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D Pereira

Publications and source records attributed to D Pereira.

At least 37 records · Page 2Linked to original sources
PubMed1993

Acute agranulocytosis after prolonged high-dose usage of intravenous dipyrone--a different mechanism of dipyrone toxicity?

Two seriously injured trauma patients presenting with intense and progressive neutropenia are described. Bone marrow examination in both cases showed virtually absent granulopoiesis but normal erythropoiesis and megakaryopoiesis, allowing the diagnosis of acute agranulocytosis. Discontinuation of only one drug (dipyrone) with no further treatment was required for normalization of blood parameters. The association of dipyrone with neutropenia is still debatable. The recent medical literature on dipyrone generation of agranulocytosis is reviewed.

Adolescent↗
PubMed1993

[The efficacy of isosorbide dinitrate administered in an intravenous bolus in acute cardiogenic pulmonary edema].

STUDY OBJECTIVE: To evaluate the efficacy, safety and tolerability of intravenous (i.v.) isosorbide dinitrate (ISDN) administered as a bolus in the treatment of cardiogenic acute pulmonary edema (CAPE). DESIGN: Clinical, prospective, open, noncontrolled trial. SETTING: Emergency room. PATIENTS AND INTERVENTIONS: Twenty two patients (15 male and 7 female), aged 54 to 80 years (68.4 +/- 6.4) with severe respiratory distress consistent with CAPE were included. The cause of CAPE was chronic ischemic cardiopathy in 13 patients, acute myocardial infarction in four, hypertensive cardiopathy in three and mitral valve disease in two. Patients were excluded from the study because of shock or systolic blood pressure equal or lower than 100 mmHg, severe aortic stenosis, hypertrophic cardiomyopathy and non-cardiogenic pulmonary edema. All patients were placed in the sitting position and received oxygen. Initial therapy consisted of an i.v. bolus of 5 to 10 mg of ISDN. Clinical data were recorded at admission and after 5, 10, 15 and 30 minutes. A new i.v. bolus of ISDN and/or another drug was administered at 5 minutes, when necessary. RESULTS: Fifteen patients treated exclusively with ISDN (in three a second i.v. bolus was necessary) improved markedly. In the remaining seven patients that needed other drugs, the improvement was not so impressive. The mean total dose of i.v. ISDN was 10.34 +/- 3.48 mg. Although all data showed a trend towards improvement, just the following were statistically significant (p < 0.05): pH increased from 7.26 +/- 0.13 to 7.32 +/- 0.9, systolic blood pressure decreased from 192.7 +/- 34.8 mmHg to 155.0 +/- 24.4 mmHg (-19%) and diastolic blood pressure decreased 110.5 +/- 12.7 mmHg to 93.2 +/- 9.1 mmHg (-16%). CONCLUSIONS: In this trial, iv ISDN administered as a bolus in doses ranging from 5 to 20 mg, was effective and safe as a first line agent in the treatment of CAPE. No serious adverse reaction were reported.

Acute Disease↗
PubMed1993

[Primary hyperaldosteronism--4 clinical cases].

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate hypertension. Serum potassium and plasmatic aldosterone values were high although plasmatic renin levels were normal. The captopril test (Lyons version), abdominal CT and iodocholesterol (NP-59) scan proved useful to exclude essential hypertension. A good therapeutical results was achieved in all cases by unilateral adrenalectomy. After surgery, diagnosis was confirmed in all cases by histological studies. At one year follow-up, all patients were asymptomatic, with no hypertension without therapeutic and the serum potassium and plasmatic aldosterone and renin values were normal.

Adenoma↗
PubMed1993

[Fever in the first 48 hours of an acute myocardial infarct treated with fibrinolytics--an indicator of nonreperfusion of the coronary vessels?].

UNLABELLED: Fever in the first days of acute myocardial infarction (AMI) is a very common clinical feature, being its prognostic value unquestionable. As infarction area reduction implies a less important fever reaction in the first days of AMI, we believe that thrombolytic therapy would result in a decline of body temperature of patients so treated. That is why we tried to identify such a correlation, and demonstrate the value of normal body temperature as indicative of reperfusion. We studied retrospectively 68 patients (10 F and 58 M, 57.1 +/- 9.6 years) survivors of AMI (I-II KK classes), with (TT) or without (NT) thrombolytic therapy. In NT group, there was an axillary temperature (AX T) higher than 37 degrees C at the first 24 hours in 21 patients (62%); TT group only had 10 patients (30%) with AX T over 37 degrees C (p < 0.01). NT group CK mean peak was 856 +/- 610 U.I./l in patients having AX T > 37 degrees C, and 436 +/- 233 U.I./l when AX T was < or = 37 degrees C (p < 0.05); in TT group there was no difference between CK peak means when AX T was > or < or = 37 degrees C (1508 +/- 1210 U.I./l vs 1406 +/- 1149 U.I./l, respectively) (NA). We established statistic difference between AX T of 15 patients which CK peak was reached after 10 hours over onset of AMI (37.59 +/- 0.36 degrees C) and those (19 p) with CK peak before 10 hours (37.17 +/- 0.60 degrees C) (p < 0.05). NT group presented then more febrile patients than did TT group. CONCLUSIONS: in NT group there was a positive relation between AX T and CK peak level; AX T > 37 degrees C was less frequent in TT group and was as much light when CK peak was more precocious. These results suggest that in thrombolytic treated patients the absence of fever in the first 48 hours may constitute one more coronary reperfusion criterion.

