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Nowadays the development of a gastro-colic fistula is usually due to malignant disease in the gastro-intestinal tract. The symptoms can vary extensively and establishing the diagnosis quite challenging. We describe the case of a gastro-colic fistula with a complicated course and review the literature., (Copyright© Acta Chirurgica Belgica.)

A 68-year-old woman presented at the Casualty Department due to collapse, anaemia, fatigue and progressive dyspnoea. She suffered from melena, indicative of a haemorrhage in the upper gastrointestinal tract. Gastroduodenoscopy revealed the presence of a polyp in the duodenum, which was endoscopically resected. Pathological investigation demonstrated that the polyp was a Brunner's adenoma, i.e. a circumscript benign submucosal nodular hyperplasia of the Brunner's glands.

A 42-year-old man was transferred to the Emergency Department after his friends had found him unresponsive and confused in his room. He had been experiencing upper abdominal complaints for a period of several months. He had taken large amounts of a calcium carbonate/magnesium subcarbonate preparation (Rennie) and had consumed at least 3 litres of dairy products per day. His behaviour was reported as being more and more abnormal during the previous few weeks. On admission he was confused and agitated and had involuntary movements of his limbs. Laboratory investigation indicated a triple acid base disorder, i.e. metabolic alkalosis, respiratory alkalosis and high anion gap metabolic acidosis, with severe dehydration. The metabolic alkalosis was caused by the intake of large amounts of dairy and antacids: milk-alkali syndrome. The metabolic acidosis was the result of hypovolaemia and pre-renal renal failure and the respiratory alkalosis was caused by hyperventilation due to the organic psychosyndrome. The patient was treated with volume expansion by isotonic saline and the administration of potassium and he was sedated with low-dose midazolam, which led to a full respiratory compensation of the metabolic alkalosis. A few days following admission, both the plasma calcium concentration and renal function returned to normal; the acid-base disorder completely normalized and the organic psychosyndrome disappeared. On gastroduodenoscopy a gastric ulcer was found; biopsies revealed a signet ring cell adenocarcinoma of the stomach.

A 76-year-old man presented with diffuse progressive abdominal pain. He had undergone endoscopic retrograde pancreaticocholangiography (ERCP) 5 weeks earlier for jaundice and increased levels of liver enzymes. A dilated biliary duct with multiple concrements had been seen, and a plastic endoprosthesis was placed. During a follow-up ERCP the stent was not found, and the obstruction was still present. Another stent was placed. Abdominal x-ray revealed migration of the first endoprosthesis to the distal jejunum and signs of ileus and free gas. CT showed that the stent was stuck in a perforated diverticulum of the sigmoid, surrounded by an abscess mass. The stent was removed by laparotomy, the perforation was closed, and a double-loop stoma was made. Two weeks after initial recovery, abdominal pain recurred. CT revealed a second dislocated stent with a perforation of the jejunum. Laparotomy was performed again with removal of the stent and repair of the perforation. Migration is a known complication of biliary endoprosthesis placement, and should be considered in cases of abdominal pain after ERCP. Perforations rarely occur and mostly affect areas of the bowel that are fixed or that present obstacles to normal elimination. Two perforations within a short period of time is an extremely rare complication of migration.

Background/aims: Treatment with ursodeoxycholic acid has been shown to decrease the rate of disease progression in patients with primary biliary cirrhosis, although the effect is modest. Since primary biliary cirrhosis has many features of an autoimmune disorder, immunosuppressives added to ursodeoxycholic acid may be of value in the treatment of primary biliary cirrhosis., Methods: A 1-year randomized, double-blind, placebo-controlled trial was carried out in 50 patients with primary biliary cirrhosis, who had already been treated with ursodeoxycholic acid for at least 1 year, but had not achieved complete disease remission. Patients were randomized to additional prednisone (30 mg per day initially, tapered to 10 mg daily after 8 weeks) and azathioprine (50 mg daily) or placebo. A subgroup of patients received cyclical etidronate and calcium. The principal aim of the study was to assess the short-term benefits and risks of the combined bile acid and low-dose immunosuppressive regimen. Primary endpoints were effects on symptoms, liver biochemistry, liver histology, bone mass and the occurrence of adverse events., Results: Pruritus (p=0.02), alkaline phosphatase, aspartate aminotransferase, IgM and procollagen-III-propeptide improved significantly (all p<0.002) in the combined treatment group as compared to the placebo group. Histological scores for disease activity and disease stage decreased significantly within the combination treatment group (p<0.001)., Conclusions: In patients with primary biliary cirrhosis receiving ursodeoxycholic acid, there is an additional beneficial effect of 1-year treatment with prednisone and azathioprine on symptoms and biochemical, fibrogenetic and histological parameters. These results strongly encourage the evaluation of this triple treatment regimen in long-term controlled trials of adequate size to document its effect on clinical events.

We examined the value of serum procollagen III amino propeptide (PIIIP) for predicting the histological progression of primary biliary cirrhosis (PBC). Serial PIIIP measurements were obtained for nine patients with histologically progressive PBC and nine patients with histologically stable early disease, assessed by repeated liver biopsies and followed for up to 13 years. The means of the follow-up PIIIP concentrations were elevated in 39% of the cases; moreover, PIIIP levels were elevated at least once during follow-up in 72% of the cases. Mean follow-up PIIIP concentrations did not differ significantly between progressive and non-progressive patients. In addition, in the progressive group, histological progression was not reflected by PIIIP levels. No difference was found between the serum PIIIP levels corresponding to the histological stages I, II and III. The individual coefficients of the correlation between serum PIIIP and biochemical variables (bilirubin, alkaline phosphatase, ASAT, albumin) and histology showed a wide distribution without a consistent trend towards positive or negative. Treatment with cyclosporin A or cyclosporin A combined with prednisone did not influence serum PIIIP levels. Treatment with penicillamine combined with prednisone, however, resulted in a significant decrease in PIIIP concentrations (p less than 0.05). We conclude that serum PIIIP measurements are of no value for predicting the histological progression of PBC.

Procollagen type III N-peptide (PIII NP) and laminin P1 fragment (LP1) have both been proposed as markers of liver fibrosis. In this study we evaluated the diagnostic application of both peptides in alcoholic liver disease and primary biliary cirrhosis. Serum concentrations of the peptides were measured by radioimmunoassay. PIII NP and LP1 levels appeared to be significantly raised in patients with alcoholic and primary biliary cirrhosis. Patients with alcohol abuse without cirrhosis had normal or slightly elevated PIII NP levels, but significantly raised LP1 levels. There was a strong correlation between PIII NP and LP1 concentrations.

Plasma lysozyme levels have been reported to reflect the functional status of the reticuloendothelial system (RES). We measured plasma lysozyme levels in 22 patients with acute hepatitis and 21 patients with cirrhosis and a mesocaval shunt. In 17 of these patients RES function was assessed by measuring the disappearance rate (t/2) of radio-labelled sulphur colloid. In acute hepatitis plasma lysozyme levels and colloid t/2 were significantly lower than in health controls and cirrhotics. In the acute hepatitis patients, the plasma lysozyme levels rose significantly two weeks after admission as the hepatitis improved. The colloid t/2 of the 17 patients with liver disease was significantly correlated with the plasma lysozyme level (r = +0.66, p = 0.005). These results suggest that in human liver disease, in comparison with animal experiments, plasma lysozyme is dependent on RES functional status in the sense that a more active RES will result in a lower lysozyme level.