Anticuerpos antifosfolípidos en pacientes con nefritis lúpica: Estudio clínico-patológico / Antiphospholipid antibodies in lupic nephritis patients: Clinical-pathologic study

Introduction: Antiphospholipid Antibodies (APA) are detected in 30 and 40% of patients with Systemic lupus erythematosus (SLE). Antiphospholipid Syndrome nephropathy (APSN) is one of renal manifestations of APS. Histological lesions of APSN have been described in SLE. Objective: To evaluate the prevalence of APA in patients with lupus nephritis (LN), its clinical and laboratory association and the presence of APSN in renal biopsies from LN patients. Patients and Methods: We retrospectively studied 28 patients with SLE diagnosis according to ACR criteria, who underwent renal biopsies with diagnosis of LN. These patients attended to our rheumatology unit for the last 2 years. Demographic, clinical and serological data were collected at the time of the first biopsy. APA (Anticardiolipin Ig G, Ig M and lupus anticoagulant) were considered positivewhen they were positive in two opportunities during the follow up. Renal biopsies were classified according to NL classification 2004. Histological features of APSN were analyzed by 2 different pathologists who were blind to clinical data. P value <0.05 was considered statistically significant. Results: Mean age was 31 years old (17-53), 86% were female and mean SLE duration was 47 months (1-180). 54% of patients were positive for APA. There was not association between APA and first creatinine level, hypertension, amount of proteinuria and active sediment. Class II LN was most frequently associated with APA. Glomerular collapse and focal cortical atrophy (FCA) were associatedwith APA (p<0.008, p<0.005). Conclusions: APA were present in 54% of patients with LN. There was not association between APA and clinical features or histological type of LN. The main histological features of APSN were glomerular collapse and FCA

[Helicobacter pylori detected in atheroma plaque]. / Detección de Helicobacter pylori en placas de ateroma.

INTRODUCTION: In general, infection and chronic inflammation have been implied as etiologic agents for atheroesclerosis and in particular coronary illness (CI). Several studies have correlated the infection of Helicobacter pylori with CI, especially with virulent strains (lineage Cag A). OBJECTIVE: Demonstrate the immunohistochemical presence of H. Pylori in atheroscletotic plaques obtained from endarterectomy of different vascular regions. MATERIAL AND METHODS: 34 atherosclerotic plaques of different vascular areas were studied, (25 men and 9 women). The tissues were fixed with 10% neutral buffered-formalin and decalcifying in formic acid 5% was used when necessary. The tissue sections were included in paraffin, cut and colored with H&E and subjected to Immunohistochemistry (IHC) of H. Pylori. Briefly, tissues were deparaffinized and thermally treated with a citrate-based solution of antigenic retrieval (ImmunoDNA Retriever with Citrate, BIO SB, Santa Barbara, CA) using a water bath at 95 degrees C for 1 hour. The IHC was conducted using a high sensitivity Biotin-Streptavidin-HRP-DAB IHC system (ImmunoDetector HRP/DAB, BIO SB). The microscopic observation evaluated the presence of mononuclear inflammatory cells and the identification of the bacteria in the wall or the vascular lumen. RESULTS: Of the 34 cases studied 14 were positive, where one could identify the bacillus in their different forms (41,17%) associated with chronic inflammation.

Detección de Helicobacter Pylori en placas de ateroma / Elicobacter Pilori detected in atheroma plague

Introducción: la infección y la inflamación crónica han sido implicadas como agentes etiológicos para la ateraesclerasis (ATE). Varios estudios han relacionado a la infección por H. Pylori (HP) con la EC, especialmente con los linajes mas virulentos (linaje Cag A). Objetivo: demostrar la presencia del HP en placas de endarterectomías, utilizando una técnica Inmunohistoquimica (lHQ) específica que revela una reacción Ag-Ac mediante un cromógeno. Material y Métodos: se estudiaron 34 placas ATE de distintos territorios vasculares. Se fijaron en formol descalcificándolas en ácido fórmico según necesidad. Fueron incluidos en parafina, cortados y coloreados con H-E y técnicas de IHQ específicas para HP. Luego fueron desparafinados y tratados térmicamente con una solución de recuperación antigénica (lnmuno DNA Retriever with Citrate) utilizando olla a presión. La IHQ se efectuó con un sistema de alta sensibilidad Biotina-Estreptavidina-Peroxidasa-DAB). La observación morfológica evaluó células inflamatorias mononucleares y la identificación de la bacteria en la pared o la luz vascular. Resultados: de los 34 casos estudiados, en 14 se pudo identificar el bacilo en sus diferentes formas (41,17%), asociado a signos de inflamación crónica. Conclusión: el HP estuvo presente en un número sustancial de lesiones ATE y se asoció con inflamación. Estudios recientes sugieren que la presencia de Hp, demostrada por técnicas de IHQ, potenciaría los FR para ATE, induciendo una respuesta celular inflamatoria crónica por irritación persistente de la pared arterial.

