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Biomedical subjects

J Pereira

Publications and source records attributed to J Pereira.

At least 109 records · Page 6Linked to original sources
PubMed1997

[Transplacental alloimmunization against specific platelet antigens: prevalence and features in a Chilean population].

BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) is a result of fetomaternal incompatibility. Platelet destruction is caused by a maternal antibody directed against a fetal platelet antigen inherited from the father and lacking on the mother's platelets. The incidence and features of transplacental alloimmunization depend on the frequency of expression of platelet specific antigens; which are highly variable among different populations. AIM: To determine the prevalence and characteristics of transplacental alloimmunization in a large group of pregnant women in Chile. MATERIAL AND METHODS: We studied 3,041 samples obtained during the third trimester of gestation. In all samples, anti platelet antibodies were screened by ELISA with platelet membranes fixed to a microtiter plate. Positive samples were further studied for antigenic specificity with the monoclonal antibody specific immobilization of platelet antigens (MAIPA) test. RESULTS: Anti platelet antibodies were found in 261 samples (8.5%). The MAIPA test identified 6 samples with antibodies directed against major platelet membrane glycoproteins, 2 anti GPIb, 2 anti GPIIb/IIIa and 2 anti GPIa/IIa. In four cases, anti HLA antibodies coexisted. Two cases corresponded to well defined platelet antigen systems: one anti HPA-1a and one anti HPA-5b. No clinical evidence of thrombocytopenia of the newborn was detected in all these cases with anti GP antibodies. CONCLUSIONS: A prevalence of platelet specific antibodies of 0.2% with only one anti HPA-1a was detected. These findings are in contrast with those of other populations but in accordance with the low frequency of the HPA-1 b/b phenotype in the Chilean population. The very low incidence of platelet specific antibodies and the lack of association with clinical thrombocytopenia in the newborn, do not support the recommendation of routine antenatal screening to all women in Chile.

Antigens, Human Platelet↗
PubMed1997

[Platelet alloimmunization in patients with oncologic blood disorders treated with multiple transfusions: prospective study in adults and children].

BACKGROUND: Refractoriness continues to be a major complication of platelet transfusion therapy in patients with multiple transfusions. Despite most cases are secondary to non-immune causes, the most serious is that associated to alloimmunization. The incidence and consequences of HLA and non-HLA (platelet specific) antibodies are unknown in our country. AIM: To prospectively determine the frequency and characteristics of post transfusion alloimmunization and the incidence of platelet specific antibodies. PATIENTS AND METHODS: Forty one adults and 24 children with a recently diagnosed malignancy and undergoing chemotherapy that required multiple transfusions were studied. Screening for antiplatelet antibodies (platelet membrane ELISA) was performed before the first transfusion, every four weeks or whenever the 1 hour corrected count increment for platelet transfusions was lower than 5000. Platelet specific antibodies were identified with a monoclonal antibody-specific immobilization of platelet antigens (MAIPA), with anti-GPIb, GPIIb/IIIa, GPIa/Iia and anti-HLA class I. RESULTS: Adult patients received an average of 10.2 +/- 5.5 units of red blood cells and 58.6 +/- 35.4 units of platelets. Children received 4.8 +/- 3.7 units of red blood cells and 9.6 +/- 6.7 units of platelets. HLA antibodies appeared in 7 of 41 adult patients (17%), platelet specific alloantibodies were found in two patients (one anti GP Ia/IIa and one anti GP Ib). Platelet refractoriness appeared in three alloimmunized patients. No child had detectable serum antibodies during follow up. CONCLUSIONS: Platelet transfusion refractoriness of immune origin occurs infrequently in our population and the presence of platelet antibodies does not mean that it will appear. The use of leukocyte depleted blood components to prevent refractoriness cannot be justified at this time.

Adolescent↗
PubMed1996

Opioid rotation in patients with cancer pain. A retrospective comparison of dose ratios between methadone, hydromorphone, and morphine.

BACKGROUND: When a change of opioid is considered, equianalgesic dose tables are used. These tables generally propose a dose ratio of 5:1 between morphine and hydromorphone. In the case of a change from subcutaneous hydromorphone to methadone, dose ratios ranging from 1:6 to 1:10 are proposed. The purpose of this study was to review the analgesic dose ratios for methadone compared with hydromorphone. METHODS: In a retrospective study, 48 cases of medication changes from morphine to hydromorphone, and 65 changes between hydromorphone and methadone were identified. the reason for the change, the analgesic dose, and pain intensity were obtained. RESULTS: The dose ratios between morphine and hydromorphone and vice versa were found to be 5.33 and 0.28, respectively (similar to expected results). However, the hydromorphone/methadone ratio was found to be 1.14:1 (5 to 10 times higher than expected). Although the dose ratios of hydromorphone/morphine and vice versa did not change according to a previous opioid dose, the hydromorphone/methadone ratio correlated with total opioid dose (correlation coefficient = 0.41 P < 0.001) and was 1.6 (range, 0.3-14.4) in patients receiving more than 330 mg of hydromorphone per day prior to the change, versus 0.95 (range, 0.2-12.3) in patients receiving ae330 mg of hydromorphone per day (P = 0.023). CONCLUSIONS: These results suggest that only partial tolerance develops between methadone and hydromorphone. Methadone is much more potent than previously described and any change should start at a lower equivalent dose.

