PubMed Health⌕ Search

Biomedical subjects

P N Herbert

Publications and source records attributed to P N Herbert.

At least 19 recordsLinked to original sources
PubMed2000

Overuse of acid-suppressive therapy in hospitalized patients.

OBJECTIVES: The aims of this study were 1) to determine the frequency of use and indications for prescription of acid-suppressive medications in hospitalized patients, and 2) to determine whether patients who are prescribed these medications for stress ulcer prophylaxis are prescribed them on hospital discharge. METHODS: The use of acid-suppressive medications (histamine-2 receptor antagonists, proton pump inhibitors, and barriers--specifically, famotidine, omeprazole, and sucralfate) was assessed in 226 patients admitted consecutively to a general medical nursing unit of an urban, community, teaching hospital. Chart review was undertaken to determine the type of medication used, timing of prescription, and indication for use. RESULTS: Of hospitalized patients, 54% were receiving acid-suppressive therapy. Histamine-2 receptor antagonists were used most frequently (62%). In all, 65% of prescriptions were not indicated as determined by consensus review. Among patients put on acid-suppressive therapy for ulcer prophylaxis, 55% were discharged on the therapy. CONCLUSIONS: There is significant overuse of acid-suppressive therapy in hospitalized patients. The problem of placing low-risk patients on ulcer prophylaxis unnecessarily is compounded by discharging these patients with the medication.

Antacids↗
PubMed1999

Lipoprotein response to a National Cholesterol Education Program step II diet with and without energy restriction.

This study examined the efficacy of a National Cholesterol Education Program (NCEP) step II diet (25% fat with < 7% saturated fat [SFA]) with and without moderate energy restriction. We tested the hypothesis that moderate energy restriction would improve the lipid profile resulting from an isoweight NCEP step II diet. Twenty hypercholesterolemic subjets (10 men and 10 postmenopausal women) consumed the following three controlled diets, each of 4 weeks' duration, as outpatients: (1) high-fat, high-saturated-fat diet to establish baseline lipids and isoweight energy requirements, (2) NCEP step II diet at isoweight energy, and (3) NCEP step II diet with an energy level 15% less than isoweight. The NCEP step II diet at isoweight energy reduced total cholesterol (TC) by 4% (P = .015), high-density lipoprotein cholesterol (HDL-c) by 13% (P < .0001), and HDL2-c by 40% (P < .0001). The TC:HDL-c ratio increased from 4.9 to 5.5 (P < .0001) and was increased in 19 of 20 subjects. Apolipoprotein B (apo B)-containing lipoproteins changed reciprocally: low-density lipoprotein cholesterol (LDL-c) decreased 4% (P = .008) and very-low-density lipoprotein cholesterol (VLDL-c) increased 29% (P < .0001). Apo B levels did not change. Compared with the NCEP isoweight diet the NCEP hypocaloric diet significantly reduced VLDL-c (-9%, P = .014) and apo B (-5%, P = .015). There was an additional reduction in TC (-4%, P = .073) and LDL-c (-4%, P = .126) with no change in HDL-c (P = .807). These data indicate that a NCEP step II diet with energy restriction produces a more desirable lipoprotein response than a NCEP step II isoweight diet. Neither NCEP step II diet improved the TC:HDL-c ratio.

Adult↗
PubMed1998

Exercise training has little effect on HDL levels and metabolism in men with initially low HDL cholesterol.

Low concentrations of high-density lipoprotein cholesterol (HDL-C) are a recognized risk factor for atherosclerotic cardiovascular disease. Exercise is often recommended to increase HDL-C, but the effect of exercise training on HDL levels and metabolism in subjects with low HDL concentrations is not well defined. The present study compared the HDL response to 12 months of supervised endurance exercise training without weight loss in 17 men aged 26 49 years with initially low ( < 40 mg/dl, N=7) or normal ( > 44 mg/dl, N=10) HDL-C levels. HDL-C levels and HDL apolipoprotein metabolism were assessed while the subjects consumed controlled diets before and after the year of training. Increases in total (5.1+/-2.8 versus 1.9+/-4.2 mg/dl, P=0.08) and HDL2 (3.8+/-2.9 versus 0.4+/-1.1 mg/dl, P=0.01) cholesterol were greater in men with normal initial HDL-C levels. Catabolic rates for HDL apolipoproteins decreased 7-14% and biological half-lives increased 10-15% after exercise training in subjects with normal HDL, but were unchanged in the low HDL-C group. HDL apolipoprotein synthetic rates were not consistently affected by exercise training in either group. Postheparin lipoprotein lipase activity increased 27%, the clearance rate of intravenous triglycerides increased 14%, and apolipoprotein B levels decreased 16% with training in subjects with normal HDL-C but were unchanged in the low HDL-C group. We conclude that the ability to increase HDL-C levels through endurance exercise training is limited in subjects with low initial HDL-C, possibly because exercise training in such subjects fails to alter triglyceride metabolism.