Introduction: In general, infection and chronic inflammation have be en implied as etiologic agents for atherosclerosis and in particular coronary illness (CI). Several studies have correlated the infection of Helicobacter pylori with CI, especially with virulent strains (lineage Cag A). Objective: Demonstrate the immunohistochemical presence of H. Pylori in atherosclerotic plaques obtained from endarterectomy of different vascular regions. Material and methods: 34 atherosclerotic plaques of different vascular areas were studied, (25 men and 9 women). The tissues were fixed with 10% neutral buffered-formalin and decalcifying in formic acid 5% was used when necessary. The tissue sections were included in paraffin, cut and colored with H&E and subjected to Immunohistochemistry (lHC) of H.Pylori. Briefly, tissues were deparaffinized and thermally treated with a citrate-based solution of antigenic retrieval (lmmunoDNA Retriever with Citrate, BlO SB, Santa Barbara, CA) using a water bath at 95°C for 1 hour. The IHC was conducted using a high sensitivity BiotinStreptavidin-HRP-DAB IHC system (lmmunoDetector HRPIDAB, BlO SB). The microscopic observation evaluated the' presence of mononuclear inflammatory cells and the identification of the bacteria in the wall or the vascular lumen. Results: Of the 34 cases studied 14 were positive, where one could identify the bacillus in their different forms (41, 17%) associated with chronic inflammation.

Detección de Helicobacter Pylori en placas de ateroma / Elicobacter Pilori detected in atheroma plague

Introducción: la infección y la inflamación crónica han sido implicadas como agentes etiológicos para la ateraesclerasis (ATE). Varios estudios han relacionado a la infección por H. Pylori (HP) con la EC, especialmente con los linajes mas virulentos (linaje Cag A). Objetivo: demostrar la presencia del HP en placas de endarterectomías, utilizando una técnica Inmunohistoquimica (lHQ) específica que revela una reacción Ag-Ac mediante un cromógeno. Material y Métodos: se estudiaron 34 placas ATE de distintos territorios vasculares. Se fijaron en formol descalcificándolas en ácido fórmico según necesidad. Fueron incluidos en parafina, cortados y coloreados con H-E y técnicas de IHQ específicas para HP. Luego fueron desparafinados y tratados térmicamente con una solución de recuperación antigénica (lnmuno DNA Retriever with Citrate) utilizando olla a presión. La IHQ se efectuó con un sistema de alta sensibilidad Biotina-Estreptavidina-Peroxidasa-DAB). La observación morfológica evaluó células inflamatorias mononucleares y la identificación de la bacteria en la pared o la luz vascular. Resultados: de los 34 casos estudiados, en 14 se pudo identificar el bacilo en sus diferentes formas (41,17%), asociado a signos de inflamación crónica. Conclusión: el HP estuvo presente en un número sustancial de lesiones ATE y se asoció con inflamación. Estudios recientes sugieren que la presencia de Hp, demostrada por técnicas de IHQ, potenciaría los FR para ATE, induciendo una respuesta celular inflamatoria crónica por irritación persistente de la pared arterial.(AU)

Introduction: In general, infection and chronic inflammation have be en implied as etiologic agents for atherosclerosis and in particular coronary illness (CI). Several studies have correlated the infection of Helicobacter pylori with CI, especially with virulent strains (lineage Cag A). Objective: Demonstrate the immunohistochemical presence of H. Pylori in atherosclerotic plaques obtained from endarterectomy of different vascular regions. Material and methods: 34 atherosclerotic plaques of different vascular areas were studied, (25 men and 9 women). The tissues were fixed with 10% neutral buffered-formalin and decalcifying in formic acid 5% was used when necessary. The tissue sections were included in paraffin, cut and colored with H&E and subjected to Immunohistochemistry (lHC) of H.Pylori. Briefly, tissues were deparaffinized and thermally treated with a citrate-based solution of antigenic retrieval (lmmunoDNA Retriever with Citrate, BlO SB, Santa Barbara, CA) using a water bath at 95ºC for 1 hour. The IHC was conducted using a high sensitivity BiotinStreptavidin-HRP-DAB IHC system (lmmunoDetector HRPIDAB, BlO SB). The microscopic observation evaluated the presence of mononuclear inflammatory cells and the identification of the bacteria in the wall or the vascular lumen. Results: Of the 34 cases studied 14 were positive, where one could identify the bacillus in their different forms (41, 17%) associated with chronic inflammation.(AU)

Syntactic comprehension deficits in agrammatism.

