PubMed Health⌕ Search

Biomedical subjects

G Encabo

Publications and source records attributed to G Encabo.

At least 37 records · Page 2Linked to original sources
PubMed1996

Clinical efficacy of bone alkaline phosphatase and prostate specific antigen in the diagnosis of bone metastasis in prostate cancer.

PURPOSE: We investigated the usefulness of bone alkaline phosphatase isoenzyme and prostate specific antigen (PSA) determined by radioimmunoassay to predict bone scan evidence of metastasis in newly diagnosed untreated and treated prostate cancer. MATERIALS AND METHODS: We analyzed bone alkaline enzyme concentrations in 350 men, including 150 controls, 100 with benign prostatic hyperplasia and 100 with prostate cancer (52 with stages T1 to 4, M0 and 48 with stages T1 to 4, M1 to 4). We also analyzed bone alkaline phosphatase enzyme concentrations in 61 stages T1 to 4, M0 prostate cancer cases during followup after radical prostatectomy or hormonal therapy, and 17 had clinical progression (9 with local, 5 with lymph node and 3 with bone metastases). Simultaneously, we analyzed PSA concentrations. RESULTS: Average bone alkaline phosphatase enzyme levels were 12, 11.1 and 10.0 ng./ml. in the control, benign prostatic hyperplasia and stage M0 prostate cancer groups, respectively (p not significant), and 83.2 ng./ml. in patients with stage M1 to 4 disease (p<0.001). Considering that to diagnose bone metastasis the cutoff for bone alkaline phosphatase enzyme and PSA is 30 ng./ml. and 100 ng./ml., respectively, clinical effectiveness was 93.7% and 81.8%, respectively. Finally, measurement of both substances at the same time increased clinical effectiveness to 97.9%. During followup a bone alkaline phosphatase enzyme level that becomes greater than 30 ng./ml. (0% in the local and lymphatic progression groups, and 100% in the bone metastasis group) indicates the need to perform a bone scan. CONCLUSIONS: We recommend the clinical use of bone alkaline phosphatase enzyme determined by radioimmunoassay and PSA measurement for the diagnosis of bone metastases and progression of prostate cancer because of the good sensitivity and specificity.

Aged↗
PubMed1995

[C-erbB-2 protein in ovarian epithelial cancer: correlation between expression in tumor tissue and blood levels].

BACKGROUND: Among 20 to 30% of the patients with ovarian cancer present overexpression of the c-erbB protein in the tumor tissue although its clinical significance has not been clearly established. In patients with a disseminated neoplasm and overexpression of c-erbB an increase in the extracellular portion of this protein may be detected in serum. The aim of this study was to determine the c-erbB protein in serum and in tumoral tissue in patients diagnosed with ovarian epithelial carcinoma. METHODS: The serum concentration of the c-erbB protein was quantified by ELISA techniques in 60 blood donor women (control group) and in 99 patients with ovarian cancer. Likewise, the expression of the c-erbB protein was determined in tumoral tissue by immunohistochemical techniques in the 99 patients with ovarian cancer. The correlation between overexpression and elevated serum values was analyzed. RESULTS: The mean c-erbB values obtained in the serum of the control group was 10.9 U/ml (SD: 2.8) with a range of 1.5-17.0. Serum determination was carried out in absence of the tumor in 49 patients being positive in 2 cases. In 7 patients the determination was performed in the presence of peritoneal implants of a diameter of less than 2 cm with none being positive. Serum determination was carried out in 43 patients in the presence of implants greater than 2 cm and 14 (32.5%) were positive. A further 153 determinations were performed during follow up of the 99 patients, 62 in tumor absence (3.2% positive), 2 in the presence of a tumor of less than 2 cm (none positive) and 89 in the presence of a tumor greater than 2 cm (34.8% positive). A correlation was found between elevated c-erbB serum values in the presence of a disseminated tumors and overexpression of tumoral tissue (p: 0.0011). CONCLUSIONS: A third of the patients with ovarian cancer and peritoneal implants of a diameter greater than 2 cm present elevated serum levels of the c-erbB.2 protein. A correlation was found between serum c-erbB positivity and overexpression of the protein in tumoral tissue.

