Citalopram-induced Raynaud's phenomenon.
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Biomedical subjects
Publications and source records attributed to M Torra.
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Although it is suspected that some patients with acute coronary syndromes (ACS) could have a sub-optimal response to aspirin (SASAR), currently a fixed dose of ASA is long-term used in all individuals. This study was designed to determine SASAR and whether a SASAR is a predictor for recurrence of ischemic events in patients on low-dose ASA with a previous ACS. One hundred patients taking ASA 100 mg/day were assessed at 1 and 6 months after a first ACS. SASAR was initially defined as a failure of the ASA treatment to significantly prolong the closure time in the Platelet Function Analyzer (PFA-100). SASAR in these samples was reconfirmed by conventional aggregometry. TXB2 levels were determined in plasma. At one month 49 patients showed SASAR in the PFA-100; only 25 of them showed SASAR by conventional aggregometry. At six months, 39 of 81 patients showed SASAR by PFA-100, but conventional aggregometry detected SASAR in only 12 of the 39 patients. TXB2 levels were significantly higher in patients with SASAR. Five patients with SASAR, by both tests, died during follow-up (p = 0.013). The PFA-100 detected a high rate of SASAR in patients with ACS. This instrument could be used to screen for suboptimal response to the antiplatelet action of ASA. Whether persistence of SASAR could relate to a higher risk of recurrence and how adjusting the dose of ASA could reduce the rate of SASAR are issues that deserve further investigations.
BACKGROUND AND OBJECTIVE: Despite the number of plans leading to lose weight among individuals in the developed countries, the prevalence of obesity has increased since 1980. The knowledge of ponderal evolution in a given population is very important because the adverse effects of obesity vary greatly among individuals and populations. The objective of the present paper was to determine the modifications in the different degrees of body adiposity in a population in Catalunya. PATIENTS AND METHODS: A measurement was made of weight and height of 24554 users aged over 14 years (10595 males and 13959 females) attended at four basic health areas (BHA): Girona 1, Girona 4, Salt and Camprodon, and a Primary Health Center (PHC) in the Girona province, for a five-year period, 1995-1999. The prevalence of the different degrees of obesity was compared with that obtained in a previous study with 6373 individuals during the 1986-1989 period (4,579 males and 1794 females). RESULTS: The prevalence of women with overweight (defined as a body mass index [BMI] > 25 kg/m2) increased from 7.3% (1986-1989, study 0) to 17.6% (1995-1999, study 1) for women aged 15 to 24 years ( p < 0.001), from 17.9 % to 28.1% for women aged 25 to 34 years (p < 0.001), and from 37.5% to 44.7 % for women aged 35 to 44 years (p < 0.001). In the latter age group, the proportion of women with obesity (BMI > 30 kg/m2) increased from 6.9% to 12.9%. Similar trends were observed among men, and the change in the 35-44 year age group (from 10.5 % of obese men to 16% [p < 0.001]), and 55 to 65 years (from 16.6% of obese men to 22.7% [p < 0.001] was particularly significant. And lastly, it is also noteworthy the proportion of individuals with low weight (BMI < 18.5 kg/m2) which increased from 7.3% to 11.6% for women aged 15 to 24 years, and from 0.3% to 2.2% for women aged 35 to 44 years. This trend was also observed for men aged 15 to 24 years (11% to 17.2%). CONCLUSIONS: The relative increase in the prevalence of overweight and obesity runs in parallel to that found in other surrounding countries. Also, it is worth mentioning that among women aged 15 to 24 years the increase in the prevalence of low weight and obesity is almost identical, which invalidates the mean and median values as a means to assess the ponderal evolution in this population. The current compartmentalization between the extreme BMIs, particularly among the youngest portion of population should be addressed from a multidisciplinary perspective.
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Serum manganese levels were determined in 250 healthy subjects (122 men and 128 women) living in Barcelona in northeastern Spain. The study was designed to assess the reference levels for serum manganese and to investigate its relationship to age and sex. The age distribution ranged from 15 to 90 years. The assays were performed by means of a graphite furnace atomic absorption spectrometry. The geometric mean of serum manganese concentration was 1.1 microg/l, ranging from 0.3 microg/l to 2.5 microg/l. In almost every case, the 95th upper percentiles of this element were < 1.8 microg/l. No correlation between the concentration of manganese and sex could be established, but in the younger population the manganese levels were nearly three times higher than the results obtained in the older population.
