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Medullary carcinoma of the breast is a fairly rare subtype of infiltrating ductal carcinoma with a more favorable prognosis than the more common forms of invasive breast cancer. However, it seems likely that medullary carcinoma is overdiagnosed, leading to less aggressive treatment than is warranted for the cancer that really exists. A review of all breast cancer cases diagnosed at Massachusetts General Hospital in Boston over a 10-year period is provided. Tumors were classified as typical or atypical medullary carcinoma (TMC, AMC), or nonmedullary carcinoma (NMC), according to their growth patterns and cellular characteristics. Results showed that only nine of the 30 cases originally diagnosed as medullary carcinoma actually fit the criteria for TMC. Seven were reclassified as AMC, and 14 as NMC. Of the latter group, 13 were infiltrating ductal carcinomas, and one was squamous cell carcinoma. Tumors for which information regarding estrogen-receptor status was known were all negative (tumor cells can be positive or negative for their receptivity to estrogen, a female hormone). Six patients with TMC had undergone mastectomy as the only treatment. Three were alive and well after at least three years, one developed metastases, and two were lost to follow-up. The remaining three TMC patients received more aggressive treatment and were alive and well. The AMC patients in this series also received aggressive treatment, and, of the five who were followed-up, two died with metastases. Results from other studies are reviewed which show, in general, improved survival for patients with typical medullary cancer. The reasons for this are not known since, in fact, some characteristics of this kind of cancer (such as its lack of estrogen receptors) are usually associated with a poorer prognosis. In summary, medullary cancer appears to be overdiagnosed, a situation that should be kept in mind by the physician when diagnosis is made. (Consumer Summary produced by Reliance Medical Information, Inc.)

OBJECTIVE: To evaluate the factors thought to be involved in the pathogenesis of acute pancreatitis associated with alcohol. BACKGROUND: The mechanism of alcohol-induced pancreatitis is believed to involve synergistic effects of various pathogenetic factors. The present study was designed to evaluate the possible contribution of pancreatic duct obstruction, physiologic exocrine stimulation, or secretory hyperstimulation to alcohol-induced pancreatic injury. METHODS: Wistar rats were allocated randomly to a control group (group 1), or to a group with pancreatic duct obstruction (group 2), physiologic exocrine stimulation (group 3), ductal obstruction and exocrine stimulation (group 4), or exocrine hyperstimulation with the cholecystokinin analogue cerulein (group 5). Three hours after this pretreatment, animals in each experimental group were randomly divided into two subgroups for intragastric administration of either water (groups 1A through 5A) or beer (groups 1B through 5B). Test solutions were instilled over 9 hours (total amount of alcohol administered, 4.8 g/kg). Twenty-four hours after beginning the test infusion, animals were killed for histologic evaluation of pancreatic edema and determination of an acinar cell necrosis score. Serum amylase levels were determined at 3, 9, and 24 hours. RESULTS: No increase in amylase levels or significant morphologic changes were found in control animals (group 1A) or in animals subjected to physiologic exocrine stimulation (group 2A). Pancreatic duct obstruction, with or without physiologic exocrine hyperstimulation (groups 3A and 4A), and exocrine hyperstimulation (group 5A) induced pancreatitis of similar severity with minor acinar cell damage. Alcohol superimposed on exocrine hyperstimulation (group 5B) increased acinar cell injury (group 5A, 0.4±0.1 points vs 5B, 1.0±0.2 points; P<.05) and serum amylase levels at 24 hours (group 5a, 41±6 U/L vs group 5B, 72±11 U/L; P<.05), whereas no differences between subgroups A and B (water vs beer) were found in groups 1 through 4. CONCLUSION: Our findings suggest that the pathogenesis of acute alcoholic pancreatitis may require a state of exocrine hyperstimulation, perhaps via cholecystokinin, but do not support a role for constriction or obstruction of Oddi's sphincter.(Arch Surg. 1994;129:1081-1085)