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Biomedical subjects

F A Soares

Publications and source records attributed to F A Soares.

At least 37 records · Page 2Linked to original sources

AIDS-related lymphoma in Brazil. Histopathology, immunophenotype, and association with Epstein-Barr virus.

The occurrence of malignant lymphoma is an increasingly important cause of morbidity and mortality in AIDS patients. The incidence of AIDS-related lymphoma in some developing countries such as Brazil is increasing as the survival of HIV infection has improved. Although there is a clear association between several types of immunodeficiency-related lymphomas and Epstein-Barr virus (EBV), the association of EBV infection in AIDS-related lymphoma in Brazil, where the incidence of AIDS is high, is unknown. Formalin-fixed, paraffin-embedded tissue from 24 cases of AIDS-related lymphoma in Brazil were analyzed for morphologic classification, immunophenotype, and EBV association using in situ hybridization studies with an EBV-EBER1 biotinylated probe. Twenty cases of AIDS-related lymphoma were classified as non-Hodgkin's lymphoma and four cases were Hodgkin's disease. Eleven non-Hodgkin's lymphomas were classified as diffuse large cell type, five cases were small non-cleaved cell, Burkitt-type, and four cases were large cell immunoblastic non-Hodgkin's lymphoma. Eighteen cases were of B-cell phenotype; one was a T-cell lymphoma, and one was classified as null. Epstein-Barr virus (EBV) was demonstrated in the majority of tumor cells of 11 of 20 (55%) of the cases non-Hodgkin's lymphomas and in 3 of 4 (75%) cases of Hodgkin's disease. AIDS-related lymphomas in Brazil are usually of large cell/immunoblastic type, but Hodgkin's disease is also seen. Both non-Hodgkin's lymphoma and Hodgkin's disease are often associated with EBV infection. The non-Hodgkin's lymphoma is predominantly of B-cell phenotype.

Adult↗

Massive intracranial immature teratoma. Report of a case with polyhidramnios and intense pelvic pain.

A case of massive intracranial immature teratoma in a female stillborn is reported. She was the product of the second pregnancy of a 25-year-old healthy woman. The pregnancy was unremarkable until the 25th week of gestation when the mother noticed a rapid enlargement of her abdomen and intense pelvic pain. Because of the pain, a cesarean section was indicated, and a stillborn weighing 2750g with macrocephaly was delivered. The cranial contents weighed 1350g and showed a huge tumoral mass with only a rim of normal brain. A histologic diagnosis of immature teratoma was made. Massive intracranial teratomas are rare tumors and their occurrence in intrauterine life is even rarer. Their histogenesis is unknown, and there is no explanation for their continuous growth during embryogenesis. A prenatal diagnosis of this rare condition can be made by ultrasound, computed tomography, or magnetic resonance imaging.

Adult↗

Severe myocarditis and esophagitis during reversible long standing Chagas' disease recrudescence in immunocompromised host.

An unusual form of reagudization of Chagas' disease, from its indeterminate phase, was documented in an immunocompromised patient. Long-standing progressive visceral aggression due to extensive intracellular proliferation of T. cruzi manifested by severe isolated right ventricular failure and esophageal ulcerations. Antiparasite chemotherapy was effective in the control of the disease.

Adult↗

Quantification and morphologic demonstration of reactive oxygen species produced by Walker 256 tumor cells in vitro and during metastasis in vivo.

