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It is not easy to understand how the electron microscopes and electron microscope techniques that we know today developed from the primitive ideas of the first microscopists of the 1930s. Newcomers to the subject in particular, their time almost fully occupied with grasping practical methods and modern computing techniques, can rarely devote much attention to the history of their subject. For some, however, this is a source of frustration: If a guide to the principal stages in the development of the subject and to the main actors and their publications were available, they would find the time to study it.

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Numerous cytoplasmic lamellar bodies were seen in many cell types in an open lung biopsy from a patient on amiodarone therapy. These membrane-bound lamellar bodies were characterized by distinct, concentric parallel membranes and peripheral granular densities. Their morphology and distribution suggest a metabolic disorder of phospholipid degradation induced by this drug. The differential diagnosis of lamellar body accumulation in the lung is discussed. This case emphasizes the desirability for ultrastructural study of lung biopsies in such potentially reversible lung disease.

The ultrastructure of spleen from four patients with idiopathic thrombocytopenic purpura (ITP) is studied. Platelets, with no evidence of degranulation and aggregation, leave the circulation by passing through gaps in the sinus wall in the marginal zones and the red pulp. They are then trapped by pseudopods of macrophages and are phagocytosed as whole elements. The endothelial cells lining the sinuses do not phagocytose platelets or other circulating blood cells. The degradation of these platelets in the phagolysosomes of macrophages is incomplete and results in the formation of myelinic‐like figures which accumulate in large numbers in these cells. This incomplete platelet breakdown may be due to a deficiency of specific lysosomal enzymes. Erythroleucophagocytosis in ITP is normal. The results are consistent with the concept that ‘self’ constituents are normally and readily destroyed by autolytic enzymes. In the case of enzyme deficiency or the presence of ‘foreign’ antigens, including altered ‘self’ antigens, these enzymes become ineffective for rapid and complete degradation of the substrate. Through macrophage‐lymphocyte interaction, antibody‐forming cells are activated against these residual substances. These antibodies, in turn, facilitate the phagocytosis of the specific ‘antigens’ by macrophages. The massive platelet phagocytosis and the presence of large numbers of germinal centres in the white pulp and plasma cells in the marginal zone and red pulp suggest that the spleen is the major site of platelet destruction, as well as the site of antiplatelet antibody synthesis.