Adult↗
PubMed1997

Effects of short-term stanozolol administration on serum lipoproteins in hepatic lipase deficiency.

We have identified a kindred in Providence, RI, deficient in hepatic triglyceride lipase (HL). The two affected brothers have coronary heart disease and elevated levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoprotein [apo] A-I. The lipoprotein lipase (LPL) activity is normal. We and others have postulated that the effects of oral anabolic steroids on HDL metabolism are mediated by HL. To test this hypothesis, we treated these two men and two controls with the oral androgen stanozolol (6 mg/d) for 2 weeks. Consistent with other reports, HL activity increased a mean of 277% in controls with a concomitant decrease in HDL cholesterol (49%), HDL2 cholesterol (90%), HDL3 cholesterol (16%), and apo A-I (41%) and no change in apo A-II. Although stanozolol failed to induce HL activity in the HL-deficient man, HDL cholesterol, HDL2 cholesterol, and apo A-I were reduced a mean of 20%, 48%, and 32%, respectively. In contrast to controls, HDL3 cholesterol (46%) and apo A-II (14%) increased in HL-deficient subjects. Stanozolol treatment also increased LPL activity (124% +/- 86%, n = 4) and decreased lipoprotein(a) ([Lp(a)] 66% +/- 3%, n = 3) in the three men with detectable levels. The data indicate that in addition to stimulation of HL activity, stanozolol treatment changes HDL cholesterol concentration and subfraction distribution by other mechanisms.

Aged↗
PubMed1997

Effect of prolonged exercise training without weight loss on high-density lipoprotein metabolism in overweight men.

This study examined the effect of exercise training without weight loss on high-density lipoprotein (HDL) metabolism in overweight men. We evaluated HDL metabolism using 125I-radiolabeled autologous HDL in 17 overweight men aged 40 +/- 7 years (mean +/- SD) before and after 1 year of exercise training. Subjects consumed defined diets in a metabolic kitchen during the metabolic studies. They performed endurance exercise under supervision for 1 hour four times weekly and maintained their pretraining body weight. Maximal oxygen uptake (VO2max) increased 27% (P < .001) with exercise training. HDL-cholesterol (HDL-C) and apolipoprotein (apo) A-I increased 10% and 9%, respectively (P < .001 for both), whereas triglycerides and apo B decreased 7% and 10%, respectively (P < .05). Postheparin lipoprotein lipase increased 11% (P = NS). Hepatic triglyceride lipase activity (HTGLA) decreased 12% (P < .05). The fractional catabolic rate (FCR) of HDL protein and of apo A-I decreased 5% and 7%, respectively (P < .05 for both). The synthetic rate of apo A-I increased 13% (P < .01). Increased HDL after exercise training is associated with both decreased HDL protein catabolism and increased HDL apo A-I synthesis. Weight loss is not required to increase HDL-C with exercise training in overweight men, but without weight loss, even prolonged exercise training produces only modest changes in HDL-C concentrations.

Adult↗
PubMed1995

Variations in plasma volume affect total and low-density lipoprotein cholesterol concentrations during the menstrual cycle.

Serum lipids are known to vary during the menstrual cycle. To determine if changes in plasma volume contribute to this effect, we determined serum lipids, lipoproteins, and estimated changes in plasma volume in 18 premenopausal women at the start of and at 5-day intervals after menstruation. Eleven men served as a comparison group. Changes in plasma volume were estimated from changes in hemoglobin and hematocrit. Total and low-density lipoprotein (LDL) cholesterol (mean +/- SD) increased 15 +/- 14 mg/dL (9% +/- 10%) and 11 +/- 13 (11% +/- 14%) within 10 days after the start of menstruation (P < .05) and then decreased toward baseline during the rest of the cycle. High-density lipoprotein (HDL) cholesterol increased 3 mg/dL, or 5%, (P < .05) on days 10 and 15 after menstruation. Plasma volume decreased 4% +/- 9% (P < .06) 10 days after the start of menstruation, and this maximum decrease in plasma volume coincided with peak increases in total, LDL, and HDL cholesterol. Except for an 8-mg/dL increase in LDL cholesterol at day 5, lipid changes were no longer significant after adjusting for changes in plasma volume. We conclude that alterations in plasma volume account for approximately half of the increase in total and LDL cholesterol during the menstrual cycle.

