There is increasing evidence that the presence of a systemic inflammatory response plays an important role in predicting survival in patients with colorectal cancer. However, it is not clear what components of the systemic inflammatory response best predict survival. The aim of the present study was to compare the prognostic value of an inflammation-based prognostic score (modified Glasgow Prognostic Score (Mgps) 0 ¼ C-reactive protein o10 mg l À1 , 1 ¼ C-reactive protein 410 mg l À1 , and 2 ¼ C-reactive protein 410 mg l À1 and albumino35 g l À1 ) with that of components of the white cell count (neutrophils, lymphocytes, monocytes and platelets using standard thresholds) in patients with colorectal cancer. Two patient groups were studied: 149 patients who underwent potentially curative resection for colorectal cancer and 84 patients who had synchronous unresectable liver metastases. In those patients who underwent potentially curative resection the minimum follow-up was 36 months and 20 patients died of their cancer. On multivariate survival analysis only TNM stage (HR 3.75, 95% CI 1.54 -9.17, P ¼ 0.004), monocyte count (HR 3.79, 95% CI 1.29 -11.12, P ¼ 0.015) and mGPS (HR 2.21, 95% CI 1.11 -4.41, P ¼ 0.024) were independently associated with cancer-specific survival. In patients with synchronous unresectable liver metastases the minimum follow-up was 6 months and 71 patients died of their cancer. On multivariate survival analysis only single liver metastasis 45 cm (HR 1.78, 95% CI 0.99 -3.21, P ¼ 0.054), extrahepatic disease (HR 2.09, 95% CI 1.05 -4.17, P ¼ 0.036), chemotherapy treatment (HR 2.40, 95% CI 1.82 -3.17, Po0.001) and mGPS (HR 1.44, 95% CI 1.01 -2.04, P ¼ 0.043) were independently associated with cancer-specific survival. In summary, markers of the systemic inflammatory response are associated with poor outcome in patients with either primary operable or synchronous unresectable colorectal cancer. An acute-phase protein-based prognostic score, the mGPS, appears to be a superior predictor of survival compared with the cellular components of the systemic inflammatory response.

Miller-Fisher syndrome is an autoimmune neuropathy characterized by ataxia, areflexia and ophthalmoplegia, and in the majority of cases the presence of high titres of anti-GQ1b ganglioside antibodies. In an ex vivo model, human and mouse anti-GQ1b antibodies have been shown previously to induce a complement-dependent alpha-latrotoxin-like effect on the murine motor endplate, i.e. they bring about massive quantal release of acetylcholine and eventually block neuromuscular transmission. Using immunofluorescence microscopy with image analysis, we show here that the late stages of this electrophysiological effect temporally coincide with the loss of heavy neurofilament (200 kDa) and type III beta-tubulin immunostaining and structural breakdown of the nerve terminal, as demonstrated by electron microscopy. Ultrastructurally, axon terminals were disorganized, depleted of vesicles, and subdivided by the infiltrating processes of capping Schwann cells. These findings provide clear pathological evidence to support a role for anti-ganglioside antibodies in mediating nerve terminal injury and further advance the view that this site may be of importance as a target in some human neuropathies.

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Hemorrhage from stoma due to ectopic varices is a rare condition, which can be seen in patients due to portal hypertension of any cause. Resnick et al. were the first to describe in the year 1968. Unfortunately, there has been no randomized controlled trials to formally assess the best management approach for such a condition, and conservative methods are temporary as they re-bleed within 1 year time. Definitive treatment requires a multidisciplinary team approach as they have a high mortality and morbidity rate. The treatment is aimed at reducing the portal-hypertension, which can be achieved with porto-systemic shunts.