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PubMedDate not supplied

Influence of AFP, CEA and PSA on the in vitro production of cytokines.

Several studies have demonstrated a decreased cytokine production in patients with cancer. Likewise, there is some evidence showing that tumor markers may play a role in immunoregulation. In this work, we have studied the in vitro production of IL-1beta, IL-6 and TNF-alpha in whole-blood cell cultures of 10 healthy subjects after polyclonal activation with lipopolysaccharide of Salmonella enteridis and phytohemagglutinin in the presence or absence of three markers, AFP, CEA and PSA. Each sample was incubated for 48 h at 37 degrees C in a humidified atmosphere of 5% CO(2). Subsequently, cytokine levels in the supernatant were determined. AFP did not significantly affect the production of the three cytokines compared to the basal value obtained on adding PBS. In contrast, CEA significantly increased the production of IL-6 (p <0.001) and TNF-alpha (p = 0.002), while PSA significantly decreased IL-1beta (p <0.001), IL-6 (p = 0.031) and TNF-alpha (p <0.0001) production. These results suggest a possible role of CEA and PSA in the production of these cytokines.

Adult↗
PubMedDate not supplied

Prognostic value of carcinoembryonic antigen, CA 19-9 and CA 72-4 in gastric carcinoma.

The prognostic value of preoperative serum levels of carcinoembryonic antigen (CEA), CA 19-9 and CA 72-4 tumor markers was investigated in patients with gastric cancer. Eighty-two patients who underwent surgical resection of gastric cancer were entered in the study. Correlation analyses showed that CA 72-4 was more frequently positive in patients with advanced tumors (p = 0.04), lymph node invasion (p = 0.02), liver metastasis (p = 0.02) and peritoneal involvement (p = 0.03). CA 19-9 was more frequently positive in patients with advanced tumors (p = 0.01) and with serosal (p = 0.04), lymph node (p = 0.008) and peritoneal involvement (p = 0.02). CEA was more frequently positive in patients with liver metastasis (p = 0.03). Low 3-year cumulative survival was significantly associated with elevated serum levels of CA 72-4 (p = 0.004), CA 19-9 (p = 0.001) and CEA (p < 0.001). Age, tumor stage and CA 72-4 provided prognostic information in the multivariate analysis. Patients with elevated serum levels of CA 72-4 showed a 4.2 times higher risk of death than patients with low levels of the marker. Our results suggest that CA 72-4 has prognostic value in gastric cancer, and patients with a high preoperative serum level of CA 72-4 have a greater risk of death due to gastric cancer.

Adult↗
PubMed2005

Activity of systemic lupus erythematosus in end-stage renal disease patients: study in a Brazilian cohort.

BACKGROUND: Dialysis has been associated with lupus remission. We studied the prevalence of systemic lupus erythematosus (SLE) as a cause of end-stage renal disease (ESRD) in the metropolitan area of Rio de Janeiro and assessed disease activity in SLE patients on dialysis. METHODS: Of 3,535 ESRD patients, 63 had SLE (1.8%). Fifty-seven entered the study (54 females, 3 males, 38 +/- 10 years). Hemodialysis consisted of 3 sessions per week of about 4 h duration, blood flow of about 400 ml/min, bicarbonate dialysate ([Ca(2+)] = 2.5-3.5 mEq/l) at 500 ml/min and cellulose acetate or polysulfone dialyzers. Activity was initially defined as: non-renal (nr) SLE disease activity index (SLEDAI) of >0; use of at least 20 mg/day of prednisone; and/or any dose of another activity-controlling drug. Fifty-seven ESRD patients without SLE were used as controls. RESULTS: Eighteen SLE patients were under drug treatment; of the remaining, 30 had an nrSLEDAI of >0 totaling 48 patients (84%) initially labeled as active. An apparent activity was also present in 21 controls (37%). Of those, 19 had an nrSLEDAI of <4. With a cutoff of >or=4, figures in each group would be 49 and 4%. Under this criterion, age was the only significant predictor of flare in our SLE ESRD population in a multivariate logistic regression model. Activity remained high in patients who were on dialysis for >5 years (7/18, 39%). CONCLUSION: SLE accounted for 1.8% of our ESRD patients. Application of SLEDAI to dialysis patients may require consideration of confounding factors related to the ESRD state. Even with a score of >or=4 as a cutoff, SLE activity in dialysis patients was high (49%) and long-lasting. Age was the major determinant of flare.