Adult↗
PubMed1991

Characterization of a new cell line (ESKOL) resembling hairy-cell leukemia: a model for oncogene regulation and late B-cell differentiation.

A B-lymphoblastoid cell line ESKOL, composed of differentiated cells resembling hairy-cell leukemia (HCL) has been established from the peripheral blood (PB) of a HCL patient. Morphologically, ESKOL cells share several features with HCL B cells. Flow cytometric analysis revealed that ESKOL cells express HC2, CD21, PCA-1, CD24, FMC7, and CD25. Analysis by Northern-blot hybridization indicated that cultured cells expressed the oncogenes c-myc, H-ras and c-fos. RNA from 3T3 cells transfected with ESKOL DNA hybridized with H-ras and c-fos DNA probes. The ESKOL cells cultured in the presence of increasing concentrations, of alpha interferon demonstrated a decrease in the rate of cellular growth and an increase in the expression of CD21, CD25, FMC7 and PCA-1. Scanning electron microscopy revealed that cells incubated in the presence of alpha interferon underwent membranous changes with a loss of villosity. These observations suggest that IFN tends to drive HC out of their developmental arrest towards maturation.

Aged↗
PubMed1991

[Assessment of the first myocardial infarctions with lead ECG --implications in the study of hospital mortality and its reduction using thrombolytic drugs].

STUDY OBJECTIVE: Correlation between mortality reduction of first Myocardial Infarction (MI) by thrombolytic therapy and MI size evaluated with the classical Electrocardiogram (ECG). DESIGN: A retrospective sequential study. SETTING: Coronary Unit patients. PATIENTS: Sequential sample of 132 patients with first MI obeying all the following criteria: 1) no previous MI; 2) age less than or equal to 70 years; 3) clinical evolution less than 12 hours; 4) no Left Bundle Branch Block in the CCU first ECG; 5) ischemic ST elevation in greater than or equal to 1 initial ECG leads. Patients were divided into Group A, with less than or equal to 3 initial ECG leads with ischemic ST elevation (n = 80), and Group B, with greater than or equal to 4 initial ECG leads with ischemic ST elevation (n = 52). Only 34 patients (25.7%) did thrombolytic therapy with IV Streptokinase (SK); 15 from Group A and 19 from Group B. MEASUREMENTS AND MAIN RESULTS: 17 patients died in MI acute phase (12.8%); 4 in Group A (5%) and 13 in Group B (24.9%). Inhospital mortality was statistically worst in Group B than in Group A (24.9% vs 5% with p less than 0.01). Creatin kinase (CK) maximal values (A = 911.5 UI; B = 1444.6 UI with p less than 0.01) and initial Heart Rate (A = 75.7; B = 86.7 with p less than 0.001) were also statistically greatest in Group B. Inhospital mortality was smaller in patients treated with SK (8.8% vs 14.3%), as in Group B (10.5% vs. 33.3%), both without statistical significance. CONCLUSIONS: Inhospital mortality and thrombolytic therapy benefit were so bigger as MI size evaluated by the number of initial ECG leads with ischemic ST elevation, by initial HR and maximal values of CK. Classical ECG can be useful by identifying patients with first MI that can more benefit with thrombolytic therapy (greater than or equal to 4 leads with ischemic ST elevation).

Aged↗
PubMed1990

The activated form of p53 is not a transactivator of the intracisternal A particle long terminal repeat promoter.

Published observations have suggested that the activated form of p53 protein could transactivate the Intracisternal A particle long terminal repeat promoter (IAP-LTR). In this paper we demonstrate that the increased expression from this promoter was due to effects of the co-transferred plasmids and not p53 per se. In transient expression experiments, co-transfer of either a p53 or a p53 frame-shift mutant plasmid with an IAP-LTR driven chloramphenicol acetyl transferase (CAT) plasmid gave a similar increase in CAT activity. Further, this increase in CAT gene activity could also be achieved by co-transfer of a plasmid containing a viral promoter alone.

