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D Alvarez

Publications and source records attributed to D Alvarez.

At least 55 records · Page 3Linked to original sources
PubMed1998

Idiopathic hypersomnia.

Identification of idiopathic hypersomnia dates back 20 years only. It typically consists of prolonged nocturnal sleep, great difficulty waking up in the morning or at the end of a nap, and constant or recurrent excessive daytime sleepiness. Complete and incomplete forms are encountered. Twenty-three subjects fulfilling ICSD criteria are reported with clinical, polysomnographic and immunogenetic data. Considering differential diagnosis is an important step in the diagnosis of idiopathic hypersomnia. Idiopathic hypersomnia is much less frequent than narcolepsy. A strong genetic component is suggested by the high proportion of familial cases. No association with HLA has been evidenced to date.

Adolescent↗
PubMed1997

Utility of tumour markers in the diagnosis of neoplastic pleural effusion.

Approximately 20% of pleural effusions are caused by neoplastic processes. Although cytology is the most specific routine diagnostic procedure, its sensitivity of 50-60% is insufficient, and thus diagnosis is usually carried out by more invasive techniques such as pleural biopsy, thoracoscopy or thoracotomy. The object of this study is to evaluate the use of determining some tumour markers in pleural fluid obtained by thoracocentesis for diagnosis of neoplastic pleural effusion. Patients (271) with pleural effusions were classified in five groups: I: neoplasms n = 88; II: tuberculosis n = 63; III: parapneumonics n = 53; IV: miscellaneous exudates n = 39 and V: transudates n = 28. The tumour markers studied were: carcinoembryonic antigen (CEA), CA 125, squamous cell carcinoma antigen (SCC), and neuron specific enolase (NSE). The tumour makers had the following diagnostic efficiencies for neoplastic origin of the pleural effusion: CEA 76% (sensitivity 31%, specificity 93%); CA 125 66% (70% and 61%); SCC 65% (48% and 80%) and NSE 53% (30% and 89%). The diagnostic efficiencies for pulmonary neoplastic origins were 68% for NSE (sensitivity 83%, specificity 53%); 65% for SCC (54% and 75%); 63% for CEA (80% and 48%) and 61% for CA 125 (79% and 42%). We believe that the routine testing of tumour markers in pleural fluid obtained by thoracocentesis would greatly increase diagnostic effectiveness and could avoid the practice of more aggressive diagnostic techniques on the patient.

Antigens, Neoplasm↗
PubMed1997

Daily variation in portal blood flow and the effect of propranolol administration in a randomized study of patients with cirrhosis.

A nocturnal increase in portal pressure and blood flow was demonstrated in patients with cirrhosis, suggesting that these hemodynamic changes may contribute to the triggering of the hemorrhagic episodes observed during the night in these patients. It is known that propranolol reduces portal flow, thus reducing the risk of variceal bleeding. In a double-blind, placebo-controlled study, we evaluated the effect of long-term propranolol administration on the daily fluctuation of systemic and splanchnic hemodynamic parameters in 14 patients with cirrhosis. Cardiac output and portal blood flow were measured by the Doppler technique. A daily fluctuation of both cardiac output and portal blood flow was observed, peaking at midnight. beta-Adrenergic blockade was manifested by a significant reduction in heart rate (-21% +/- 4%, P < .01) and cardiac output (-12% +/- 2%, P < .05). A significant decrease in portal blood flow (-20% +/- 4%, P < .01) was also observed in these patients. Propranolol administration blunted the time-related changes in cardiac output and portal blood flow. In contrast, patients receiving placebo had a nocturnal peak of both parameters similar to that observed under basal conditions. Our study shows that chronic propranolol administration abolishes the nocturnal peak of portal blood flow in patients with cirrhosis and indicates a preventive effect of propranolol in these patients.

Adrenergic beta-Antagonists↗
PubMed1997

Hemostatic and hemodynamic effects of vasopressin analogue DDAVP in patients with cirrhosis.

