62 resultados para Acute Disease

em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"


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The effect of viable splenic lymphoid cells and their constituents (filtrate) on carrageenan-induced acute pleurisy was investigated in rats. Suspensions of lymphoid cells administered intravenously to recipients just prior to initiation of pleurisy enhance both the volume of exudate and cell accumulation in the pleural cavity 3 h after the irritation. Similar results were observed when filtrate of disrupted lymphoid cells was injected either 30 or 5 min before the carrageenan, but not when administered 30 min afterwards. Suspensions of bone marrow cells, on the contrary, were ineffective in producing an enhancement of the parameters studied. When administered into the pleural cavity together with carrageenan, the lymphoid cell filtrate augmented the inflammatory response to the irritant. Nevertheless, it was ineffective, per se, to elicit any local change. It is suggested that lymphoid cells may play a pro-inflammatory role in the initiation of the process by enhancing both the fluid and the cellular components of inflammation.

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A simple and sensitive chemiluminescence assay for the demonstration of the activity of intracellular myeloperoxidase (MPO) is described, which is useful for the distinction between myeloid and lymphoid commitment in blasts from acute leukemia patients. When the cut-off point was settled at 13 mV of chemiluminescence all cases of acute myeloid leukemia (AML) were distinguished from those of acute lymphoid leukemia. In addition, this technique was able to demonstrate MPO activity in AML poorly differentiated (FAB-M0) which usually does not stain for MPO in classical cytochemistry preparations and could be negative also by immunocytochemistry with anti-MPO monoclonal antibody. Therefore the method here described presented a higher sensitivity than the immunocytochemistry procedure with anti-MPO.

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Neurocysticercosis (NCC) is an infection of the central nervous system (CNS) caused by the metacestode larval form of the parasite Taenia sp. Many factors can contribute to the endemic nature of cysticercosis. The inflammatory process that occurs in the tissue surrounding the parasite and/or distal from it can result from several associated mechanisms and may be disproportionate with the number of cysts. This discrepancy may lead to difficulty with the proper diagnosis in people from low endemic regions or regions that lack laboratory resources. In the CNS, the cysticerci have two basic forms, isolated cysts (Cysticercus cellulosae = CC) and racemose cysts (Cysticercus racemosus = CR), and may be meningeal, parenchymal, or ventricular or have a mixed location. The clinical manifestations are based on two fundamental syndromes that may occur in isolation or be associated: epilepsy and intracranial hypertension. They may be asymptomatic, symptomatic or fatal; have an acute, sub-acute or chronic picture; or may be in remission or exacerbated. The cerebrospinal fluid (CSF) may be normal, even in patients with viable cysticerci, until the patients begin to exhibit the classical syndrome of NCC in the CSF, or show changes in one or more routine analysed parameters. Computed tomography (CT) and magnetic resonance imaging (MRI) have allowed non-invasive diagnoses, but can lead to false negatives. Treatment is a highly controversial issue and is characterised by individualised therapy sessions. Two drugs are commonly used, praziquantel (PZQ) and albendazole (ABZ). The choice of anti-inflammatory drugs includes steroids and dextrochlorpheniramine (DCP). Hydrocephalus is a common secondary effect of NCC. Surgical cases of hydrocephalus must be submitted to ventricle-peritoneal shunt (VPS) immediately before cysticidal treatment, and surgical extirpation of the cyst may lead to an absence of the surrounding inflammatory process. The progression of NCC may be simple or complicated, have remission with or without treatment and may exhibit symptoms that can disappear for long periods of time or persist until death. Unknown, neglected and controversial aspects of NCC, such as the impaired fourth ventricle syndrome, the presence of chronic brain oedema and psychic complaints, in addition to the lack of detectable glucose in the CSF and re-infection are discussed. © 2011 Bentham Science Publishers.