Chloramphenicol O-Acetyltransferase↗
PubMed1990

[Angioimmunoblastic lymphadenopathy with dysproteinemia. The first reported case at the "Santo Tomás" Hospital].

Description of the first case of angio-immunoblastic lymphadenopathy with dysproteinemia diagnosed in a male patient 64 years old and which preceded the development of a lymphoma. The importance of this study is the association that may exist between certain drugs and the development of angioimmunoblastic lymphadenopathy, which occurred in our patient with the use of diphenylhydantoin. This disease can present itself up to 22 years after exposure to the agent.

Biopsy↗
PubMed1990

[Prognostic significance of angina pectoris before myocardial infarction].

The AA analysed the incidence of previous angina to myocardial infarction (PA) (42.3%) and post myocardial infarction angina (PMIA) (46.39%) in 97 patients that survived the acute phase of myocardial infarction, all discharged from the CCU of the Funchal's Hospital Center Cardiological Department (Madeira Island), whose 25 of them (26.8%) presented both. They met 14 positive Treadmill tests in the 30 patients that were submitted to sub-maximal protocols. They concluded that the presence of PA and positive treadmill tests can identify a patient group with increased risk of PMIA, suggesting that patients with PA have also an increased isquemic risk.

Aged↗
PubMed1990

[Effect of intravenous administration of SO4Mg in the acute phase of myocardial infarct].

Fifty four patients (p) with acute myocardial infarction (40M; 14F) were entered into a prospective study where they received either intravenous magnesium sulphate (group A-27 p) or placebo (group B-27 p). The incidence of arrhythmias necessitating treatment was greater in group B (37%) than in group A (15%). Mortality was 18.5% in group B and 3.7% in group A. These results suggest that magnesium sulphate administration reduces the incidence of arrhythmias and death after acute myocardial infarction.

Aged↗
PubMed1989

[Therapeutic effectiveness of intravenous magnesium sulfate in tachyarrhythmia. Apropos of 4 clinical cases].

This is a report about four patients with tachyarrhythmias successfully treated with intravenous magnesium sulfate. In two cases (supraventricular tachycardia and torsade de pointes) because they were resistant to other antiarrhythmic drugs, and in the remaining two cases (paroxistic atrial fibrillation) because they presented characteristic features of magnesium depletion. The efficacy, the rapid onset of action and the absence of adverse reactions must be emphasized and the authors suggest that larger and randomized trials should be carried out, in order to establish the real place of magnesium sulfate in the antiarrhythmic armamentarium.

Adult↗
PubMed1989

[Risk and follow-up after myocardial infarct at a peripheral hospital].

AIM: Analysing the influence of clinical and paraclinical "markers" in long term prognosis (LTP) of Acute Myocardial Infarction (AMI), in terms of mortality, post AMI Angina, post AMI Heart Failure and non fatal recurrent AMI in patients of a Post AMI Consultation of a peripherical hospital. DESIGN: A) Retrospective study (series A and B) of the average incidence of 17 "markers" of bad post AMI TLP so as to identify those that had a discriminating value with regards to death after hospital discharge. B) Prospective study so as to determine its influence in those patients followed in a post AMI Consultation (series C), with regards to mortality, post AMI Angina, post AMI Heart Failure and non fatal recurrent AMI. PARTICIPANTS: Series A - 97 survivors of AMI treated on the CCU of Madeira's Hospital Center in its 1st year. Series B - 91 survivors of AMI treated of AMI treated on the CCU of Madeira's Hospital Center in its 2nd year. Series C - 88 survivors of AMI treated on the CCU of Madeira's Hospital Center after this period and followed up since then at the post AMI consultation. RESULTS: A) Significant statistical differences were observed in the series A and B, with regards to late mortality, in 5 of those "markers" (aged greater than or equal to 70 years, Auricular Fibrillation and Killip III class during the acute phase of the AMI, frequent ectopic ventricular beats before discharge and a survival probability of less than or equal to 60% at 5 years after AMI). B) It was observed that bearers of greater than or equal to 1 of these 5 clinical "markers" of the series C had significant statistical differences in relation to non bearers with regards to mortality, post AMI Angina, post AMI Heart Failure and non fatal recurrent AMI. CONCLUSIONS: It is considered that those 5 post AMI clinical "markers" allows identification of the very bad cases of post AMI LTP in peripherical hospitals. This identification can lower the ratio cost benefit of the indispensable diagnostic techniques for stratification of post AMI risk, through the rationalization of its use. A Study of its accessibility with regards to peripherical hospitals and a AMI national register became important to evaluate the problem of the Portuguese AMI survivors in terms of Public Health.

