This condition must be considered as a secretory neurosis, either inborn or provoked by errors of diet and life. In cases of long duration it is possible that secondary glandular proliferation may occur, and it is certain that a secondary slight gastric dilatation sometimes ensues. It is the commonest form of indigestion. The characteristic symptom is a burning or gnawing pain in the epigastrium, which begins one or two hours after a meal, or sometimes even later, so that it is described by the patient as "preceding" a meal. It seldom occurs at night. The patient has generally discovered that the pain is relieved by food, by bicarbonate of soda, or by vomiting. Natural vomiting is uncommon, but some patients have been taught by experience to provoke it with the finger. Flatulence (the gas being partly derived from the carbonates of saliva and bile), substernal heartburn, and acid eructations are common. Occasionally severe attacks of gastric (probably pyloric) spasm occur, generally associated with paroxysmal pyrosis.
These symptoms are due to a rapid and excessive secretion of gastric juice. Free hydrochloric acid is found earlier after a test-breakfast (even within ten minutes) than under healthy conditions; the total acidity at the height of digestion, expressed in terms of hydrochloric acid, commonly rises to 03 per cent, occasionally even to 0.6 per cent, or it lies between 70 and 100 on Ewald's scale. It is probable, also, that in some severe cases secretion continues even after digestion is completed (cp. hyper-secretion). Before dietetic treatment is undertaken, it must be made clear that the symptoms are due to hydrochloric acid and not to organic acids. Though organic acids set free by bacterial or toruloid action can notably increase the total acidity of the contents of the stomach, this occurs on a large scale only in cases of pyloric obstruction and gastric dilatation, a condition which as a rule is sufficiently obvious. A total acidity above normal (above 60 on Ewald's scale) after a test-dinner establishes the diagnosis.
If this perversion of secretion is considered in relation to digestion, it will be clear that the normal allowance of time during which starch digestion can continue in the stomach is curtailed by this premature rise of acidity. It ceases when hydrochloric acid amounts to 0.12 per cent. Protein-digestion however is usually well performed, but Boas has recorded cases, in which pepsin was absent and protein-digestion delayed. Theoretically it might be supposed that in consequence of the excessive acidity of the chyme as it enters the duodenum the pancreatic digestion of fat would be delayed, but in practice I do not think that there is evidence of this, though a dislike for fat is occasionally noted. As a rule the stomach is emptied at any rate within normal limits of time, but in severe cases there is delay, which is probably due to pyloric spasm, and occasionally some degree of dilatation results. Perhaps the delay of digestion, which occurs when much starch is taken, may also tend to produce this result. After long continuance of hyperacidity some degree of chronic gastritis may supervene, manifested by a greater tendency to vomit and the appearance of mucus in the vomit. These points, which must be realized in prescribing a suitable diet, present the malady only in its simplest form. Many cases however are complex, and the associated conditions and antecedents must be reckoned up and weighed. Associated with hyperacidity there is often a real gastric hyperaesthesia, either a primary sensory neurosis or a secondary result of continued hyperacidity, and the mere contact of food with the gastric mucosa will then excite pain or discomfort. A loose right kidney and gastroptosis in women are not uncommon associations and add greatly to the difficulty of treatment. Although hyperacidity is commonly associated with gastric ulcer, hyperacidity does not in that association present the characteristic symptoms described above, and gastric ulcer is rarely present and need seldom be suspected, when those typical symptoms are clearly marked. In pure hyperacidity it may be noted that easily digested foods are as likely to produce pain as indigestible articles, and that a large meal may be better borne than a small one. From duodenal ulcer there is greater difficulty of distinction, and the symptoms of such an ulcer and those of hyperacidity may have a close resemblance. The possibility of the co-existence of the two conditions must always be borne in mind, and the occurrence of haematemesis or melaena in a patient who has long suffered from hyperacidity should cause no surprise. The occurrence of pain in the back and rigidity of the right rectus should be noted in this connexion.
Further if treatment is to be precise, some idea must be gained as to the cause of the hyperacidity. It is clear that it arises in some cases from gross causes, such as imperfect mastication, food bolting, hurried meals immediately followed by active movement, excess of protein in the diet, abuse of alcohol, of gastric stimulants and I believe of tobacco. Habitual overfeeding certainly plays a part in the causation in some cases. Some go so far as to regard hyperacidity as being mainly due to long continued excess of protein food. Hemmeter for example suggests that it is an "adaptive process," meaning that the power of the glandular structures to secrete acid has been increased in response to the excessive stimulus of excess of meat in the diet. Certainly it is not a common condition in hospital classes, of whose diet bread and butter are the chief constituents. Such cases as seem to arise from one or more of these avoidable causes afford great satisfaction in treatment. But a history of such a faulty life is by no means so commonly obtained as in cases of dilatation and chronic gastritis. Hyperacidity often occurs without any obvious avoidable cause.
The general health is usually good. But in many cases an obvious nervous defect underlies the condition. Though it is more common in men than in women, its subjects are usually high-strung and excitable, apt to hurry when no haste is needed. They may belong to the leisured class and voluntarily adopt a strenuous life, but commonly they are tied to an occupation which entails quick meals, train-catching, excitement and worry. This is often found to be a serious obstacle to successful treatment. It is aggravated by shock, emotion or work under pressure, and in some patients it occurs in attacks only under such influences, so that in quiet times any kind of food can be taken with impunity. As in all gastric and intestinal neuroses, idiosyncrasies as regards certain articles of diet may come to light when treatment is begun, and these will add to the difficulty.