Diagnostic laparoscopic cholecystectomy.
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Biomedical subjects
Publications and source records attributed to H M Spiro.
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We review acid rebound, the seemingly paradoxical increase in acid secretion resulting from administration of an antacid. Primarily a laboratory observation, the demonstration of the phenomenon was a major contributing factor to the swift, and possibly unjustified, fall from grace of calcium carbonate in the therapy of peptic ulcer disease despite years of apparently successful use. Calcium, as carbonate or other salts, causes an increase in gastric acid secretion owing, at least in part, to direct ionic stimulation. Another possible mode of action involves antral alkalinization with subsequent gastrin release. Other antacids, notably magnesium hydroxide and aluminum hydroxide, may therefore also cause rebound, but the data in this area are less convincing. Despite the demonstration that acid rebound occurs, no one has thoroughly investigated its clinical import. What limited data actually exist suggest no obvious clinically significant deleterious effect from use of calcium carbonate in peptic ulcer. Because of calcium carbonate's excellent acid-neutralizing capacity, its venerable past record in treating ulcer disease, and recent observations that low-dose antacids heal peptic ulcers, it is appropriate to reevaluate acid rebound, to focus on its clinical significance, if any.
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In this article, the author comments on the following topics: whether peptic ulcer is a disease or just the sign of another process; whether the crater has a multifactorial origin; the ubiquity of Helicobacter pylori and the conclusion that a specific strain will doubtless prove to be the cause of some, but not all, ulcers; the inherent definitional problem of "nonulcer dyspepsia"; and the controversy over how much gastric acid needs to be reduced to speed the healing of peptic ulcer.
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We evaluated 50 consecutive patients with symptomatic gallstones for the clinical features of biliary pain with particular reference to the timing of their painful episodes. Thirty-eight of the 50 patients were able to provide the time of onset of biliary pain in the 24-h cycle. The time of onset of biliary pain displays significant circadian periodicity (p = 0.0032), with its peak at 00:25 h. Forty-five patients had more than 1 episode of pain. Of these 84% had either all or over half of their attacks of biliary pain at the same clock time. Twenty-two patients with renal colic (a close parallel to biliary pain) and 31 patients with episodic abdominal pain from miscellaneous causes showed no circadian or other periodicity in the time of onset of pain. In only 1 of these patients did the abdominal pain recur consistently at the same clock time. "Typical" biliary pain has its onset at night and tends to recur at the same clock time. It is steady and relatively mild, lasting 1-5 h, it is felt in the right upper quadrant or the epigastrium, may radiate to a variety of sites, is associated with some additional symptoms, and is not usually related to meals. The chronobiological and other features of biliary pain reported here should be useful in the diagnostic evaluation of abdominal pain.
This essay tells the stories of six physicians with inflammatory bowel disease (IBD) to emphasize how important denial and control become when a physician is a patient. Guilt at the supposed psychosomatic "origin" of IBD suggests that we as physicians should never blame our patients for getting sick.
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We review the rise, in the 1930s, and the decline, in the 1960s, of medicine's attention to psychosomatic considerations in ulcerative colitis. Both the rise and decline of interest in psychosomatics resulted from trends outside of the published work which directly contested the issue. In particular, the "rise" period coincided with the heyday of the psychosomatic movement and the "fall" with the autoimmune theory, the introduction of steroids, and other trends. Finally, we offer a general critique of the way the debate over the psychosomatic hypothesis was conducted.
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