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J M Valle

Publications and source records attributed to J M Valle.

At least 19 recordsLinked to original sources
PubMed2000

Pulmonary valve endocarditis: mid-term follow up of pulmonary valvectomies.

Four males aged 20-37 years (three drug addicts and one with a congenital mixed pulmonary valve lesion) were diagnosed in 1989, 1991 and 1993 with pulmonary valve endocarditis without tricuspid infection. Three patients were positive for hepatitis B, C or both, and one patient was HIV-positive. The predominant organism in blood cultures was Staphylococcus aureus. Antibiotic treatment of pulmonary valve endocarditis had failed; thus partial or total valvectomies were performed. Postoperatively, all patients were cured of infection and initial recovery was good. At mid-term follow up (5-10 years) there were no recurrences, and tolerance of the resultant pulmonary insufficiency was good. Slight to severe tricuspid valve insufficiency developed, together with right ventricular dilatation, in all cases. Hepatomegaly was apparent in two cases and peripheral edema in one. Despite treatment, the latter patient remained in moderate right ventricular failure, and may require homograft valve replacement. The other three patients remained in good clinical condition. Eradication of the infection was achieved in all patients. It is concluded that pulmonary valve resection is the treatment of choice for pulmonary valve endocarditis when antibiotic treatment has failed. Complete resection of all affected tissue should be performed in these cases. Analysis of preoperative data did not permit differentiation of those patients likely to develop right heart failure.

Adult↗
PubMed1999

Lymphocyte populations in tuberculous pleural effusions.

Different systemic and local responses to mycobacterial antigens suggest an active compartmentalization of responsive lymphocytes to tubercular antigens. This fact, observed in pleuritic processes, raises doubts about the accuracy of information obtained in the study of cells taken solely from peripheral blood. For this reason we decided to study the concept of compartmentalization in 140 patients suffering from pleural effusions. Patients were classified into six groups according to the aetiology of the effusion: group I, tuberculous, n = 23; group II, paraneoplastic, n = 41; group III, metapneumonic empyematous, n = 5; group IV, transudate, n = 38; group V, miscellaneous exudate, n = 19; group VI, unknown aetiology, n = 14. In each group we studied the lymphocyte population by using flow cytometry with doubly fluorescent monoclonal antibodies: B [expressing human lymphocyte antigen (HLA)-DR on the surface], T (CD3+), CD4+ and CD8+, and the subpopulation of activated T lymphocytes (together expressing CD3 and HLA-DR on the surface) (CD3+DR+). The study of these subpopulations in peripheral blood did not yield valuable results, but the CD3+DR+ population in pleural fluid demonstrated a diagnostic efficiency of 84% [positive predictive value (PPV) 51%, negative predictive value (NPV) 96%] at a cut-off value of 80.4 cells/mm3. The CD3+DR+ pleural fluid/peripheral blood ratio demonstrated an efficiency of 83% (PPV 50%, NPV 96%), and showed a statistically significant difference (P < 0.02) with regard to all the diagnostic groups, with the exception of the paraneoplastic effusions. The lymphocytic subpopulations study confirms the concept of compartmentalization in tuberculous pleuritis, as shown by the greater number of activated T lymphocytes present in pleural fluid in comparison with peripheral blood in tuberculous pleuritis, a 98% efficiency of adenosine deaminase (ADA) determination in pleural fluid versus a 50% value in peripheral blood, predominance of helper cells (CD4+) in pleural fluid and suppressor cells (CD8+) in peripheral blood, a greater CD4+/CD8+ ratio in pleural fluid than in peripheral blood, and a significant correlation of ADA-CD3+DR+ in pleural fluid, which does not occur in peripheral blood.

Adenosine Deaminase↗
PubMed1998

Tuberculous pleurisy: a study of 254 patients.

OBJECTIVES: To determine the age at which tuberculous pleural effusions occur, the radiological and biochemical characteristics of the effusions, the sensitivities of the various diagnostic tests, and the utility of combining clinical, radiological, and analytic data in diagnosis. METHODS: We studied the case histories of 254 patients in whom tuberculous pleural effusions were diagnosed with certainty between January 1, 1989, and June 30, 1997, in a Spanish university hospital in a region with a high incidence of tuberculosis. RESULTS: The mean (+/-SD) age of the patients was 34.1+/-18.1 years, and 62.2% were younger than 35 years. The effusion was on the right side in 55.9% of patients, on the left side in 42.5% of patients, and on both sides in 1.6% of patients. In 81.5% of patients, less than two thirds of the hemithorax was affected. Associated pulmonary lesions were detected in 18.9% of patients, of whom 14.6% exhibited cavitation. In 93.3% of the effusions, more than 50% of leukocytes were lymphocytes, and almost all had the biologic characteristics of exudates (98.8% had high total protein contents, 94.9% had high cholesterol levels, and 82.3% had high lactate dehydrogenase levels). All but 1 effusion (99.6%) had an adenosine deaminase (ADA) concentration higher than 47 U/L, 96.8% (123/127) of the effusions had high ADA2 levels, and 89% (73/82) of the effusions had high interferon gamma levels. Adenosine deaminase 2 contributed 72.2%+/-12.5% (mean +/- SD) of total ADA activity. Total ADA activity was significantly correlated with ADA2 (r = 0.83) and with interferon gamma (r = 0.30) levels. Definitive diagnosis was based on the observation of caseous granulomas in pleural biopsy tissue samples in 79.8% of patients, on the results of biopsy cultures in 11.7% of patients, and on pleural effusion cultures in the remaining 8.5% of patients. Results of the tuberculin skin test were positive in only 66.5% of patients. CONCLUSIONS: In these patients, lymphocyte-rich exudative pleural effusions occurred, on average, at a young age, with no preference for either the right or the left side; normally affected no more than two thirds of the hemithorax; and were generally unaccompanied by pulmonary infiltrates. High ADA concentration was a highly sensitive diagnostic sign and was caused by a rise in ADA2 concentration. The most sensitive criterion based on pleural biopsy was the observation of caseous granulomas, and culture of biopsy material further increased overall sensitivity. Negative skin test results were no guarantee of the effusion being nontuberculous. This, together with the low mean age of the patients and the low frequency of associated pulmonary lesions, suggests that tuberculous pleural effusion is a primary form of tuberculosis in this region.

Adenosine Deaminase↗
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↗
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↗
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

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↗