Haemorrhagic small bowel melanoma metastasis: a clinical rarity.

We report on a clinical case with haemorrhagic small bowel metastases in a malignant melanoma patient with anaemia, diagnosed using small bowel video capsule endoscopy (VCE). A 67-year-old male patient with a previous diagnosis of malignant melanoma presented with anaemia and vertigo on admission. The standard diagnostic protocol for gastrointestinal (GI) bleeding investigation including a gastroscopy, colonoscopy and small bowel capsule endoscopy, as well as abdominal sonography and a restaging protocol including chest-abdomen-pelvis CT (CAP-CT), echocardiography and ECG was applied. Gastroscopy and colonoscopy were not conclusive in determining the bleeding source. VCE provided evidence for numerous haemorrhagic small bowel metastases. The CAP-CT was unremarkable for small bowel findings. Due to a diffuse metastatic disease diagnosed in heart, brain, liver, spleen and bone metastasis, the patient was treated in a conservative/palliative manner. VCE can provide precious information about GI bleeding of unknown origin when classical diagnostic methods are non-conclusive.

Quantitative gene expression of cytokines in peripheral blood leukocytes stimulated in vitro: modulation by the anti-tumor nerosis factor-alpha antibody infliximab and comparison with the mucosal cytokine expression in patients with ulcerative colitis.

Emerging data indicate that alterations in cytokine synthesis play a role in inflammatory bowel disease (IBD) pathogenesis. In this study, we quantified mRNA expression of the main acute-phase cytokines and T-cell cytokines in biopsies from patients with established ulcerative colitis (UC) and compared it with that obtained in biopsies from normal controls. Quantification of cytokine gene expression was also evaluated in in vitro phytohemagglutinin (PHA)-treated peripheral blood leukocytes (PBLs) at the RNA and protein levels. The in vitro influence of the anti-tumor necrosis factor-alpha (TNF-alpha) antibody infliximab (INFL) on PHA-treated PBLs was also evaluated. Analyzing inflamed specimens from UC patients compared with control samples, interleukin (IL)-6 was sharply the most induced cytokine. Interestingly, similar results were found in activated PBLs, where acute-phase cytokines were more abundantly expressed compared with T-cell cytokines. IL-6 was confirmed to be the most induced with a maximum increase of 1110-fold after 4 h of PHA stimulation, followed by TNF-alpha and IL-1beta as well as interferon-gamma (IFN-gamma). Surprisingly, analyzing cytokine-mRNA expression from activated PBLs, the time kinetics and quantity of IFN-gamma was more similar to that of the acute-phase proteins than to that of the T-cell cytokines, which were upregulated after 1 h. The upregulation of cytokine-mRNA was translated into protein as demonstrated by enzyme-linked immunosorbent assay. IFN-gamma was also strongly expressed in the RNA from UC biopsies. TNF-alpha protein was not detectable at all in INFL-treated cultures. INFL did not induce a reduction of TNF-alpha-mRNA nor of IL-1beta-mRNA, but it reduced IFN-gamma- mRNA and, to a lesser extent, IL-6-mRNA; it also reduced the T-cell-derived cytokine IL-2. The in vitro model of PHA-stimulated PBLs may mimic inflammation processes observed in vivo. INFL may reduce inflammation in vivo through inhibition of both monocyte and T-cell activation.