gency department because of sudden onset of epigastric pain and melena. Blood tests showed a slight increase in cardiac troponin I, and electrocardiogram revealed low QRS voltages with no abnormality consistent with acute myocardial injury. At echocardiography, an initial diastolic dysfunction and left ventricular wall thickening with a sparkling appearance of the myocardium were found. An urgent upper gastrointestinal endoscopy showed an active bleeding Dieulafoy’s lesion in the duodenal bulb, which was successfully treated with epinephrine injection and argon plasma coagulation; two clean-based irregular ulcers in the second tract of the duodenum were also found. The clinical course was characterized by the recurrence of episodes of massive hematochezia and melena, requiring multiple blood transfusions. Colonoscopy and upper endoscopy results were nondiagnostic, and thus capsule endoscopy was performed. It showed various findings throughout the entire small bowel, such as multiple patchy red plaque lesions (mucosal hematoma, l" Fig. 1), thickened folds causing, in some instances, intraluminal stenosis (l" Fig. 2), irregular-shaped ulcerations (l" Fig. 3), and polypoid protrusions or masses, some of which had ulcerations and visible vessels (l" Fig. 4). Histopathologic evaluation of biopsy specimens from the stomach, duodenum, and proximal jejunum revealed a massive deposition of amorphous eosinophilic material in the lamina propria and muscularis mucosae. Congo red stain was positive and demonstrated green birefringence under polarizing microscopy The spectrum of small-bowel lesions of AL-type amyloidosis at capsule endoscopy

Indeterminate cell histiocytosis (ICH) is a proliferation of indeterminate CD1a+, CD68+, S100+ and CD207- dermal dendritic cells. We describe a 39-year-old man who developed diffuse ICH and, 6 years later, acute myeloblastic leukaemia (AML). He was treated with cyclophosphamide, etoposide and vinblastine until 2003. In August 2004, he presented dyspnoea, hyperpyrexia and infiltration of the lung parenchyma, compatible with an AML invasion, and died after a course of induction chemotherapy. Cytomorphology and immunophenotype analyses suggested an ICH clonal evolution. The leukaemogenic role of etoposide is discussed. ICH has previously been reported in association with B-cell malignancy, but only one case has shown systemic progression.