Administration, Oral↗
PubMed1996

Comparison of antibodies raised against the peptide 10-24 of chicken riboflavin carrier protein (cRCP) by classical and multiple antigen peptide (MAP) approaches.

Riboflavin carrier protein is an essential protein required for the growth and development of the embryo and hence for the maintenance of pregnancy. Our efforts to delineate the antigenic determinants of chicken riboflavin carrier protein (cRCP) resulted in the identification of a bioneutralization epitope in the region 10-24 of cRCP. The present work compares the properties of the antibodies raised against the peptide epitope by classical and multiple antigen peptide (MAP) system approaches. The extent of cross-reaction of the antibodies to the MAP construct with the parent protein was found to be significantly less as compared to the antibodies raised against the peptide-diphtheria toxoid conjugate. Furthermore, the bioneutralizing ability of the antisera to the MAP construct was also found to be very poor. The results suggest that there are serious limitations in the ability of antibodies raised against MAP constructs to cross-react with the native proteins.

Amino Acid Sequence↗
PubMed1996

Normal mitochondrial DNA and respiratory chain activity in familial dysautonomia fibroblasts.

Familial dysautonomia (FD), an autosomal recessive disease mapped to chromosome 9q31, is a sensory and autonomic neuropathy of unknown etiology. We have previously reported light microscopic pleiomorphic changes in cells suggestive of altered plasma membranes, an increase in globotriaosylceramide (Gb3), reflected by an increase in Gb3 on the surface of the plasma membrane, and a decrease in the rate and amount of ganglioside synthesized. In unrelated studies, we demonstrated that storage of glycospingolipids (GSL) is deleterious to mitochondrial function. Recently, mitochondrial dysfunction has been associated with neurodegenerative disease, superimposed on an autosomal inheritance pattern. We have now probed Southern blots of total FD fibroblast DNA, digested with BamHI, EcoRII, and/or PvuII, with purified placental 32P-labeled mitochondrial DNA. The sizes of all FD mitochondrial DNAs were normal (16,569 bp), some containing previously identified BamHI polymorphisms. Lactate/pyruvate ratios, and activities of Complexes II and III, matched those of control cells. Electron microscopy revealed morphologically normal mitochondria, in conjunction with a normal oxidative state, determined using the redox dyes Mito Tracker CMXR and CMXR-H2 and fluorescence microscopy. We conclude that mitochondrial dysfunction, due to GSL accumulation, changes in mitochondrial DNA, or mutation of a chromosome 9q gene involved in mitochondrial function, is neither a primary nor a secondary cause of FD, as determined by a study of FD fibroblasts.

Blotting, Southern↗
PubMed1996

Mesenteric arteriovenous fistula causing portal hypertension and bleeding duodenal varices.

We report a case of portal hypertension associated with a non-traumatic arteriovenous fistula, presenting with bleeding duodenal varices. The patient was admitted for melaena. Emergency endoscopy showed oesophageal varices with no signs of recent bleeding and with no blood in the upper gastrointestinal tract. Arteriography of the coeliac axis and superior mesenteric artery failed to detect any bleeding source. Endoscopy was repeated because of persistent bleeding and revealed active bleeding from varices in the distal duodenum. The patient underwent surgery and a large paraduodenal varicose vein associated with an arteriovenous fistula was found. Resection of the paramural varix and surgical occlusion of the arteriovenous fistula were effective in the control of bleeding. Liver biopsy revealed mild portal fibrosis without cirrhosis. Three years after surgery the patient still has oesophageal varices but has not had recurrent bleeding. There was regression of intraduodenal varices.

Aged↗
PubMed1996

Hemostatic disorder of uremia: the platelet defect, main determinant of the prolonged bleeding time, is correlated with indices of activation of coagulation and fibrinolysis.

