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

Splenectomy specimens from 65 dogs with severe, diffuse, sustained, and pro gressive splenomegaly were examined. The clinical signs, hematology, and se rum chemistry values in for the dogs were not useful diagnostic features. M icroscopic changes in the spleens were distinctive and consisted of 1) myel oid metaplasia, 2) histiocytosis, 3) erythrophagocytosis, and 4) thrombosis with segmental infarction. Ultrastructural features suggested proliferativ e changes in the splenic reticular cells and macrophages (reticular meshwor k) that described a continuum from reactive changes associated with immunol ogic damage of erythrocytes to neoplastic proliferation of histiocytic comp onents. Thirty percent of the dogs survived 12 months. Approximately one ha lf (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 patholog y was consistently present, and a specific cause of death was often not evi dent. Distinctive histologic changes in the splenic tissues-including mitot ic activity, erythrophagocytosis, giant cell formation, thrombosis/infarcti on, and the proportion and distribution of histiocytic and hematopoietic ce lls-were statistically evaluated for prognostic relevance. The presence of giant cells was the only reliable prognostic feature, and that was indicati ve of a fatal outcome. These descriptive changes of myeloid metaplasia in t he canine spleen are compared with the human clinical and pathologic syndro mes 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.