Aged↗
PubMed1987

Effect of a sublethal dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin on interscapular brown adipose tissue of rats.

The effect of a sublethal dose (15 micrograms/kg) of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in selected tissues of male Sprague-Dawley rats by histological techniques 1, 3, 7 and 14 days after TCDD dosage. Histology of the heart, muscle, white adipose tissue, pancreas and the thyroid was unremarkable and that of the liver was found in agreement with previous reports. However, considerable changes were seen in interscapular brown adipose tissue (IBAT) of TCDD-treated rats. Initial accumulation followed by depletion of lipids, appearance of glycogen, cellular, mitochondrial and nuclear transformations were observed. In conjunction with other experiments it is concluded that a sublethal dose of TCDD alters fat and glucose metabolism in IBAT.

Adipose Tissue, Brown↗
PubMed1986

Histopathology of interscapular brown adipose tissue, thyroid, and pancreas in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats.

The time course of histological changes was studied in rats lethally intoxicated (150 micrograms/kg) with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In addition to TCDD-caused tissue damage described by others, the thyroid, pancreas, and interscapular brown adipose tissue (IBAT) were identified as tissues affected by TCDD. Because histological changes in the thyroid and pancreas occurred late (7 days after dosing), these effects are viewed as secondary due to altered hormonal homeostases. Both light and electron microscopic examination of IBAT identified this tissue as a target in TCDD toxicity. Histological changes in IBAT are characterized by three phases: (1) "fatty" IBAT (Days 1 to 3 after dosing); (2) fat depletion accompanied by glycogen accumulation (Days 4 to 7 after dosing); and (3) complete fat and glycogen depletion together with massive cellular damage (Days 8 to 14), particularly affecting the mitochondria. It is concluded that brown adipose tissue is a primary target in TCDD toxicity. It seems that destruction of brown adipose tissue by TCDD leads to an energy imbalance resulting in reduced oxygen consumption which forces animals to contribute a greater proportion of energy to the maintenance of their body temperature by anaerobic pathways. It is suggested that this less efficient energy utilization is the cause of a wasting syndrome.

Adipose Tissue, Brown↗
PubMed1985

Structure and polymorphism of class I MHC antigen mRNA.

We have used cDNA cloning and primer extension techniques to determine the complete nucleotide sequence of HLA-B7 mRNA. The 5'-untranslated sequence of the mRNA is rather short and the putative promoter has weak homology to the conventional "TATA" sequences. The 5' end and the polyadenylation site define the transcription unit of the B7 gene to be about 3.5 kb long. Comparison of the translated nucleotide sequence of this cDNA with the amino acid sequence of the heavy chain of the B7 antigen showed two amino acid differences. In addition, comparison with the sequences of the coding and untranslated regions of several HLA and H-2 genes showed that the class I histocompatibility molecules consist of four variable segments separated by three regions of homology. Analysis of the DNA polymorphisms revealed that in the variable segments the majority of the nucleotide substitutions are nonsilent, while in the homology regions the majority of substitutions are silent. Further analysis of the nature of the amino acid substitutions revealed the predominance of nonconservative replacements/changes in both the variable segments and the homology regions except the transmembrane part of the molecule. Selection at both the protein and the codon levels contributes to the pattern of mutations found in class I histocompatibility molecules.

Amino Acid Sequence↗
PubMed1981

Three cDNA clones encoding mouse transplantation antigens: homology to immunoglobulin genes.

We constructed cDNA libraries from poly(A)+ RNA isolated from cell lines of two different inbred strains of mice, and screened the libraries with a cDNA clone encoding a human transplantation antigen. Three cDNA clones were identified, sequenced and found to encode amino acid sequences highly homologous to portions of a known mouse transplantation antigen. Comparison of the cDNA sequences of mouse transplantation antigens with the constant region domains of the mouse immunoglobulin mu gene reveals a striking homology, which suggests that the two genes share a common ancestor. Antibody genes undergo DNA rearrangement during B cell differentiation that are correlated with their expression. In contrast, DNA blots with these cDNA probes suggest that the genes for the transplantation antigens are not rearranged in the genomes of liver or embryo cells, which express these antigens, as compared with sperm cells, which do not express these antigens. In Bam Hl-digested liver DNAs from different inbred strains of mice, 10-15 bands of hybridization were found. Accordingly, the genes encoding the transplantation antigens appear to constitute a multigene family with similar gene numbers in different mice.

Amino Acid Sequence↗