George B. Jerzy Glass

Correlative study of hydrochloric acid, pepsin, and intrinsic factor secretion in newborns and infants

The developmental patterns of secretion of hydrochloric acid, pepsin, and intrinsic factor were studied, following Histalog stimulation, in gastric juice of infants 12 hr to 3 months old. In the first day of life, the outputs of hydrochloric acid, intrinsic factor, and pepsin were very low, but in no instance was achlorhydria found. The outputs of these three glandular secretory components then showed a gradual increase until the third week after birth, followed by a short decline in the third to fourth week, and a second sustained rise continuing into the second and third month of life.A good correlation was observed between the outputs of hydrochloric acid and intrinsic factor in gastric juice of the neonate following Histalog stimulation; and a somewhat poorer correlation between that of intrinsic factor and pepsin.When secretory outputs were recalculated for body weight, those of intrinsic factor in infants 2–3 months old were at levels comparable to that observed in older children and adults; those of hydrochloric acid, at the lower range of normal, or slightly below adult levels; and that of pepsin, well below adult values.On serial determinations, one infant showed intrinsic-factor activity, throughout the period of study, that was well below that of other infants of comparable age. The possible relationship of this case to juvenile pernicious anemia is discussed.

Atrophic gastritis: Structural and ultrastructural alterations, exfoliative cytology and enzyme cytochemistry and histochemistry, proliferation kinetics, immunological derangements and other causes, and clinical associations and sequellae

Our main purpose in this review article is to present some of the vast amount of information on the subject of atrophic gastritis available at the present time. Various areas of research pertaining to this entity, including that from the authors laboratory, are reviewed in this article, encompassing histological and ultrastructural abnormalities, enzyme histochemistry, and exfoliative cytology and cytochemistry of chronic gastritis, with emphasis on the diagnostic significance of these laboratory methods. The altered cell proliferation kinetics in atrophic gastric lesions is also discussed, as well as its significance in the proliferation and reduction of glandular cells of the gastric mucosa. Furthermore, some of the more recent evidence of immunological mechanisms and other causes of chronic gastritis, such as chronic alcoholism and bile reflux, is reviewed, as well as the effects of partial gastrectomy on the gastric mucosa. The important associations and sequellae of atrophic gastritis, such as gastric ulcer, gastric polyps, and gastric cancer, are discussed in detail.

