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Biomedical subjects

M Bursztyn

Publications and source records attributed to M Bursztyn.

At least 19 recordsLinked to original sources
PubMed2006

Moderate renal insufficiency at 70 years predicts mortality.

BACKGROUND: Glomerular filtration rate (GFR) diminishes with age. Kidney function in the elderly is often assessed by serum creatinine alone, although it is insensitive in this age group. Formulae for predicting GFR are not widely used. AIM: To study the effect of low predicted GFR on mortality. DESIGN: Longitudinal cohort study. SETTING: The community-based Jerusalem Seventy Year Olds Longitudinal Study. METHODS: We studied 445 subjects, all aged 70 years, using questionnaires, a medical examination with history-taking, and standard laboratory tests. Moderate renal insufficiency was defined as a predicted GFR of <60 ml/min, based on the Cockcroft-Gault (CG) and the Modification of Diet in Renal Disease (MDRD) equations. RESULTS: Predicted GFR was normally distributed, with a mean +/- SD of 62.4 +/- 15.27 ml/min. Predicted GFR was <60 ml/min in 221 (46%), most of whom had normal serum creatinine. Twelve-year mortality was 38.7% in these 221 vs. 27% in the other 204. The survival advantage was already evident after 3 years. Under Cox proportional hazard analysis using numerous common risk factors as independent variables, lower predicted GFR had a significant mortality risk (hazard ratio 2.108, 95%CI 1.43-3.12, p = 0.0002). DISCUSSION: In community-dwelling elderly people, moderate renal insufficiency as assessed using the CG equation is a strong and independent predictor of mortality. Most of these at-risk patients have 'normal' serum creatinine.

Age Factors↗
PubMed2005

Normal ambulatory blood pressure: a clinical practice-based comparison of two recently published definitions.

The European Society of Hypertension (ESH) has issued guidelines for the detection and treatment of hypertension. According to these guidelines, normal 24-h ambulatory blood pressure (ABP) is defined as lower than 125/80 mmHg. Another publication of ESH recommendations for blood pressure (BP) measurement defines normal awake and asleep blood pressure as lower than 135/85 and 120/70 mmHg, respectively. Our aim was to investigate the compatibility of these two recently proposed ABP cutoffs in clinical practice. We analysed 1495 consecutive ABP measurements. In all, 56% of the subjects were female; age 58 +/- 16 years; body mass index 27 +/- 4 kg/m(2); clinic BP 151+/-22/84 +/- 13 mmHg. Two-thirds were treated for hypertension, and 11% for diabetes. Subjects were classified as having normal 24-h BP if the corresponding value was <125/80 mmHg. Normal awake-sleep BP was diagnosed if awake BP was <135/85 mmHg and sleep BP was <120/70 mmHg. Concordance between the cutoffs was found in 93% of the subjects. Among the 7% discordant subjects, 4.5% were hypertensive applying the 24 h, but not awake-sleep, BP values, whereas only 2.5% were hypertensive according to awake-sleep, but not 24 h, BP values (P < 0.005). In Conclusion, in real-life ABP measurement, a good agreement was found between two recently issued ABP normality definitions. However, some subjects are classified as hypertensive only according to one of these methods, more often by the 24-h cutoff of 125/80. This discordance may be significant in large-scale clinical BP monitoring.

Blood Pressure↗
PubMed2004

Hyperplastic gastropathy as a presenting manifestation of systemic lupus erythematosus.

A patient is described who had severe hyperplastic gastropathy as the presenting manifestation of systemic lupus erythematosus (SLE). Aggressive immunosuppressive therapy with systemic corticosteroids and immunoglobulins resulted in complete remission of lupus, and a prompt clinical and radiological regression of hyperplastic gastropathy. Hyperplastic gastropathy is an uncommon gastric illness, which is usually idiopathic but rarely is associated with Helicobacter pylori infection, cytomegalovirus infection or lymphocytic gastritis. Three previous case reports have noted a response of idiopathic hyperplastic gastropathy to systemic corticosteroid treatment, yet none of the presented patients had a systemic inflammatory disease. The presented case is the first in the medical literature in which hyperplastic gastropathy is directly linked to the development of clinical and laboratory manifestations of SLE. We suggest that hyperplastic gastropathy be added to the list of rare gastrointestinal manifestations of SLE, and that autoimmune disease be considered a possible cause of hyperplastic gastropathy. As such, any patient with symptomatic idiopathic hyperplastic gastropathy accompanied by other evidence of systemic inflammation should be considered for SLE evaluation and immunosuppressive treatment.

