Italian journal of gastroenterology and hepatology最新文献

Neuroendocrine tumours of the gastroenteropancreatic tract are growths originating either from the cells of the diffuse (neuro)endocrine system, such as gastric carcinoids and islet cell tumours, or from nerve structures, such as duodenal paragangliomas. A great deal of cellular and clinical information is available whereas data concerning the genetic and molecular basis of diffuse (neuro)endocrine system tumours of the gastroenteropancreatic tract are very few and fragmentary. The present paper reviews some genetic and molecular investigations of potential interest. As far as concerns the genetic background of diffuse (neuro)endocrine system tumours, the frequent loss of heterozygosity for the locus of Multiple Endocrine Neoplasia type 1 in tumour samples suggests a potential role of the Multiple Endocrine Neoplasia gene. With regard to the molecular background, no mutation of the p53 or retinoblastoma susceptibility (Rb) genes has been demonstrated. Useful data have been generated by in situ analysis of the proliferation activity of tumours.

Positron emission tomography is an in vivo tracer and imaging technique that utilizes short-lived positron emitting radionuclides (11C, 15O, 13N, 18F) with half-lives ranging between 2 min and 2 hours. These radionuclides are interesting from the labelling viewpoint since they are natural constituents of most biologically active compounds. The short half-life is an advantage with regard to the irradiation dose to the patient but it is also a limitation since it requires the production of these radionuclides in close vicinity to the positron emission tomography camera.

Gastrointestinal endocrine neoplasms are rare tumours that have been classified by the peptides they secrete and the resulting clinical syndromes. The incidence of these tumours is estimated to be less than 1-1.5 cases/100,000 of the general population. These gastrointestinal endocrine cells are characterized by similar cytochemical and ultrastructural characteristics, contain amines and they are capable of uptake of amine precursors to amines or peptides. The function of these cells is the neuroendocrine regulation of normal homeostatic mechanisms including vasomotor tone as well as carbohydrate, calcium and electrolyte metabolism. Each amine precursor uptake and decarboxylation cell normally synthesizes, stores and secretes its single amine or polypeptide and is responsive to its environment for stimulation or suppression in the related clinical syndrome.

Background: The excessive accumulation of cholesterol absorbed from bile by the gallbladder impairs its contractility and favours gallstone formation. The total low plasma and high density lipoprotein cholesterol concentrations are associated with gallstone disease.

Aims: To investigate the effect of plasma lipoproteins on gallbladder cholesterol and phosphatidylcholine absorption from bile and to establish whether cholesterol absorption is Brefeldin A-sensitive.

Methods: Gallbladder mucosa lipid absorption rates were measured using: 1) in vitro isolated intra-arterially perfused pig gallbladder model with and without plasma lipoproteins perfusing the vascular tree; 2) human gallbladder fragments mounted in Ussing chambers with plasma lipoproteins at different concentrations in the serosal side; 3) pig gallbladder fragments mounted in Ussing chambers in the presence and absence of Brefeldin A.

Results: Total lipoproteins and high density lipoprotein significantly increased the release of biliary cholesterol and phosphatidylcholine in plasma and significantly decreased the tissue accumulation of cholesterol absorbed from bile. The scavenger effect of plasma lipoproteins on cholesterol absorbed from bile was concentration dependent. Brefeldin A did not influence gallbladder absorption of biliary cholesterol.

Conclusions: Biliary cholesterol is absorbed by gallbladder mucosa via a Brefeldin-insensitive pathway and is removed by plasma lipoproteins.

The association between mixed cryoglobulinaemia and chronic hepatitis C virus infection has recently been described. Cryoglobulinaemic glomerulonephritis, a complication of mixed cryoglobulinaemia, is usually treated with immunosuppressive therapy, but, given the presence of viral infection, this therapy is no longer recommended. This report concerns a case of a 30-year-old patient with cryoglobulinaemic glomerulonephritis, refractory to steroid treatment, in whom recovery from hepatitis C virus infection was obtained as well as from cryoglobulinaemic glomerulonephritis after interferon therapy. The clinical symptoms and laboratory tests were normal after prolonged interferon therapy and, 3 years after the end of treatment, the patient is free from disease.

Many syndromes reflecting impaired metabolism have been described in association with primary neoplastic diseases. Hypercalcaemia secondary to malignancy without bone metastases and with normal parathyroid glands has been described as "pseudohyperparathyroidism". Differentiation from primary hyperparathyroidism is difficult and care should be taken to exclude an occult malignancy prior to surgical exploration for a parathyroid adenoma. Hypercalcaemia associated with hepatocellular carcinoma is not uncommon. Nevertheless, we describe a rare case of coma with persistent hypercalcaemia in a cirrhotic patient not previously known to have hepatocellular carcinoma.