BACKGROUND: Because little is known about micronutrient/antioxidant intake and asthma severity, we investigated dietary intake and plasma/serum levels of micronutrients/antioxidants in a group of asthma patients with various degrees of severity, and compared the results with healthy subjects. METHODS: A case control study was carried out on 118 asthma patients and 121 healthy subjects. The severity of the disease was classified by division of patients into four groups. Normal dietary micronutrient/antioxidant intake was estimated from a food frequency questionnaire. Plasma/serum levels of vitamins C, E, and A, selenium, magnesium, zinc, and platelet glutathione peroxidase (GSH-Px) activity were also determined. RESULTS: No differences in daily micronutrient/antioxidant intake were seen between patients and healthy subjects. The severity of the disease showed no significant relationship with micronutrient/antioxidant intake. There were no differences in plasma/serum levels in any of the micronutrients/antioxidants between healthy subjects and asthmatics. Nor were any differences found between asthma groups in severity in the biochemical measures, except in platelet GSH-Px activity, which was significantly lower in the most severe groups. CONCLUSIONS: In this study, we found no evidence of any association between micronutrient/antioxidant intake or plasma/serum levels of micronutrients/antioxidants and asthma. Reduction of platelet GSH-Px activity in the most severe patients suggests that these patients have a diminished capacity to restore part of the antioxidant defences.
BACKGROUND: Increased plasma levels of alpha-1-acid glycoprotein (AGP) were reported in major depressive disorder. However, the relationship between AGP levels, severity of depression, treatment response and antidepressant levels are still unclear. METHODS: Plasma AGP levels were measured in 36 subjects with major depressive disorder before and after a 6-week treatment with imipramine and in 30 controls. Free imipramine plasma levels of depressed patients were measured at 6 weeks. Comparative analysis between depressed patients and controls, between non-responders (N = 12) and responders (N = 24), and between severely depressed patients (N = 14) and moderately depressed patients (N = 22) were made. RESULTS: Depressed patients had significantly higher mean values of AGP than control subjects. Imipramine non-responders and specially severely depressed patients had significantly greater increases of AGP levels during treatment than other depressed subgroups. There was no correlation between baseline AGP levels and severity of depression or free imipramine levels. LIMITATIONS: The most significant limitations of this study are the small sample size and the fact that all the subjects were out-patients. Results should not be generalized to in-patient populations. CONCLUSIONS: Depressed patients showed high baseline concentrations of AGP. AGP levels did not predict either free imipramine plasma levels or differential response after 6 weeks of treatment with imipramine. A greater increase of AGP during treatment was associated with severity of depression and treatment non-response. CLINICAL IMPLICATIONS: The relationship between high plasma levels of AGP, severity of depression and lack of treatment response is clarified. The influence of imipramine levels is minimized.
To compare the effects of sodium fluoride and etidronate in severe postmenopausal osteoporosis, we conducted a 3 year, prospective, trial in 118 postmenopausal osteoporotic women with at least one vertebral fracture, who were randomly assigned to receive sodium fluoride (25 mg twice daily, as enteric-coated tablets) plus calcium (1000 mg/day) or intermittent etidronate (400 mg/day for 14 days) followed by calcium (1000 mg/day for 76 days). Lateral spine X-ray films and dual-energy X-ray absorptiometry (DXA) measurements of the lumbar spine and proximal femur were performed at enrollment and yearly. Nonvertebral fractures were recorded every 6 months. Thirty-one women in the fluoride group and 47 in the etidronate group completed the trial. At 36 months, the mean change from baseline of the lumbar bone density in the fluoride group was 8.5 +/- 2.04% (p = 0.001) and in the etidronate group was of 3.6 +/- 0. 84% (p < 0.001). The changes in the fluoride group were significantly higher than in the etidronate group (p = 0.01). Both groups showed nonsignificant changes in femoral neck bone density. There was no significant difference between groups in the cumulative proportion of women with new vertebral fractures, with an incidence in the fluoride group of 16% vs. 17% in the etidronate group. However, the number of new vertebral fractures was significantly lower in the fluoride group (6 fractures) than in the etidronate group (19 fractures) (p = 0.05). The number of patients with nonvertebral fractures was similar in both groups. A high incidence of side effects, mainly gastrointestinal symptoms and lower extremity pain syndrome, was observed in the fluoride group. Etidronate was well tolerated. We conclude that, in women with severe osteoporosis, although sodium fluoride is more favorable than cyclical etidronate for increasing lumbar bone mass, no differences were observed in the incidence of fractures.
The authors have developed a simple isocratic high-pressure liquid chromatographic (HPLC) assay for the simultaneous determination of lamotrigine and other frequently coadministered antiepileptic drugs in serum samples. Lamotrigine extraction was performed on a reversed-phase Oasis HBL preparation column. The eluates containing butalbital as internal standard were separated with a 7-microm Chromsystems C18 250 x 4.0 mm I.D. reversed-phase column at a temperature of 40 degrees C using a mobile phase consisting of pH 3.8 phosphate-acetonitrile buffer (55:45, v/v), at a flow rate of 0.8 mL/min. Ultraviolet detection was carried out at 210 nm. Measurement of the peak:height ratio allowed quantitative determination of the samples. The method was linear over a concentration range of 0.2 to 20 microg/mL for lamotrigine. Recovery was >90%. Within-day and between-day coefficients of variation ranged from 1.8% to 6.7%. The mean lamotrigine concentration was 8.01 +/- 5.63 microg/mL. After studying sera from 130 patients treated with lamotrigine the authors confirmed that associated antiepileptic therapy affected the serum lamotrigine levels, which were significantly higher in patients under valproic acid treatment.