Adult↗
PubMed1993

Adiposity and cardiovascular risk factors in men with obstructive sleep apnea.

STUDY OBJECTIVE: To assess anthropometric characteristics of patients with obstructive sleep apnea (OSA) and their relationship to cardiovascular risk factors (dyslipidemia, hypertension, glucose intolerance) and severity of breathing abnormalities during sleep. DESIGN: Case series. SETTING: Referral-based sleep disorder center serving Rhode Island and Southeastern Massachusetts. PATIENTS: Forty-five men, 26 to 65 years old, with OSA diagnosed by clinical and polysomnographic criteria. RESULTS: By national health survey criteria, 51 percent of patients were in the upper fifth percentile for weight, whereas 91 to 98 percent were in the upper fifth percentile for skinfold thicknesses (triceps, subscapular, triceps plus subscapular). Severe upper body obesity, as defined by a waist-hip ratio (WHR) greater than or equal to 1.00, was present in 51 percent of the patients. The WHR, however, did not correlate significantly with the severity of respiratory disturbances during sleep. The patients had higher prevalences of hypertension and impaired glucose tolerance than expected, but normal prevalences of hypercholesterolemia, low high-density lipoprotein cholesterol, and overt diabetes mellitus. Skinfold thicknesses correlated more closely with the severity of OSA than did body mass index (BMI) or neck circumference. CONCLUSION: Men with OSA have a marked excess of body fat that is not always reflected in measurements of body weight or BMI. Also, upper body obesity, hypertension, and impaired glucose tolerance occur more frequently than expected in this population. Severe adiposity may not only promote development of the respiratory abnormalities of OSA, but also may contribute directly to the increased cardiovascular risk associated with OSA.

Adult↗
PubMed1992

The MspI restriction fragment length polymorphism 3' to the apolipoprotein A-II gene: relationships with lipids, apolipoproteins, and premature coronary artery disease.

In previous studies, a restriction fragment length polymorphism (RFLP) has been identified using MspI restriction endonuclease in the 3' region of the apo A-II gene. The rare variant site for this MspI (M2) has been reported to be associated with higher levels of HDL cholesterol and apo A-II. We have studied the frequency and lipid associations of this RFLP in a population of 168 coronary artery disease (CAD) male and female patients, who had more than 50% narrowing of one or more arteries prior to age 60 years, as well as 255 aged-matched males and females from the Framingham Offspring Study. We also studied 31 kindreds in which the proband had premature CAD. The frequency of the M2 allele was higher in CAD cases (0.20) than in the controls (0.13) (P less than 0.05). In general, those subjects carrying the M2 allele had lower HDL cholesterol and apo A-I plasma levels; however, this difference was only significant (P less than 0.02 and 0.002, respectively) in females with CAD. No cosegregation of the M2 allele with hypoalphalipoproteinemia was found in 31 kindreds studied. However, in both generations there was a trend for those subjects carrying the M2 allele to have lower HDL cholesterol levels than those carrying the M1 allele. Sequence analysis of the apo A-II gene of subjects homozygous for either the M1 (n = 1) or the M2 allele (n = 2) revealed that this RFLP is due to a T----C single base mutation 528 bp 3' to the apo A-II gene. In the subjects homozygous for the M2 allele no other mutations were found within the coding region of the apo A-II gene that could result in changes in the primary sequence of the protein. These data indicate that the MspI RFLP 3' to the apo A-II gene is somewhat more frequent in the CAD group. However, there was no significant association between this RFLP and any of the parameters examined. In conclusion, this DNA marker lacks the specificity to be clinically useful for CAD risk assessment in the population studied.

Adult↗
PubMed1992

Lipids in psychological research: the last decade.

We review the recent literature examining lipid changes during stressful experiences, and the psychological and constitutional differences that influence lipid levels at rest and that may modulate lipid response to stress. Mild forms of chronic or episodic stress are apparently not associated with alterations in lipids and lipoproteins, but severe forms of real or perceived stress do appear to alter lipid levels. Acute laboratory stress is frequently associated with short-term alterations in lipids and lipoproteins, but the significance of these changes is unclear. Several individual characteristics, such as heightened neuroendocrine or autonomic reactivity to stressors, Type A component behavior, and other aspects of personality, appear to be associated with an atherogenic lipid profile. Stress may influence lipid concentrations and metabolism through a variety of physiological and behavioral mechanisms, but none have been clearly elucidated. Future research should concentrate on understanding these mechanisms.

