This paper reports on two patients with carcinoid tumours of the gall bladder who presented to the Aberdeen hospitals during the period 1970 to 1990 and reviews all previously reported cases in published works.

Coagulopathy is a well recognised complication of peritoneovenous shunting for ascites. The relative contributions of primary fibrinolysis and disseminated intravascular coagulation remain controversial. Plasminogen activating activity was significantly lower in malignant ascites (n = 10, median < 0.02 (range < 0.02-1.26) IU/ml) than in alcoholic ascites (n = 10, 1.07 (0.30-1.49) IU/ml) (p < 0.05). Fibrinolytic activity was determined by a balance between tissue plasminogen activator and plasminogen activator inhibitor-1. There was no significant difference between the two groups in the concentration of tissue plasminogen activator (34 (12-64) ng/ml in malignant ascites v 29 (12-43) ng/ml in alcoholic ascites), but the concentration of plasminogen activator inhibitor-1 was significantly higher in malignant ascites (736 (213-1651) ng/ml) than in alcohol ascites (29 (12-43) ng/ml) (p < 0.05). Malignant ascites contained significantly higher concentrations of urokinase (0.7 (< 0.1-1.3) ng/ml v 0.2 (< 0.1-0.6) ng/ml in alcoholic ascites) and plasminogen activator inhibitor-2 (33 (< 6-140) ng/ml v 9 (< 6-28) ng/ml alcoholic ascites). The plasminogen activating activity of alcohol ascites may lead to primary fibrinolysis after peritoneovenous shunting. The considerably lower activity found in malignant ascites may explain why coagulopathy after shunting is less pronounced in this group of patients.

A prospective surveillance programme for patients with longstanding (> = 8 years), extensive (> = splenic flexure) ulcerative colitis was undertaken between 1978 and 1990. It comprised annual colonoscopy with pancolonic biopsy. One hundred and sixty patients were entered into the programme and had 739 colonoscopies (4.6 colonoscopies per patient; 709 patient years follow up). Eight eight per cent of examinations reached the right colon. There was no procedure related death. One Dukes's A cancer was detected. Forty one patients (25%) defaulted. Of these 25 remain well; 13 are unaccounted for, and one died from colonic cancer. One patient had colectomy for medical reasons, and another died of carcinoma of the pancreas. Retrospectively an additional 16 eligible patients were identified who had not been recruited. Of these, 14 remain well, two are unaccounted for. None developed colonic cancer. Four patients refused colonoscopy. All remain well. Over the same period seven other cases of colonic cancer were found in association with ulcerative colitis, two in patients who had erroneously been diagnosed as having only proctitis and were therefore not entered into the programme, but were found at operation to have total colitis, one in a patient with colitis of seven years duration, and four patients who had previously attended the clinic but had been lost to follow up before 1978 and then had represented with new symptoms during the surveillance period. Thus, of the nine colitis related cancers diagnosed in this centre during the study period only one was detected by the surveillance programme. The results of this large study, a a review of published works, cast doubts on the effectiveness of colonoscopic surveillance programmes in detecting colorectal cancer in patients with ulcerative colitis.

Primary oesophageal involvement by lymphoma in two patients, one with Hodgkin's disease and one with non-Hodgkin's lymphoma is reported. In both, there were no manifestations of the disease outside the oesophagus, which is exceptionally rare. In the patient with non-Hodgkin's lymphoma, the oesophageal tumour was the first manifestation of lymphoma. Shortly after admission he developed a tracheo-oesophageal fistula from which he died before treatment could be started. In the patient with Hodgkin's disease, isolated oesophageal lymphoma was the first relapse after a 13 year interval free of disease. As he had previously received mediastinal irradiation he was treated with combination chemotherapy that resulted in long term survival (> five years). Several other long term survivors have been described but only after radiotherapy or surgery. These findings suggest that systemic chemotherapy may be equally successful in treating isolated primary oesophageal lymphoma, thus offering an alternative for those patients in whom local treatment is contraindicated.