Adult↗
PubMed1978

Pyocephalus of the newborn child.

3 cases of pyocephalus (ventricular empyema) in newborn children are described and 16 cases from the literature are analyzed. Half of the previously published cases of pyocephalus are secondary to cerebral abscesses. Neuroradiological findings and especially the necroscopic study of a case demonstrated the existence of membranous blockages inside the ventricles which may make the circulation of CSF impossible. Our treatment of choice consists of repeated punctures and evacuations of purulent content and topic as well as parenteral administration of antibiotics. Further CSF derivative measures are almost always necessary. By these means, we believe the high mortality of these cases could be lowered.

Anti-Bacterial Agents↗
PubMed1985

Acute renal failure complicating viral hepatitis in the absence of severe hepatic insufficiency.

Four patients (2 were HBsAg positive) with acute icteric viral hepatitis (VH) developed acute renal failure (ARF) in the course of their illness and in the absence of other complications. Their peak serum creatinine values (4.7-10, mean 7 mg/dl) were reached either before or simultaneously with their maximum serum aminotransferase values (1,390-2730, mean 2,032 mU/ml). Apart from VH no other factors responsible for precipitating ARF could be identified. In the HBsAg-negative patients, serological investigations for infectious mononucleosis, cytomegalovirus infection, and leptospirosis were negative. In 2 patients liver biopsy showed changes consistent with VH. Proteinuria was absent in all cases, making glomerulonephritis unlikely. The urinary sodium excretion was uniformly high (57-104, mean 78 mmol/l in random samples). Two patients required short courses of dialysis. All cases recovered completely with return of serum creatinine to normal values after a mean duration of 25 days. After a normal serum creatinine level had been achieved, 1 case was lost to follow-up, and the other 3 cases maintain normal renal and liver function tests 9 months (mean) after the initial episode. Otherwise uncomplicated VH is a potential cause of ARF, even in the absence of severe hepatic insufficiency. The mechanism of ARF in VH is unknown, but vasoconstriction phenomena induced by endotoxemia might contribute.

Acute Kidney Injury↗
PubMed1995

Increased plasma endothelin concentration in atherosclerotic renovascular hypertension.

The aim was to investigate circulating levels of immunoreactive endothelin (ir-ET) in atherosclerotic renovascular hypertension (RVH), and to assess the role of the kidneys in its overall plasma concentration. We studied 16 hypertensive patients with renal artery stenosis evidenced by angiography and admitted to hospital for the diagnostic evaluation of RVH by renal vein plasma renin activity (PRA) determinations. The right femoral vein was catheterized to simultaneously measure PRA and ir-ET in both renal veins and inferior vena cava below the origin of the renal veins. RVH was present in 9 patients as indicated by diagnostic PRA renal vein ratios and the remaining 7 patients were considered to have essential hypertension (EH). Patients with RVH showed a marked increase in systemic plasma ir-ET concentration (10.3 +/- 0.9 pg/ml). Despite a significant increase of PRA in the vein of the ischemic (IK) versus the contralateral (CK) kidney in patients with RVH, no significant differences in ir-ET concentration were observed between both kidneys. These results indicate that patients with RVH have increased circulating levels of ir-ET. However, the higher systemic plasma ir-ET do not arise from the renal circulation, since plasma ir-ET is significantly higher in systemic circulation than in renal veins.

Creatinine↗
PubMed1992

Comparative studies of furosemide effects on membrane potential and intracellular chloride activity in human and rabbit ciliary epithelium.

