970 resultados para parathyroid hyperplasia


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Objectivo: É fundamental os enfermeiros identificarem o tecido de hipergranulação e compreenderem o que pode traduzir em termos do ambiente biológico da ferida. É uma entidade comum nas feridas complexas, que se for gerida consegue-se controlar a cicatrização que se encontra estagnada. Com esta Revisão Sistemática da Literatura apoiada num estudo de caso, identificaram-se as intervenções de Enfermagem para a gestão de feridas complexas com tecido de hipergranulação. Metodologia: Foi efectuada uma pesquisa no motor de busca EBSCO, seleccionando bases de dados específicas e utilizados os descritores: “HYPERGRANULATION” or “OVERGRANULATION” or “HYPERTROPHIC GRANULATION” oy “HYPERPLASIA OF GRANULATION TISSUE” and “WOUND” and “ASSESSMENT”. Recorreu-se ao método PI©O e seleccionados um total de 13 artigos. Conclusão: Os cuidados de Enfermagem, o modus operandi, face às feridas com tecido de hipergranulação é ainda algo ambíguo e empirista. Com base nas evidências científicas existentes sobre a problemática definiram-se directrizes para a prática clínica.

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In 9 of 491 patients (1.8%) who underwent prostatic arterial embolization (PAE) for benign prostatic hyperplasia from March 2009-November 2013, prostatic arteries arose from the external iliac artery via an accessory obturator artery (AOA). Computed tomography angiography performed before the procedure identified the variant and allowed planning before the procedure. The nine AOAs were catheterized from a contralateral femoral approach. Bilateral PAE was technically successful in the nine patients. There was a mean decrease in international prostate symptom score of 6.5 points and a mean prostate volume reduction of 15.1% (mean follow-up, 4.8 mo) in the nine patients.

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The aim of this study is to report a clinical case of asymptomatic female Caucasian children with torpedo maculopathy. A 5-year-old girl was referred to our clinic for routine evaluation. The ophthalmic examination revealed best-corrected visual acuity of 20/20 in both eyes, without any changes in the biomicroscopy. Fundus examination showed normal findings in one eye, whereas in the contralateral eye it disclosed, in the temporal sector of the macular region, a whitish, atrophic, oval chorioretinal lesion with clearly defined margins. Posterior evaluations documented the stability of the lesion. Torpedo maculopathy diagnosis is based on its characteristic shape and peculiar location. The differential diagnosis has to be established versus choroidal lesions (melanoma and nevus), congenital or iatrogenic hyperplasia of the retinal pigment epithelium (RPE) and particularly versus the congenital pigmented lesions associated with Gardner's syndrome.

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Os autores fazem a revisão da clínica, do registo da sintomatologia e impacto na qualidade de vida, dos meios auxiliares ao diagnóstico e das atitudes terapêuticas da Hiperplasia benigna da Próstata. Fundamentados nestes dados propõem Orientações Terapêuticas e Recomendações, para quando e como enviar os doentes portadores desta patologia a Urologia. Assim, segundo os critérios definidos neste trabalho, devem ser enviados à Urologia os doentes com sintomatologia importante ou grave, idade inferior a 50 anos, antecedentes de diabetes ou alterações neurológicas, micção francamente alterada, globo vesical, toque rectal com palpação prostática suspeita de neoplasia, hematúria, infecção urinária, insuficiência renal, ou PSA> 4 nglml para idade inferior a 70 anos.

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Os autores descrevem um caso de um doente de 23 anos com linfoma de 1-Iodgkin de celularidade mista num estádio II-B que após quimioterapia desenvolveu uma massa mediastínica, cuja histologia revelou tratar-se de uma hiperplasia do timo.

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Severe chronic kidney disease may lead to disturbances, such as hyperphosphatemia, increased secretion of fibroblast growth factor -23 (FGF -23) and vitamin D deficiency. These may increase plasmatic levels of parathyroid hormone, and decrease plasmatic levels of calcium. Altogether, these may contribute to the development of secondary hyperparathyroidism, and to abnormalities in mineral metabolism. Kidney transplantation is the best option to improve longevity and quality of life in end -stage chronic kidney disease patients. Vitamin D deficiency has been associated with cardiovascular disease, which is the leading cause of death in chronic kidney disease. Therefore, diagnosing this deficiency may be pivotal for minimizing mortality in chronic kidney disease, because pharmacological treatments for this deficiency may be prescribed. Calcitriol is indicated for the treatment of vitamin D deficiency, both in chronic kidney disease and in kidney transplanted patients. However, calcitriol may increase the plasmatic levels of calcium and phosphorous, which can lead to vascular calcifications, that have been associated with cardiovascular mortality. Selective vitamin D receptor activators are indicated for the treatment of vitamin D deficiency in chronic kidney disease. These have the advantage of being associated with lower increases of plasmatic levels of calcium and phosphorous. These drugs also seem to have additional effects that may minimise patient morbidity and mortality, especially due to potentially reducing cardiovascular events. Unfortunately, there are few studies about the use of these drugs in kidney transplanted patients. Here we present a review about the physiology of vitamin D, the consequences of its deficiency in chronic kidney disease and in kidney transplanted patients, and about the diagnosis and treatment of this deficiency. Finally, we discuss the new line of research about the efficacy and safety of selective vitamin D receptor activators in kidney transplanted patients.

