Happy Accidents: Serendipity in Major Medical Breakthroughs in the Twentieth Century

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Authors: Morton A. Meyers
Tags: Reference, Health & Fitness, Technology & Engineering, Biomedical
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caused by a regressive wish to be dependent on others, the feelings stimulating increased gastric motility and secretion in anticipation of being fed by idealized parents. When the wish cannot be gratified through normal adult relationships, it was concluded, an ulcer results. In Stress and Disease, an influential medical textbook published in 1968, Harold G. Wolff, a well-known psychiatrist, described excess gastric secretion as a reaction to rampant “competitive striving” and other pressures of contemporary society, despite the fact that stressful life events had not been shown to be more common in patients with ulcers than in the general population.
    Nevertheless, the stress-acid theory of ulcers gained further credibility when safe and effective agents to reduce gastric acid, known as H2 blockers, were introduced in the 1970s. Acid inhibitors, such as cimetidine (Tagamet) and ranitidine (Zantac), became so popular and were taken over such extended periods that they became the world's biggest-selling prescription drugs. By 1992 the worldwide market for prescription ulcer medications amounted to $6 billion a year. Ulcers affect one in ten adults in the Western world. These acid inhibitors are effective at easing symptoms, but they fail to prevent ulcers from recurring.
    S WIMMING A GAINST THE T IDE OF “C ERTAINTY ”
    No one ever even considered a bacterial cause for ulcers. Gastroenterologists invariably thought the stomach a sterile environment. Gastric juices are so acidic, a tooth immersed in a container of the fluid overnight would have its enamel dissolved. It was taken as doctrine that bacteria could not survive and flourish in such a harsh, inhospitable environment. It is nevertheless a curious historical fact that, over the years, spiral bacteria were glimpsed in specimens of the human stomach but were dismissed as either contaminants or opportunists that had colonized the tissue near ulcers. In 1954 a widely respected gastroenterologist reported finding no spiral bacteria in more than a thousand biopsy specimens of the stomach, and this report provided what was considered “conclusive” evidence that gastric bacteria, if present, were incidental. 3
    The overthrow of long-held but false concepts frequently is initiated not by those at the top of their fields but rather by those at the fringes. And technological advances in the 1970s opened a new door. Flexible fiberoptic gastroscopes enabled doctors to take targeted biopsy samples from a larger area of the stomach. In 1979 J. Robin Warren, a staff pathologist at the Royal Perth Hospital in Western Australia, was examining biopsy samples from patients with gastritis when he made a puzzling observation: there were unexpectedly large numbers of curved and spiral-shaped bacteria. He then used a special stain to make their number and shape more evident and saw that stomach cells near the bacteria were damaged.
    Warren persisted in his systematic observations over the next two years. The bacteria were present in many gastric biopsies, usually in association with persistent stomach inflammation, termed chronic superficial gastritis. They were sited, often in colonies, beneath the mucus layer, indicating that they were not contaminants from the mouth, and were thriving within the mucus. Furthermore, Warren noted that the bacteria were all the same, not varied, as would be expected of secondary invaders.
Slightly Crackers
Later, reflecting on his discovery of what would be identified as H. pylori in the stomach, Warren commented: “It was something that came out of the blue. I happened to be there at the right time, because of the improvements in gastroenterology in the seventies…. Anyone who said there were bacteria in the stomach was thought to be slightly crackers.” 4
    The fact that the bacteria settle particularly in the gastric antrum (the lower part of the stomach), as well as local variations in bacterial density, may explain why previous biopsies had

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