Gastric Ulcer and Gastritis THE term gastritis has often been used to describe
dyspepsia in patients who have no radiological evidence convincing evidence that gastritis is a of abdominal symptoms or even presignificant disposes to ulceration has been hard to obtain. J OSKE et aU claimed that 40% of 221 patients with microscopic evidence of chronic atrophic gastritis obtained of an ulcer. But cause
by peroral gastric biopsy had had dyspepsia, a symptom which they attributed to the gastritis; while COGHILL2 found that only 19% of a similar group of 200 patients had abdominal symptoms. Much of the difference between these two results can probably be attributed to the methods of selection used in collecting the patients, and to the variations in microscopic grading and assessment of disability. Furthermore, since chronic gastritis seems to become comparatively common with increasing age, the concurrence of abdominal pain and gastritis could well be fortuitous. It has often been claimed that gastric ulceration is primarily caused by reduced mucosal resistance,34 perhaps associated with chronic gastritis,5 but there is
of determining whether or not the gastritis antedates chronic ulceration. Acute gastric ulcers causing haemorrhage have been found only in areas of damaged mucosa, the microscopic picture, usually of atrophic gastritis,6suggesting that the mucosal damage preceded ulceration. MACKAY and HISLOP7 have described 9 cases illustrating the concept that active chronic atrophic gastritis may be associated with a tendency to recurrent chronic ulceration, often associated with bleeding. To be convincing, MACKAY and HISLOP’S argument should be backed by evidence that chronic gastric ulcers which heal without leaving severe diffuse atrophic gastritis are comparatively resistant to further breakdown. MACKAY and HISLOP’S patients all had severe hypochlorhydria, presumably due to diffuse gastritis; thus conceivably a somewhat paradoxical situation might exist in which gastric-ulcer patients with a low acid secretion would be more liable to recurrence than patients with less severe gastritis and higher levels of add output. Using a different approach, CAPPER and his colleagues8 monitored the pH of the gastric mucosa at operation through a gastrotomy incision during continuous histamine stimulation. They found that chronic ulcers were constantly sited in an alkaline area which was continuous with the pyloric mucosa and that, if the ulcer was high in the body of the stomach, then the alkaline area could be very large. But if the ulcer healed, then the alkaline area at the site of the ulcer seemed to be replaced by acid-secreting and pepsin-secreting cells. Thus a healing ulcer might be associated with a rising acid output in response to histamine stimulation-a no means
1. Joske, R. A., pinckh, E. S., Wood, I. J. Q. Jl Med. 1955, 24, 269. 2. Coghill, N. F. Post-grad. med. J. 1960, 36, 733. 3. Illingworth, C. F. W. J. R. Coll. Surg. Edinb. 1956, 2, 14. 4. Marks, I. N., Shay, H. Lancet, 1959, i, 1107. 5. Tanner N. C. Post-grad. med. J. 1954, 30, 448. 6. Langman, M. J. S., Hansky, J. H., Drury, R. A. B., Jones, F. A.
1964, 5, 550. 7. 8.
Mackay, I. R., Hislop, I. G. ibid. 1966, 7, 228. Capper, W. M., Laidlaw, C. D’A., Buckler, K., Richards, D. Lancet, 1962, ii, 1200.
situation which would give some support to MACKAY and HISLOP’S suggestion that persisting atrophic change leads to recurrence. Parallel with the interest in gastritis as a cause of ulcer, the cause of the gastritis itself has come in for renewed consideration; and COGHILL2 has reviewed evidence suggesting associations with age, alcohol consumption, and the drinking of excessively hot beverages. The typical area of spread of gastritis from the pylorus proximally has suggested that it is caused by duodenal reflux-experimental evidence in support of this belief was provided by LAWSON,9 who found that gastritis ensued when duodenal reflux was induced in dogs. JAMES and PICKERING 10 observed that bile-staining of the gastric aspirate 11is common in patients with gastric ulcer; and DU PLESSis reported that the concentration of bileacid conjugates in the gastric contents of fasting patients tended to be much higher in gastric ulcer than in duodenal ulcer or patients without dyspepsia. Conceivably, as DU PLESSis suggests, the comparatively alkaline duodenal contents act by altering the physical characteristics of gastric mucus so that it becomes a weaker barrier. Acid and pepsin might then cause gastritis which simultaneously leads to reduced acid production and increased liability to ulcer. That the ulcer should appear in the presence of a falling total acid output is perhaps not as unreasonable as may at first appear, since hydrogen-ion concentration may well be much more important than the volume secreted and, as ROWLANDS 12 has pointed out, a 50% reduction of acidity in terms of normality may merely represent a change in pH from 1.1to 15.
Crumbling Edifice THE extreme unrest of junior hospital medical staff exposes the failure of successive Governments to provide the money that is needed for an effective hospital service, and the equal failure of the medical profession’s leaders insist that the service must not only be nourished but also be remoulded. The sources of this unrest must be grasped if it is to be eradicated. Hospitals have insufficient doctors. This is not to
exclusively a hospital problem, nor even exclusively a British problem-though in Britain it has been exacerbated by adoption of the Willink report, in which the profession all too readily acquiesced. But the shortage is at its most acute in the hospital service owing to the survival of the myth, systematically formulated in the early years of the National Health Service, that nearly all medical work not undertaken by consultants can and must be carried out by transients "-those who will become consultants here or abroad, or leave subsequently the hospital service to engage in other work. Perpetuating this myth has involved heavy dependence on several thousand Commonwealth graduates to occupy junior posts; and it is beginning to dawn on the countries from "
9. Lawson, H. H. ibid. 1964, i, 469. 10. James, A. H., Pickering, G. W. Clin. Sci. 1949, 8, 181. 11. du Plessis, D. J. Lancet, 1965, i, 974. 12. Rowlands, E. N. Post-grad, med. J. 1960, 36, 714.