Adult↗
PubMed2002

Non-dipping in diabetic patients: insights from the siesta.

Non-dipping, ie failure to lower blood pressure during sleep, has been found to be more prevalent in diabetic than in non-diabetic subjects. However, the reasons remain to be clarified. Diabetic patients may wake up more frequently during the night (for instance, due to nocturia). This may result in inclusion of awake blood pressure measurements in the night-time average and thus erroneously raise this average, causing misclassification of patients as non-dippers. However, non-dipping in diabetes may be due to blunted effect of sleep itself on blood pressure secondary to autonomic neuropathy. We undertook this study in order to further clarify this question. We studied 23 diabetic patients, and 23 matched controls who underwent 24-h ambulatory blood pressure monitoring, and reported taking an afternoon nap. Afternoon nap, by virtue of its short duration, is devoid of interruptions, and thus can be used as a model for tiled, non-interrupted sleep. We found that, both in diabetic patients and controls, blood pressure declined during the afternoon nap in a similar magnitude to the night-time decline. However, this decline was significantly blunted in the diabetic patients (13.9 +/- 2.2% decline in diastolic blood pressure during naptime in the diabetic patients, as compared with 24 +/- 2.3% decline in diastolic blood pressure during the siesta in the control group, P < 0.02). The blunted decline of blood pressure during the nap in diabetic patients demonstrates that non-dipping is due to the blunted effect of sleep itself. This can be another facet of autonomic dysfunction seen in diabetes mellitus.

Blood Pressure↗
PubMed2001

Atrophy or hypertrophy in chronic renal ischemia: role of the IGF-I system.

To examine the role of insulin-like growth factor-1 (IGF-1) in renal atrophy of rats with two-kidney, one-clip (2K1C), in which the clipped kidney atrophies, and in the one-kidney, one-clip (IK1C) model of renovascular hypertension, in which it hypertrophies, we studied levels of IGF-I, mRNA, and protein in 2K1C, IK1C, and unilateral nephrectomy (NPX) in rats by solution-hybridization RNase protection, and radioimmunoassay, respectively, both cross-reactively and longitudinally at 3, 10, and 30 days after clipping. Three days after clipping, there were no differences in blood pressure or kidney size; however, 10 and 30 days postoperation, the clipped kidney shrank in the 2K1C model. The nonclipped 2K1C and the clipped lK1C and unilateral nephrectomy kidneys increased in weight (P < .05. At day 3 the IGF-I levels were lower (557 +/- 54, 335 +/- 61 ng/g in control and clipped 2K1C, P < .05, v 1,074 +/- 186, 1,109 +/- 54, and 1,154 +/- 200 ng/g kidney, nonclipped 2K1C, 1K1C, and NPX, respectively). At 30 days the IGF-I levels were 300 +/- 24 ng/g in control (P < .05) v clipped 2K1C, 160 +/- 19, 218 +/- 20 ng/g in nonclipped 2K1C and 406 +/- 33 and 470 +/- 34 ng/g in 1K1C and NPX, respectively (P < .05) v control and clipped 2K1C. Kidney mRNA was increased in the clipped 2K1C. In conclusion, the kidney that had higher IGF-I levels early in nonclipped 2K1C, 1K1C, and nephrectomy hypertrophied, and the kidney (clipped 2K1C) that failed to increase IGF-I atrophied. IGF-I levels are dissociated from the local mRNA message.

Animals↗
PubMed2001

Maternal component in the familial aggregation of hypertension.

