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Biomedical subjects

E Ribera

Publications and source records attributed to E Ribera.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Acute myelofibrosis: apropos of a case with immunocytochemical and ultrastructural studies].

We report a case of acute myelofibrosis. This is a rare myeloproliferative disorder characterized by pancytopenia, minimal or absent anisopoikilocytosis, bone marrow fibrosis with hyperplasia and immaturity of the three main cellular lines with megakaryocyte predominance, absence of splenomegaly and rapidly fatal course. We discuss its relationship with acute megakaryocytic leukemia, as its blast elements correspond to megakaryocytes when ultrastructural and antifactor VIII immunoperoxidase techniques are used; these techniques disclose alpha granules and cell demarcating membranes.

Aged↗
PubMed1989

Adenosine deaminase in body fluids: a useful diagnostic tool in tuberculosis.

The performance of a colorimetric ADA determination in body fluids other than serum in the diagnosis of tuberculosis was assessed in 1063 patients from whom pleural (600), peritoneal (136), pericardial (77), or cerebrospinal (250) fluids were obtained. In exudative pleuroperitoneal and pericardial effusions, an ADA decision level of 0.71 mu kat/L displayed a sensitivity of 1.00, and was higher than those of histologic (0.83) and bacteriologic (0.62) studies. At this level, ADA reached a specificity of 0.92 and efficiency of 0.94. In cerebrospinal fluid, an ADA catalytic concentration above 0.15 mu kat/L strongly suggests tuberculous meningitis in patients older than 7 years (sensitivity 1.00, specificity 0.99 and efficiency 0.99). ADA results obtained with a UV-method were closely correlated with those of the colorimetric method in pleuroperitoneal effusions (r = 0.989) and in cerebrospinal fluids (r = 0.905). Sample blanks should be processed, otherwise false positive results may be found in non-tuberculous cerebrospinal fluids (5.3%) and pleuroperitoneal effusions (3.8%).

Adenosine Deaminase↗
PubMed1989

Autoimmune neutropenia and thrombocytopenia associated with development of antibodies to human immunodeficiency virus.

We report on two patients with acute human immunodeficiency virus (HIV) infection, who developed an infectious mononucleosis-like clinical episode with thrombocytopenia and granulocytopenia. In both cases we detected the presence of IgG antigranulocyte antibodies and in one case the presence of IgG, IgM and IgA antiplatelet antibodies. The mechanisms of these cytopenias are discussed. The association between such autoimmune cytopenias and acute HIV infection has not been previously reported. We suggest testing for HIV seroconversion in patients with a seronegative infectious mononucleosis-like syndrome belonging to groups with a high risk for HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Acute interstitial secondary to tricuspid endocarditis caused by Staphylococcus aureus].

The kidney diseases in patients with bacterial endocarditis and intravenous drug addicts (IVDA) tend to be of glomerular origin. Interstitial nephritis has been related to drug toxicity and only occasionally has it been described in other associations. We describe a 27-year-old patient IVDA with tricuspid endocarditis caused by S. Aureus whose first manifestations was acute renal failure. The renal biopsy showed an interstitial nephritis. It was treated with antibiotic and hemodialysis, obtaining the cure and normal levels of plasmatic creatinine.

Acute Disease↗
PubMed1988

Functional modulation of hepatitis B core antigen-specific T lymphocytes by an autoreactive T cell clone.

Hepatitis B core (HBc)Ag-specific T cells present in the peripheral blood of a patient with chronic active hepatitis B were expanded by co-cultivation for 7 days with rHBcAg. After cloning at 1 cell/well in the presence of PHA and IL-2, five HBcAg-specific CD4+ cloned lines were obtained. All five lines proliferated and produced IL-2, IFN-gamma, and TNF in a dose-dependent fashion in response to HBcAg, but not to HBV envelope Ag. The cloned lines and derivative clones were HLA class II (DR1) restricted. All T cell clones were able to induce anti-HBc production by autologous B cells in response to HBcAg (helper effect). The proliferative response and the helper effect of the HBcAg-specific T cell lines and clones were augmented by co-cultivation with an autologous, autoreactive (HLA-DQ1 specific) T cell clone, even in the absence of HBcAg, and the autoreactive T cells directly stimulated anti-HBc secretion by autologous B cells, presumably due to the release of Ag-nonspecific factors. These findings define a model immunoregulatory circuit the physiologic significance of which remains to be determined.

Adult↗
PubMed1988

Adenosine deaminase activity in rheumatoid pleural effusion.

The activity of adenosine deaminase was studied in nine cases of rheumatoid pleural effusion, showing an increase in enzyme activity in all. Rheumatoid arthritis seems unique, however, as it cannot be differentiated from pleural tuberculosis on the basis of this test. Selective increase of adenosine deaminase in both conditions is attributed to stimulation of T lymphocytes in the pleural fluid.

Adenosine Deaminase↗
PubMed1988

High level of interferon gamma in tuberculous pleural effusion.