BACKGROUND: Pulmonary endothelial damage can be caused by agents that generate oxidants, e.g., bleomycin, hyperoxia, neutrophils or x-irradiation. In animals with intravascular cancer cells, there is increased tumor cell arrest and the subsequent formation of metastatic tumors at the sites of such endothelial injury. We have previously shown that Walker 256 (W256) tumor cells, stimulated with phorbol esters (phorbol 12-myristate 13 acetate) or the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine, generate chemiluminescence that is inhibitable by catalase. Such activated cells can injure cultured endothelial monolayers. The purpose of the present study was to quantify and obtain morphological confirmation of the generation of reactive oxygen species by W256 cells in vitro, and to determine if this phenomenon could be morphologically detected in vivo during the metastatic process. EXPERIMENTAL DESIGN: The production of oxidants from W256 cells was quantitated in vitro by the scopoletin fluorescence assay, by a ferrithyiocyanate colorimetric assay (Thurman reaction), and confirmed morphologically, in vitro and in vivo, by the formation of cerium perhydroxide (Ce[OH]2OOH) deposits from cerium chloride (CeCl3). To demonstrate generation of reactive oxygen species in vivo, we examined W256 cells collected from the pulmonary circulation and at sites of spontaneous metastasis in the lung after intramuscular tumor transplantation, or cells arrested in the lungs after intravenous injection. The specificity of the CeCl3 reaction was confirmed by blocking in the presence of catalase. RESULTS: As measured by the loss in scopoletin fluorescence and by generation of ferrithiocyanate 5 x 10(6) activated W256 cells produced an equivalent of 18 nM of H2O2 per hour A. Ce-[OH]2OOH deposits were identified in vitro on the surface of W256 cells, and at points of attachment between W256 cells and cultured endothelial cell monolayers. In vivo, CeCl3-derived deposits were seen on circulating W256 cells and on W256 cells that had arrested in the lungs following the intravenous injection of activated or non-activated W256 cells, or in spontaneous pulmonary metastases which formed after intramuscular tumor inoculation. Pretreatment of tumor-bearing animals with phorbol 12-myristate 13 acetate increased the number of CeCl3-derived deposits more than 2 fold. Catalase inhibited the formation of the electron-dense deposits in vitro and in vivo. CONCLUSIONS: These data provide morphologic evidence that cancer cells can produce reactive oxygen species in vivo and suggest that free radicals might contribute to endothelial damage during the metastatic process.

Animals↗

Thoracic lymph node metastasis and carcinomatous lymphangitis after inoculation of Walker 256 tumor through the trachea.

1. Experimental models of carcinomatous lymphangitis have not been described. This is an important clinical entity which usually results in the patients' death, although its natural history is still controversial. This study was undertaken to investigate whether the pattern of lung involvement after Walker 256 tumor inoculation through the trachea is a good model of carcinomatous lymphangitis. 2. Fifty male Wistar rats were inoculated through the trachea with 2.5 x 10(6) Walker 256 tumor cells and killed in groups of 5 animals each at 6 h and on days 1, 3, 7, 14, 21, 28, 35, 45, and 60 of the experiment. The lungs and thoracic lymph nodes were examined by light microscopy. 3. There were no tumors in the 25 animals killed before the 21st day of the experiment. The remaining 25 rats were sacrificed after 3 weeks of the experiment; 52% of them displayed thoracic lymph node metastases, and 40% developed a mild carcinomatous lymphangitis. The lung involvement did not correlate with respiratory distress, tumor dissemination or additional histological abnormalities. 4. We conclude that invasion of the lung is possible after intratracheal tumor cell inoculation, and that spreading follows a lymphatic pattern. This finding establishes this approach as a viable experimental model of carcinomatous lymphangitis. New approaches to increase the intensity and frequency of lung involvement, as well as the development of respiratory distress should be pursued in order to improve the efficiency of this model.

Animals↗

Pulmonary tumor embolism to arterial vessels and carcinomatous lymphangitis. A comparative clinicopathological study.

A prospective study of 222 consecutive autopsies of cancer cases was undertaken to investigate whether carcinomatous lymphangitis and pure arterial tumor embolism of the lungs are different clinicopathological entities. The lungs were removed as a block and 15 sections (three from each lobe) were analyzed. A protocol containing clinical (ie, dyspnea, cyanosis, right ventricular failure, engorgement of jugular veins, and peripheral edema as main cause of death) and morphological (ie, right ventricle thickness and dilatation, vascular sclerosis, pulmonary infarct) data were carefully recorded in each case. Arterial tumor embolism was detected in 19 cases (8.5%) and carcinomatous lymphangitis in 44 cases (19.8%). We found no differences in relation to signs and symptoms of arterial tumor embolism and carcinomatous lymphangitis, but respiratory distress as the main cause of death was significantly more frequent in the cases with arterial involvement by tumor emboli. Morphologically, however, right ventricular hypertrophy-dilatation, histological signs of pulmonary hypertension, and hemorrhagic infarcts were more prevalent in the cases with arterial tumor embolism. This study permits us to conclude that although arterial tumor embolism and carcinomatous lymphangitis are clinically similar diseases, they are morphologically different entities. Our results suggest that the most probable pathogenesis of pulmonary endarteritis and subsequent pulmonary hypertension is the injury to the vascular endothelium caused by the arrest of tumor emboli.