Furosemide (1 mM), a potent loop diuretic, caused a 10-mV (n = 14) depolarization of the intracellular potential difference (PDI) of isolated rabbit ciliary epithelium (CE), but produced a 9-mV (n = 5) hyperpolarization of PDI of isolated human CE. In rabbit CE, furosemide consistently depolarized PDI by 13, 7 and 8 mV in HCO3(-)-free Ringer, Na(+)-free Ringer and after BaCl2 treatment, respectively. The depolarization of PDI was reduced to 2 mV (n = 11) in Cl(-)-free conditions. A hyperpolarization of PDI caused by furosemide that was quantitatively similar to that seen in normal Ringer also occurred in human CE during immersion in HCO3(-)-free Ringer, Na(+)-free Ringer and after BaCl2 treatment. There was a small hyperpolarization (3 mV) of PDI in Cl(-)-free conditions. Human or rabbit tissue-cultured nonpigmented ciliary epithelial cells were loaded with the Cl(-)-sensitive fluorophore 6-methoxy-N-(3-sulfopropyl) quinolinium (SPQ) in hypotonic solution (145 mosm) for 4 min at 37 degrees C. Furosemide decreased intracellular Cl- fluorescence activity of both human and rabbit ciliary epithelial cells by 30 +/- 5 (n = 8) and 25 +/- 7% (n = 13), respectively, when the cells were immersed in Cl(-)-rich solution. It is suggested that a furosemide-sensitive Cl- movement exists in both rabbit and human CE, although the mode of Cl- movement to the aqueous across CE may differ between these species.

Animals↗
PubMed1993

Erythrocyte ion fluxes in essential hypertensive patients with left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity and mortality in essential hypertension (EH). Several hemodynamic and nonhemodynamic factors have been involved in the development of LVH in hypertension, including abnormalities in cellular ion mobilization. METHODS AND RESULTS: We measured different ion transport systems in erythrocytes from 50 patients with EH classified as having or not having LVH measured by M-mode echocardiography. Thirty-two EH patients (64%) exhibited criteria of LVH, and 18 (36%) did not. When the two groups were compared, patients with LVH were older (44.7 +/- 7.4 versus 37.6 +/- 9.2 years; P < .01) and exhibited higher rates of erythrocyte Na(+)-H+ exchange (9.8 +/- 4.1 versus 7.1 +/- 2.6 mmol.[L.cells.h]-1; P < .05) and higher intraerythrocyte Na+ content (8.5 +/- 1.3 versus 7.5 +/- 0.8 mmol/L per cell; P < .01). Systolic and diastolic blood pressure values, as well as biochemical, hormonal, and other erythrocyte ion transport systems studied did not differ between EH with or without LVH. The results of a multiple linear regression analysis using left ventricular mass index (LVMI) as the dependent variable showed that Na(+)-H+ exchange and the maximal rate of the Na(+)-K(+)-Cl- cotransport were the only two independently significant parameters associated with an increased LVMI. CONCLUSIONS: The increased rate of the erythrocyte Na(+)-H+ exchange and the decreased maximal rate of the Na(+)-K(+)-Cl- cotransport system are both associated with the presence of LVH in EH patients. These abnormalities of ion transport pathways tend to increase the intracellular Na+ content and may be involved in the pathogenesis of LVH in EH.

Adult↗
PubMed1994

Increased activity of the Mg2+/Na+ exchanger in red blood cells from essential hypertensive patients.

