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There are five stages in the development of the cat's gastric glands: 1. During the stage of the indifferent epithelium from day 19 to day 24, the anlage of the stomach develops with all layers; 2. The stage of gland formation from day 24 to day 41 is the beginning of the gland buds. They develop in connection with endocrine cells on day 34 into primitive oxyntic and primitive mucous cells. The latter form the basis for all other cells, including the surface mucous cells; 3. During the stage of gland evagination from day 42 to 55, the anlagen are separated into primitive pits and tubules, while the cells continue to differentiate and the first intermediate cells are seen; 4. The stage of gland branching from day 56 to birth is characterized by the formation of additional glands at the bottom of the pits which change the ordinary anlagen into branched glands. During this stage, the cardiac glands are formed; 5. In the stage of gland maturation from birth to the 9th week, the peptic cells are formed and the glands start functioning. The oxyntic cells show carbonic-anhydrase activity and signs of acid secretion, and, between the weeks 4 and 8, the peptic cells contain pepsinogen, producing a negative reaction to PAS and a positive reaction to HID. Mucous cells and mucous neck cells produce PAS- and AB-positive mucin.

We have recently shown that antigastric autoantibodies occur in a considerable number of Helicobacter pylori (H. pylori) infected patients. Particularly, autoantibodies to canaliculi within parietal cells of human gastric body mucosa are strongly associated with H. pylori gastritis. In this study we analyzed the implications of this type of autoantibody for histological and for clinical parameters of the disease. 126 patients with upper abdominal complaints were included in our study. Several histological and clinical parameters were evaluated. Presence of anticanalicular autoantibodies is significantly correlated with a higher degree of gastritis in the body mucosa, with atrophic changes in the gastric mucosa, with elevated fasting gastrin levels and a decreased pepsinogen I/pepsinogen II ratio. These data indicate, that the host's autoimmune response to canaliculi of parietal cells is of relevance for the pathogenesis and outcome of H. pylori gastritis.

Most undesired side effects in therapy with non-steroidal antiinflammatory drugs (NSAID) mainly effect the gastric and duodenal mucosa. The radioimmunological determination of pepsinogen A and C (pepsinogen group I and II) is qualified for inclusion of the functional and morphologic state of the gastroduodenal mucosa. By determination of the pepsinogens group A and C the influence and the gastroduodenal compatibility of the non-steroidal antiinflammatory drug lonazolac Ca (LCa) [Irritren] were examined in a dosage of 600 mg/d during a 2-weeks therapy. 31 patients with various painful rheumatic diseases and 10 healthy probands as a control group were examined. The results show that the treatment with LCa did not significantly effect mean and median of pepsinogen A- and -C levels in serum. Only in 3.7% of the cases a contemporary increase of pepsinogen A and C occurred, which could be estimated as a beginning superficial gastritis. In addition the beneficial clinical efficacy of LCa was documented by a significant decrease of a tripartite pain score from 2.1 to 1.4. The results point to a very good proportion of clinical efficacy and gastroduodenal side-effects of LCa.

Pepsinogen values were determined in helminth free (n = 12) and naturally raised farmed fallow deer (n = 10-12) from birth (June 1992) to 11 (May 1993) and 15 months (September 1993) of age respectively in 4 weekly intervals. At birth the plasma pepsinogen value was 0.708 +/- 0.197 U Tyrosin/l and decreased thereafter until 14 weeks of age to 0.139 +/- 0.061 U Tyrosin/l in both groups. From the 18th week of age the naturally raised fallow deer, infected with gastrointestinal nematodes, had significantly higher pepsinogen values than the helminth free kept animals. Maximum pepsinogen levels in the naturally raised fallow deer were determined in November 1992 (0.813 +/- 0.336 U Tyrosin/l) and in June 1993 (1.050 +/- 0.163 U Tyrosin/l). In helminth free animals no further decrease of plasma pepsinogen values was seen from 14th week of age onwards: it was 0.202 +/- 0.110 U Tyrosin/l. There was no influence of sex on the plasma pepsinogen values in both groups.

Therapy with non-steroidal anti-inflammatory drugs often causes gastroduodenal side effects. Changes in the gastric mucosa were studied by determination of serum pepsinogen I and pepsinogen II by the means of radioimmunoassay. 41 patients with degenerative rheumatic diseases were divided into two groups, 21 patients receiving 600 mg S(+) ibuprofen daily (3 x 200mg) and 20 patients receiving 900 mg S(+) ibuprofen daily (3 x 300 mg) over a 14-day period. No significant increase occurred in mean and median values of pepsinogen I and II. Indeed, no changes in serum pepsinogen I and II were noted in 80% of the patients in the higher dosage group and in more than 90% of the lower dosage group. None of the gastroduodenal side effects frequently reported during therapy with non-steroidal anti-rheumatic drugs occurred.

Early indications of the development of gastroduodenal lesions can be obtained with the radioimmunological determination of pepsinogen I in serum. The influence of the non-steroidal anti-inflammatory drug Acemetacin in depot form on the course of the pepsinogen levels in serum was examined during 14 day therapy. Mean and median of pepsinogen I in the whole group of 26 patients did not increase significantly. Likewise no increases of the single pepsinogen levels in serum were seen in 85%. Only 4 patients showed increases of about 20 to 27% compared with the initial values. These results indicate that Acemetacin with prolonged action is well tolerated and has only mean influence on the integrity of the mucosa.

Gastroduodenal lesions of the mucosa are known to be the most frequent side effect during therapy with non-steroidal antiinflammatory drugs (NSAIDs). We investigated the radioimmunological determination of serum-pepsinogen I as an indicator for the quality of the gastroduodenal mucosa. A good correlation was found between the endoscopy findings of 78 patients and contemporary determinations of serum-pepsinogen. Further, a follow-up of pepsinogen I was made during the treatment of 107 patients with degenerative rheumatic diseases with eight different NSAIDs. The results recommend the determination of pepsinogen I as an indicator of gastroduodenal mucosal changes under therapy with NSAIDs; this determination gives a deciding factor for the gastrolesive potency of an NSAID.

We compared examinations of uropepsinogen with the histologic status of the gastric mucosa in a prospective study of 199 patients. It was tested whether a determined value of uropepsinogen is defining the histologic status of the gastric mucosa. This question must be answered negative.