Eleven agrammatic and 16 fluent aphasic patients were given a comprehension task consisting of simple, active and passive reversible sentences. The purpose of the study is to reconsider the comprehension disorders in agrammatism, and particularly of passive reversible sentences, to test to what extent Grodzinsky's trace deletion hypothesis (TDH) is generalizable to other types of NP-movement, and finally to ascertain whether the pattern of impairment observed in agrammatism differs from that of fluent aphasic patients. The study confirms that trace analysis may be selectively impaired in agrammatism. However, this deficit is not the only mechanism underlying comprehension disorders and cannot be said to occur in all agrammatic patients. Comprehension disorders also involve the processing of clitic object pronouns which also underly NP-movement. Finally, the impairment found in fluent aphasic patients differs, both in type and severity, from that of agrammatic patients, thus confirming the peculiar aspects of the agrammatic comprehension deficit suggested by Grodzinsky's TDH.

The social and vocational outcome of spinal cord injury patients.

Functional status, perception of adjustment, occupational outcome and social functioning were investigated in a group of spinal cord injury (SCI) patients (mean age 34, range 10-74 years) seen at a specialised spinal unit over the period January 1984-December 1988. Functional status was assessed using a standardised scale measuring patients' performance of specific tasks, and other measures of outcome were investigated by a structured interview. Almost two thirds (68%) of the patients were independent according to the standardised scale (33% quadriplegic and 84% paraplegic). Patients' autonomy appeared to be threatened by architectural barriers in and about the house: approximately one third (34%) of those classified as 'independent' on the standardised rehabilitation scale used needed some help in their everyday life. A negative occupational outcome emerged: compared to the pre-morbid situation, 43 patients (44%) were worse off; 48 (49%) did not experience substantial changes--though it must be noted that 68% of these (33/48) were virtually unemployed (ie student, home maker, retired, unemployed) before the injury; and for 6 (7%) some improvement took place. With a multivariate analysis age was the only statistically significant predictor of poor occupational outcome, with older patients being worse off irrespective of the extent of disease and functional autonomy. The paper discusses these results and stresses the need for integrating results based on the use of standardised rehabilitation scales with the analysis of potential barriers influencing a patient's ability to exploit his/her autonomy.

Sindrome de Sweet un paciente de 79 años / Sweet's syndrome in a 79 year old patient

1. Se presenta un típico caso de Síndrome de Sweet en una paciente de sexo femenino, de 79 años, considerándose la de más edad relatada hasta ahora. Se hace el diagnóstico clínico por la morfología, topografía, etc., juntamente con la sintomatología dolorosa y la evolución de las lesiones. 2. El laboratorio informa leve leucocitosis neutrofílica. 3. El estudio histopatologico muestra el típico infiltrado neutrofílico y edema en dermis papilar, compatible en Dermatosis Aguda Febril Neutrofílica o Síndrome de Sweet papilar, compatible con Dermatosis Aguda Febril Neutrofílica o Síndrome de Sweet. 4. El tratamiento corticoideo y antihistamínico arrojó buenos resultados. Clínicamente no había datos de interés, pero se propone mantener a la paciente bajo control, por ser el Sweet considerado un processo eventualmente paraneoplásico

Sindrome de Sweet un paciente de 79 años / Sweets syndrome in a 79 year old patient

1. Se presenta un típico caso de Síndrome de Sweet en una paciente de sexo femenino, de 79 años, considerándose la de más edad relatada hasta ahora. Se hace el diagnóstico clínico por la morfología, topografía, etc., juntamente con la sintomatología dolorosa y la evolución de las lesiones. 2. El laboratorio informa leve leucocitosis neutrofílica. 3. El estudio histopatologico muestra el típico infiltrado neutrofílico y edema en dermis papilar, compatible en Dermatosis Aguda Febril Neutrofílica o Síndrome de Sweet papilar, compatible con Dermatosis Aguda Febril Neutrofílica o Síndrome de Sweet. 4. El tratamiento corticoideo y antihistamínico arrojó buenos resultados. Clínicamente no había datos de interés, pero se propone mantener a la paciente bajo control, por ser el Sweet considerado un processo eventualmente paraneoplásico (AU)