As early as 1872, the development of necrosis of the fatty bone marrow was observed in a case of acute pancreatitis (1). Since that time, sporadic cases of intramedullary fat necrosis associated with bone destruction have been reported in conjunction with acute and subacute pancreatitis, traumatic pancreatitis, and pancreatic carcinoma (2–7). In most reports the clinical and pathologic features were emphasized, although in some cases the authors were able to show that the osseous changes were accompanied by corresponding radiologic manifestations. More recently, however, Immelman and his associates have stressed in two publications the roentgen features of intramedullary fat necrosis and bone necrosis in cases of chronic calcific pancreatitis (6, 7). Since 1945 we have collected a series of cases of documented chronic pancreatitis with radiographic bone changes which we considered the result of previous intramedullary fat necrosis and bone infarction. Though the pathogenesis of this process is as yet not fully clarified, we wish to present our cases at this time in the hope of stimulating further interest in this subject. Conceivably, additional observations may lead to a better understanding of the entire disease process and its incidence, as well as its relationship to other types of intramedullary fat necrosis and bone infarction. Case Reports Case I: W. S., a 47-year-old Negro male alcoholic, was first observed at Grady Memorial Hospital in 1944 with clinical evidence of pancreatic insufficiency and diabetes. On occasion, he had experienced vague episodes of joint and lower extremity pain. At that time the serum amylase was reported as 242 Somogyi units. Abdominal films showed extensive pancreatic lithiasis, and radiographs demonstrated evidence of aseptic necrosis of the humeral and femoral heads (Figs. 1 and 2). The clinical course was complicated by a severe urinary tract infection, with eventual fatal septicemia. Autopsy disclosed renal papillary necrosis as well as evidence of acute and chronic pancreatitis. There was no laboratory or clinical sign of syphilis or sickle-cell disease. Case II: J. L., a 50-year-old Negro male alcoholic, was treated at Grady Memorial Hospital in 19.53 because of left hip pain of three months duration. Radiologic examination demonstrated bilateral aseptic necrosis of the femoral heads (Fig. 3). Two years later the patient was readmitted with symptoms of acute pancreatitis which had developed following excessive alcohol intake. During this hospitalization an epigastric mass developed which was clinically thought to represent a pancreatic pseudocyst. Pancreatic lithiasis was demonstrated roentgenographically. There was no evidence of diabetes or pancreatic insufficiency or of syphilis or sickle-cell disease. Case III: W. B., a 57-year-old Negro male alcoholic, was admitted to Grady Memorial Hospital in 1952 because of jaundice.