To assess maternal versus paternal contributions to the familial aggregation of hypertension, we examined family history data from 344 hypertensive probands (69 African American, 153 US Caucasian, 122 Greek Caucasian) ascertained without respect to parental hypertension status. The proportion of hypertensive mothers (81.7, 65.0 and 84.8% for African Americans, US Caucasians and Greek Caucasians, respectively) of these probands was significantly greater than the proportion of hypertensive fathers (50.0, 44.9 and 48.3%, respectively) in all three ethnic groups. The lifetime risk of hypertension was significantly greater for mothers compared with fathers of these hypertensive probands (p<0.001). Examination of the proband's siblings indicated that maternal history of hypertension was associated with greater lifetime risk for hypertension than paternal history (p<0.01). In conclusion, we observe a consistent maternal component in the inheritance of hypertension. Although we cannot separate a maternal genetic from epigenetic or environmental effect, our findings suggest that genetic research should include studies of the mitochondrial as well as nuclear genome. Furthermore, when assessing a patient's risk for hypertension, particular attention should be paid to the maternal family history.

Adult↗
PubMed2001

The effect of the fast of Ramadan on ambulatory blood pressure in treated hypertensives.

Every year, millions of Moslems throughout the world fast from sunrise till sunset daily during the month of Ramadan, that is, experience repeated cycles of fasting-refeeding. Studies in animal models have shown that repeated cycles of fasting-refeeding may cause or exacerbate hypertension. Changes in sleeping patterns as well as changes in medication timing may also influence ambulatory blood pressure. We undertook this study in order to examine the effect of the Ramadan fast on treated hypertensive subjects. Seventeen hypertensive subjects were examined, and 24-h blood pressure monitoring was carried out twice, before and during the last week of the Ramadan. All continued their medications, which were all once-daily preparations. Twenty-four hour mean blood pressure as well as average awake and average asleep blood pressure were compared. There was no difference between mean blood pressure before and during the Ramadan (138.5 +/- 18.5/77.2 +/- 8.1 mm Hg vs 136.4 +/- 20.4/75.7 +/- 5.9 mm Hg, P-nonsignificant). Blood pressure load also did not differ before and during Ramadan (systolic load 49% vs. 44%, diastolic load 21% vs. 18%, P-nonsignificant). Weight was reduced by 1.4 +/- 1.6 kg (P < 0.002). We conclude, that according to our findings, treated, hypertensive patients may be assured that, with continuation of previous medications, traditional fasting during the month of Ramadan can be safely undertaken.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Dipping status may be determined by nocturnal urination.

Nondipping, ie, failure to reduce blood pressure by >/=10% during the night, is considered an important prognostic variable of 24-hour ambulatory blood pressure monitoring. However, some people wake up at night to urinate. Usually, 24-hour ambulatory blood pressure monitoring-derived blood pressure includes these rises in the nighttime blood pressure mean. We identified 97 subjects undergoing 24-hour ambulatory blood pressure monitoring who reported waking up at night to urinate. We assessed the 24-hour ambulatory blood pressure monitoring first using total daytime and total nighttime means and then using actual daytime awake and nighttime asleep (as reported by the patient) means. Nocturnal decline in blood pressure was 14.4+/-8.5/11.8+/-6.1 mm Hg with the first method and 17.1+/-8.3/13.8+/-5.9 mm Hg with the second one (P<0.00001). Although the absolute difference between the nocturnal blood pressure declines calculated by the 2 methods was small, the effect on nocturnal dip was profound. Average systolic blood pressure dipping was 10.1% by the total day-total night method and 12.0% by the actual day awake-night asleep method (P</=0.00001), and that of diastolic blood pressure was 14.2% and 16.7%, respectively (P</=0.00001). The prevalence of systolic blood pressure nondipping decreased from 42.2% by the first method to 31.9% by the second method (P</=0.0056), and that of diastolic blood pressure nondipping decreased from 22.6% to 11.3% (P</=0.00001). Inclusion of awake blood pressure measurements during the night obscured the normal dipping pattern in people who woke up to urinate. Thus, taking into account people's actual behavior increases the accuracy of the results.

Blood Pressure↗
PubMed2001

Chronic exogenous hyperinsulinaemia-induced hypertension in pregnant rats: effect of chronic treatment with l-arginine.