The painful rib syndrome consists of three features: pain in the lower chest or upper abdomen, a tender spot on the costal margin, and reproduction of the pain on pressing the tender spot. This is a common cause for referral to a general medical/gastroenterology clinic, accounting for 3% of new referrals in Lincoln. Seventy six consecutive patients were studied. The mean age was 48 years and 70% were women. Forty three per cent had been investigated, often extensively, before referral, and eight had had a non-curative cholecystectomy. The case notes from all patients were reviewed and a follow up questionnaire was sent after a mean period of four years to those 72 still alive, of which 56 replied. Thirty nine (70%) still had the pain although all except three had learnt to live with it. Despite a firm diagnosis being given, 25 (33%) patients were referred again to hospital by their general practitioner. All further investigations were negative apart from the finding of gall stones in three patients. The four patients who died had died from unrelated causes. The painful rib syndrome is common but underdiagnosed. It is a safe, clinical diagnosis requiring no investigation. Systematic firm palpation of the costal margin in recommended in all patients presenting with pain in the lower chest or upper abdomen.

A 14 year old girl with multiseptate gall bladder and cystic dilatation of the biliary tree is presented. This is the 20th published case report of patients with multiseptate gall bladder and only the second to be associated with a choledochal cyst. The cystic spaces of the gall bladder did not communicate with the neck of the gall bladder or the rest of the biliary tree, and this unusual feature has not been previously described. A multiseptate gall bladder with a normal biliary tree commonly causes symptoms suggestive of cholecystitis, although gall stones are seldom present. Diagnosis is confirmed by an oral cholecystogram or ultrasound scan that may show the fine intraluminal septae, and these features should be looked for in patients with biliary symptoms without biliary calculi. Cholecystectomy is curative for the isolated gall bladder anomaly but hepaticojejunostomy may be necessary for an associated choledochal cyst.

The secretory response of gastric acid to pure ethanol and alcoholic beverages may be different because the action of the non-ethanolic contents of the beverage may overwhelm that of ethanol. Pure ethanol in low concentrations (< 5% vol/vol) is a mild stimulant of acid secretion whereas at higher concentrations it has either no effect or a mildly inhibitory one. Pure ethanol given by any route does not cause release of gastrin in humans. Alcoholic beverages with low ethanol content (beer and wine) are strong stimulants of gastric acid secretion and gastrin release, the effect of beer being equal to the maximal acid output. Beverages with a higher ethanol content (whisky, gin, cognac) do not stimulate gastric acid secretion or release of gastrin. The powerful stimulants of gastric acid secretion present in beer, which are yet to be identified, are thermostable and anionic polar substances. The effect of chronic alcohol abuse on gastric acid secretion is not as predictable. Chronic alcoholic patients may have normal, enhanced, or diminished acid secretory capacity; hypochlorhydria being associated histologically with atrophic gastritis. There are no studies on the acute effect of alcohol intake on gastric acid secretion in chronic alcoholic patients. The acid stimulatory component of beer and wine needs to be characterised and its possible role in the causation of alcohol induced gastrointestinal diseases needs to be investigated.

An elderly woman with chronic ulcerative colitis who developed proximal muscle weakness, increased serum creatine phosphokinase activity, and histological and electromyographic abnormalities characteristic of polymyositis is described. Treatment with corticosteroids and 5-acetylsalicylic acid was followed by a remission in bowel symptoms, improvement in muscle power, and reversal of electromyographic changes. An autoimmune link between the two disorders seems likely.