The incidence of bacterial infections in cirrhotic patients admitted to hospital is very high. In several studies, 30% to 50% of cirrhotics presented bacterial infections at admission, or developed this type of complication during hospitalization. Most bacterial infections in cirrhotic patients are hospital-acquired. Between 15% to 35% of cirrhotics admitted to hospital develop nosocomial infections; these figures contrast sharply with the hospital-acquired infection rate in the general hospital population (5% to 7%). Urinary tract infections (12% to 29%), spontaneous bacterial peritonitis (7% to 23%), respiratory tract infections (6% to 10%) and bacteraemia (4% to 9%) are the most frequent bacterial infectious complications seen in cirrhotic patients. However, since spontaneous bacterial peritonitis is the most characteristic bacterial infection in cirrhosis, this report will focus (mainly) on this infectious complication.

In patients with gastro-enteropancreatic neuroendocrine tumours the localization of all the neoplastic lesions and an accurate staging of the diseases have important therapeutic implications. Somatostatin receptor scintigraphy with In-111 pentatreotide has proved to be useful in detecting gastro-enteropancreatic tumours; however, the role of abdominal single photon emission computed tomography has not yet been definitively established. In a series of 52 patients with gastro-enteropancreatic tumours (9 non-functioning islet cell carcinomas, 4 insulinomas, 3 somatostatinomas, 2 VIPomas, 1 glucagonoma and 33 carcinoids) we compared somatostatin receptor scintigraphy with the results of computed tomography and magnetic resonance imaging performed within one month. Four and 24-hour total body planar images and 4-hour abdominal single photon emission computed tomography were acquired after the i.v. injection of approximately 250 MBq of In-111 pentatreotide. Only abdominal localizations were considered: planar scans detected 16 extrahepatic lesions in 13 patients and 54 liver sites in 21 patients; single photon emission computed tomography visualized 31 extrahepatic lesions and 89 liver metastases in 27 and 28 patients, respectively; computed tomography and magnetic resonance imaging detected 11 extrahepatic lesions in 10 patients and 73 liver sites in 21 patients. In-111 pentatreotide single photon emission computed tomography was the only imaging method able to localize tumoural lesions in 13 patients; all these localizations were then histologically verified. The scintigraphic positivity did not depend on the site or on the presence of hormonal hypersecretions. In conclusion, our results indicate that single photon emission computed tomography is more sensitive than planar images and computed tomography/magnetic resonance imaging in detecting abdominal gastro-enteropancreatic tumours and their metastases; it is able to increase both the number of visualized lesions and that of patients with positive findings. Single photon emission computed tomography is particularly useful in patients in whom tumoural lesions have not been already localized; it should be the first imaging modality in patients with gastro-enteropancreatic tumours: its initial use will result in more information and proper management.

We describe a fatal case of Wolman's disease in a 5-month-old Italian infant with severe gastrointestinal symptoms in whom the diagnosis was made from intestinal biopsy findings at the age of 3 1/2 months. Abdominal CT scan, elevated blood acid phosphatase levels and histologic findings confirmed the diagnosis.

Background: Prostate-specific antigen has been considered a specific and sensitive marker of prostate cancer. In recent years, it has been reported that prostate-specific antigen may also be found in pancreatic tissue; however, very little evidence of serum levels of this protein in pancreatic disease has been forthcoming.

Aims: To explore the possibility that pancreatic diseases may influence both total and free serum prostate-specific antigen.

Patients and methods: A total of 72 females were studied: 44 patients with acute pancreatitis: 6 with chronic pancreatitis: 12 with pancreatic carcinoma and 10 healthy volunteers. Total and free serum prostate-specific antigen were measured using commercial kits.

Results: In patients with acute pancreatitis, total and free serum prostate-specific antigen were detectable in two out of the 44 patients (5%). In patients with chronic pancreatitis, total and free serum prostate-specific antigen were undetectable, whereas 4 out of the 12 patients (33%) with pancreatic carcinoma had detectable serum levels of total and free prostate-specific antigen.

Conclusions: Female patients with acute pancreatitis and especially those with pancreatic cancer may have detectable serum levels of total and free prostate-specific antigen. Further studies are necessary to understand why these molecules are elevated in patients with pancreatic diseases, thus affecting the specificity of prostate-specific antigen determination as a prostate tumour marker.