Desmopressin (DDAVP), a synthetic analogue of vasopressin, has been shown to improve the bleeding time in patients with cirrhosis. The duration of this effect and the hemodynamic changes associated with DDAVP have not been studied so far. To evaluate these issues, 14 cirrhotics with portal hypertension were studied in basal conditions and after DDAVP (0.3 uk/kg). In 8 patients, hemostatic tests were done at basal conditions and 1, 3, 6 and 24 hs after drug administration. In the remaining 6 patients, mean arterial pressure, cardiac output, portal and femoral blood flows were evaluated. Hemodynamic parameters were measured by Doppler ultrasound. DDVP caused a marked decrease in bleeding time at 1, 3, 6 and 24 hs (14 +/- 9 vs 8 +/- 3, 7 +/- 4, 6 +/- 4 and 8 +/- 4 min, respectively); the decrease was maximal and statistically significant at 6 hs (55 +/- 15%, p < 0.02) after DDAVP infusion. Bleeding time reduction was observed in every patient studied. In the hemodynamic study, DDAVP caused a mild but significant decrease in mean arterial pressure (12 +/- 8%, p < 0.05); no significant changes were observed in the rest of hemodynamic parameters studied. These findings show that DDAVP can be used to shorten the bleeding time for a period of at least 24 hs in patients with cirrhosis, without deleterious hemodynamic effects. This beneficial effect may be of potential relevance in the medical management of patients with chronic liver diseases.

Bleeding Time↗
PubMed1997

[Abortions caused by anticardiolipin antibodies: prevention by low-dose acetylsalicylic acid].

BACKGROUND: It is a very well-known fact the relationship between pregnancy with history of fetal losses and positive aCL, and many treatments have been tried in order to prevent it. We present a study about the treatment of these pregnant women with ASA at low doses. PATIENTS AND METHODS: We have followed-up a group of 28 women with previous abortions and positive aCL. They were treated with ASA (50 mg/day) since beginning until end of pregnancy. We measured aCL levels monthly. RESULTS: 24 cases of pregnancy (86%) were successfully, 3 cases were fetal losses and 1 case was a fetal malformation. IgG aCL were positive in 16 patients before treatment, and IgM aCL in 11 cases. One patient had both of them. 18 patients became negative after pregnancy. We have not found any relationship between the level of aCL and fetal losses. CONCLUSIONS: In our study, ASA at low doses (50 mg/day) is a safe and effective treatment in achieving successful pregnancies, and reducing aCL levels in patients with history of fetal losses.

Abortion, Habitual↗
PubMed1996

Analysis of complement C3 deposition and degradation on Klebsiella pneumoniae.

The majority of Klebsiella pneumoniae serum-resistant strains activate complement and bind C3b, the opsonic fragment of C3, without C5b-9 formation and bacterial killing. The mechanisms leading to C3b deposition without cell death were studied, and the results indicate that serum-resistant strains activate principally the alternative pathway and that serum-sensitive strains activate both the alternative and classical pathways. Bacterial molecules implicated in C3b deposition are the outer membrane porin proteins and smooth and rough lipopolysaccharides. Porins activate both complement pathways, and the rough lipopolysaccharide activates the classical pathway, causing deposition of C3b in serum-sensitive strains. The smooth lipopolysaccharide of serum-resistant strains activates only the alternative pathway, impeding the binding of C1q to porins (S. Albertí, G. Marqués, S. Camprubí, S. Merino, J. M. Tomás, F. Vivanco, and V. J. Benedí, Infect. Immun. 61:852-860, 1993; S. Albertí, F. Rodríguez-Quinónes, T. Schirmer, G. Rummel, J. M. Tomás, J. P. Rosenbusch, and V. J. Benedí, Infect. Immun. 63:903-910, 1995) and rough lipopolysaccharide molecules and thereby preventing activation of the classical pathway. After its deposition, C3b is quickly degraded to iC3b on both types of strains, but the higher-level deposition of C3b on serum-sensitive strains, resulting from activation of both the alternative and classical complement pathways, supports further complement activation and killing of serum-sensitive strains.

Bacterial Proteins↗
PubMed1996

Adenosine deaminase (ADA) isoenzyme analysis in pleural effusions: diagnostic role, and relevance to the origin of increased ADA in tuberculous pleurisy.