Arousal↗
PubMed1992

Decreased HDL2 and HDL3 cholesterol, Apo A-I and Apo A-II, and increased risk of myocardial infarction.

BACKGROUND: A large and consistent body of evidence supports the judgment that elevation of total plasma blood cholesterol is a cause of myocardial infarction (MI) and that high levels of low density lipoprotein (LDL) cholesterol have a positive relation and high levels of high density lipoprotein (HDL) cholesterol an inverse relation with MI. At present, however, the roles, if any, of the major subfractions of HDL, namely, HDL2 and HDL3, have not been clarified. In addition, the relation of plasma apolipoprotein concentrations to MI and whether they provide predictive information over and above their lipoprotein cholesterol associations is unknown. METHODS AND RESULTS: We evaluated these questions in a case-control study of patients hospitalized with a first MI and neighborhood controls of the same age and sex. Cases had significantly lower levels of total HDL (p less than 0.0001) as well as HDL2 (p less than 0.0001) and HDL3 (p less than 0.0001) cholesterol. These differences persisted after controlling for a large number of demographic, medical history, and behavioral risk factors and levels of other lipids. There were significant (p less than 0.0001) inverse dose-response relations with odds ratios for those in the highest quartile relative to those in the lowest of 0.15 for total HDL, 0.17 for HDL2, and 0.29 for HDL3 cholesterol levels. Levels of LDL and very low density lipoprotein cholesterol and triglycerides were also higher among cases than controls, but only for triglycerides was the difference statistically significant after adjustment for coronary risk factors and other lipids (p = 0.044). Apolipoproteins A-I and A-II were both significantly (p less than 0.0001) lower in cases, and differences remained even after adjustment for coronary risk factors and lipids. There were significant dose-response relations for both apolipoprotein A-I (p = 0.026) and A-II (p = 0.002). Neither apolipoprotein B nor E was significantly related to MI after adjustment for lipids and other coronary risk factors. When all four apolipoproteins were taken together, there was an increased level of prediction of MI over the information provided by the lipids and other coronary risk factors (p = 0.003), but this appeared present only for the individual apolipoproteins A-I (p = 0.027) and A-II (p = 0.011). CONCLUSIONS: These data indicate that both HDL2 and HDL3 cholesterol levels are significantly associated with MI. They also raise the possibility that apolipoprotein levels, especially A-I and A-II, may add importantly relevant information to determination of risk of MI.

Age Factors↗
PubMed1991

Effects of exercise and lovastatin on serum creatine kinase activity.

Vigorous physical activity and lovastatin (Mevacor) a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, have both been independently associated with elevated creatine kinase (CK) levels. To determine the effect of lovastatin plus exercise on serum CK activity, we measured CK levels before and after maximal treadmill exercise in 14 men (51.6 +/- 17.3 years, mean +/- SD) and 6 women (48.5 +/- 7.4 years) before and after 4 weeks of lovastatin treatment (20 mg/d). Blood samples were obtained before, immediately after, and 24 hours after exercise. Individual subjects were exercised for the same duration on each test. Preexercise CK levels and the average CK response to treadmill exercise did not differ before and after lovastatin treatment. In two men taking lovastatin, however, CK levels increased by 183% and 242% 24 hours after exercise during lovastatin administration. We conclude that low-dose lovastatin treatment plus exercise does not affect average CK activity but that this combination may markedly increase CK levels in certain individuals.

Adult↗
PubMed1991

High density lipoprotein metabolism in endurance athletes and sedentary men.