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OBJETIVO: Conhecer os efeitos do diabetes e o impacto de seu tratamento medicamentoso em curto e longo prazo sobre os vasos da coróide e membrana de Bruch. MÉTODOS: Foram estudados 30 ratos Wistar, divididos em 3 grupos experimentais: grupo controle (GC), grupo diabético (GD) e grupo diabético tratado (GT), estudados 1 mês (momento M1) e 12 meses (momento M2) após o início do experimento. O diabetes foi induzido por aloxana endovenosa, na dose de 42 mg/kg. O GT foi tratado com hipoglicemiante oral (acarbose) e insulina subcutânea. Após o sacrifício, os olhos foram preparados para exame ao microscópio eletrônico de transmissão, interessando a ultra-estrutura da membrana de Bruch e os vasos da coróide. RESULTADOS: O exame ultra-estrutural da coróide dos ratos diabéticos mostrou depósitos na membrana de Bruch, acúmulo de vesículas, glicogênio e corpos densos no citoplasma das células endoteliais. O grupo mais afetado foi de ratos diabéticos de 12 meses (GDM2). Os animais com menor intensidade de alterações foram os ratos tratados por 12 meses (GTM2). CONCLUSÃO: Os ratos diabéticos desenvolveram alterações degenerativas na membrana de Bruch e vasos da coróide. Estas alterações foram mais evidentes nos animais submetidos à doença crônica, mas também ocorreram agudamente. O tratamento a curto prazo não foi capaz de evitar os processos degenerativos. A longo prazo, o tratamento inibiu a progressão destes processos.

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The primary complex like Ghon was observed in a child's clinical roentgenographic study. C.S., white, male, 6 years old, was born in Curitiba (PR), Brazil and living in Guaratingueta (SP), Brazil, developed common cold, bimodal diary fever, chills, shake and sweats. Dyspnea, cough with general lymphadenopathy. Foot and right shoulder arthralgias. Six months ago visited a cave, equitation practice, dog and cat contacts and no transfusion, frontal sweats, fever (38.4 degrees C). T.A. was 8/6, tachycardia in generalized lymphadenopathy. Cardiopulmonary system was normal, mesogastric tumoral mass, hepatosplenomegaly and no ascites. Bone marrow with eosinophilia; nodule demonstrated presence of P. brasiliensis, hypoalbuminemia; hyperglobulinemia; anemia; leukocytosis with eosinophilia. Immunodiffusion with exoantigen 43 kd of P. brasiliensis was 1/32. Primary complex like Ghon was observed in interstitial pneumonia followed by mediastinal and mesogastric mass (35 to 40 days). Clavicular osteolytic lesions (45 to 60 days) appeared during paracoccidioidomycosis therapy. Recovery was observed 2 months after treatment of acute infantile paracoccidioidomycosis.

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IgG, IgM and IgA antibodies to GP43 (glycoprotein fraction of Paracoccidioides brasiliensis) were measured by ELISA in 63 samples from 23 patients with paracoccidioidomycosis before and twice after chemotherapy was started. Antibodies against P. brasiliensis were detected by indirect immunofluorescence (IF) (IgG, IgM and IgA isotypes), counterimmunoelectrophoresis (CIE) and complement fixation. Two control groups composed of 19 healthy individuals and 12 patients with other diseases (six with histoplasmosis, three with tuberculosis and three with other mycoses). The highest efficiency percentages were found with IgG and IgA- ELISA (100%), IgG-IF (96.2%), CIE (94.4%) and the lowest with CF (75.9%). Highest positive and negative predictive values (100%) were observed for IgG and IgA ELISA. IgG and IgM-ELISA antibodies are more often found in patients with acute than chronic disease (P = 0.01). Four to six months after treatment follow-up showed decreased levels of IgG and IgM-ELISA for acute cases and decreased titres of CIE for chronic cases in relation to pretreatment levels. This study suggests that IgG-ELISA anti-GP43 represents a good marker to monitor clinical response to therapy.

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BAKGROUND AND OBJECTIVES: Negative pressure pulmonary edema has been defined as non-cardiogenic edema, with transudation of fluid to the interstitial space of the lungs due to an increase in negative intrathoracic pressure secondary to obstruction of the upper airways. This is the case of a healthy patient who underwent general anesthesia and developed acute pulmonary edema after extubation. CASE REPORT: A 23-year old female patient, physical status ASA II, underwent gynecologic videolaparoscopy under general anesthesia. The procedure lasted 3 hours without intercurrence. After extubation the patient developed laryngeal spasm and reduction in oxygen saturation. The patient improved after placement of an oral cannula and administration of oxygen under positive pressure with a face mask. Once the patient was stable she was transferred to the recovery room where, shortly after her arrival, she developed acute pulmonary edema with elimination of bloody serous secretion. Treatment consisted of elevation of the head, administration of oxygen via a face mask, furosemide and fluid restriction. Chest X-ray was compatible with acute pulmonary edema and normal cardiac area. Electrocardiogram (ECG), echocardiogram and cardiac enzymes were normal. The condition of the patient improved and she was discharged from the hospital the following day, asymptomatic. CONCLUSIONS: Acute pulmonary edema associated with obstruction of the upper airways can aggravate surgical procedures with low morbidity, affecting mainly young patients. Early treatment should be instituted because it has a fast evolution and, in most cases, resolves without lasting damages. © Sociedade Brasileira de Anestesiologia, 2008.