Recent studies have shown that maternal hyperinsulinaemia is a risk factor for the development of hypertension in pregnancy. Experimentally, pregnant rats with chronic exogenously induced hyperinsulinaemia (P-INS rats) have increased blood pressure at the end of gestation. This is associated with a blunted elevation of the excretion of the urinary metabolites of nitrate (UNO(x)). In the present study, we aimed to evaluate the mechanism(s) of the increase in blood pressure in this model. Four groups were studied: normal pregnant rats (P rats), P-INS rats, P-INS rats treated with L-arginine (2 g/l in the drinking water) (L-ARG rats) and hyperinsulinaemic virgin rats (V-INS rats). Systolic blood pressure (SBP), UNO(x) excretion (on ingestion of a controlled low-nitrate diet), urine noradrenaline (norepinephrine) and plasma endothelin levels were evaluated. Rats were killed on day 22 of pregnancy. Five P-INS rats were not killed at this time, in order to measure SBP 30 and 60 days after delivery. Fetal number and fetal body weight were evaluated. At the end of pregnancy, a 10+/-3% increase in SBP was found in P-INS rats, contrasting with a fall of -15+/-4% in P rats (P<0.01). In the L-ARG group at the end of pregnancy, SBP values had fallen by -14+/-2%, to values comparable with those of P rats. The increase in UNO(x) excretion was 175+/-38% in P rats, 106+/-12% in L-ARG rats and 41+/-8% in P-INS rats (P<0.01 compared with P and L-ARG groups). No differences were found in the urinary excretion of noradrenaline or in the plasma levels of endothelin-1 between the pregnant groups. Fetal number was similar in all groups, but fetal body weight was lower for P-INS rats compared with P and L-ARG rats. Thus the blood pressure response to L-arginine strongly suggests that a decrease in NO availability may be the main pathogenic mechanism involved in the development of hypertension in this model.

Animals↗
PubMed2000

Subpressor dose of L-NAME unmasks hypertensive effect of chronic hyperinsulinemia.

We previously found that chronic exogenous hyperinsulinemia without sugar supplementation does not elevate blood pressure. This may be partially explained by the ability of insulin to release nitric oxide and cause vasodilatation. To test this hypothesis, we studied 4 groups of rats: 9 rats (body weight, 213+/-14 g) treated with a gradual increase of a sustained-release subcutaneous insulin pellet; 9 rats (body weight, 213+/-9 g) treated with N:(G)-nitro-L-arginine methyl ester (L-NAME) in drinking water 50 mg/L; 19 rats (body weight, 217+/-11 g) treated with the combination of L-NAME and insulin; and 9 control rats (body weight, 218+/-11 g). Blood pressure was followed weekly for 6 weeks, and then rats were studied in metabolic cages. Weight gain was not different during the 6 weeks. Renal function did not differ between the 4 groups, but 24-hour urinary nitrite/nitrate excretion was lower (P<0.02) in L-NAME-treated and higher in insulin-treated rats. Plasma insulin doubled (P<0.002) in the insulin-treated rats, but there was no hypoglycemia and, by week 6, fructosamine levels were 2.1+/-0.2, 2.1+/-0.2, 2.3+/-0.1, and 2.3+/-0.2 mmol/L in control rats and rats treated with L-NAME, insulin, and L-NAME plus insulin, respectively. Systolic blood pressure, which did not differ at baseline, at week 3 was 122+/-17, 118+/-17, and 118+/-24 mm Hg in the control, L-NAME, and insulin groups and 136+/-14 mm Hg (P<0.03) in the combination group. At week 6, systolic blood pressure was 128+/-14, 127+/-15, and 118+/-13 mm Hg in the control, L-NAME, and insulin groups, respectively, and 150+/-14 mm Hg (P<0.0005) in the combination group. In a subsequent experiment, L-arginine 2 g/L abrogated the effects of L-NAME and insulin combination. In conclusion, chronic exogenous hyperinsulinemia does not affect blood pressure but may cause hypertension when endothelial function is compromised.

Animals↗
PubMed1999

The siesta in the elderly: risk factor for mortality?

