ABSTRACT
Bone metastasis, a very common sequelae of cancer, is often associated with great morbidity. Understanding the biology of bone metastases may lead to therapeutic interventions to target the metastases. In addition to replacing bone marrow elements, the presence of tumour cells in bone modulates the normal bone remodelling process. Some tumours result in primarily osteolytic bone lesions, whereas others are associated with osteoblastic bone lesions. In either case, the resulting changes in the bone structure result in weakened bone that induces pain and is predisposed to fracture. The mechanisms through which cancer cells modulate bone remodelling are not clearly defined, but ongoing research using a variety of animal models will hopefully provide clues to prevent or slow the progress of bone metastases.
ABSTRACT
We report the case of an 18-year old man with hemolytic-uremic syndrome (HUS) having a classic clinical presentation and diagnostic renal pathology without evidence of microangiopathic hemolytic anemia (MAHA) by peripheral blood smear. Indirect evidence of hemolysis was suggested by mild anemia, elevation of serum lactate dehydrogenase, and examination of the patient's bone marrow. We postulate that in this case the inability to detect schistocytes in the peripheral smear reflected a low degree of hemolysis. Review of the literature revealed that evidence of fragmented erythrocytes by peripheral smear is not always present in HUS, yet this observation has received little attention. Thus, the diagnosis of HUS need not include overt evidence of MAHA as is traditionally taught.