Carcinoma↗

Pulmonary leukostasis without hyperleukocytosis: a clinicopathologic study of 16 cases.

Pulmonary leukostasis is a serious, almost always fatal, complication usually reported to occur in patients with acute granulocytic leukemias when the peripheral white blood cells exceed 50,000/mm3. We report a clinicopathologic study of 16 leukemic patients with pulmonary leukostasis and with less than 50,000/mm3 circulating leukocytes. The results demonstrated that hyperleukocytosis per se cannot be the cause of pulmonary leukostasis, but that other factors, such as the presence of circulating blasts and the affinity of neoplastic cells for the pulmonary endothelium, may be related to the development of acute respiratory distress in patients with leukemia.

Adolescent↗

Increased numbers of pulmonary megakaryocytes in patients with arterial pulmonary tumour embolism and with lung metastases seen at necropsy.

AIMS: To compare the number of pulmonary megakaryocytes in patients with local malignant disease without metastases with the numbers in patients with pulmonary tumour emboli without lung metastases and with those with pulmonary metastases. METHODS: The prevalence of pulmonary megakaryocytes was studied in 40 necropsies divided into four groups of 10 cases each: normal lungs (I); localised malignancies (II); pulmonary tumour embolism without lung metastases (III); pulmonary tumour embolism and lung metastases (IV). Five fragments (one of each pulmonary lobe) of tissue lung were collected, embedded in paraffin wax, sectioned, and stained by an immunohistochemical method to detect factor VIII related antigen. The number of megakaryocytes was evaluated in 500 high power fields/case. RESULTS: No differences were observed between groups I and II or between groups III and IV, but there was a 3.5-fold increase in the number of megakaryocytes in the groups with pulmonary tumour embolism or lung metastases compared with those with local neoplasms or normal lungs. CONCLUSIONS: An increased number of pulmonary megakaryocytes correlated with the presence of tumour cells in the microcirculation of the lungs or parenchymal metastases, but not with local malignancies without lung disease. The permanent siting of tumour emboli may stimulate megakaryocytes to migrate to the lungs, and may increase the release of platelets into the pulmonary circulation.

Cell Count↗

A prospective study of the morphological aspects of tumor involvement of the pulmonary vessels.

A prospective morphological study of tumor involvement of the pulmonary vessels (TIPV) was undertaken on 203 consecutive autopsy cases of malignancies. The lungs were removed as a block and 15 sections (3 from each lobe) were analyzed. Site of origin, histological type and staging of the tumor, topographic distribution of the tumor emboli in the lungs, right ventricular hypertrophy and dilatation, pulmonary infarct, pulmonary vascular sclerosis and lung metastases were recorded in each case. TIPV was detected in 84 (41.4%) cases, the highest frequency reported until now. In 28 cases, TIPV was considered to be the main cause of death. The breast, liver, and pancreas were primary sites in more than 50% of the cases in which TIPV was observed. TIPV was more prevalent in epithelial neoplasms and showed a strong correlation with advanced disease. There was no significant difference among topographic regions of the lungs. The cases with TIPV were correlated with a high frequency of right ventricular hypertrophy and dilatation, vascular sclerosis and pulmonary metastases but not with pulmonary infarcts.

Female↗

Clinical aspects of tumour involvement of the pulmonary vessels.