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Coumarins represent an important class of phenolic compounds with multiple biological activities, including inhibition of lipidic peroxidation and neutrophil-dependent anion superoxide generation, anti-inflammatory and immunosuppressor actions. All of these proprieties are essential for that a drug may be used in the treatment of inflammatory bowel disease. The present study examined intestinal anti-inflammatory activity of coumarin and its derivative, the 4-hydroxycoumarin on experimental ulcerative colitis in rats. This was performed in two different experimental settings, i.e. when the colonic mucosa is intact or when the mucosa is in process of recovery after an initial insult. The results obtained revealed that the coumarin and 4-hydroxycoumarin, at doses of 5 and 25 mg/kg, significantly attenuated the colonic damage induced by trinitrobenzenesulphonic acid (TNBS) in both situations, as evidenced macroscopically, microscopically and biochemically. This effect was related to an improvement in the colonic oxidative status, since coumarin and 4-hydroxycoumarin prevented the glutathione depletion that occurred as a consequence of the colonic inflammation. © 2008 Pharmaceutical Society of Japan.

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Introduction: Obstructive sleep apnea syndrome is related to cardiopulmonary complications in children. It is important to know its patophysiology and possible complications to help reduce risks in this group. Aims: To report three cases of severe cardiorespiratory complications of obstructive sleep apnea managed in the intensive care unit (ICU). Case report: Two children with no previous diagnosis of obstructive sleep apnea syndrome suffered acute congestive heart failure and acute lung oedema with need of ICU and improved after adenotonsillectomy. In a third case, the patient had acute lung oedema as a complication after adenotonsillectomy. Conclusions: Paediatricians and otolaryngologists must be aware of the clinical manifestations of severe sleep apnea. Early referring to treatment and special attention at pre and post surgical periods are essentials to avoid serious complications.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The number and activity of natural killer (NK) cells were studied in 34 untreated patients with paracoccidioidomycosis, 20 with the chronic form of the disease and 14 with the acute form. NK cells were detected with monoclonal antibody Leu-11c and the cytotoxic activity was measured using a single cell assay against K562 target cells. Both groups of patients had an increased number of circulating NK cells, their cytotoxic activity being significantly lower than in the healthy controls. These findings may be of importance in the immunological disturbances associated with paracoccidioidomycosis since NK cells exert important immune effector functions and may play a role in resistance against Paracoccidioides brasiliensis.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Desde a década de 1970 não se notificavam casos autóctones de doença de Chagas aguda em São Paulo. em março de 2006 a Vigilância Epidemiológica registrou óbito por doença de Chagas aguda, em Itaporanga, de paciente de seis anos de idade. Exame histopatológico post mortem realizado no Hospital das Clínicas da Faculdade de Medicina de Botucatu confirmou o diagnóstico. Consultamos prontuários de hospitais e entrevistamos profissionais de saúde envolvidos além de familiares do paciente. Descrevemos medidas adotadas in loco para identificar a via de transmissão, reservatórios e vetores. Discutimos as possíveis fontes de infecção. Na região não foram identificados outros casos humanos, vetores ou reservatórios vertebrados infectados por Trypanosoma cruzi. Salientamos a importância de manter a vigilância, mesmo em áreas onde a transmissão de doença de Chagas está interrompida e naquelas ainda infestadas por triatomíneos. Deve-se admitir a hipótese diagnóstica de doença de Chagas quando observados: edema palpebral (uni ou bilateral), insuficiência cardíaca, miocardite, pericardite, anasarca, quadros similares aos de síndrome nefrótica ou glomerulonefrite sem causas outras aparentes, em pacientes com dados epidemiológicos positivos. Encontro, mesmo em raras ocasiões, de triatomíneos na região ou ainda contato com alimento contaminável com formas infectantes de T. cruzi.