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This study investigated the clinical, radiographic, and pathologic features of breast hamartoma. The patients ranged in age from 18 to 89 years, with a mean age of 45 years, and a median age of 43 years. Seventy-five percent of the patients were asymptomatic, other than reporting a breast lump. In two patients, the lesions recurred at 7 and 18 months after the initial resection. The clinical diagnoses were fibroadenoma in 10 cases, carcinoma in 5 cases, hamartoma in 4 cases, and phyllodes tumor and lipoma in 2 other cases. Mammograms were available in 12 cases, the majority of which showed a well-defined mass of homogeneous density. Grossly, these lesions were oval to round, well-circumscribed masses, ranging in size from 1 to 7 cm in maximum dimension (mean, 3.9 cm). The microscopic appearance of these tumors corresponded to their gross appearance. Lesions that were grossly firm, rubbery, and white consisted largely of dense fibroconnective tissue with variable amounts of glandular elements with little adipose tissue. Softer, pale, yellow lesions contained more adipose tissue. A consistent and important diagnostic feature was the presence of both lobules and ducts, in contrast to fibroadenoma in which lobules are often absent or rare. The current trend of mammographic breast screening has made us aware that mammary hamartomas are not uncommon. These lesions may go unrecognized by the pathologists because they show all the constituents of normal breast tissue and may be reported as "no pathological diagnosis" or "normal breast tissue," which are inappropriate diagnoses for a lesion that presents as a palpable and a well-circumscribed mass.

In four of five patients with thrombotic thrombocytopenic purpura (TTP) in whom serial tests of hemostatic function were performed, severe thrombocytopenia, normal plasma fibrinogen concentrations and mildly increased concentrations of fibrinogen/fibrin degradation products were observed. Widespread platelet thrombi were found in arterioles and capillaries. Fibrin could be seen around some of the platelet clumps and was the main component in a small number of the thrombi in two patients. The observations show that TTP is a disorder in which intravascular platelet consumption results in disseminated platelet thrombosis. The coagulation system is apparently activated secondarily to platelet aggregation and variable quantities of fibrin are incorporated into the thrombi. Clinical improvement resulted from combined therapy with corticosteroids, heparin and drugs that suppress platelet function.