An integrated residency in internal and preventive medicine.

The importance of preventive and population-based principles in clinical practice is widely acknowledged. The challenge of imparting these principles in either undergraduate or postgraduate medical education has, however, not been fully met. The necessary skills are provided comprehensively by preventive medicine residency programs, but at the expense of clinical training. Sequential residencies in primary care and preventive medicine, the currently available means of obtaining thorough preparation in both clinical and population-based principles, represent an inefficient, generally unappealing, and non-integrated approach. In response to these concerns, and in an effort to make preventive medicine training appeal to a wider audience, the authors developed and implemented a residency program fully integrating internal and preventive medicine. The program meets, and generally exceeds, the requirements of both specialty boards over a four-year period. The program provides extensive training in clinical, preventive, and public health skills, along with case management and cost-effective care, conferring the MPH degree and leading to dual board eligibility. The model is ideally wed to the demands of the modern health care environment in the United States, is extremely attractive to applicants, and may warrant replication both to train academic and administrative leaders and to raise the standards of preventive and public health practice in primary care.

Does acid suppression by antacids and H2 receptor antagonists increase the incidence of atrophic gastritis in patients with or without H. pylori gastritis?

Currently there is controversial evidence that suggests that the accepted incidence of atrophic gastritis of 1.2 to 3.3% in patients with Helicobacter pylori gastritis may be increased by the long-term suppression of acid by a proton pump inhibitor (omeprazole). The purpose of this study is to show whether lesser forms of acid suppression by antacids or H2 receptor antagonists may have an influence on the development of atrophic gastritis. The authors recently reported a study in which a cohort of 36 patients with symptoms of dyspepsia were followed clinically for a period of 7 to 19 years. In that report all subjects underwent upper endoscopy with two biopsy specimens each from the antrum and fundus, on at least two occasions, 7 to 19 years apart. A diagnosis of atrophic gastritis was based on the interpretation of these biopsies by two gastrointestinal pathologists. The presence of H. pylori colonization was determined by tissue sampling and by a campylobacter-like organisms test of the antrum. Of the 36 patients in the authors' previous report, 33 had adequate baseline and follow-up data on medications consumed throughout the period of the study. In their current report they now present the findings of a retrospective review in which they correlate the presence of atrophic gastritis with the sole use of antacids and H2 receptor antagonists throughout the period of the study. In the cohort of 33 patients evaluated from the previous report, the authors found that atrophic gastritis had developed in all 28 patients positive for H. pylori, and in none of the 5 patients negative for H. pylori (p < 0.0001). A retrospective analysis of this previously studied cohort of 33 patients revealed that the use of antacids and H2 receptor antagonists did not predict the development of atrophic gastritis in either H. pylori-negative or -positive subjects. In a retrospective analysis of a cohort of 33 patients followed for an average of 11.7 years, atrophic gastritis developed in H. pylori-positive but not in H. pylori-negative subjects, irrespective of the use and duration of antacids or H2 receptor antagonists.

Long-term symptom patterns, endoscopic findings, and gastric histology in Helicobacter pylori-infected and -uninfected patients.

There is a paucity of data on the long-term behavior of dyspepsia, endoscopic findings, and gastroduodenal histology in patients with or without Helicobacter pylori colonization. We evaluated these parameters during a period of 7 to 19 years (average, 12.3 years) by baseline and follow-up studies. In 36 patients studied, the pattern of gastroduodenal dyspepsia and esophagogastroduodenoscopy findings remained essentially unchanged in 67% and 56% respectively. Dyspepsia patterns did not correlate significantly with either endoscopic or histologic findings, including the severity or location of gastritis in the fundus or antrum, or the presence or absence of H. pylori gastritis. Of 36 patients with adequate biopsies of the fundus and antrum, H. pylori colonization with gastritis was present in 73% but not in 27%. Progression to various degrees of atrophic gastritis was noted in 100% with, and in none without, H. pylori gastritis. In the fundus, atrophy progressed from 14% to 56%, but intestinal metaplasia did not change. In the antrum, atrophy increased from 22% to 64% and intestinal metaplasia increased from 17% to 36%. No patient demonstrated dysplasia, but severe atrophy was seen in the fundus (6%) and antrum (11%). Only two patients (5%) had severe loss of glandular elements and very low pepsinogen I, and thus can be considered to have developed advanced gastric atrophy.

Gastroduodenal dyspepsia: a personal view integrating clinical, endoscopic, histological and management criteria. The spiro syndrome.