The rise in adenosine deaminase (ADA) activity in the pleural fluid of tuberculous pleurisy patients, though used for diagnosis, is of unknown origin. In this work, we determined ADA activity and the activities of 2'-deoxyadenosine deaminase and ADA-2 in 350 patients. We also considered whether the results throw light on the origin of high pleural fluid ADA in tuberculous pleurisy and estimated the diagnostic efficiency of 2'-deoxyadenosine deaminase, ADA-2 and total ADA activities with and without the inclusion of the 2'-deoxyadenosine deaminase/ADA activity ratio in a combined criterion. The 350 pleural effusions were classified by previously established criteria as transudates (60 males/18 females) or as tuberculous (49 males/27 females), neoplastic (50 males/39 females), parapneumonic (36 males/19 females), empyematous (11 males/3 females), or miscellaneous (25 males/13 females) exudates. Total ADA, ADA-2 and 2'-deoxyadenosine deaminase activities were, respectively, 127.5 +/- 2.9, 103 +/- 29.5 and 42.8 +/- 14 U.L-1 in tuberculous exudates. With diagnostic thresholds of 47, 40 and 22 U.L-1 respectively, the sensitivities of ADA, ADA-2 and 2'-deoxyadenosine deaminase for tuberculosis were 100, 100 and 95%; their specificities 91, 96 and 92%; and their efficiencies 93, 97 and 93%, respectively. One hundred and one effusions (all 76 tuberculous, 12 neoplastic, 4 parapneumonic and 9 empyematous exudates) had total ADA levels > 47 U.L-1; of these, 8 neoplastic, 1 parapneumonic and all the tuberculous exudates had a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49. The criterion of simultaneously having ADA > 47 U.L-1, ADA-2 > 40 U.L-1 and a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49 was satisfied by all the tuberculous effusions but only eight others (all neoplastic) (sensitivity 100%, specificity 97%, efficiency 98%). We conclude that: 1) high total ADA activity in tuberculous pleural effusions is due mainly to an increase in ADA-2, and, therefore, originated from the only known source monocytes and macrophages; 2) ADA-2 was a more efficient diagnostic marker of tuberculous pleurisy than total ADA activity, although the difference was not statistically significant; and 3) among effusions with high total ADA the 2'-deoxyadenosine deaminase/ADA activity ratio differentiates tuberculous effusions from empyemas and parapneumonic effusions, but fails to discriminate well between tuberculous and neoplastic effusions.

Adenosine Deaminase↗
PubMed1996

The etiology of pleural effusions in an area with high incidence of tuberculosis.

To investigate the etiology of pleural effusions in our region, we undertook a prospective study of patients with this condition in our centers. During a 5-year period, we studied 642 pleural effusion patients aged 57.1 +/- 21.1 years, of whom 401 were men aged 56.5 +/- 21 years and 241 were women aged 57.8 +/- 21.4 years; the male/female ratio was 1.6:1. The most frequent cause of pleural effusion was tuberculosis (25%), followed by neoplasia (22.9%) and congestive heart failure (17.9%). The etiology of 48 cases (7.5%) remained uncertain. In the neoplastic effusion group, the most frequent locations of the primary tumor were lung (32.6%), breast (11.5%), lymphoma (10.8%), and ovary (7.5%); in 21 cases (14.3% of the neoplastic group), it was not possible to identify the primary tumor. The 111 patients aged younger than 40 years with tuberculous effusions made up 69.4% of tuberculous effusion cases and the same percentage of patients younger than 40 years; the proportion of effusions that were tuberculous peaked in the 11- to 30-year-old age group and declined steadily thereafter. Of the patients with neoplastic effusions, 83% were older than 50 years; the proportion of effusions that were neoplastic rose steadily from zero in the 0- to 30-year-old age group to a peak among 60- to 70-year-olds. The age-wise distribution of effusions secondary to congestive heart failure was similar to that of neoplastic effusions. Of the effusions secondary to congestive heart failure, 86% (99/115) affected the right pleura or both, and 83% of effusions secondary to pulmonary thromboembolism (15/18) affected the right side. Neoplastic, tuberculous, parapneumonic, empyematous, and other exudative effusions showed no preference for either side. Of the 97 bilateral effusions, 77 (79.4%) were secondary to heart failure (59, 60.8%) or neoplasia (18, 18.6%). We conclude that in our region, the most frequent cause of pleural effusion is tuberculosis, followed by neoplasia and congestive heart failure. We suggest that all those interested in pleural disease should determine the etiologic pattern of pleural effusion in their region with a view to the adoption of regionally optimized diagnostic and therapeutic attitudes.

Adolescent↗
PubMed1996

Clinical implications of white coat hypertension.

