Tratamiento prolongado con interferón alfa2 combinante de la hepatitis crónica por virus B

Tesis doctoral original inédita leída en la Universidad de Autónoma de Madrid, Facultad de Medicina. Fecha de lectura: 20 de noviembre de 198

Detection of Neuroendocrine Tumours by Enteroscopy: A Case Report

We present the case of a 62-year-old patient who developed melenas and in whom conventional endoscopic tests could not detect any bleeding lesion. In our case, capsule endoscopy and enteroscopy were the pivotal elements in establishing the diagnosis of a neuroendocrine tumour with an atypical location. As a result, it was possible to surgically remove the lesions at an early stage of the malignancy without metastatic disease and without the need for adjuvant therapy. Our case demonstrates the need for these new techniques in tumours of atypical location and aggressive course. Otherwise, this malignancy may be underdiagnosed until an advanced stage

Effect of C-reactive protein on Fcγ receptor II in cultured bovine endothelial cells

A B S T R A C T The major CRP (C-reactive protein) receptor on leucocytes has been identified as the low-affinity IgG receptor Fcγ receptor II (CD32). Our aim was to assess whether inflammation may modify the presence of the CD32 receptor in BAEC (bovine aortic endothelial cells). Confocal microscopy experiments showed a weak expression of the CD32 receptor in control BAEC that was slightly increased by 10 µg/ml CRP. Incubation of BAEC with TNF-α (tumour necrosis factor-α) did not modify the fluorescence signal of CD32. Addition of CRP to TNF-α-incubated BAEC enhanced the fluorescence signal of the CD32 receptors. The CD32 receptors showed a perinuclear cytoplasmic localization in BAEC. An alteration of the NO (nitric oxide)-dependent vasorelaxation has been defined as endothelial dysfunction. Endothelial dysfunction has been associated with the presence of superoxide anion and with a reduction in the expression of the eNOS (endothelial NO synthase). A concentration of CRP similar to that detected in patients with cardiovascular risk (10 µg/ ml) failed to modify the generation of superoxide anion stimulated by TNF-α. Western blot experiments showed that TNF-α decreased the expression of the eNOS protein, which was partially protected by treatment with 10 µg/ml CRP. The protective effect of 10 µg/ml CRP on eNOS expression in TNF-α-incubated BAEC was prevented by an antibody against CD32 receptors. In conclusion, the present results suggest that, although CRP has been associated with inflammation, CRP may protect the expression of eNOS protein against pro-inflammatory mediators such as TNF-α