I am presenting my view on how to approach the difficult subject of dyspepsia, based on my personal experience and the writings and teachings of Howard M. Spiro. Symptoms arising from the esophagus, and called esophageal dyspepsia, are separated from symptoms arising from the stomach, designated as gastroduodenal dyspepsia. The holistic approach to patients with dyspepsia, and designated Spiro syndrome, is the main purpose of this report. I am introducing a newly defined classification, and criteria, using an interchangeable, standardized nomenclature, to be used by the clinician, endoscopist, and pathologist for diagnosing and managing the causes of gastroduodenal dyspepsia. There are five clinical/endoscopic/histological categories to be considered as possible causes of gastroduodenal dyspepsia. Often these entities are found to be asymptomatic, or a combination may cause symptoms: (1) idiopathic dyspepsia--normal endoscopy and histology; (2) congestive gastropathy/duodenopathy; (3) gastritis/duodenitis; (4) peptic ulcer crater, and (5) gastric cancer. I believe this holistic, unifying approach to diagnosis and management of dyspepsia will enhance the communication between physicians and help standardize the terminology for clinical investigation.

The Yale-Affiliated Gastroenterology Program: 1965-1995. A community-university model of collaboration.

The Yale-Affiliated Gastroenterology Program (YAGP) originated in 1965 from the informal arrangements of two gastroenterologists, one university based and the other in a community hospital. Conceived at a time when there was little central authority, either on a national or on a hospital/medical school level, its links were forged by the personal relationships of its directors. The process of growth remained informal and flexible enough for the directors to meet the special requirements of their own community and hospital. YAGP provided an important model for improving medical care and education in community hospitals since it addressed personnel needs, contributed to the education of physicians, and fostered clinical research in digestive diseases. YAGP evolved its own standards and its own accreditation mechanism, but faltered when the Accreditation Committee on Graduate Medical Education provided national rather than local criteria. Increased controls by hospitals and medical schools led to more formal ties and programs, and YAGP ceased to matter. Still, there may be lessons from what was in its time an innovation, on a local and state level rather than on a national level.

Ulcerative colitis and scleroderma. A coincidental relationship?

Speculation continues that ulcerative colitis is an autoimmune disorder that is frequently associated with other diseases with a similar underlying pathogenic mechanism. In 1965 we reported a patient with ulcerative colitis and scleroderma in support of this hypothesis. Now we supply a follow-up of over 30 years to describe how each disease acted independently, evidence, we believe, that the association was primarily fortuitous.

Endoscopic treatment of Dieulafoy's lesion of the duodenum.

Dieulafoy's lesion is an often unrecognized cause of catastrophic upper gastrointestinal hemorrhage, typically seen in otherwise asymptomatic patients. Although the lesion is most often found in the stomach, it has rarely been reported to occur in the jejunum and duodenum. Endoscopic treatment has recently been attempted to arrest the bleeding from these lesions, when found in the stomach, with satisfactory results. We report a patient with a bleeding duodenal Dieulafoy lesion who was successfully treated with endoscopic injection of epinephrine (1:10,000) and electrocoagulation. Endoscopic treatment of Dieulafoy's lesion should be attempted before surgery and, as in other causes of acute nonvariceal hemorrhage, be considered the treatment of choice.

No acid, no polys--no "active" gastritis, no dyspepsia. A proposal.

The current dilemma in characterizing non-ulcer dyspepsia (NUD) is due to the very nature of the term which has forced the dependence for diagnosis primarily on symptomatology and the absence of an ulcer crater as ascertained by radiographs or endoscopy. I propose a new classification which I believe is consistent and well founded, based on the presence of histologic gastritis and acid secretion of the stomach. Four categories are presented: (a) normal histology, (b) "active" gastritis, (c) "inactive" gastritis, and (d) atrophic gastritis with achlorhydria. Acid secretion is present in categories a-c. The classification is dependent on the presence of the "poly" to denote active gastritis, round cells to classify inactive gastritis, and the loss of parietal and chief cells with achlorhydria to define gastric atrophy. I propose that polys and acid, which characterize active gastritis, are necessary for producing dyspepsia and/or gastroduodenal mucosal injury, and provide a rationale for treatment. The accepted causes of active gastritis include acid-peptic disease, Campylobacter pylori, and aspirin/nonsteroidal anti-inflammatory drug (NSAID) medication.

A multicenter study of ranitidine treatment of duodenal ulcers in the United States.