Epidemiological, clinical, and experimental evidence suggests a relation between Mg2+ metabolism and essential hypertension. The aim of the present study was the detection of abnormalities of the erythrocyte Mg2+/Na+ exchanger in essential hypertensive patients. We studied 66 untreated essential hypertensive patients and 36 normotensive control subjects. Maximal efflux rates of total Mg2+ efflux and the Na(+)-dependent and Na(+)-independent components of Mg2+ efflux were determined in Mg(2+)-loaded red blood cells. Mg2+/Na+ exchanger was calculated as the Na(+)-dependent component of the Mg2+ efflux. Mean values of Mg2+/Na+ exchanger were clearly elevated in hypertensive subjects with respect to normotensive control subjects [184.7 +/- 15.7 versus 84.4 +/- 6 mumol(L.cell.h)-1; P < .001]. This elevation was due primarily to the increased total Mg2+ efflux [324.2 +/- 21.9 versus 257.9 +/- 17.3 mumol(L.cell.h)-1; P < .05], whereas the Na(+)-independent component was not significantly different between the groups [154.5 +/- 11.8 versus 173.4 +/- 15.5 mumol(L.cell.h)-1; P = NS]. Moreover, total erythrocyte Mg2+ content was slightly reduced in hypertensive patients with respect to normotensive control subjects (1.84 +/- 0.04 versus 2.07 +/- 0.04 mmol/L.cell; P < .001). Using the 99% confidence limits of the normotensive population as the normal range, 30 (45.5%) hypertensive subjects showed values of Mg2+/Na+ exchanger higher than 160 mumol(L.cell.h)-1. The Mg2+/Na+ exchanger was inversely correlated with basal intraerythrocyte Mg2+ content (r = -.323; P = .001). From a clinical point of view, we found a positive correlation between diastolic blood pressure values and Mg2+/Na+ exchanger (r = .246; P < .05) in the sample of essential hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Erythrocyte sodium transport, intraplatelet pH, and calcium concentration in salt-sensitive hypertension.

We evaluated changes in erythrocyte sodium transport systems, platelet pH, and calcium concentration induced by low and high salt intakes in a group of 50 essential hypertensive patients classified on the basis of their salt sensitivity. Patients received a standard diet with 20 mmol NaCl daily for 2 weeks supplemented in a single-blind fashion by placebo tablets the first 7 days and NaCl tablets the following 7 days. Salt sensitivity, defined as a significant rise (P <.05) in 24-hour mean blood pressure obtained by ambulatory blood pressure monitoring, was diagnosed in 22 (44%) patients. The remaining 28 (56%) were considered to have salt-resistant hypertension. In the entire group of hypertensive patients, high salt intake promoted a significant increase (P <.05) in the maximal rate of erythrocyte NA(+)-Li(+) countertransport (from 271 +/- 19 to 327 +/- 18 microM/(L cells/h) and of the Na(+)-dependent HCO3(-)-CL(-) exchanger (from 946 +/- 58 to 1237 +/- 92 microM/L cells/h) as well as in platelet pH (from 7.15+/-0 0.01 to 7.19+/-0.02 and calcium concentration (from 49+/-2 to 57 +/-2 nmol/L). Depending on salt sensitivity, high salt intake promoted opposing changes in some of the sodium transport systems studied. Salt-sensitive patients increased the maximal rate of the erythrocyte Na(+)-K(+) pump (fom 7.0 +/- 0.4 to 8.8 +/- 0.4 mmol/(L cells/h), Na(+)-K(+)-Cl(-) cotransport (from 416 +/- 37 to 612 +/- 41 micromol/(L cells/h), Na(+)-Li(+) countertransport (from 248 +/- 20 to 389 +/- 17 micromol/(L cells/h) at the end of the high salt period. Conversely, salt-resistant patients decreased the Na(+)-K(+) pump (from 8.0 +/- 0.4 to 6.9 +/- 0.3 mmol/(L cells/h) and Na(+)-K(+)-Cl(-) cotransport (from 578 +/- 53 to 481 +/- 43 micromol/(L cells/h). We conclude that modulation of erythrocyte sodium transport systems by high salt intake depends on salt sensitivity. The Na(+)-K(+) pump, Na(+)-K(+)-Cl(-) cotransport, and Na(+)-Li(+) countertransport increase in salt-sensitive patients, whereas the activity of these sodium transport systems tends to decrease in salt-resistant patients. Independent of salt sensitivity, high salt intake promotes a significant increase in the erythrocyte Na(+)-dependent HCO3(-)-Cl(-) exchanger, platelet pH, and calcium concentration in essential hypertensive patients.

Adult↗
PubMed1997

Oral calcium supplementation reduces intraplatelet free calcium concentration and insulin resistance in essential hypertensive patients.