Plasma chromium levels were determined in 243 healthy subjects. The study group consisted of 134 men and 109 women, ages 19-71 yr, all residing in Barcelona in northeastern Spain. The study was designed to assess the reference levels for plasma chromium and to investigate its relationships to age and sex. The assays were performed by means of a graphite-furnace atomic absorption spectrometer. The mean plasma chromium concentration was 3.01 +/- 1.45 nmol/L, ranging from 0.6 to 6 nmol/L. The upper reference values in the 0.95 percentile for this population was 5 nmol/L. No significant differences were observed with respect to the subjects' sex.
Serum and urine fluoride levels were determined in 250 healthy subjects (15-90 years, 122 men and 128 women) residing in Catalonia, Spain, and in 150 patients (20-81 years, 84 men and 66 women) with chronic renal failure undergoing regular dialysis treatment, living in the same geographical area, to determine normal range and to investigate its relationships to age, sex and renal function. Serum and urine fluoride were determined by a fluoride ion specific electrode system. Mean (+/- S.D.) serum fluoride concentration was 17.5 +/- 9.5 micrograms/l, ranging from 1 to 47 micrograms/l, in the control group and 58 +/- 31 micrograms/l, ranging from 28 to 185 micrograms/l, in renal patients. Urine fluoride concentration in the healthy group was 671 +/- 373 micrograms/24 h, ranging from 156 to 1900 micrograms/24 h. Fluoride status in the patient group was significantly greater than the control group. There was significant correlation between serum fluoride and age. No sex related difference was found.
The present study was undertaken to evaluate the fluoride status in the general healthy population of Barcelona. Serum and urine fluoride ionic concentration was determined in a random sample of 250 subjects (age range 15-90 yr) by the Orion fluoride electrode system to determine the normal range of fluoride in this population. The results obtained show that in the general population of Barcelona, fluoride ionic serum concentration ranges between 1 and 47 microg/L (x = 17.5 +/- 9.7 microg/L) and fluoride ionic urine concentration ranges between 156 and 1990 microg/24 h (x = 671 +/- 373 microg/24 h). The mean serum fluoride concentration of the younger population was shown to be significantly greater (p < 0.05) than that of the older group. No sex-related difference was found.
BACKGROUND: This study was designed to determine current lead exposure in the Barcelona population and to evaluate the changes occurred during the last 10 years. Blood lead concentration was investigated in a random sample of 694 healthy subjects (age range: 0-65 years). PATIENTS AND METHODS: Adults were random selected from a group of blood donors. Samples of children analysed were selected from subjects with a preoperatory analyses without any disease that could modify blood lead levels. Lead levels were determined by atomic absorption spectrometry. RESULTS: Blood lead concentration was 4.06 +/- 1.4 micrograms/dl in umbilical cord, 8.9 +/- 2.9 micrograms/dl in the paediatric population and 7.8 +/- 4.2 micrograms/dl in the total of adults analyzed. There was statistical differences between the younger subjects and the older population. In 1984 the results found were 18.6 +/- 6.6 micrograms/dl. CONCLUSIONS: The results obtained show that in the last 10 years a reduction on the blood lead levels was occurred. This reduction is parallel with a diminish in the lead petrol concentration in the ambient air.
BACKGROUND & AIMS: Because osteopenia increases morbidity of primary biliary cirrhosis (PBC), the effects of cyclical etidronate vs. sodium fluoride on bone mass were compared in patients with PBC. METHODS: Thirty-two women with PBC were randomly assigned to receive etidronate (400 mg/day during 14 days every 3 months) or fluoride (50 mg/day, enteric-coated tablets). Bone mineral density of the lumbar spine and proximal femur were measured initially and every 6 months. Bone fractures were also evaluated. RESULTS: Sixteen patients were allocated into each group, which were comparable with respect to the severity of PBC and osteopenia. Thirteen patients with etidronate and 10 patients with fluoride completed 2 years in the study. In the etidronate group, bone mineral density increased in the lumbar spine (P = 0.02) and did not change in the proximal femur. In the fluoride group, lumbar bone mineral density did not change but femoral bone mass decreased, particularly in the Ward's triangle. Two patients in the fluoride and none in the etidronate group developed new vertebral fractures, and the number of new nonvertebral fractures was similar in both groups. Neither treatment impaired liver function or cholestasis. CONCLUSIONS: Cyclical etidronate is more effective and better tolerated than sodium fluoride in preventing bone loss in PBC.