Treatment of duodenal ulcer with the histamine H2-receptor antagonist, ranitidine, was assessed in a double-blind, randomized, multicenter trial in which patients were treated for two consecutive 4-week periods with ranitidine 150 mg b.i.d. or a placebo. All patients were allowed to take antacids as necessary for symptoms. Three hundred eighty-two patients were entered and 355 completed the first 4-week trial period. Ranitidine significantly improved healing at 2 weeks (37 versus 19%, p less than 0.01) and at 4 weeks (73 versus 45%, p less than 0.01), with better relief of pain and lower use of antacids. In the second 4-week trial period, 124 unhealed patients from the first 4 weeks were re-randomized. Ranitidine treatment resulted in a greater healing rate regardless of previous treatment (p less than 0.05). In this trial, side effects were uncommon and not different between placebo and the tested drug. One case of hepatitis in the ranitidine treated group was presumed on the evidence to be non-A non-B. Ranitidine is effective and appears to be safe in the treatment of duodenal ulcer and its symptoms.

Sulfasalazine-induced pulmonary disease.

Sulfasalazine has been widely used in the treatment of inflammatory bowel disease. Although a high incidence of side effects has been reported, pulmonary complications are rare. The clinical, radiographic, and histological abnormalities that occurred in a patient three months after initiation of sulfasalazine are described. A review of the literature suggests that the possibility of drug-induced pulmonary disease should be considered in any patient with inflammatory bowel disease receiving treatment with sulfasalazine who develops symptoms or radiographic evidence of pulmonary disease. Transbronchial biopsy may be useful in confirming the type of pulmonary injury.

Duodenal epithelial thymidine uptake in patients with duodenal ulcer or endoscopic duodenitis.

To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [3H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [3H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [3H]thymidine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [3H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation.

Hydrogen peroxide colitis: a report of three patients.

We have seen three patients with acute ulcerative colitis after hydrogen peroxide enemas. The colitis is probably the result of the explosive entrance of gas into the loose connective tissues of the mucosa and submucosa of the rectum and sigmoid. Fortunately, it is transitory in nature, but it should be distinguished from ulcerative, ischemic, or pseudomembranous colitis.

Is gastroduodenitis part of the spectrum of peptic ulcer disease?

Gastroduodenitis should be included with duodenal ulcer and gastric ulcer in the spectrum of clinical disorders that have different pathogenetic mechanisms but a similar clinical picture. Published results of a clinical, endoscopic, radiologic, and histologic study of 100 patients presenting with gastrointestinal symptoms revealed that 61% had classic and 39% had atypical manifestations of peptic ulcer disease. We could not clinically distinguish the 24 patients with ulcer crater (40% of the classic group) from the 25 patients with acute gastroduodenitis without crater (41% of the classic group). Preliminary data of a prospective study compared the treatment responses of 19 patients with gastroduodenitis and 39 patients with peptic ulcer disease. These patients were diagnosed endoscopically and restudied after treatment with a bland diet and antacids seven times per day for 8 weeks. The responses to therapy in gastroduodenitis and peptic ulcer were as follows: endoscopically, 63 and 80%, respectively; histologically, 74 and 65%, respectively; symptomatically, 47 and 65%, respectively. Preliminary data on the duodenal epithelial thymidine uptake revealed an increased proliferative index in duodenitis patients but not in patients with peptic ulcer or control subjects.

The effectiveness of panendoscopy on diagnostic and therapeutic decisions about chronic abdominal pain.

To evaluate the impact of panendoscopy on diagnosis and management, we asked several gastroenterologists to state their diagnoses, management plans, and confidence in these plans before performing endoscopy in patients with chronic abdominal or thoracic pain; and to repeat the same decisions after endoscopy. To evaluate acceptance of the procedure, patients were later interviewed about their discomfort during its performance. To check the way that changes in diagnosis may have affected patient management, we formed six diagnostic groups that roughly correspond to differing treatments. The postendoscopic diagnostic groupings revealed two unsuspected cancers and disagreed with the original classification in 38 (45%) of 84 patients. Dramatic or substantial changes in management occurred in 37 (44%) patients, but often did not correspond to changes in diagnosis. Conversely, management was often unchanged despite alterations in diagnosis. Patients expressed about equal preferences for barium meal as for panendoscopy, and 75% would have agreed to a repeat endoscopy without hesitation. Although the ultimate benefits of postendoscopy management changes were not ascertained, we believe that these results support the use of panendoscopy in patients with persistent and unexplained symptoms.