Injection sclerotherapy is now the accepted first line treatment for bleeding oesophageal varices, although it is associated with an impressive list of rare complications. The main problem concerns the strategy for uncontrollable or recurrent bleeding. Patients with uncontrolled bleeding may be referred for surgery after considerable blood loss and are then extremely difficult to assess. The effects of blood loss on liver function can lead to an unduly pessimistic assessment of liver status. An effective choice of emergency surgical procedure may require considerable surgical expertise. Oesophageal transection and devascularisation are satisfactory for many patients with oesophageal varices secondary to cirrhosis and should nearly always control bleeding. Difficulties arise in patients who are grossly obese and in those who have undergone extensive surgery in the upper abdomen. Problems may also be encountered in those treated by repeated sclerotherapy, which may have caused severe inflammatory change and thickening around the lower oesophagus and upper stomach. We believe that an emergency mesocaval shunt using either a vein graft or a synthetic material such as polytetrafluoroethylene is the procedure of choice for this difficult group of very sick patients. The surgical exposure is satisfactory and not unduly prolonged in even the largest patients and the technique does not interfere with any subsequent transplant operation. There is a greater choice in the management of the patient with less urgent bleeding from recurrent varices after sclerotherapy. Repeat sclerotherapy may be effective for small oesophageal varices while liver transplantation may be indicated in the patient with deteriorating liver function. A selective distal splenorenal shunt should be considered for patients with intact splenic and left renal veins and a mesocaval vein graft for the remainder. We would therefore suggest that surgery should still be considered for the management of portal hypertension, particularly in the following circumstances: (1) Uncontrollable bleeding during the initial course of sclerotherapy; (2) Life threatening haemorrhage from recurrent varices; (3) Bleeding from ectopic varices not accessible to sclerotherapy; (4) Uncontrollable bleeding from oesophageal ulceration secondary to injection sclerotherapy; (5) Severe, symptomatic hypersplenism; (6) For patients who live in communities remote from blood transfusion facilities and adequate medical care. The management of the complications of portal hypertension continues to pose problems. We believe that the best results should come from a combined management approach using injection sclerotherapy as primary treatment and surgery for complications and for haemorrhage from unusual anatomical sites.

The motor function of the colon is probably the least understood of the various hollow viscera of the human body. This is partly because of the marked variability of colonic motor function and the short recording periods usually used, generally not exceeding three hours. Most of the data available on human colonic motility originate from investigations conducted in the most distal portions of the viscus, because of technical difficulties in reaching its proximal portions. Although attempts have been made to solve these problems through the ingestion of radiotelemetric pressure sensors, these efforts have been hampered by intermittent signal loss and the inability to control the location of the capsule within the gastrointestinal tract. To overcome these problems, techniques have recently been developed that permit prolonged recordings (24 hours or more) of myoelectrical and contractile activity of the human colon, with both perfused and solid-state manometric systems. The present paper reviews the current experience in 24 hour recording from the human colon, with a primary emphasis on the more forceful propulsive contractile activity associated with the so called mass movements.

Polymerase chain reaction is a highly sensitive technique for the detection of hepatitis B virus-DNA and hepatitis C virus-RNA in serum, liver tissue, and peripheral mononuclear blood cells. In chronic hepatitis B, it is particularly useful for identification of infectious subjects who are hepatitis B surface antigen positive and anti-hepatitis B e antigen antibody-positive, and for follow up of hepatitis B virus infections in liver transplantation programmes. Polymerase chain reaction detection of hepatitis C virus-RNA in serum may be the only means of confirming acute hepatitis C infection and also of identifying viraemia in the chronic disease, particularly in anti-hepatitis C virus antibody-negative individuals. It can also be used for direct evaluation of mother to child hepatitis C virus transmission. As in hepatitis B, polymerase chain reaction can be used for monitoring reinfection with hepatitis C virus after liver transplant, and has proved invaluable in identification of different hepatitis C virus genotypes. The efficacy of antiviral treatment can also be monitored using polymerase chain reaction. Polymerase chain reaction has thus shown numerous advantages for disease detection and monitoring despite the limitations imposed, for example, by possible contamination problems and semiquantitative evaluations.

The hepatitis B virus (HBV) belongs to a group of viruses termed hepadnaviruses. The 3.2 kb genome encodes for a variety of proteins involved in viral replication (p-gene), transactivation (x-gene), or encodes for structural proteins (c- and s-genes). Several viral and non-viral functions determine the clinical course of HBV infection. The hepatitis D virus resembles a viroid and requires the HBV as a helper virus. The interaction between the viruses is not well understood. More information on the interaction between the human host and viruses is needed to help improve the treatment.