Splenic myeloid metaplasia, histiocytosis, and hypersplenism in the dog (65 cases).

Splenectomy specimens from 65 dogs with severe, diffuse, sustained, and progressive splenomegaly were examined. The clinical signs, hematology, and serum chemistry values in for the dogs were not useful diagnostic features. Microscopic changes in the spleens were distinctive and consisted of 1) myeloid metaplasia, 2) histiocytosis, 3) erythrophagocytosis, and 4) thrombosis with segmental infarction. Ultrastructural features suggested proliferative changes in the splenic reticular cells and macrophages (reticular meshwork) that described a continuum from reactive changes associated with immunologic damage of erythrocytes to neoplastic proliferation of histiocytic components. Thirty percent of the dogs survived 12 months. Approximately one half (53%) of the dogs with complete postmortem evaluations showed multiorgan involvement with a tissue distribution and cell morphology consistent with histiocytic neoplasia. For the remaining dogs (47%), only splenic pathology was consistently present, and a specific cause of death was often not evident. Distinctive histologic changes in the splenic tissues-including mitotic activity, erythrophagocytosis, giant cell formation, thrombosis/ infarction, and the proportion and distribution of histiocytic and hematopoietic cells-were statistically evaluated for prognostic relevance. The presence of giant cells was the only reliable prognostic feature, and that was indicative of a fatal outcome. These descriptive changes of myeloid metaplasia in the canine spleen are compared with the human clinical and pathologic syndromes of 1) agnogenic myeloid metaplasia, 2) hemophagocytic syndromes, and 3) hypersplenism. These diseases in humans produce histopathologic changes in the spleen that are similar to those observed in the canine splenic tissue we examined in this study.