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Lesions involving the intra-hepatic biliary ducts in schistosomiasis have been reported in the literature, both in mice and man, but there are no data concerning their quantitative, evolutionary or post curative chemotherapeutic aspects on record. In order to obtain such data an investigation on this subject was attempted. Mice infected with 50 Schistosoma mansoni cercariae were submitted to a liver biopsy at the 9th week post-infection, and treated with 400mg/bw praziquantel immediately afterwards. Infected and non-infected controls were submitted to the same procedures. By 19 weeks from cercarial exposure all surviving animals were sacrificed. The biliary ducts were counted on histological sections and the results were expressed as biliary ducts/portal spaces. This quantitative evaluation was compared with that from normal controls and revealed hyperplasia as the main biliary duct change (p<0.007) in schistosomiasis. Hyperplastic changes underwent only mild partial and not statistically significant regression after specific chemotherapy (p>0.05). Infected and untreated animals presented ductal changes that did not differ from those of the treated group. Measurements of serum bilirrubin (total and direct), and gamma-glutamyl-transpeptidase (gamma-GT) did not reveal significant differences when animals from the several groups were compared. Thus, bile ducts exhibit a proliferative response in relation to neighboring S. mansoni injury to portal areas, but although these lesions are histopathologically impressive, they lack a functional or prognostic significance.

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Introduction Celiac disease is an autoimmune disorder that involves gluten intolerance and can be triggered by environmental factors including hepatitis B virus (HBV) infection. This study aimed to describe the prevalence of celiac disease in individuals with HBV infection and to describe the clinical and laboratory characteristics of celiac disease associated with HBV. Methods This cross-sectional study included 50 hepatitis B patients tested for IgA anti-endomysial antibodies (EMAs) and tissue anti-transglutaminase (TTG) between August 2011 and September 2012. Results Fifty patients were included with a mean age of 46.0 ± 12.6 (46.0) years; 46% were female and 13% were HBeAg+. Six patients had positive serology for celiac disease, four were EMA+, and five were TTG+. When individuals with positive serology for celiac disease were compared to those with negative serology, they demonstrated a higher prevalence of abdominal pain (100% vs. 33.3%, p = 0.008), lower median creatinine (0.7mg/dL vs. 0.9mg/dL, p = 0.007) and lower mean albumin (3.6 ± 0.4g/L vs. 3.9 ± 0.3g/L, p = 0.022). All individuals with positive serology for celiac disease underwent upper digestive endoscopy, and three of the patients exhibited a macroscopic pattern suggestive of celiac disease. Histologically, five patients demonstrated an intra-epithelial lymphocytic infiltrate level > 30%, and four patients showed villous atrophy associated with crypt hyperplasia on duodenal biopsy. Conclusions An increased prevalence of celiac disease was observed among hepatitis B patients. These patients were symptomatic and had significant laboratory abnormalities. These results indicate that active screening for celiac disease among HBV-infected adults is warranted.

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BACKGROUND: Diffuse panbronchiolitis is a clinical pathologic condition characterized by chronic inflammation of respiratory bronchioles, with clinical features that position it as a differential diagnosis among the sinopulmonary syndromes. METHODS AND RESULTS: We present 4 cases (1 Black, 2 Japanese descendants, and 1 Japanese), living in Brazil, in which the diagnosis was made by the clinical and radiological features and confirmed by transbronchial biopsy. The clinical findings included chronic sinusitis, productive cough, rhonchi, and wheezes. The pulmonary function tests showed an obstructive pattern. High resolution computerized tomography showed a diffuse nodular pattern, airway ectasia, and airway wall thickening. The biopsy showed interstitial accumulation of foam cells and lymphoid cells in the walls of respiratory bronchioles: 2 of our cases had bronchus-associated lymphoid tissue hyperplasia. We searched for the HLA Bw54 in all of our patients, but only 1 was positive. A low dose macrolide treatment was introduced, resulting in with clinical and functional improvement. A score that rated the extent of nodules, airway ectasia, mucus plugging, and airway wall thickening was applied on pre- and post-treatment High resolution computerized tomography results, revealing an improvement in tomographic pattern related to that observed in the pulmonary function tests. CONCLUSION: We conclude that diffuse panbronchiolitis is a systemic disease that is not exclusive to the Asian population, whose clinical and radiological features should be better known by occidental pulmonary physicians.