Carcinoma↗
PubMed1995

[Final results of complete hormone blockade versus monotherapy in prostatic metastatic cancer. PSA implications].

Of 102 patients with metastatic prostate cancer, 52 were treated with orchidectomy and 50 with CHB; 22 of these received a LHRH analog + Flutamide and 28 orchidectomy + Flutamide. No differences were seen in either arm in terms of age (69.9 vs 70.2 years) or initial PSA (493.3 vs 486.5 ng/ml) variables. After three months treatment, CHB achieved a decrease of PSA higher than monotherapy (52.9 vs 34.5 ng/ml) p<0.01 as well as minimum PSA level during follow-up (41.2 vs 17.5 ng/ml) (p<0.001). Initial clinical response rates were higher in the group treated with complete blockade (42.3% vs 52%) (p=n.s.). Overall, no significant differences were seen between the actuarial curves of biological progression, clinical progression and survival, with expected mean values of 13 vs 12, 14 vs 15 and 34 vs 28 months, respectively. However, when survival was considered as a function of bone disease dissemination, a greater survival rate was seen in patients with minimal M1 disease (p<0.05), and there were no differences between the M2 and M3 arms.

Actuarial Analysis↗
PubMed1994

[Prostate-specific antigen as an evaluation method in the treatment of hormone-refractory cancer of the prostate].

Out of 62 patients with hormone-refractory metastatic prostate cancer, 34 received rescue treatment with estramustine phosphate and 28 received non-steroidal symptomatic treatment. All patients undergoing symptomatic treatment experienced increased PSA levels while in 16 (47%) patients treated with estramustine phosphate, PSA decreased between 13-96%. In 11 cases (32.3%) the decline in PSA was higher than 50%. In 5 (14.7%) the decline was lower than 50% and in 18 cases (53%) PSA levels were increased. SCR rate was 82%, 60% and 6% respectively while OCR were 36.4%., 0% and 0% respectively. No clinical response was seen in patients undergoing symptomatic treatment. A decline in PSA levels higher than 50% 12 weeks after treatment appears to be a "good prognosis" factor related to the best clinical response rates and survival.

Estramustine↗
PubMed1994

[The concept of biologic progression in metastatic cancer of the prostate hormonally treated].

A total of 110 patients with hormone-treated metastatic prostate cancer were monitored quarterly with serial PSA determinations. At the first control, 6 patients had progressed clinically, 5 of which had decreased PSA ranging between 9-77%. After a period of response, 69 patients progressed clinically, of which 1 showed no elevation of PSA levels, 14 showed progression concurrent with PSA increase, and 54 showed a period of gradual elevation of PSA over a range of 2-31 months. The probability of biological progression when the first rise occurred ranged between 72-96%, which after a second increase ranged between 92-100%, and all patients with three consecutive increases progressed clinically.

Androgen Antagonists↗
PubMed1994

Pericardial and myocardial localization of antimyosin in a case of acute myocarditis.

A 60-yr-old immunodepressed woman presented with acute perimyocarditis and cardiac tamponade complicating meningococcic infection. We had the opportunity to study her cardiac condition by injecting antimyosin during the acute phase. Images at 48 hr showed unexpected findings, with obvious localization of the tracer in the pericardial fluid, as well as myocardial uptake. Possible mechanisms for pericardial activity are discussed.

Antibodies, Monoclonal↗
PubMed1991

Diagnostic value of ascites gamma interferon levels in tuberculous peritonitis. Comparison with adenosine deaminase activity.

