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Aim The changes in the management and outcome of rectal cancer in Oxford were studied over a 10-year period. Method Rectal cancer data using a prospectively collected data base were divided into curative (global) and palliative groups. The global curative group was further divided into those with and without (selected group) the following features: emergency cases, local excision, salvage surgery for recurrence or incomplete local excision, metastatic disease, perioperative death, hereditary cancer, inflammatory bowel disease-related cancer, and synchronous cancer. Results Between 1994 and 2003, 709 cases of rectal cancer were treated, 532 for cure and a selected group of 393 after removing patients with the aforementioned exclusions. For the selected group, the average follow-up was 51.2 months, overall survival 65.4% and cancer-specific survival 75.3%. There was no 2-year survival difference between each of the 10-year periods of study. Two-year local recurrence was 5.6% for the first 5-year period and 2.3% for the second ( P = 0.11). MRI staging increased during the 10 years (0% in 1994; 66.7% in 2003) as did use of definitive chemoradiotherapy (dCRT) (0% in 1994; 64.7% in 2003). The anastomotic leakage rate was significantly higher in the second 5-year period (2.6% vs 9.6%; P = 0.01). Conclusion Despite increasing use of MRI and dCRT, 2-year survival and local recurrence were not significantly different within the 10 years studied. [ABSTRACT FROM AUTHOR]

A male patient with portal hypertension, portal vein thrombosis, spontaneous splenorenal shunt formation, and encephalopathy, thought to have post-hepatitis B cirrhosis, is described. His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels. [ABSTRACT FROM AUTHOR]