The stress ulcer syndrome

Summary o 1. In 3% of 2,297 men who sustained intracranial, spinal cord and intra-abdominal combat wounds gastrointestinal bleeding developed. 2. Gastrointestinal bleeding was more common following intra-abdominal trauma than intracranial trauma. 3. Subtotal gastric resection and vagotomy and removal of localized deep ulcer craters controlled gastrointestinal bleeding, if nonoperative management failed. The indication for and type of operation should be tailored to the overall clinical condition of the patient and pathologic lesion encountered. 4. The stress ulcer of the stomach or duodenum has been the dominant grossly visible clinical feature to the surgeon. The gross and microscopic pathologic lesions that we encountered included several related stages of what has been called the stress ulcer syndrome. These included microscopic epithelial necrosis; grossly visible superficial erosion and deep ulceration of stomach, small bowel or colon; and hemorrhagic necrosis of the entire gut. Because of the varied and generalized nature of these pathologic lesions, we prefer to use the descriptive term “acute gastrointestinal focal necrosis syndrome” (AGFNS), rather than the commonly used term “stress ulcer.” 5. That the AGFNS is probably initiated very early following trauma is suggested by the advanced chronic inflammatory histopathologic changes found in operative specimens. 6. No increase in urinary steroid excretion was found following trauma, which speaks against the role of the adrenals in initiating gastrointestinal lesions of stress. 7. Net acid output was below normal in the first 24 hours, perhaps due to initiation of back diffusion of hydrogen ions immediately following trauma. This acid output increased gradually on subsequent post-trauma days in all patients in whom prospective measurements were made. Therefore, prophylactic antacid therapy may be important to protect against initial acid back diffusion and subsequent increased net acid output. 8. A serum protein leak into the gastric content was found in all patients following trauma, but was greater in those who oozed larger amounts of blood into the stomach lumen or who bled grossly. This suggests all of our patients had some degree of permeability derangement of the gastrointestinal mucosal barrier. 9. No decrease in gastric sialic acid and other oligosaccharides was found following trauma, which suggested that the previously postulated deficiency of the gastric mucus barrier was not a primary causative factor. 10. The output of SGP and NSGP showed a gradual increase after trauma. This was the largest in grossly bleeding patients, in those oozing blood into the stomach and just prior to bleeding. Also, the output of individual carbohydrates (fucose, hexosamines, sialic acid) increased just prior to the bleeding. These findings can be considered as a manifestation of focal necrosis of the gastric surface epithelium preceding the bleeding and associated with shedding of mucous cells into the lumen. The focal denudation of the gastric mucosa from protective mucus layer at the time of increased gastric output in turn may contribute to a potentiation of existing gastric mucosal damage due to trauma of multifactorial pathogenesis. The less marked increase in the carbohydrate content of gastric juice which occurs at a later date in nonbleeding patients may be related in part to mucosal cell regeneration seen at that time histologically. 11. Clinically evident gastrointestinal bleeding is only a partial manifestation of the AGFNS. In a large portion of post-trauma patients in whom no gross bleeding was recognized, the chemical assay of heme in gastric juice showed the presence of 5–60 ml of blood/L of gastric content. The mechanism appears to be similar to that of gross bleeding as shown by its association with serum protein leakage and changes in gastric mucosubstances. It should be recognized as an equivalent of gross gastrointestinal bleeding and searched for and managed accordingly. 12. Bile reflux was associated in our patients with blood entry into the stomach. However, clinically significant gastrointestinal bleeding and increased serum protein leak into the stomach did not correlate with the presence of bile in gastric contents.

Effects of Salicylates on the Canine Stomach: A Morphological and Histochemical Study

The acute and chronic effects of aspirin (100 to 300 mg per kg) administered orally for 1 to 4 weeks were determined in 3 dogs bearing total gastric fistulae and in 2 intact dogs. Serial gastroscopic examinations were carried out in the fistula-bearing dogs permitting visual inspection and procurement of biopsy specimens, and autopsy specimens were available in 4 dogs. Histochemical techniques and in vivo radioautography using Na235S04 for sulfated mucin incorporation were employed. Aspirin induced systemic signs of toxicity in all animals with three fatalities. One dog died of hematemesis due to bleeding jejunal erosions, and 1 died from a perforated gastric ulcer. Gross lesions included hemorrhagic mucosal erosions and, with higher doses, larger erosions and generally shallow ulcers. The most common histopathological changes were degeneration or necrosis of surface epithelium and mucosal hemorrhages. The fresh ulcers and larger erosions exhibited signs of acute inflammation; older lesions showed early stromal and epithelial repair. In grossly normal areas, a cuboidal regenerative-type surface epithelium and numerous mitoses in the crypts were frequently found, suggesting a chronic response to sustained, aspirin-induced damage. Intracellular mucin was reduced in both damaged and regenerating epithelium.

Intestinal Absorption of Vitamin B12 in Humans as Studied by Isotope Technic.

Summary The scintillation measurements of the hepatic uptake of C060-B12 following its oral and parenteral administration to 20 normal humans, indicate that the efficiency of intestinal absorption of vit. B12 decreases sharply on increase of the intake. The peak of the absorption curve of vit. B12 was found at the oral dose of 0.5 μg, at which the hepatic uptake was found equivalent to 90.5 ± 5.8% of that observed following intramuscular injection of a similar dose of this vitamin. With the increase of the dose, a progressive decline in absorption followed a hyperbolic regression curve, so that at the oral dose of 50 μg B12 the hepatic uptake was equivalent to only 3.0 ± 0.7% of that found after intramuscular injection of a similar dose of this vitamin. The data obtained indicate that the increment in the oral dose of vit. B12 from 0.5 to 50.0 μg, results apparently in an increase of the amount absorbed of only 1.0 μg. It is suggested that in addition to Castles gastric intrinsic factor, an intramural “intestinal B12-acceptor” exists, which may be responsible for the partial mucosal block to the absorption of vit. B12 in the intestine of normal humans. The role of this hypothetic acceptor in the absorption of vit. B12 might be analogous to that of apoferritin in intestinal absorption of iron.