OBJECTIVE: To determine the clinical implications of mild white coat hypertension (WCH). SUBJECTS AND METHODS: We studied 102 subjects (54 men, 48 women), 51 of whom were normotensive and 51 slightly hypertensive. None had ever received antihypertensive therapy. An ambulatory blood pressure (ABP) record (Accutracker II), a 24-h electrocardiogram and an echocardiogram were obtained from each, and each was examined by funduscopy. WCH subjects were compared with sustained hypertension (SH) subjects and with normotensives. RESULTS: Fifty-three percent of the hypertensives qualified as WCH. The ultrasonographic characteristics and the ABP variables of the WCH group differed significantly from those of normotensives, but not from those of the SH group. The prevalence of left ventricilar hypertrophy (LVH) in the SH group (62.5%) did not differ significantly from its prevalence in the WCH group (40.7%), but the prevalence among normotensives (17.6%) was significantly lower than in either of the other two groups. The WCH and SH groups did not differ significantly as regards the prevalence of hypertensive retinopathy (33.3% in the former, 58.3% in the latter). For no non-LVH, non-retinopathic subject, whether normotensive or hypertensive, were more than 18% of daytime diastolic ABP measurements > or = 90 mmHg. Ultrasonographic findings were no better correlated with ABP than with in-clinic BP measurements. Fundus findings correlated well with in-clinic BP and with numerous ABP parameters. Retinopathy, with or without LVH, was efficiently predictable among hypertensives on the basis of body mass index and the 24-h maximum of systolic BP. CONCLUSIONS: Myocardiac remodelling and vascular retinopathy develop early and in parallel in hypertensives, and both developments appear to involve determinants including body mass index and 24-h maximum systolic BP. WCH subjects, as defined by current ABP-based criteria, have cardiac and retinovascular characteristics different to normotensive subjects. Stricter criteria are needed to discriminate between hypertensives with and without the systemic developments that constitute the immediate source of risk to the hypertensives individual.

Adult↗
PubMed1995

Vasodilatory effects of propylthiouracil in patients with alcoholic cirrhosis.

BACKGROUND/AIMS: An experimental study has shown that propylthiouracil increases portal blood flow in normal rats. Whether propylthiouracil has a similar effect in patients with alcoholic cirrhosis remains to be demonstrated. The aim of this study was to evaluate the effects of oral propylthiouracil (300 mg) on systemic and portal hemodynamics in patients with alcoholic cirrhosis. METHODS: Plasma propylthiouracil levels were also measured by high performance liquid chromatography in five patients with alcoholic cirrhosis. In eight patients with cirrhosis, mean arterial pressure, cardiac output and portal blood flow were evaluated before and after placebo and propylthiouracil administration. Hemodynamic measurements were performed by the Doppler technique. The plasma peak level of propylthiouracil was achieved at 1.4 +/- 0.1 h in patients with alcoholic cirrhosis. This time was chosen to express hemodynamic changes. RESULTS: Propylthiouracil administration caused a significant increase in portal blood flow (+16.5%, p < 0.05) in patients with alcoholic cirrhosis. This effect was associated with a mild and significant rise in cardiac output (from 5.8 +/- 0.2 to 6.1 +/- 0.3 l/min, p < 0.05) and a decrease in peripheral vascular resistance (from 1171 +/- 69 to 1070 +/- 67 dyn . s-1 . cm-5, p < 0.01). A significant correlation was observed between changes in portal blood flow and peripheral vascular resistance (r = 0.79, p < 0.05). No significant changes were observed after placebo. CONCLUSIONS: Our findings show that propylthiouracil has a vasodilatory effect in patients with alcoholic cirrhosis. We postulate that this effect could be the mechanism by which propylthiouracil decreases hypermetabolic state, and increases oxygen delivery to the liver, in patients with alcoholic liver diseases.

Female↗
PubMed1995

Value of adenosine deaminase in the diagnosis of tuberculous pleural effusions in young patients in a region of high prevalence of tuberculosis.

