. This review concludes with two major implications of the restenosis research: certain clinical, technical, and pharmacologic factors, if addressed, may predictably decrease the rate of restenosis and certain clinical and morphologic factors may increase the risk of restenosis; these factors may be less readily modified (eg, diabetes, lesion calcification) and thus must be considered in the decision for angioplasty.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMedDate not supplied

Increased urinary catechol estrogen excretion in female smokers.

Premenopausal female smokers show significantly increased estrogen 2-hydroxylation, which may account in part for the anti-estrogenic effects of cigarette smoking. We have measured five major urinary estrogens, including estradiol (E2), estrone (E1), 16 alpha-hydroxyestrone (16 alpha OHE1), estriol (E3), and 2-hydroxyestrone (2OHE1), in premenopausal female smokers and non-smokers, to determine whether increased C-2 hydroxylation affected the urinary excretory patterns in these subjects. While total measured estrogen excretion in the follicular phase did not differ significantly between the two groups, urinary 2OHE1 among the smokers constituted a significantly greater proportion of the total (31.1 vs 18.2%, P less than 0.02). This difference was largely caused by significantly increased urinary 2OHE1 and decreased E3 observed in smokers. A urinary catechol estrogen index, defined by [2OHE1]/[E3], was significantly elevated in smokers compared with non-smokers (1.67 +/- 0.21 vs 0.56 +/- 0.08, P less than 0.001), and this urinary index correlated strongly with radiometrically determined estrogen 2-hydroxylation (r = 0.84, P less than 0.01). Ratios of the various estrogen metabolites did not vary substantially throughout the menstrual cycle. Urinary estrogen indices as described here may therefore be useful in demonstrating differences in estrogen metabolism, specifically 2-hydroxylation vs 16 alpha-hydroxylation, in selected populations.

Adult↗
PubMedDate not supplied

Radioimmunoassay of 16 alpha-hydroxyestrone in human urine.

A radioimmunoassay for the quantitation of the sum of free, glucuronidated and urine is described. The method is reliable and accurate. Using this method, urinary excretion of 16 alpha-hydroxyestrone was determined in normal men, premenopausal women, and postmenopausal women. The values were compared to the urinary excretion of estrone and estradiol. In two women, the urinary excretion of the three estrogens was measured in daily samples throughout a normal menstrual cycle. We conclude that 16 alpha-hydroxyestrone is a quantitatively important urinary estrogen. Inclusion of the measurement of 16 alpha-hydroxyestrone should yield a more accurate assessment of estrogen metabolism.

Estradiol↗
PubMedDate not supplied

P450 enzymes of estrogen metabolism.

Endogenous and exogenous estrogens undergo extensive oxidative metabolism by specific cytochrome P450 enzymes. Certain drugs and xenobiotics have been found to be potent inducers of estrogen hydroxylating enzymes with C-2 hydroxylase induction being greater than that of C-16 hydroxylase. Oxygenated estrogen metabolites have different biological activities, with C-2 metabolites having limited or no activity and C-4 and C-16 metabolites having similar potency to estradiol. Pathophysiological roles for some of the oxygenated estrogen metabolites have been proposed, e.g. 16 alpha-hydroxyestrone and 4-hydroxyestrone. These reactive estrogens are capable of damaging cellular proteins and DNA and may be carcinogenic in specific cells.

Animals↗