BACKGROUND: Endurance athletes have higher high density lipoprotein (HDL) concentrations than sedentary controls. To examine the mechanism for this effect, we compared HDL apoprotein metabolism in 10 endurance athletes aged 34 +/- 6 years (mean +/- SD) and 10 sedentary men aged 36 +/- 8 years. METHODS AND RESULTS: Subjects were maintained on controlled diets for 4 weeks, and metabolic studies using autologously labeled 125I HDL were performed during the final 2 weeks. Lipids and lipoproteins were measured daily during these 2 weeks, and the average of 14 values was used in the analysis. HDL cholesterol (58 +/- 14 versus 41 +/- 10 mg/dl), HDL2 cholesterol (26 +/- 10 versus 12 +/- 8 mg/dl), and apolipoprotein A-I (apo A-I) (144 +/- 18 versus 115 +/- 22 mg/dl) were higher in the athletes, whereas triglyceride concentrations (60 +/- 18 versus 110 +/- 48 mg/dl) were lower (p less than 0.01 for all). Postheparin lipoprotein lipase activity was not different, but hepatic triglyceride lipase activity was 27% lower (p less than 0.06) in the athletes. The athletes' mean clearance rate of triglycerides after an infusion of Travamulsion (1 ml/kg) was nearly twofold that of the inactive men (5.8 +/- 1.5 versus 3.2 +/- 0.9%/min, p less than 0.001). There was no differences in HDL apoprotein synthetic rates, whereas the catabolic rates of both apo A-I (0.15 +/- 0.02 versus 0.22 +/- 0.05 pools per day, p less than 0.01) and apolipoprotein A-II (apo A-II) (0.15 +/- 0.02 versus 0.20 +/- 0.04 pools per day, p less than 0.05) were reduced in the trained men. Apo A-I and apo A-II half-lives correlated with HDL cholesterol in each group (r greater than 0.76, p less than 0.05 for all) but not consistently with lipase activities or fat clearance rates. This relation between apoprotein catabolism and HDL cholesterol was strongest at HDL cholesterol concentrations of less than 60 mg/dl. CONCLUSIONS: We conclude that higher HDL levels in active men are associated with increased HDL protein survival. The mechanisms mediating this effect require better definition, and other factors appear to contribute to HDL cholesterol and protein concentrations among individual subjects.

Adult↗
PubMed1991

Lipid and lipoprotein responses to episodic occupational and academic stress.

We examined the effects of psychological stress on plasma lipid, lipoprotein, and apolipoprotein levels in three related studies. In the first study, tax accountants (N = 20) and a comparable control group (N = 20) were assessed during and after the tax season. In the second and third studies, first-year medical students (N = 24 and N = 16) were assessed at midsemester and immediately before the examinations. Across studies, the stressors induced significant psychological distress. There were no corresponding changes in lipid and lipoprotein levels. Mean stress-induced change in total cholesterol level was -0.04 mmol/L (-1.6 mg/dL) (95% confidence interval, -0.23 to 0.16 mmol/L [-9 to 6 mg/dL]) for the accountants and 0 mmol/L (0 mg/dL) (95% confidence interval, -0.16 to 0.21 mmol/L [-6 to 8 mg/dL]) and 0.10 mmol/L (4 mg/dL) (95% confidence interval, -0.18 to 0.39 mmol/L [-7 to 15 mg/dL]) for medical students in the second and third studies, respectively. In all studies, change in total cholesterol level correlated with change in total serum protein levels (r = .42 to .60). These results suggest that commonly occurring stressful situations do not produce significant changes in plasma lipid and lipoprotein levels.

Accounting↗
PubMed1990

Effects of n-3 fatty acids in essential hypertension.

We examined the effects on blood pressure, plasma lipoproteins, and platelet function when marine oil supplements (rich in n-3 fatty acids) or vegetable oil supplements (rich in n-6 fatty acids) were added to the usual diets of patients with mild essential hypertension. In a randomized, double-blind, parallel-group study, patients received 50 g of either marine oil (n = 8) or vegetable oil (n = 8) daily for 6 weeks following a baseline observation period. Diastolic blood pressure declined during treatment with fish oil (mean +/- SEM, 96 +/- 2 v 89 +/- 2 mm Hg, P = .02), but did not change with vegetable oil (92 +/- 1 v 94 +/- 1 mm Hg). Systolic blood pressure did not change significantly during either treatment. Serum triglycerides declined (by approximately 30%) in patients receiving only marine oil, but total cholesterol, LDL-, HDL-, HDL2-, and HDL3-cholesterol-subfractions and apolipoproteins A-I and B were unchanged in both treatment groups. Bleeding time increased by 33% during treatment with marine oil but did not change with vegetable oil supplements. Marine oil did not alter in vitro platelet aggregation thresholds. The lack of a significant correlation between blood pressure changes and platelet membrane fluidity, plasma renin activity, aldosterone, norepinephrine, or epinephrine suggests that these variables did not mediate the antihypertensive effect of the marine oil. We conclude that large doses of marine oil reduce diastolic blood pressure, lower triglycerides, and increase bleeding time in patients with mild hypertension.

Adult↗