Volume 66 - 2003 - Fasc.2 - Symposium
Diagnosis and therapeutic problems of primary sclerosing cholangitis
Primary sclerosing cholangitis (PSC) leads to a progressive destruction of the intra- and extrahepatic bile ducts. The cause is unknown but genetic and immunological mechanisms may play a role. The median survival time from diagnosis to death is about 12 years. MRCP is almost equal to ERCP for diagnosing PSC and shows the typical localised or multifocal strictures and interfering segments of ectatic bile ducts. Liver histology can be helpful in making the diagnosis but is often unspecific and there is a large sampling variability.
The treatment of PSC is disappointing. The combination of ursodeoxycholic acid with endoscopic dilatation is probably the best treatment. Patients with cirrhosis and/or recurrent cholangi- tis should be evaluated for liver transplantation as the outcome after liver transplantation is good, especially if there is no cholan- gio-carcinoma present and if the Child-Pugh score is not too high. There is also a need to treat the complication of PSC such as osteo- porosis, cholangitis and the development of cholangiocarcinoma. (Acta gastroenterol. belg., 2003, 66, 155-159).
Endoscopic therapy of chronic pancreatitis
Chronic pancreatitis (CP) is a rare disease in western countries (incidence 2-10/100.000/year). It ultimately leads to irreversible damage of the pancreas with exocri- ne and endocrine insufficiency. Pain is the major clinical symptom and is present early in the course of the disea- se in most of the cases (1-3).
With the exception of the rare hereditary CP which is associated with a mutation in the cationic trypsinogen gene on chromosome 7 (4,5), the etiology of CP has not already been demonstrated. Chronic alcoholism is a pre- cipitating factor and it dramatically increases the proba- bility of CP development but the disease can develop in non-alcoholic subjects and is then qualified of "idio- pathic" CP.
Early multi-system organ failure associated with acute pancreatitis : a plea for a conservative therapeutic strategy
The mortality of severe acute pancreatitis still ranges between 10 and 20%. Nowadays, infected pancreatic necrosis is the leading cause of death. Despite advances in intensive care therapy, howe- ver, early and worsening multi-system organ failure remains a source of substantial morbidity and still accounts for 20 to 50% of the deaths. In recent years, the systemic inflammatory response syndrome and the relevant cascades of inflammatory mediators have been implicated as the key factor in the emergence of remote tissue damage. Early multi-system organ failure that supervenes in the first week is typically associated with a sterile necrotizing process. There are no pathophysiological, clinical or economical data to support the practice of debridement of sterile necrosis to prevent or to control early multi-system organ failure. This issue has never been addressed in a controlled study. Besides intensive care support, non-surgical therapeutic modalities including urgent endoscopic sphincterotomy for impacted stones, antibiotic pro- phylaxis for the prevention of pancreatic infection and early jejun- al nutrition have been specifically developed hopefully to attenuate multiple organ failure, to obviate the need of surgical drainage and to improve survival. Fine needle aspiration of necrotic areas must be incorporated in any conservative therapeutic strategy in order to identify and not to jeorpardize those with infected necrosis that remains an absolute indication for drainage.
A specific treatment of acute pancreatitis is still lacking, so far. However, there is ample experimental and pathophysiological evi- dence in favour of immunomodulatory therapy in severe acute pancreatitis. The administration of one or several antagonists of inflammatory mediators possibly combined with a protease inhi- bitor may at last provide the opportunity to interfere with the two major determinants of prognosis : the severity of multiple organ failure and the extent of necrotic areas that creates the culture medium for bacterial superinfection. These benefits remain to be substantiated in a controlled study, however. (Acta gastroenterol. belg., 2003, 66, 177-183).
Biopsy of focal liver lesions : guidelines, comparison of techniques and cost-analysis
When a focal liver lesion is discovered, differentiation between a benign and malignant nature and further characterization are mandatory to guide further treatment. Histology remains the gol- den standard. Improving imaging techniques such as contrast enhanced Doppler ultrasonography, spiral CT and new MRI pro- cedures are promising, but not 100% accurate. When there is any doubt, biopsy should be performed. Fine Needle Aspiration Biopsy (FNAB) has a high sensitivity and specificity (90-95%) in expe- rienced hands, but has a high insufficient sampling rate (up to 15%). In a series of 245 Fine Needle Tru-cut Biopsies (FNTCB) of focal solid liver lesions performed at our institution, sensitivity and specificity for the diagnosis of malignancy were 86% and 100% respectively, with an overall accuracy of 88%. Positive predictive value was 100%, but negative predictive value was rather low (56%). Insufficient sampling rate was low (2.5%), and a more accurate histological characterization was possible compared to FNAB. Finally, the cost-analysis of different biopsy techniques is presented for the Belgian situation according to used materials, pathology procedures and hospitalization. (Acta gastroenterol. belg., 2003, 66, 160-165).
Pathophysiology of acute pancreatitis : a multistep disease*
Acute pancreatitis is an inflammatory disease diagno- sed mainly in presence of acute abdominal pain associa- ted with a concomitant rise of serum amylase and lipase levels (1-3). In western countries, gallstone migration into the common bile duct and alcohol abuse account for most of the aetiologies of the disease (4-7). The injury is usually mild in 70 to 80% of cases, but 10-20% of the patients have a severe injury and, among them, 15 to 25% will die (4,8).
Early severity indexes in acute pancreatitis
Severe acute pancreatitis was defined at the Atlanta symposium (1) as an attack in which a complication occurs, and so severity cannot be determined until the patient has been discharged from hospital and the pre- sence or absence of complications has been documen- ted. However a prediction of severity may be made at the start of the hospital admission, based on a variety of cli- nical biochemical and radiological features.
Early prediction of severity for individual patients with acute pancreatitis is important for three reasons. First, it is helpful to identify as soon as possible those patients who are most severely ill, who will require aggressive management in the intensive care unit or high dependency area. Second, specific therapy targeted to those patients with severe disease, or predicted severe disease, is becoming a clinical reality. Such therapy should not be offered to patients with mild pancreatitis, who will recover without complications, and who may suffer complications of the treatment offered. There is good evidence to support the use of endoscopic sphincterotomy in patients with gallstones and predicted severe pancreatitis and growing evidence for the use of enteral nutrition in patients with severe disease of any cause (2-8). Selection of these patients for treatment depends on early identification of those at risk of complications. Third, it is helpful when reporting studies of patients with pancreatitis to characterise the group of patients by indicating the numbers who meet criteria of predicted severity at the outset.
NASH-NAFLD Management Summary of the discussion
Considering the male : female ratio of the disease, Prof. James estimates that the ratio is 40:6O.The mild excess of females having this disease is probably due to the higher frequency of mild obesity in this gender.
A high prevalence of NASHrelated cirrhosis is expected.
The presence of NASH is not restricted to developed countries. In India e.g., obesity and secondary diabetes mellitus are very frequent. A possible genetic explana- tion could make Indians more susceptibe for obesity and type 2 diabetes mellitus, resulting in a high prevalence of NASH in this population.