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The macrolide tacrolimus (FK506) is a powerful immunosuppressive drug that acts early in the T-cell activation process and inhibits cytokine gene transcription. Data from several trials in liver transplantation have shown the efficacy of tacrolimus in the prevention of allograft rejection and its potent hepatotrophic effect, which could explain its great success in liver transplantation. However, tacrolimus is not devoid of adverse effects (mainly nephrotoxicity and neurotoxicity) requiring careful blood level monitoring, which is an essential aid in the adjustment of drug dosing. Several methods of analysis are available to measure tacrolimus in whole blood. A new assay based on the enzyme-linked immunosorbent assay (ELISA) technology has been developed. The INCSTAR PRO-TRAC FK506 is a sensitive immunoassay (range, 0.5 to 60 ng/ml), which uses a mouse monoclonal antibody to FK506. Samples are extracted into methanol and dried under nitrogen. The reconstituted extracts are analyzed by ELISA by using 2-h incubation. The aim of this study was to evaluate the ELISA method in routine monitoring of liver transplant patients and to compare the whole blood results with those obtained by Abbott microparticle enzyme immunoassay (MEIA) IMx. Precision studies with 20 samples from 4.37 and 17.1 ng/ml gave within-run total coefficients of variance of 14.4 and 17.4%, respectively. A total of 63 blood samples was analyzed. The mean +/- SD were 9.68 +/- 5.92 and 10.52 +/- 7.54 ng/ml by ELISA and MEIA assays, respectively. There was an acceptable correlation between the methods: ELISA = 1.419 + 0.785 MEIA; Sy x x = 2.639; r = 0.804. Serial tacrolimus measurements (n = 13) in two patients with bilirubin levels > 20 mg/dl yielded mean +/- SD (range) of 11.64 +/- 7.59 ng/ml (2.60-25.40 ng/ml) and 15.55 +/- 10.78 ng/ml (3.60-34.4 ng/mL) by ELISA and MEIA assays, respectively. These discrepancies in concentrations can result from variation in matrix or different cross-reactivities or both in the two tests. We concluded that the INCSTAR PRO-TRAC FK506 is suitable for routine whole blood tacrolimus monitoring.
Concentrations of cadmium and zinc were determined in the liver and in the kidney (cortex and medulla) of subjects from the general population of Barcelona (Spain) by atomic absorption spectrometry. Tissues were collected from necropsies of 50 selected subjects without any occupational exposure to heavy metals. Cadmium levels calculated on a fresh tissue basis were 14.6 +/- 5.9 micrograms/g (2.4-31) in the kidney cortex, 8.6 +/- 4.3 micrograms/g (1.5-16.7) in the kidney medulla and 0.98 +/- 0.50 micrograms/g (0.32-2.32) in the liver. Zinc concentrations ranged between 18-53 micrograms/g, (mean +/- S.D.: 38.0 +/- 10 micrograms/g) in the kidney cortex, 25.0 +/- 7.7 micrograms/g (12-42 micrograms/g) in the kidney medulla and 41.7 +/- 18.3 micrograms/g (20-84 micrograms/g) in the liver. The aim of the present work was to study the association of cadmium and zinc in the kidney and in the liver of a human population with cadmium accumulation from an environmental origin. The results obtained showed a significant correlation between cadmium and zinc concentration in the liver (r = 0.86, P < 0.001), but not in the kidney.
The serum levels of testosterone, sex hormone binding globulin, and free testosterone index were measured in 51 epileptic men (age 18-45) in order to assess the possible effects of antiepileptic drugs on sexual dysfunction. An analytical gas chromatography-mass spectrometry method was developed to assess the urinary excretion of testosterone, epitestosterone, androsterone, etiocholanolone, 11-OH androsterone and 11-OH etiocholanolone and to evaluate if the catabolism of testosterone had been increased. Twenty normal healthy males of similar age, 18-45 years, served as control group. Patients receiving polytherapy (n = 34) or monotherapy with carbamazepine (n = 8) or phenytoin (n = 9) showed higher levels of sex hormone binding globulin and testosterone, and lower levels of free testosterone than did the controls (P < 0.03). Urinary excretion of the metabolites androsterone and 11-OH androsterone was significantly reduced (P < 0.02) in the polytherapy group, while the monotherapy group showed only significant differences (P < 0.02) in the elimination of 11-OH androsterone. Our results suggest that an induction of the hepatic synthesis of sex hormone binding globulin may be the mechanism by which the antiepileptic drugs lower the levels of free testosterone in serum. However, the reduced excretion of androsterone and the normal levels of etiocholanolone show that the antiepileptic drugs do not produce an increase in the main catabolism pathway of testosterone.