We evaluated the effect of oral calcium supplementation on blood pressure, calcium metabolism, and insulin resistance in essential hypertension. After receiving a standard diet with 500 mg of calcium per day during a 4-week period, 20 nondiabetic, essential hypertensive patients were randomized in a double-blind fashion to receive oral calcium supplementation (1500 mg of calcium per day) or placebo for 8 weeks. At the end of the 4-week period of low-calcium diet and after the 8-week period of intervention, we measured blood pressure (by both office and 24-hour ambulatory blood pressure monitoring), calcium-regulating hormones [urinary hydroxyproline and serum osteocalcin, parathormone, and 1,25(OH)2-vitamin D3], intraplatelet free calcium concentration, fasting plasma glucose and insulin levels, and the insulin-sensitivity index (euglycemic-hyperinsulinemic clamp). Compared with patients maintained at low calcium intake, essential hypertensive patients under oral calcium supplementation significantly reduced serum osteocalcin (from 22.2 +/- 1.9 to 17.9 +/- 2.0 micrograms/L; P = .0015), parathormone (from 4.20 +/- 0.38 to 3.30 +/- 0.36 pmol/L; P = .0003), and 1,25(OH)2-vitamin D3 (from 98.0 +/- 11.0 to 61.6 +/- 5.7 pmol/L; P = .0062). Likewise, we found a significant reduction in intraplatelet free calcium concentration (from 35.9 +/- 1.2 to 26.5 +/- 0.8 nmol/L; P = .0005) and fasting plasma insulin levels (from 71.8 +/- 5.9 to 64.6 +/- 6.2 pmol/L; P = .05) and a significant increase in the insulin-sensitivity index (from 2.89 +/- 0.77 to 4.00 +/- 0.95 mg.kg-1.min-1; P = .0007). None of these parameters were significantly modified in patients maintained at low calcium intake. Office and 24-hour mean values of systolic and diastolic blood pressure did not change after 8 weeks of oral calcium supplementation or placebo.

Administration, Oral↗
PubMed1999

Effect of alcohol abstinence on blood pressure: assessment by 24-hour ambulatory blood pressure monitoring.

Several studies have shown that cessation of alcohol drinking reduces blood pressure (BP). However, attempts to reproduce these findings by ambulatory BP monitoring (ABPM) have shown inconsistent results. The aim of the present study was to assess the effect of 1 month of proven abstinence from alcohol on the 24-hour BP profile in heavy alcohol drinkers. Forty-two men who were heavy drinkers (>100 g of pure ethanol per day) were consecutively admitted to a general ward for voluntary alcohol detoxification. On the day of admission, they received a total dose of 2 g/kg of ethanol diluted in orange juice in 5 divided doses, and a 24-hour ABPM was performed. A new 24-hour BP monitoring in the same environmental conditions was performed after 1 month of proven alcohol abstinence while the subjects were receiving the same amount of fluid but without the addition of alcohol. After 1 month of proven alcohol abstinence, BP and heart rate (HR) significantly decreased. The reduction was 7.2 mm Hg for 24-hour systolic BP (SBP) (95% CI, 4.5 to 9.9), 6.6 mm Hg for 24-hour diastolic BP (DBP) (95% CI, 4.2 to 9.0), and 7.9 bpm for HR (95% CI, 5.1 to 10.7). The proportion of alcoholic patients considered hypertensive on the basis of 24-hour BP criteria (daytime SBP >/=135 mm Hg or daytime DBP >/=85 mm Hg) fell from 42% during alcohol drinking to 12% after 1 month of complete abstinence. Abstinence did not modify either the long-term BP variability, assessed by SD of 24-hour BP, or its circadian profile. We conclude that abstinence in heavy alcohol drinkers significantly reduces BP assessed by 24-hour ABPM and that this reduction is clinically relevant. These results show that heavy alcohol consumption has an important effect on BP, and thus cessation of alcohol consumption must be recommended as a priority for hypertensive alcohol drinkers.