Effect of Prolonged Administration of Parietal Cell Antibodies from Patients with Atrophic Gastritis and Pernicious Anemia on the Parietal Cell Mass and Hydrochloric Acid Output in Rats

Mild atrophic lesions were produced in gastric mucosa of rats injected for 6 to 8 weeks with immunoglobulin G processed from sera of patients with atrophic gastritis and pernicious anemia, containing circulating parietal cell antibody. These changes consisted of thinning of the mucosa, decrease of the mucosal volume, and significant reduction of parietal cell mass, but without signs of inflammation and delayed hypersensitivity reaction. No similar lesions were observed in control animals. The parallel between the reduction of the parietal cell mass and decrease of the mucosal volume, as well as decrease in the intrinsic factor activity of the gastric juice of rats treated for 8 weeks with parietal cell antibodies containing immunoglobulin G, suggests concomitant reduction of peptic cell mass under these circumstances. Rats treated with parietal cell antibodies also demonstrated a profound decrease of the hydrochloric acid output, which was more pronounced than was warranted by the coexisting reduction of the parietal cell mass. This was not seen in control animals. The possible implications and limitations of this study in regard to the problem of gastric atrophy and gastric anacidity in man are discussed.

Passage of serum albumin into the stomach. Its detection by paper electrophoresis of gastric juice in protein-losing gastropathies and gastric cancer.

ConclusionsThe presence of serum albumin in the gastric lumen can be readily diagnosed by paper electrophoresis of the gastric juice. While small amounts of albumin are present in the gastric juice under normal conditions, a massive leakage of serum albumin into the stomach occurs often in gastric cancer, Menetriers disease, and in some cases of gastric atrophy. Paper electrophoresis of the gastric juice has definite clinical significance for the detection of these conditions.

Erosive Gastritis and Acute Gastroduodenal Ulcerations as Source of Upper Gastrointestinal Bleeding in Liver Cirrhosis

This retrospective study was initiated to compare the frequency of acute gastric mucosal lesions (AGML) (including erosive gastritis and acute gastroduodenal ulcerations) in patients with and without

Histochemical Study of the Mucosubstances in the Canine Stomach I. The Resting Mucosa

SummaryTwo sulfated compounds of epithelial origin were identified in the dog gastric mucosa by histochemical and autoradiographic (35SO4) technics. One is a sulfated glycoprotein produced by the surface epithelium and the other a chondroitin sulfate A- or C-like material occurring in chief cells and pyloric glands; both glycoprotein and acid mucopolysaccharide probably contribute to the sulfated fractions found chemically in dog gastric juice. A sialidase-susceptible mucin was found predominantly within superficial cells of the fundus and autrum, and this may be the source of the sialic acid found in the secretions. A strictly neutral glycoprotein was found in the mucous neck and parietal cells, perhaps indicating a relationship between these two cellular elements. In cells containing neutral and acidic mucins, the vicinal hydroxyl and anionic groups were judged to be in close proximity. Strong staining for basic protein was found in parietal cells and a less intense reaction in surface epithelium. Sulfur-containing amino acids were identified by direct and indirect technics in the surface epithelium.

DIFFERENTIATION OF MACROCYTIC ANEMIAS AND DIAGNOSIS OF PERNICIOUS ANEMIA AND SPRUE IN REMISSION BY ACCELERATED MEASUREMENT OF HEPATIC UPTAKE OF RADIOACTIVE Co60B12

Excerpt The differential diagnosis of various types of macrocytic anemia often presents difficult clinical problems. Many cases of dietary folic acid or B12deficiency and sprue cannot be distinguis...