Several parameters of primary hemostasis and markers of activation of coagulation and fibrinolysis were measured in 48 patients with severe (creatinine clearance < 20 ml/min) chronic renal failure (CRF) without dialysis and disease or drugs affecting hemostasis. Bleeding time (BT) was prolonged in 25/48 patients, and was correlated with age of patients, severity of renal failure, hematocrit, impairment in platelet aggregation-secretion and decrease in platelet ATP content. Defects in von Willebrand factor played no role in the prolongation of the BT. Multivariate analysis showed that only platelet dysfunction and severity of renal disease were independent predictors of the BT in uremia. The platelet functional disorder was significantly correlated with a reduction in platelet ATP and ADP. High levels of plasma thrombin-antithrombin complexes (TAT), prothrombin fragment F1 + 2, fibrinogen and factor VIIc were observed in patients with CRF, as described in prethrombotic states. Plasmin-antiplasmin complexes (PAP), fibrinogen and fibrin degradation products (FgDP, FnDP) were significantly increased, and the activity of plasminogen activator inhibitor (PAI-1) was slightly reduced, denoting an activation of fibrinolysis. A negative correlation was found between platelet levels of ATP and ADP with plasma TAT, F1 + 2 and PAP. Furthermore, plasma PAI-1 activity was negatively correlated with the BT and was lower in patients with prolonged BT as compared with controls and patients with normal BT. These links between primary hemostasis and activation of coagulation and fibrinolysis suggest that increased intravascular generation of thrombin and/or plasmin is an important mediator of the defects in primary hemostasis, prolongation of the BT and, probably, bleeding in CRF.

Adolescent↗
PubMed1996

[Activated C protein resistance: laboratory study and prevalence of the defect in the Chilean population].

Activated protein C resistance (APCR) or Factor V Leiden has been recently described as the most prevalent hemostatic abnormality associated with venous thrombosis. In patients with familial thrombophilia, the prevalence of APCR is 19-60% and around 20% in sporadic venous thrombosis. APCR is usually measured by the degree of prolongation of Activated Partial Thromboplastin Time (APTT) on patient's plasma, induced by addition of APC in comparison to normal plasma. At the molecular level the defect is caused by a single-point mutation in the gene for factor V (FV) (G1.691-->A), that predicts the replacement of Arg506 by Glutamine. This mutation makes activated factor V resistant to inactivation by APC. Since the prevalence of the defect is highly variable among different populations, the objective of this work was to study its frequency in our population and in patients with thrombophilia. We defined the normal range for APTT ratio (APTT + APC/APTT - APC) in a group of 73 healthy volunteers in whom the presence of FV Q506 mutation was searched using Mull enzyme digestion of PCR amplified genomic fragment containing the nucleotide 1.691. The lower limit of APTT ratio established in this group was 2.13. APCR was found in 6 out of 159 control subjects (3.8%) and in 14/50 (28%) of patients with thrombosis. In 13 cases as a single defect and in one associated to type I protein C deficiency. All the APCR patients and control subjects were heterozygotes by gene analysis. The results demonstrate that in our population APCR is also the most common defect associated with thrombosis, in accordance with a high prevalence in the population. The ability to screen for this defect will permit the identification of carriers that would benefit of preventive therapy at risk situations.

Base Sequence↗
PubMed1996

[Hemophilia A: analysis of intron 18 and intron 7 of factor VIII gene and their role in a diagnostic strategy for carrier detection in a Chilean population].

Hemophilia A is an X-linked disorder of coagulation caused by a deficiency of factor VIII. A larger number of different mutations in the VIII gene have been identified. Thus, the detection of female carriers, depends upon the analysis of DNA polymorphisms in and near the factor VIII gene. Our aim was to develop a strategy, earlier reported, for carrier testing in families at risk of hemophilia A. In this study, we analyzed the DNA polymorphisms in 26 affected families, with use of the factor VIII intragenic polymorphisms identified by the restriction enzymes BclI and AlwNI, and by differential hybridization with sequence-specific oligonucleotide probes recognizing BclI and AlwNI polymorphism. While the DNA polymorphism detected by BcilI site in intron 18 of the factor VIII gene was informative for 38% families studied, the AlwNI/intron 7 polymorphism provided additional information (4%). The carrier status of the remaining 58% could be determined utilizing the other polymorphisms suggested by strategy. The two polymorphic sites used combined with the other polymorphisms, intragenic and extragenic, can generate levels of informativeness greater than 98%. We concluded that the strategy for carrier testing would be a good alternative in genetic counselling for hemophilia A, but its limitations must be carefully taken into account.

Chile↗
PubMed1995

Platelet autoantibodies in patients with chronic liver disease.

