In vitro studies have found a potential for acid rebound to occur due to antacid overuse, however the significance of this finding has been called into question. Properties of antacids
When an excess amount of acid is produced in the stomach, the natural mucous barrier that protects the lining of the stomach can degrade, leading to pain and irritation. There is also potential for the development of acid reflux, which can cause pain and damage to the esophagus. Antacids contain alkaline ions that chemically neutralize stomach gastric acid, reducing damage to the stomach lining and esophagus, and relieving pain. Some antacids also inhibit pepsin, an enzyme that can damage the esophagus in acid reflux.Antacids do not directly inhibit acid secretion, and thus are distinct from acid-reducing drugs like H2-receptor antagonists or proton pump inhibitors. Antacids do not kill the bacteria Helicobacter pylori, which causes most ulcers. Interactions
Antacids are known to interact with several oral medications, including fluoroquinolone and tetracycline antibiotics, iron, itraconazole, and prednisone. Metal chelation is responsible for some of these interactions (e.g. fluoroquinolones, tetracyclines), leading to decreased absorption of the chelated drug. Some interactions may be due to the pH increase observed in the stomach following antacid ingestion, leading to increased absorption of weak acids, and decreased absorption of weak bases.
Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system, first described by Edwin Bickerstaff in 1951. It may also affect the peripheral nervous system, and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome. Signs and symptoms
In order to diagnose Bickerstaff brainstem encephalitis, ataxia and ophthalmoplegia must be present. These are also diagnostic features of Miller Fisher syndrome, and so Bickerstaffs is only diagnosed if other features are present which exclude Miller Fisher syndrome. These may include drowsiness, coma or hyperreflexia. When the condition is defined in this way, a number of other features are commonly but not always found: among these are weakness of the limbs, the face, and/or the bulbar muscles; abnormalities of the pupils; and absent reflexes.Like some other autoimmune diseases, the condition usually follows a minor infection, such as a respiratory tract infection or gastroenteritis. Pathophysiology
The clinical features and course of the condition, the associated auto-antibodies against relevant antigens, and the response to treatment, all suggest that Bickerstaff brainstem encephalitis is an autoimmune disease. However, each of these criteria fails to fit a substantial proportion of patients, and there is no single test or feature which is diagnostic of Bickerstaff brainstem encephalitis. It is, therefore, possible that a proportion of cases are due to other causes, such as infection or lymphoma, but remain undiagnosed. It is also possible that there is more than one autoimmune disease that can cause an illness that would currently be diagnosed as Bickerstaffs.