The involvement of the pulmonary vessels by tumour emboli may lead to a clinical picture defined as 'subacute cor pulmonale'. Information about this syndrome has been limited to case reports and a few series. A study of 214 autopsied cancer patients was undertaken to investigate the clinical signs and symptoms of tumour involvement of the pulmonary vessels (TIPV). The lungs were removed as a block and 15 sections (3 from each lobe) were analyzed. Clinical data about right ventricular failure, dyspnoea, cough, pleuritic chest pain, cyanosis, engorgement of jugular veins, peripheral oedema, haemoptysis and haemoptoic sputum were obtained from the medical records of each patient. Tumour emboli were detected in 89 cases, and no respiratory symptoms were recorded in 39. The presence of dyspnoea and cyanosis were highly significant in the group with TIVP, and right ventricular failure and peripheral oedema showed slight significant differences between the patients with and without TIPV. The classical picture of subacute cor pulmonale was observed in 13 patients and TIPV was considered to be the main cause of death in 29 cases. Our results indicate that although the development of subacute cor pulmonale was rare in patients with cancer, TIPV may be suspected when the patient presents respiratory distress and should be included in the differential diagnosis of dyspnoea in cancer patients.

Humans↗

Fulminant disseminated pulmonary adiaspiromycosis in humans.

A case of fulminant disseminated pulmonary adiaspiromycosis is reported. The patient, a 35-year-old black male farm worker, presented with a four-week history of generalized weakness, unproductive cough, evening fever, and a weight loss of 8 kg. He died 12 days after hospitalization of respiratory failure due to granulomatous lung disease. The clinical and radiographic findings were indistinguishable from those of miliary tuberculosis. Microscopic examination of material obtained at autopsy revealed the large fungus characteristic of adiaspiromycosis in the center of suppurative granulomas throughout the lungs. This is believed to be the first fatal case of pulmonary adiaspiromycosis reported in humans, and it may have been occupationally acquired.

Adult↗

Accumulation of brown adipose tissue and nutritional status. A prospective study of 366 consecutive autopsies.

Increased amounts of brown adipose tissue have been reported to occur in association with several diseases. The objective of the present study was to determine whether brown adipose tissue accumulation is related to nutritional status. Histologic sections of periadrenal tissue prospectively obtained at consecutive autopsies from 366 adults were examined. The cases were separated into three groups: malnourished (101 autopsies), normotrophic (128 autopsies), and obese (137 autopsies), according to the Quetelet index. Of these patients, 89 had brown adipose tissue accumulation, 35 were malnourished, 32 were normotrophic, and 22 were obese. The results showed a correlation between brown adipose tissue and patient nutritional status and a higher brown adipose tissue accumulation in malnourished patients. Cardiovascular disease was the most common type of illness present in the cases with brown adipose tissue accumulation.

Adipose Tissue, Brown↗

Pulmonary tumor embolism to alveolar septal capillaries. An unusual cause of sudden cor pulmonale.

Although metastatic spread of tumor to the lungs is common, subsequent production of cor pulmonale is not. The involvement of pulmonary alveolar capillaries causing sudden cor pulmonale is very rare. We describe a patient who presented with chest pain and sudden shortness of breath. Autopsy disclosed diffuse pulmonary microembolism to septal capillaries caused by tumor cells from a squamous cell carcinoma of the cervix. To our knowledge, this is the second report of this kind of pulmonary tumor embolism.

Carcinoma, Squamous Cell↗

Pulmonary tumour embolism from squamous cell carcinoma of the oesophagus.

Pulmonary tumour embolism and subacute "cor pulmonale" have been reported in association with tumours of different origins. Even though these features were first described in a patient with carcinoma of the oesophagus, the frequency and importance of oesophageal tumours as the source of pulmonary tumour embolism have not been studied. In the present investigation, the lungs of 16 autopsied patients with squamous cell carcinoma of the oesophagus were studied prospectively. The lungs were removed as a block and 15 sections (3 from each lobe) were analysed. Pulmonary tumour embolism was detected in 7 cases. The lymphatic vessels were involved in all of them, and were associated with arteries and arterioles in 2. 2 patients presented a classical picture of subacute cor pulmonale, and dyspnoea was present in 3 other cases. The present study permitted us to conclude that carcinomas of the oesophagus frequently evolve toward carcinomatous lymphangitis and that pulmonary tumour embolism should be included in the differential diagnosis of the dyspnoea presented by the patients.

Carcinoma, Squamous Cell↗