Metastatic Calcification induced by Hytakerol in Rats infected with Plasmodium berghei.

vitamin D, other derivatives of irradiated ergosterol, and parathyroid hormone induce metastatic calcifications in many organs (Vanderveer, 1931; von Brand et al., 1932; Engel, 1952; Baker et al., 1954; Haas et al., 1958). It is also known that several disease conditions, such as metastatic tumors, chronic renal disease, and hyperparathyroidism, are associated with abnormal tissue calcifications (Eisenstein et al., 1960). More rarely have studies involving parasites been reported. It has, however, been found that structures originating from the host, such as the wall of Trichinella cysts (von Brand et al., 1933, 1938; Wantland, 1934, 1935, 1936, 1938), readily calcify under the influence of the above compounds, as do tissues degenerating as a sequel of a parasitic invasion, such as the damaged tissue due to a larval tapeworm migrating through the liver (von Brand et al., 1933). Parasites, in general, seem liable to artificial calcification only after they have died (Otto and von Brand, 1941). Still less information is available concerning the possible influence of parasitic infections on the experimental production of metastatic calcifications in the tissues of the host. Von Brand and Holtz (1933) described an increased susceptibility to calcification of canary birds infected with Plasmodium praecox. It was considered worth while to examine this question further, employing a mammalian malaria species, Plasmodium berghei. In the present investigation, the effects produced by large amounts of a dihydrotachysterol concentrate on organ calcifications in the host were studied during the malarial infection in rats.