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The complement system is an important humoral defense mechanism that plays a relevant role against microbial agents, inflammatory response control, and immunocomplex clearance. Classical complement pathway activation is antibody-dependent. The C4 component participates in the initial step of activation, and C4 expression is determined by 2 pairs of allotypes: C4A and C4B. Deficiencies in C4 allotypes have been associated with several diseases. The aim of the present review is evaluate the reported data in the literature regarding specific C4A and C4B deficiencies and characterize their clinical relevance. We searched the MEDLINE and LILACS databases. Papers referring to total C4 deficiency without allotype evaluation and case reports of primary C4 deficiency were not included. Deficiencies in C4 allotypes have been associated with Mycobacterium leprae infection, erythema nodosum, systemic sclerosis with anti-topoisomerase I antibodies, intermediate congenital adrenal hyperplasia with DR5 genotype, diabetes mellitus type 1 with DR3,4 genotype, and diabetes mellitus with antibodies against islet cells. C4 allotype deficiency is also related to C4B deficiency and autoimmune-associated diseases, such as systemic lupus erythematosus, or diseases with an autoimmune component, such as autism. Some reports associate C4A with thyroiditis after delivery as well as limited and systemic sclerosis without anti-topoisomerase I antibodies. However, the studies with C4A and C4B have been concentrated in isolated populations, and some of the studies could not be reproduced by other authors.

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PURPOSE: To establish the Southern blotting technique using hybridization with a nonradioactive probe to detect large rearrangements of CYP21A2 in a Brazilian cohort with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CAH-21OH). METHOD: We studied 42 patients, 2 of them related, comprising 80 non-related alleles. DNA samples were obtained from peripheral blood, digested by restriction enzyme Taq I, submitted to Southern blotting and hybridized with biotin-labeled probes. RESULTS: This method was shown to be reliable with results similar to the radioactive-labeling method. We found CYP21A2 deletion (2.5%), large gene conversion (8.8%), CYP21AP deletion (3.8%), and CYP21A1P duplication (6.3%). These frequencies were similar to those found in our previous study in which a large number of cases were studied. Good hybridization patterns were achieved with a smaller amount of DNA (5 mug), and fragment signs were observed after 5 minutes to 1 hour of exposure. CONCLUSIONS: We established a non-radioactive (biotin) Southern blot/hybridization methodology for CYP21A2 large rearrangements with good results. Despite being more arduous, this technique is faster, requires a smaller amount of DNA, and most importantly, avoids problems with the use of radioactivity.

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Dissertação de mestrado em Bioquímica Aplicada

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El cáncer es una enfermedad común de causa de muerte en el mundo entero. Si bien el éxito en el tratamiento de casi todas las formas de esta enfermedad depende de su diagnóstico temprano seguido de resección quirúrgica, los enfoques en investigación sobre compuestos inhibitorios de la carcinogénesis podrían ser aplicados a implementar estrategias de quimioprevención poblacionales. Se sabe que el carcinoma de páncreas exocrino ocupa el cuarto lugar como causa de muerte en el hombre en los Estados Unidos. Se presupone que su incidencia es similar en nuestro país. La causa del cáncer de páncreas es desconocido en la mayoría de los casos. Los estudios epidemiológicos si bien no dan datos certeros tienden a señalar que componentes de la dieta son factores de riesgo en la génesis del cáncer de páncreas (Rogers y Longnecker, 1988). Se conoce que el cáncer de páncreas es clínicamente silencioso y sólo manifiesta síntomas tardíamente, cuando ya se ha producido la invasión y metástasis (Pour, 1991). De ahí que haya interés por desarrollar modelos multifactoriales que puedan aportar datos para comprender las causas y el mecanismo de desarrollo del cáncer en el hombre. Trabajos realizados en el laboratorio del Programa Centro de Biología Celular y Desarrollo (CEBYD-CONICET), Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Director Dr. Benito Monis, han permitido establecer que la nitrosometilurea (NMU) induce la proliferación de poblaciones celulares exocrinas del páncreas de rata con la formación de estructuras nodulares atípicas, múltiples, de crecimiento expansivo que aumenta en número y tamaño con la edad, a los que identificaron con la sigla FACH (Focal Acinar Cell Hyperplasia). Este proceso hiperplásico es primariamente del epitelio acinar, aunque se han observado con notable menor frecuencia la aparición de estructuras ductulares neoformadas y aislados focos microscópicos de células con apariencia de hepatocitos (transdiferenciación o metaplasia hepatocítica). Los nódulos son con mayor frecuencia acidófilos aunque pueden observarse focos basófilos. Estos últimos son de dimensión microscópica. Excepcionalmente se han encontrado lesiones cancerosas en páncreas en el numeroso grupo de ratas inyectadas con NMU y estudiadas luego de la muerte natural en el laboratorio, por lo cual se infiere que las lesiones proliferativas que el NMU induce en páncreas de rata no posee tendencia a la transformación maligna. Este es el concepto central en las investigaciones sobre carcinogénesis pancreática en curso en el laboratorio CEBYD y sobre el cual proponemos el presente plan de trabajo. Además, hemos aislado células de un osteosarcoma inducido en la rata por la NMU (en curso) que han sido mantenidas tanto "in vivo" como "in vitro" para su caracterización y para el estudio de agentes inhibitorios de la carcinogénesis. El propósito del presente plan de trabajo es probar posibles agentes quimioterapéuticos en ambos modelos experimentales desarrollados en nuestro laboratorio.