BACKGROUND: During the siesta, blood pressure declines like it does during night sleep. Because cardiovascular and cerebrovascular events cluster during the morning hours, when hemodynamic changes from nocturnal baseline are maximal, we hypothesized that an additional sleep period during the day (the siesta) may increase cardiovascular and cerebrovascular events, and thus mortality. METHODS: A prospective population-based cohort study of 455 70-year-old residents of Jerusalem, Israel, using self-reported siesta at baseline and 6 1/2 years of total mortality data. RESULTS: The prevalence of the practice of the siesta was 60.7%. It was more prevalent among men than women (68% vs 51%, P<.001) and in survivors of previous myocardial infarction than in those without previous myocardial infarction (78% vs 58%, P = .009). After 6 1/2 years of follow-up (1990-1996), 75 subjects died. For those who practiced the siesta, total mortality was 20% vs 11% for those who did not (P = .01; risk odds ratio, 2.0; 95% confidence interval, 1.1-3.4). In a multiple logistic regression model that included several lifestyle descriptors, risk factors, and diseases, the siesta remained predictive of mortality (P = .03; risk odds ratio, 2.1; 95% confidence interval, 1.1-3.9).

Aged↗
PubMed1999

Mortality in the Jerusalem 70-year-olds longitudinal study: does nifedipine have a role?

BACKGROUND: Short-acting nifedipine was found to be associated with increased mortality in elderly patients in some studies. METHODS: We examined effects of long-acting nifedipine in a longitudinal study of Jerusalem 70 year olds (448 participants). RESULTS: After follow-up of 6.5 years (1990-1996) 70 subjects died. We examined the effects of baseline variables on total mortality. Hypertensives had higher mortality than normotensives, 21.2% versus 13.8%, p = 0.01. Diuretic-treated patients (n = 72), mostly hypertensive (n = 71), had significantly higher mortality than non-diuretic-treated patients (n = 375), 45.5% versus 14.1%; p < 0.001. Although nifedipine-treated patients had a higher prevalence of coronary heart disease diagnosis than diuretic-treated patients (52% versus 35%), their relative risk of mortality was 0.8 (CI 0.4-1.4) of that of diuretic-treated patients. A multiple logistic regression model, including gender, systolic blood pressure, creatinine, cholesterol, diagnosis of congestive heart failure, cardiovascular arrest, diabetes, previous myocardial infarction, physical activity, nifedipine, other calcium channel and beta blockers and diuretics, found only serum creatinine and diuretic therapy associated with total mortality, p = 0.004 and p < 0.02, respectively. When interaction terms were added to account for drug combinations, diuretic therapy lost significance, but the combination of diuretics and beta blockers (probably representing a more severe form of hypertension) became significant, p = 0.03. CONCLUSION: Long acting nifedipine is not associated with increased mortality in elderly hypertensives.

Aged↗
PubMed1998

Expression of alpha2-adrenergic receptors in normal and atherosclerotic rabbit aorta.

Alpha2-adrenergic receptors (alpha2-ARs) in vascular smooth muscle cells are known to mediate vasoconstriction; however, it is unknown which of the 3 subtypes of alpha2-AR (alpha2A, alpha2B, or alpha2C) is expressed in vascular tissue. We have used subtype-specific probes in in situ hybridization and RNase protection assays to analyze the expression of alpha2-AR in the thoracic aorta of New Zealand White (NZW) and Watanabe heritable hyperlipidemic (WHHL) rabbits, a model for atherosclerosis. We found that the alpha2A-AR mRNA was in endothelial and smooth muscle cells in both NZW and WHHL aorta. In addition, the shoulders and subendothelial regions of the atherosclerotic lesions in WHHL aorta showed abundant expression of alpha2A-AR mRNA. Antibodies to macrophage (RAM-11) and smooth muscle cell (HHF-35) antigens were used to localize macrophage and smooth muscle cells in aortic sections from WHHL rabbits. The expression of alpha2A-AR mRNA within the lesions of WHHL rabbits correlated with the presence of infiltrating macrophages. We discuss the potential role of alpha2A-ARs in macrophage function and in promoting atherosclerosis.

Animals↗