[Coronary cineangiography in survivors of acute myocardial infarction: is it really necessary?].
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Biomedical subjects
Publications and source records attributed to R Bassan.
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We have studied 7 patients with T gamma-lymphoproliferative disorders, in whom 78-88% of circulating nonadherent lymphocytes had the morphology of large granular lymphocytes (LGL) as assessed by light and transmission electron microscopy. The main common features of the membrane phenotype of these LGL expansions included expression of T3, HNK-1 and AB8.28. Other monoclonal antibody-defined surface markers of LGL (OKM1, B73.1, N901) were variably expressed or absent in these patients. Patients' LGL had little or no natural killer (NK) activity but mediated antibody-dependent cellular cytotoxicity (ADCC). Exposure to interferons (type B or gamma) for 20-72 hr resulted in no appreciable induction of cytolytic activity. In contrast, culture in the presence of interleukin-2 (IL-2) for 3 days resulted in the expression of strong cytolytic activity in all the patients tested against an NK-susceptible (K562) and an NK-resistant (Daudi) target. The expression of T3 antigen, the low levels or lack of native NK activity and the induction of consistent cytotoxicity by prolonged exposure to IL-2 led us to suggest that the cells expanding in these subjects are related to the effectors involved in lymphokine-activated killer (LAK) activity.
In a prospective study 51 consecutive patients who survived the acute phase of inferior wall myocardial infarction underwent coronary arteriography. Eleven patients developed some degree of atrioventricular (AV) block in the acute phase of infarction that disappeared within a few days and was considered by electrocardiographic analysis to be located in the AV node. Patients with AV block during acute myocardial infarction had a significantly higher prevalence of left anterior descending coronary artery obstruction (91 versus 55%, p less than 0.05) than did patients without AV block and the obstruction preceded the exit of the first septal perforator branch in 73% of cases with heart block and in 30% of cases without block (p less than 0.01). The sensitivity, specificity and predictive values were 31, 95 and 91%, respectively, for the existence of left anterior descending coronary artery obstruction when AV block occurred during acute inferior myocardial infarction, and 40, 90 and 73%, respectively, for the occurrence of the coronary artery obstruction before the exit of the first septal perforator branch. Patients with inferior myocardial infarction and left anterior descending coronary artery obstruction have a sixfold greater chance of developing heart block in the acute phase of infarction than do patients with inferior infarction without such obstruction (p less than 0.05). These findings also support the observations that the proximal AV conduction system usually has a dual arterial blood supply from both the right and left anterior descending coronary arteries, and may explain the transient behavior of heart block and lack of necrosis of the AV node seen in these patients.
We have studied five patients with chronic lymphocytosis consisting of large granular lymphocytes (LGL). The increased numbers of LGL in these patients had little or no natural killer activity, mediated antibody-dependent cellular cytotoxicity, and were induced to kill tumour lines after culture for 3 days with interleukin 2 (IL-2). Patients' LGL showed considerable reactivity with HNK-1 and AB8.28 monoclonal antibodies (MoAb), whereas positivity for OKM1 and N901 was found in only two subjects, and only one patient reacted with B73.1. No appreciable reactivity has been found with anti-Tac MoAb in the four patients tested. In the absence of stimulation, the patients' LGL produced no IL-2 and only minimal amounts of IL-1 and interferon (IFN). On stimulation with lipopolysaccharides (for IL-1) or phytohaemagglutinin A (PHA) (for IL-2 and IFN), they produced IL-1 and IFN in amounts similar to those produced by normal lymphocytes, but only modest levels of IL-2. These results indicated that proliferating LGL, like normal LGL, have a secretory capacity. The lack of constitutive lymphokine production, the lack of Tac receptor expression, and the defect in IL-2 production after PHA stimulation do not support the hypothesis of an autocrine proliferation sustained by a known growth factor.
6 patients with a chronic, clinically heterogeneous proliferative disorder of the large granular lymphocytes (LGL) were investigated. In each case the majority of peripheral blood lymphocytes reacted with HNK-1, OKT3 and T11 monoclonal antibodies, whereas morphology and other immunological features varied from case to case. 2 cases were of particular interest. 1 patient had an expansion of HNK-1 stained, large agranular rather than granular lymphocytes; another patient's LGL simultaneously expressed HNK-1, OKT4 and T8 antigens. The heterogeneous features of these abnormally expanded cell populations are similar to those of the normal cell subsets from which they are likely to have originated.
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We have investigated 10 patients with T gamma-lymphoproliferative disorders (T gamma LPD) for cell migratory capacity. Large granular lymphocytes (LGLs) expanding in these subjects expressed natural killer cell markers (HNKI, B73.1, AB8.28, N901, OKM1) to a variable extent. The patients' LGLs mediated antibody-dependent cellular cytotoxicity, while appreciable natural killer activity was only measurable in 3 patients. The migratory capacity of T gamma LPD was examined by using nitrocellulose filters. The patients' LGLs migrated into filters and showed responsiveness (in 9 of 10 patients) to activated serum, used as chemoattractant, as normal LGLs do. No clearcut correlation emerged between in vitro migratory capacity and disease aggressiveness or involvement of abdominal organs. These results confirm in T gamma LPD the migratory potential of LGLs and suggest the possibility that acquisition of enhanced locomotor capacity is not a crucial determinant of disease aggressiveness in T gamma LPD.
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Twelve cases of T gamma LPD (lymphoproliferative disorders of Fc gamma receptor-bearing T cells) involving an expansion of large granular lymphocyte/natural killer (LGL/NK) cells were investigated for the expression of LGL/NK-associated markers and for T beta gene rearrangement. All the cases selected were classified as T gamma LPD on the basis of morphology, function, and phenotype of the circulating cells. 10 to 12 cases displayed clonal rearrangements of the T beta locus and expression of the T3 antigen, whereas the 2 remaining cases displayed the germline configuration of the T beta gene and no expression of the T3 antigen. T8, Mol, B73.1, and N901 antigens were variably expressed among both T beta+T3+ and T beta-T3- T gamma LPD cases. We suggest that individual T gamma LPD cases represent the clonal expansion of cells frozen at different stages of differentiation/activation within an individual hematopoietic LGL/NK lineage.
A defective formation of E rosette from peripheral lymphocytes was observed in five patients with Gaucher disease. Evidence is shown that the reduction of E rosetting capacity is due to serum factors since it was induced in normal lymphocytes incubated with patients' sera. It is likely that ferritin, found elevated in the patients, might be involved in this inhibitory phenomenon. This disfunction might play a role in the high incidence of cancer in Gaucher patients.
Fourteen patients with idiopathic thrombocytopenic purpura (ITP) refractory to steroids and/or splenectomy were treated with danazol (200 mg 3 times a day) for 2 months. The following responses were achieved: excellent (platelet count greater than 100 X 10(9)/l) in 5 patients; good (greater than 50 X 10(9)/l, but less than 100 X 10(9)/l) in 2 patients, and poor in (no increase of platelet count) 7 patients. In three cases remission lasted more than 7 months. Danazol was well tolerated and in most patients better suited than steroids for long-term intake.
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A patient with concurrent multiple myeloma and B-cell chronic lymphocytic leukemia (CLL) is presented. Immunologic studies showed an identity between the myeloma protein and surface immunoglobulin of CLL cells.
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A case of childhood chronic neutropenia due to myelokathexis is reported. This extremely rare condition (the fourth case in the literature) has been diagnosed from the characteristic bone marrow abnormalities in the neutrophils.