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Background: To alert for the diagnosis of the 22q11.2 deletion syndrome (22q11.2DS) in patients with congenital heart disease (CHD). Objective: To describe the main CHDs, as well as phenotypic, metabolic and immunological findings in a series of 60 patients diagnosed with 22q11.2DS. Methods: The study included 60 patients with 22q11.2DS evaluated between 2007 and 2013 (M:F=1.3, age range 14 days to 20 years and 3 months) at a pediatric reference center for primary immunodeficiencies. The diagnosis was established by detection of the 22q11.2 microdeletion using FISH (n = 18) and/or MLPA (n = 42), in association with clinical and laboratory information. Associated CHDs, progression of phenotypic facial features, hypocalcemia and immunological changes were analyzed. Results: CHDs were detected in 77% of the patients and the most frequent type was tetralogy of Fallot (38.3%). Surgical correction of CHD was performed in 34 patients. Craniofacial dysmorphisms were detected in 41 patients: elongated face (60%) and/or elongated nose (53.3%), narrow palpebral fissure (50%), dysplastic, overfolded ears (48.3%), thin lips (41.6%), elongated fingers (38.3%) and short stature (36.6%). Hypocalcemia was detected in 64.2% and decreased parathyroid hormone (PTH) level in 25.9%. Decrease in total lymphocytes, CD4 and CD8 counts were present in 40%, 53.3% and 33.3%, respectively. Hypogammaglobulinemia was detected in one patient and decreased concentrations of immunoglobulin M (IgM) in two other patients. Conclusion: Suspicion for 22q11.2DS should be raised in all patients with CHD associated with hypocalcemia and/or facial dysmorphisms, considering that many of these changes may evolve with age. The 22q11.2 microdeletion should be confirmed by molecular testing in all patients.

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Definite hyperplasia of cells occurs in the skin lesions of the infectious myxoma of rabbits, more visible in such stages in which the intercellular basophilic substance is rather scanty (fig. 2). The increase in number of cells is the result of simplified forms of mitosis (modified type of mitosis, pseudoamitosis) which might readily be mistaken for amitosis in their final stages. Budding (figs. 20, 28, 29, 30) as well as constriction of the nucleus (figs. 18, 31, 32), and the formation of giant-cells (figs. 33, 34) are not rare. During the entire process the nuclear membrane does not desintegrate as in typical mitosis. Division of the cytoplasm following division of the nucleus has been demonstrated (fig. 17). Typical mitosis is practically absent. The cells which undergo hyperplasia present remarkable changes in their dimension, shape, and structure. The nucleus and cell-body are considerably enlarged (figs. 6, 7, 8). The shape of the nucleus is modified (figs. 8, 10, 15). Hypertrophy of nuclein, either as an intranuclear network (spireme?, figs. 9, 23), or in the form conspicuous, deeply staining masses which appear not to be homogeneous but to be composed of small particles closely clumped ("mulberries"?, figs. 12, 13, 14, 25, 26) occurs in most cells. While some of these pictures are probably related to necrosis of the cells as started by most of the previous workers, it is lekely that some of them may represent developmental stages of the modified mitosis (pseudoamitosis) here reported. In fact, fine cytological details not ordinarily preserved in necrotic cells (figs. 35, 36, 37) may be demonstrated in the socalled myxoma-cells subtted to approved cytological methods of study (fixation in B-15 and P. F. A.-3, staining in iron-hematoxylin).