The thrombocytopenia in chronic liver disease (CLD) has been attributed mainly to hypersplenism, although other factors such as reduced mean life span with increased platelet turnover have also been demonstrated. Immunological abnormalities have been described in the pathogenesis and progression of CLD. In this sense, many studies have reported elevated levels of platelet associated IgG (PAIgG) in patients with CLD, and it has been suggested that PAIgG could represent true antiplatelet antibody. In this study we used a glycoprotein (GP)-specific immunoassay (MACE) to determine whether PAIgG or circulating antiplatelet antibodies, reacted against the GPIIb/IIIa or GPIb/IX complexes, in patients with CLD. Thirty-six patients with CLD of diverse etiology were studied (20 female, mean age 53 years, range 38-75 years). 23 out of 36 patients (64%) had anti-GP antibodies in MACE. Particularly, 12 had anti-GPIb, 4 anti-GPIIb/IIIa, and 7 had both types of autoantibodies. The existence of these anti-GP antibodies was not related with the blood platelet count or etiology of CLD. These data show that in patients with CLD of diverse origin, there is a high prevalence of autoantibodies reacting specifically with platelet membrane GP, which constitutes the first evidence of the specific nature of platelet-bound IgG in CLD. These findings suggest that in patients with CLD, an immune mechanism may participate in inducing or aggravating the thrombocytopenia.

Adult↗
PubMed1995

Comparative ultrastructure and immunolabeling of MHC-II antigens of alveolar macrophages obtained from patients with paracoccidioidomycosis and other lung diseases.

Samples of alveolar macrophages (AM) obtained by bronchoalveolar lavage from patients with either paracoccidioidomycosis, silicosis, sarcoidosis, or allergic alveolitis were investigated by electron microscopy and immunocytochemistry to compare cellular ultrastructure and expression of MHC-II antigens in the AM cell surface. All samples of AM obtained from patients with these pathologies showed heterogeneous structural features. Although, this morphological diversity is also present in AM of healthy donors, our observations seem to indicate that in the diseases studied this morphofunctional diversity is associated with additional ultrastructural characteristics inherent to each disease. In paracoccidioidomycosis the proportion of vacuolated macrophages is significantly lower than in other diseases; this might indicate that in paracoccidioidomycosis the proportion of activated AM is smaller. We observed significant differences in the expression of MHC-II antigens. Silicosis, sarcoidosis, and allergic alveolitis do not differ significantly in the quantity of immunolabeled AM or in the distribution of the label. The percentage of AM from paracoccidioidomycosis that exhibit the MHC-II molecule is very low with poor immunolabeling. In this disease the low expression of the MHC-II molecule could be related to a decrease of the antigen presenting function by AM.

Alveolitis, Extrinsic Allergic↗
PubMed1995

Administration of subtoxic doses of t-butyl alcohol and trichloroacetic acid to male Wistar rats to study the interactive toxicity.

Tertiary butyl alcohol and trichloroacetic acid (TCA) are known to be contaminants in drinking water. In order to evaluate the interactive toxicity of t-butyl alcohol (TBA) with TCA, young male Wistar rats were dosed through water at a dose level of TBA (0.5% v/v), 25 ppm TCA and a combined dose of TBA+TCA (0.5% v/v TBA, 25 ppm TCA) for a period of 10 weeks ad libitum and were maintained on normal diet. The control animals received plain water and normal diet. There was remarkable loss of body weight and significantly decreased liver triglycerides in the treatment groups in the order of TBA+TCA, TCA, TBA and increased liver weights were observed. Serum succinate dehydrogenase (SDH) levels were significantly increased in TCA- and TBA+TCA-treated groups. There was no significant change in serum alanine (GPT), aspartate (GOT) aminotransferase, serum alkaline (ALP) and acid (ACP) phosphatase levels as well as liver glutathione (GSH) and liver and serum cholesterol levels in the treated groups. But serum triglycerides, liver glycogen, serum glucose (only in TBA- and TCA-treated animals) were significantly high in the treated groups. Lipid peroxidation measured by diene conjugation was significant in TBA+TCA-treated group and kidney GSH levels were significantly low in the treated groups. These results show that interaction of TBA+TCA does bring about alteration in biochemical parameters which may play a pivotal role in toxic responses on long-term exposure.

Alanine Transaminase↗
PubMed1995

Thickening of the pituitary stalk: a finding suggestive of intrasellar tuberculoma? Case report.

We describe the case of a patient with an exclusively intrasellar mass, disclosed because of a left sixth nerve palsy and headaches. No other manifestation of disease, namely, endocrinological, was present. The lesion was approached transsphenoidally, and the pathological examination revealed a tuberculoma. Complete removal was achieved, and the patient started postoperative antituberculous therapy. In some circumstances, thickening of the infundibulum and the pituitary stalk could preoperatively suggest the diagnosis of hypophysial tuberculoma.

Antitubercular Agents↗