By injecting sodium caseinate into mice, Kuczynski (1923) and Letterer (1926) were able to produce changes corresponding to generalised amyloidosis in man. Several reports on experimental amyloidosis have been published subsequently, but it would seen that very little attention has been given to the relationship between amyloidosis and the endocrine glands. The observation has been made in human subjects that a persistent febrile condition seems to promote the production of amyloid degeneration (Peräsalo 1948). Experimental amyloidosis in mice was produced by us more rapidly when the animals were kept at supernormal temperature (Peräsalo, Kuusisto & Latvalahti 1949). Changes pointing to the general adaptation syndrome were also seen both in the parenchymatous organs and in the blood picture of the test animals. These observations seemed to indicate the need of investigations of the rôle played by the endocrine glands in the development of experimental amyloidosis. When in the autumn of 1949. I entered upon this experimental study, I found no reference to this subject in the literature. The endocrine system appears to have a very great influence on the protein metabolism, with which amyloidosis also is connected. The adrenal cortex occupies a significant position in Selye’s (1948) theory on the general adaptation syndrome. It has also been found to play an important part in various infectious and allergic conditions and in so-called collagen diseases. It may therefore be assumed that this endocrine gland, at least, is a contributing factor in the etiology of amyloidosis.
No takes yet. Share an insight, caveat, or question.
J Latvalahti (1953) studied this question.