Primary splenic lymphoma with filiform ultrastructure.

A case of primary large cell splenic lymphoma of B lineage exhibiting filiform cell appearance is reported. The patient presented with massive splenomegaly, and following spontaneous splenic rupture, died of adult respiratory distress syndrome. The clinical aspects of the case, notably a lymphoma arising as a primary tumour in the spleen, with spontaneous spleen rupture and rapid fatal outcome, in combination with the filiform appearance of the lymphoma on electron microscopic examination, constitute an unusual combination of features. As far as is known, this B cell neoplasm is only the second primary splenic lymphoma of filiform type to be recorded.

Malignant fibrous histiocytomas of salivary glands.

The light microscopic, immunohistological and ultrastructural findings in two cases of malignant fibrous histiocytoma arising in salivary glands are presented and the features of seven previously reported cases are reviewed. This neoplasm is extremely rare in this site and may pose problems in diagnosis. It has to be distinguished from other spindled cell tumours, in particular from epithelial tumours of predominantly spindled cell pattern; immunohistological markers for histiocytic cells may be of value. The histogenesis of this neoplasm is controversial but our electron microscopic findings support an origin from mesenchymal cells which differentiate along a broad fibrohistiocytic spectrum.

Ultrastructural study of bleomycin-induced pulmonary changes in mice.

The pulmonary changes produced in mice given bleomycin intraperitoneally (twice weekly for 4 weeks, total dose 240 mg/kg) were examined by light and electron microscopy. Bleomycin damaged the pulmonary vessels and produced type I pneumocyte necrosis, resulting in non-uniform pulmonary fibrosis. The sequence of events leading to pulmonary fibrosis may be arbitrarily divided into three phases: firstly, a focal perivascular lesion consisting of interstitial oedema with plasma cell and lymphocyte infiltration; followed by the middle proliferative phase characterised by type I pneumocyte necrosis, intra-alveolar fibrin deposition, an increase in the numbers of type II pneumocytes and fibroblasts and an overall decrease in the alveolar diameter. The third phase consisted of organisation, with intra-alveolar and interstitial collagen formation and the synthesis of elastin. These phases, although occurring sequentially, did not bear a constant time relationship to the dosage schedule, for new early focal lesions continued to appear throughout the period of the experiment. These ultrastructural changes are not specific for bleomycin, but represent a general reaction of the lung to injury. The exact mechanism whereby bleomycin produces the lung damage has yet to be ascertained.