Annamaria Nemeth

Mechanisms of vagal nerve in gastric mucosal defense: unchanged gastric emptying and increased vascular permeability.

Gastric cytoprotection in response to different agents (prostaglandins, carotenoids, etc.) failed to occur after surgical vagotomy. Decreased gastric emptying and the increased vascular permeability were tested in ethanol-treated rats without and with bilateral surgical vagotomy. The experiments were carried out on Sprague–Dawley rats. The animals were fasted for 24 h before experiments. Bilateral surgical vagotomy or only laparatomy were carried out at 30 min before administration of ethanol (96%, 1 ml). The animals were killed at 0, 1, 5, 15, and 60 min after ethanol administration, when the number and severity of gastric mucosal lesions were noted. In another series of experiments, the animal received Evans blue (1 mg/100 g) i.v. 15 min before killing. The gastric contents were collected and the glandular mucosa was scraped. Evans blue was extracted in chloroform, and its concentration was spectrophotometrically measured. It has been found that (a) both number of lesions and severity of ethanol-induced gastric mucosal damage were larger at each time period in surgically vagotomized rats than in rats with intact vagal nerves; (b) the increased vascular permeability was significantly higher in gastric mucosa at an early period in surgically vagotomized rats compared to rats with intact vagal nerve; (c) the increased vascular events preceded the development of macroscopic appearance of gastric mucosa damage in both groups of animals; and (d) the time-related response were the same in both groups of animals. It is concluded that increased vascular permeability, but not gastric emptying, probably has some role in the failure of the development of gastric cytoprotection in surgically vagotomized rats.

The real face of juvenile polyposis syndrome

Colorectal cancers are mostly sporadic; some cases of familial clustering and autosomal dominant conditions are also known to occur. Juvenile polyposis syndrome (JPS) is an autosomal dominant condition caused by the mutation of the SMAD4 or the BMPR1A genes. JPS is characterized by hamartomatous polyps developing in the upper and lower intestine. Contradicting previous studies, many of these polyps can go through malignant transformation.This paper reports the case of a male patient who was continuously treated for juvenile polyposis. During the eighteen years of treatment, more than hundred polyps were endoscopically removed from his gastrointestinal tract. The patients care was interrupted for eight years due to insufficient compliance. He was subsequently referred to our Department of Gastroenterology in severe clinical condition caused by metastatic colorectal cancer. He died after a short palliative therapy at the age of 31. His first-degree accessible relatives were further examined for juvenile polyposis syndrome. Several gastrointestinal polyps of different histological origin were observed in the deceased patients brother, who subsequently had to undergo a left lateral hemicolectomy. Genetic analyses revealed mutations of the BMPR1A gene in the clinically affected brother, the brothers daughter, and in the deceased probands daughter.Indebt genetic analyses helped customize and deliver care to a very specific group of individuals. We were able to identify potential family members on whom preventive care and treatment could be focused and simultaneously prevented unnecessary clinical and invasive procedures on those who were healthy. Furthermore, these analyses helped prevent future unnecessary trauma or distress on the analyzed family.

Serum beta-crosslaps concentration and its correlation to the bone mineral density of patients with inflammatory bowel disease

Background: Patients with inflammatory bowel disease (IBD) have decreased bone mineral density (BMD). According to the reported data, the metabolic bone disorder of patients with Crohns disease (CD) is more severe than that of patients with ulcerative colitis (UC). Beta-CrossLaps is a C-telopeptide breakdown product of type 1 collagen, reflecting the bone resorption. Aims: The aim of the present study was to determine the clinical relevance of serum beta-CrossLaps (bCL) measurement in patients with inflammatory bowel diseases (IBD). Patients and methods: 50 IBD patients (27 UC, 23 CD) and 45 healthy controls (HC) were studied. The male/female ratio was 28/22 in the IBD group, and 12133 in the HC group. The mean age in IBD and HC groups were 37.5 and 31.5 years, resp. Bone mineral density of the lumbar spine. femoral neck and the distal third of radius was measured by DEXA method (Hologic QDR 4500C). Serum bCL was determined by immunoassay (Elecsys, Roche). Results: Serum bCL levels of healthy subjects (0.276~0.146: meanz Sfr) were within the reference range provided by the manufacturer (0-0.35 ng/ml). The difference in bCL concentration between the CD and HC groups was significant (0.425~0.27 vs. 0.276~ 0.146; p=0.007), while the bCL levels ofUC and HC groups was not different (0.278~0.208 vs. 0.276 ~0.146). Serum bCL levels and the lumbar spine BMD z-scores corraleted significantly in patients with CD (r= 0.51, p=0.019). There were no significant correlations between the serum bCL and z-scores at the femoral neck and the distal third of radius in patients with CD and UC, resp. Conclusion: There is a significant correlation between serum bCL concentration and the bone mineral density of CD patients. Serum bCL level correlates to the bone mineral density of the lumbar spine (z-score). Serum bCL measurement may be a useful laboratory marker for the assessment of the metabolic bone disease in patients with lBO, particularly in those with CD.