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Results of the complex diagnosis and surgical treatment of 180 patients with perforation of gastroduodenal ulcers were analyzed. It was shown that in pathogenesis of perforations of chronic gastroduodenal ulcers the leading place belonged to oxidizing stress. A pathogenetically grounded method of treatment of perforations of chronic gastroduodenal ulcers is an excision of the perforated ulcers in combination with vagotomy, but the method of treatment of perforations of "silent" ulcers is videolaparoscopic suture with endoscopic transgastgric chemical vagotomy.

The results of examinations and treatment of 338 patients operated by reason of perforated gastric and duodenal ulcer (PGDU). It was established, that parenteral and oral nutrition in PGDU patients after traditional surgical operation did not improve patients' trophic state. Performance of early enteral nutrition with Pevzner's diet and nutritive maintenance during all postoperative period in patients, operated by low-invasive methods, has favorable influence on patients' trophic state.

Experiments were performed in 18 male rats followed by a histological investigation of the obtained material. The application of the 30% solution of ethyl alcohol was proved to cause irreversible dystrophic alterations of nerve fibers in the gastric wall when injected subserously and there were no irreversible destructive alterations in other organ tissues. Results of treatment of 82 patients with perforated pyloro-duodenal ulcers after suturing the perforated opening in combination with chemical denervation of the gastric acid-producing zone with 30% solution of ethyl alcohol injected subserously were analyzed. Reliably decreased acid-proteolytic activity of the gastric body was found to result in stable remission and low percentage of recurrent diseases. The method can be recommended for wide practical use due to its simplicity and low percentage of recurrences of ulcer disease of the duodenum against the background of preserved helicobacteriosis of the stomach.

To investigate the distribution and origin of alpha-smooth muscle actin (ASMA)-positive stromal cells in the perforation of human gastroduodenal ulcers. Perforative lesions of 24 surgically resected gastroduodenal ulcers were examined immunohistochemically for ASMA, HCD, CD34, CD31, CAM5.2 and HMW-CK, and double staining of ASMA and CAM5.2 was also performed. In addition, to determine the cell source of collagen, in situ hybridization of collagen I mRNA was performed. In the normal gastroduodenal wall, the reticular network of CD34-positive stromal cells was identified in the muscularis mucosa, submucosa, muscular propria, and subserosa. In the subepithelial area, many myofibroblasts were observed, whereas no CD34-positive stromal cells were seen. In areas neighboring ulcerative lesions, no CD34-positive stromal cells were observed, but a significant number of myofibroblasts were present there. In the deep layer of ulceration, numerous fusiform or stellate stromal cells strongly positive for ASMA and CAM5.2 were observed in the subserosal area around the perforation. In the same site, many cells co-expressing ASMA and CAM5.2 were identified by double staining. In contrast, in the surface layer of ulceration, stromal cells expressing only ASMA were observed. The cytokeratin-positive subserosal myofibroblastic cell in human gastroduodenal ulcer is a novel type of myofibroblast.

The authors report corticosteroïd-therapy of giant cell arteritis of a woman who presented a gastric ulceration induced by indometacin. They point out interest of H2 receptor antagonist coupled with steroid-therapy.

Basal and pentagastrin stimulated acid output was measured in 80 normal and 179 duodenal ulcer subjects of Chinese, Indian and Malay origin. Basal and maximally stimulated acid output was significantly higher in duodenal ulcer patients compared with normal subjects. There was however considerable overlap and less than one in four duodenal ulcer patients were hypersecretors. The acid output (and hence the parietal cell mass) was lower than in Caucasian subjects and this was possibly related to weight differences. The acid output did not differ significantly in the Chinese, Indian and Malay subjects, suggesting that parietal cell mass in the three racial groups is closely similar. The difference in frequency of duodenal ulcer disease in the three racial groups is thus not related to gastric secretory capacity.

The amylase:creatinine clearance ratio in patients suffering from acute pancreatitis or acute duodenal perforation was higher than normal in both groups of patients. These findings cast doubt on the value of this parameter as a specific index of acute pancreatitis. The mechanism or mechanisms underlying the increased amylase excretion have not been determined. However, the markedly elevated urinary excretion of lysozyme observed in some patients suggests, by analogy, that diminished tubular reabsorption of amylase may contribute towards the elevated amylase:creatinine ratio.

It was felt that the apparent specificity of the amylase-to-creatine clearance ratio (ACCR) in several previous studies of pancreatitis might reflect a failure to utilize adequately ill control subjects. The ACCR and the renal clearances of beta 2-microglobulin (B2-m), similarly related to creatinine (BCCR) as well as the urinary concentration of albumin, were compared in 27 patients with acute pancreatitis, 8 with a perforated peptic ulcer and 7 with mild biliary colic, during the first 5 days in hospital. Acute pancreatitis was graded as mild (6), moderate (14) or severe (7), using a combination of clinical data, diagnostic peritoneal lavage and multiple criteria. Further assessment of the severity of the acute illness was obtained from measurement of C-reactive protein (C-RP). Lowest C-RP levels were found in the patients with mild pancreatitis and biliary colic, and highest levels in the patients with severe pancreatitis and perforated ulcer (P less than 0.002). Similarly, ACCR and BCCR levels were significantly lower in the two mild groups than in the two severe ones (P less than 0.01 and less than 0.002 respectively), although plasma amylase was raised only in patients with pancreatitis and plasma B2-m was similar in all groups. Electrophoresis of urine showed dense bands of tubuloprotein in patients from both severe groups. Urine albumin was higher in severe pancreatitis than in perforated ulcer (P less than 0.1), perhaps indicating a more specific glomerular lesion in pancreatitis. Thus a rise in amylase clearance appeared to be related to the severity of the acute illness, and may be a component of a non-specific tubuloproteinuria. In this study patients with a perforated peptic ulcer had increases in ACCR similar to those seen in patients with severe pancreatitis, and we are therefore doubtful whether ACCR has any role in the clinical diagnosis of pancreatic disease.

Perforation of ulcer occurred after distinct impairments in protective mechanisms of gastric mucosal membrane; this suggestion was corroborated by studies of glycoprotein content in blood serum of patients with perforating gastroduodenal ulcer within the early postoperation period. Studies of the glycoprotein in blood serum and urine within the later periods after the operation showed that the mucosal protective barrier was completely restored in some patients, thus protecting against the ulcer exacerbation, while recurrence of the disease was observed in the patients with deteriorated protective mechanisms in gastric mucosal membrane.