It has been observed that T-lymphocytes of patients with tuberculosis produce interferon gamma (IFN gamma) in vitro. Based on this idea, we studied IFN gamma in pleural fluid and serum. We studied 80 patients with pleural effusion; 30 patients with tuberculous pleurisy had high IFN gamma concentrations in pleural fluid. Patients with malignant pleural effusions, nonspecific pleural effusion, parapneumonic effusions and pleural transudates had low levels. The IFN gamma levels were higher in those with massive tuberculous effusion and apparent pulmonary lesion on x-ray film. We found that the T4/T8 lymphocyte ratio was higher in pleural fluid than in peripheral blood. Numbers of T3 and T4 lymphocytes were higher in tuberculous pleural effusions compared with those in other patients. There is no correlation between IFN gamma levels and lymphocyte subsets in pleural effusion. Perhaps pleural T-lymphocytes produce IFN gamma after stimulation by mycobacterial antigens and this lymphokine activates macrophages, increasing their bactericidal activity against Mycobacterium tuberculosis.

Humans↗
PubMed1987

Intrahepatic, nucleocapsid antigen-specific T cells in chronic active hepatitis B.

Hepatitis B core antigen (HBcAg)-specific T cell lines were established from hepatic lymphomononuclear cells derived from five patients with chronic active hepatitis B. No hepatitis B virus envelope antigen-specific cell lines were established. Proliferation in response to recombinant and native HBcAg, but not to native hepatitis B surface antigen containing the pre-S(2) region, confirmed the specificity of the five T cell lines. All cell lines represented mixed populations of CD4+ and CD8+ T cells. The CD4+ subset provided antigen-specific help to autologous B cells with respect to anti-HBc production and to CD8+ cells with regard to HBcAg-induced proliferation and suppressor activity. The CD8+ subset contained suppressor cells that selectively inhibited the proliferative response of autologous HBcAg-specific CD4+ cells without inhibiting CD4+ cells of unrelated specificity (tetanus toxoid). Moreover, the CD8+ cells were also capable of suppressing HBcAg-stimulated antibody to HBcAg production without showing inhibition of total immunoglobulin production stimulated by pokeweed mitogen. The cytotoxic potential of the T cell lines was established in a lectin-dependent cytotoxicity system; natural killer cytotoxicity was completely absent. Our data suggest that the lesional T cells present at the site of hepatocellular injury in chronic active hepatitis B are primarily HBcAg-specific lymphocytes of the helper and suppressor/cytotoxic phenotypes and that both are functionally competent.

Antibody Formation↗
PubMed1987

Activity of adenosine deaminase in cerebrospinal fluid for the diagnosis and follow-up of tuberculous meningitis in adults.

We studied the activity of adenosine deaminase in the cerebrospinal fluid of 40 normal controls and 205 patients who were grouped according to disease (tuberculous, viral, and purulent meningitis; neoplasms; stroke; and miscellaneous). The mean enzyme value was clearly higher for the patients with tuberculous meningitis (15.7 +/- 4.3 U/liter) than for the other patients (1.4 +/- 1.5 U/liter). The sensitivity of the test for diagnosing tuberculous meningitis was 1 and specificity, 0.99. The enzyme activity, as well as progression of the disease, was studied in 32 patients with tuberculous meningitis. A significant rise in levels of enzyme was observed during the first 10 days of therapy, was followed by a gradual decline, and reached normal values after three to four months of treatment. Two patients showed substantial increases that coincided with the development of complications. The test proved to be a simple and reliable method for early diagnosis and follow-up of tuberculous meningitis.

Adenosine Deaminase↗
PubMed1986

Adenosine deaminase activity in the diagnosis of lymphocytic pleural effusions of tuberculous, neoplastic and lymphomatous origin.

We studied the activity of adenosine deaminase in 74 lymphocytic pleural effusions which were divided into four groups according to the aetiology: tuberculous (38 cases), neoplastic (17), lymphomatous (7) and miscellaneous (12). The mean enzyme value was significantly higher in the tuberculous cases (93.81 +/- 29.56 U/I) than for the other three groups and significantly higher in pleural effusions of lymphomatous origin than in the neoplastic and miscellaneous groups. Based on the lowest value of enzyme activity found in the tuberculous group (50 U/I), the test had a sensitivity of 1 and a specificity of 0.97.

Adenosine Deaminase↗
PubMed1986

Adenosine deaminase activity in the diagnosis of tuberculous peritonitis.

We studied the activity of adenosine deaminase in the peritoneal fluid of 66 patients who were divided into five groups according to causes of ascites as follows: tuberculous peritonitis (group I), septic peritonitis (group II), secondary to malignant tumours (group III), miscellaneous conditions (group IV), and control subjects of transudates (group V). In patients with tuberculous peritonitis the enzyme activity was significantly higher than for the rest of the groups (p less than 0.001), and enzyme concentrations in all patients were well above the upper non-tuberculous value. Adenosine deaminase activity in the peritoneal fluid has proved to be a simple and reliable method for early diagnosis of tuberculous peritonitis.

Adenosine Deaminase↗