The value of ascites gamma interferon concentration and ascites adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a prospective study of 86 patients with ascites, including 16 with tuberculous peritonitis. Gamma interferon concentration was higher in tuberculous peritonitis than in the other causes of ascites (p less than 0.0001), and a cut-off between 3 and 9 u/ml reached a sensitivity and a specificity of 100%. The mean (+/- SD) gamma interferon level in tuberculous ascites was 39.3 +/- 18.3 u/ml in patients seronegative for HIV and 14.2 +/- 4.7 u/ml in patients with AIDS (p = 0.01). Adenosine deaminase activity in tuberculous ascites was also higher than in the other causes of ascites (p less than 0.0001), and a cut-off of 40 u/l reached a sensitivity of 100% and a specificity of 97%. The two false positives for adenosine deaminase test were true negatives for the gamma interferon test. There was no significant correlation between gamma interferon concentration and adenosine deaminase activity either in tuberculous ascitis or in any other group. This study suggests that ascites gamma interferon determination may be very useful in the screening of tuberculous peritonitis, but its cost makes it advisable to use adenosine deaminase activity as a routine test, at least in areas where tuberculosis is endemic.

Adenosine Deaminase↗
PubMed1990

[Gamma interferon and adenosine deaminase in pleuritis].

The concentration of gamma interferon (IFN gamma) and adenosine deaminase (ADA) activity were measured in the pleural fluid of 162 patients to compare their diagnostic significance and to establish a possible correlation between both tests. The IFN gamma levels in tuberculous pleural effusions were quite variable, with a mean of 93 U/ml and a median of 48 U/ml. They were higher than 2 U/ml in all cases, whereas no case of nontuberculous effusion showed higher values. ADA activity was higher than 43 U/l in all tuberculous effusions, with a mean value of 80 U/l, higher than in any other group except lymphoma. In three pleural effusions associated with lymphoma, one with mesothelioma, one with adenocarcinoma and four with empyema, ADA activity was higher than 43 U/l. In these patients, IFN gamma levels were low. There was no correlation in the whole series or in any group between IFN and ADA. Both parameters can be very useful for the diagnosis of tuberculous pleuritis. The measurement of IFN gamma is more specific, although the experience with this test is more limited than with ADA. It has the additional shortcoming of a high cost and it requires facilities for radionuclide use. Therefore, we think that ADA measurement should be considered as a routine test while IFN gamma measurement should be reserved for reference institutions.

Adenosine Deaminase↗
PubMed1990

Lymphocyte proliferation and gamma-interferon production after "in vitro" stimulation with PPD. Differences between tuberculous and nontuberculous pleurisy in patients with positive tuberculin skin test.

T-lymphocytes previously sensitized by an antigen undergo blastic transformation and produce IFN tau when stimulated by the same antigen. We studied the lymphoblastic response to PPD and IFN tau production in pleural fluid and peripheral blood of 41 patients (15 with tuberculous pleural effusion, 13 with nontuberculous pleurisy and positive tuberculin skin test, and 13 with tuberculin-negative nontuberculous pleurisy). In tuberculous pleuritis, pleural lymphocyte blastic response and IFN tau production were higher than those of peripheral lymphocytes, whereas in tuberculin-positive nontuberculous patients, peripheral lymphocyte response and IFN tau production were higher than those of pleural lymphocytes. Tuberculous pleural fluid lymphocytes underwent greater blastic transformation and produced more IFN tau than pleural lymphocytes of tuberculin-positive nontuberculous patients, whereas the opposite occurred in peripheral lymphocytes. In tuberculin-negative nontuberculous patients, there was no lymphoblastic response in either the pleural fluid or peripheral blood. These results concur with the concept of immunologic compartmentalization. In tuberculous pleuritis, there would be clonal expansion of PPD-responding T-lymphocytes in the pleural compartment. This expansion of PPD-specific lymphocytes would not occur in nontuberculous pleuritis, but lymphocytes sensitized to other antigens would accumulate in the pleural compartment.

CD4-Positive T-Lymphocytes↗