BACKGROUND: Pleural biopsy is usually considered important for the diagnosis of pleural effusions, especially for distinguishing between tuberculosis and neoplasia, even though tuberculous pleural fluid contains sensitive biochemical markers. In regions with a high prevalence of tuberculosis, and in patient groups with a low risk of other causes of pleurisy, the positive predictive value of these markers is increased. The criteria for performing a pleural biopsy under these circumstances have been investigated, using adenosine deaminase (ADA) as a pleural fluid marker for tuberculosis. METHODS: One hundred and twenty nine patients with a pleural effusion aged < or = 35 years (mean (SD) 25.2 (4.9) years) were studied. Seventy three were men. Eighty one effusions (62.8%) were tuberculous, 12 (9.3%) parapneumonic, and 10 (7.7%) neoplastic, five were caused by pulmonary thromboembolism, four by systemic lupus erythematosus, seven by empyema, three following surgery, one was the result of asbestosis, and one of nephrotic syndrome. In five cases no definitive diagnosis was reached. ADA levels were determined by the method of Galanti and Giusti. RESULTS: The diagnostic yield of procedures not involving biopsy was 94.5% (122/129). Pleural biopsy provided a diagnosis in a further two cases, but not in the remaining five. All tuberculous cases had pleural fluid levels of ADA of > 47 U/l (mean (SD) 111.1 (36.6) U/l). The only other cases in which ADA exceeded this level were six of the seven patients with empyema. Cytological examination of the pleural fluid diagnosed eight of the 10 neoplastic cases, compared with six diagnosed by pleural biopsy. CONCLUSIONS: In a region with a high prevalence of tuberculosis procedures not involving pleural biopsy have a very high diagnostic yield in patients with a pleural effusion aged < or = 35 years, making biopsy necessary only in cases in which pleural levels of ADA are below 47 U/l, pleural fluid cytology is negative and, in the absence of a positive basis for some other diagnosis, neoplasia is suspected.

Adenosine Deaminase↗
PubMed1995

Sulfation pathway of thyroid hormone metabolism in selenium-deficient male rats.

Male Sprague-Dawley rats were fed a selenium-deficient yeast-based laboratory diet or a control diet for 6 wk. The tissue type I 5'-monodeiodinase (5'-MDI) activity and the immunoassayable 5'-MDI were significantly (P < 0.05) reduced in the liver and the kidney but not in the thyroid of selenium-deficient rats. The mean serum concentrations of thyroxine sulfate (T4S), 3,3',5'-triiodothyronine sulfate (T3S), and reverse T3 sulfate (rT3S) (ng/dl) were significantly increased in selenium-deficient rats (15.7, 59.4, and 22.8, respectively, n = 12) compared with control rats (< 1.0, 18.5, and 9.1, respectively, n = 12, P < 0.01). Kinetic studies were carried out during a constant infusion of unlabeled sulfated iodothyronines (T4S, T3S, or rT3S, n = 5-6/group) at a rate of 1 microgram/h by Alzet minipump for 48 h. The data showed that elevated serum concentrations of T4S or T3S in the selenium-deficient rat are due both to reduced metabolic clearance rate (MCR, mean, l.kg-1.day-1, 7.4 for T4S and 4.5 for T3S in selenium deficiency vs. 12 and 9.2, respectively in controls, P < 0.05) and increased production rate (mean, microgram.kg-1.day-1, 1.2 for T4S, and 2.7 for T3S in selenium deficiency vs. 0.12 and 1.7, respectively, in the controls, P < 0.05). However, the increased serum rT3S concentration in selenium-deficient rats is due mainly to reduced MCR (mean, l.kg-1.day-1, 34 vs. 67 in controls, P < 0.05) and its daily production rate remained unchanged in selenium deficiency (mean, microgram.kg-1.day-1, 7.6 vs. 6.1 in the control group, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Bronchiolitis obliterans organizing pneumonia secondary to amiodarone: a rare aetiology.

Bronchiolitis obliterans organizing pneumonia (BOOP) is a clinicopathological entity with well-defined diagnostic criteria, the aetiology of which is generally unknown. Among the adverse pulmonary effects of the drug amiodarone, BOOP is the least commonly reported in the literature. In this article we describe a case of amiodarone-induced BOOP.

Amiodarone↗
PubMed1995

Acute respiratory failure as the first sign of Arnold-Chiari malformation associated with syringomyelia.

We report a rare case of acute respiratory failure in a previously asymptomatic patient showing clinical signs of inferior cranial nerve palsy together with weakness and muscular atrophy of the upper limbs. Magnetic resonance imaging revealed Arnold-Chiari malformation associated with platybasia, basilar impression, syringomyelia and Klippel-Feil syndrome. Episodes of apnoea required tracheostomy and recurred upon tentative closure of the tracheostome, but remitted upon decompression of the posterior fossa. This case involved both obstructive mechanisms and dysfunction of the respiratory centre. Patients with respiratory failure not explained by pulmonary pathology should be checked for underlying neurological disease.

Abnormalities, Multiple↗