Adult↗
PubMed2000

Renin-angiotensin system genetic polymorphisms and salt sensitivity in essential hypertension.

We evaluated the association between salt-sensitive hypertension and 3 different genetic polymorphisms of the renin-angiotensin system. Fifty patients with essential hypertension were classified as salt sensitive or salt resistant, depending on the presence or absence of a significant increase (P<0.05) in 24-hour ambulatory mean blood pressure (BP) after high salt intake. The insertion/deletion (I/D) angiotensin-converting enzyme (ACE) gene, the M235T angiotensinogen (AGT) gene, and the A1166C angiotensin II type 1 (AT1) receptor gene polymorphisms were determined with the use of standard polymerase chain reaction methods. Twenty-four (48%) patients with significantly increased (P<0.05) 24-hour mean BP with high salt intake (from 107.3+/-9.4 to 114.8+/-10.6 mm Hg) were classified as salt sensitive. In the remaining 26 patients (52%), high salt intake did not significantly modify 24-hour mean BP (from 107.6+/-10 to 107. 8+/-9 mm Hg), and they were classified as having salt-resistant hypertension. We did not find any significant association between either M235T AGT or A1166C AT1 receptor genotypes and the BP response to high salt intake. However, patients with essential hypertension homozygous for the insertion allele of the ACE gene (II) had a significantly higher BP increase with high salt intake (9. 8+/-8.1 mm Hg for systolic BP and 5.2+/-4.2 mm Hg for diastolic BP) than that observed in patients homozygous for the deletion allele (DD) (1.2+/-5.9 mm Hg for systolic BP; P=0.0118 and -0.2+/-4.2 mm Hg for diastolic BP; P=0.0274). Heterozygous patients (ID) exhibited an intermediate response. The prevalence of salt-sensitive hypertension also was significantly higher (P=0.012) in II (67%) and DI patients (62%) compared with DD hypertensives (19%). We conclude that a significant association exists between the I/D polymorphism of the ACE gene and salt-sensitive hypertension. Patients with II and DI genotypes have significantly higher prevalence of salt sensitivity than DD hypertensives.

Adult↗
PubMed2001

Endothelial dysfunction in salt-sensitive essential hypertension.

The aim of this study was to evaluate endothelium-dependent and -independent vasodilation, as well as endothelium biochemical markers, in a group of essential hypertensive patients classified on the basis of salt sensitivity. Changes in forearm blood flow in response to acetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA) infusion were determined by means of strain-gauge plethysmography. Moreover, plasma and urinary concentrations of nitrates, cGMP, and endothelin were measured during low (50 mmol/d) and high (250 mmol/d) salt intake. Salt-sensitive hypertension was diagnosed in 26 patients who exhibited a significant increase in 24-hour mean blood pressure assessed by ambulatory blood pressure monitoring after 1 week of high salt intake. Nineteen patients were considered salt resistant. Compared with salt-resistant hypertensives, salt-sensitive patients presented a significant lower (P=0.005) maximal acetylcholine-induced vasodilation (21+/-6.3 versus 28+/-7.5 mL. 100 mL(-1). tissue. min(-1)). On the contrary, maximal sodium nitroprusside-induced vasodilation did not significantly differ between groups (22.4+/-4.5 versus 23.9+/-5.3 mL. 100 mL(-1). tissue. min(-1)). The decrease in maximal acetylcholine-induced vasodilation promoted by the coadministration of L-NMMA was significantly more pronounced in salt-resistant compared with salt-sensitive patients (P=0.003). Finally, high salt intake promoted a significant decrease in 24-hour urinary nitrate excretion in salt-sensitive patients (from 443+/-54 to 312+/-54 micromol/d; P=0.033) compared with salt-resistant hypertensives (from 341+/-50 to 378+/-54 micromol/d). We conclude that salt-sensitive hypertension is associated with endothelial dysfunction characterized by a defective endothelium-dependent vasodilation. Impairment of the L-arginine-nitric oxide pathway may be responsible for this abnormal endothelial response.

Acetylcholine↗