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Amyloidosis as a manifestation and origin of presenile and senile degeneration

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By Schwartz P • • May 20, 1976

All essential attributes of the amyloidosis in aged persons ("senile amyloidosis") correspond to the condition which in younger individuals develops after infections, particularly following tuberculosis and lymphogranulomatosis, as so-called secondary amyloid degeneration, and also manifests many features of the so-called primary amyloidosis, not connected with infections.

Amyloid depositions in the brain, cardiac muscle, and in pancreatic islets (the "senile amyloidotic triad") dominate the morbid anatomic aspect. However, we know no organ or tissue which necessarily remains spared. The number of involved organs and tissues, in general, increases with the progressive aging of the patients. In those persons living long enough, amyloidosis affects every individual and probably all organs and tissues.

Contrary to the so-called secondary amyloidosis, in many cases of senile amyloidosis the spleen, liver and kidney remain intact.

In the so-called Alzheimers disease, in which both clinically and pathoanatomically a particularly destructive cerebral amyloidosis in relatively young persons prevails, just as in the common senile dementia of aged persons, the brain condition is associated with a systemic amyloid degeneration of many other organs.

Several cerebral and cardiac lesions due to amyloid accumulations can probably be diagnosed electrographically. Thus, through these already known morbid anatomical observations we have the promise of an essential enrichment of diagnostic perspectives.

In general, the etiologic manifoldness of amyloidosis presently seems to be incomparable. Infections, ionizing radiation, traumatic lesions in human pathology, the introduction of chemically definable substances, infections, and stress consequent to social burdening, proved effective in spontaneous and experimental amyloid degeneration of animals.

The demonstration of a tuberculous infection with the help of postmortem radiographs, as well as with the employment of histologic and microbiologic procedures to provide the evidence of acid fast bacilli in calcified remnants of pulmonary foci, proved to be eminently successful methods in the exploration of causes of senile tuberculosis and amyloidosis: Tuberculosis, after its invasion of the organism in early childhood, with its toxic and immunobiologic influences, holds it under its spell for an entire, even very long life and can be considered the most frequent cause of senile amyloidosis.

Chromosomal disturbances, with their hereditary manifestations, or, as in cases of mongoloid idiocy, associated with individual deformations, may present as amyloidoses.

Amyloid deposits in human pathology may develop by the transformation of normal structures, like cartilage, osteoid tissue, vascular elastic fibers, and also from scar hyalin and from fibrin.

We observed the disappearance of cerebral and cardiac amyloid accumulations producing typical defects. Amyloidosis represents one of the most frequent spontaneous diseases of animals.

Source: Fortschr Med 1976 May 20;94(15):890-6

PMID: 134966, UI: 77004695

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