= Solution
\b[Historical “amyloid disease” denotes the waxy or lardaceous visceral change, especially in the <spleen>, <liver> and <kidneys>; modern <amyloidosis> denotes deposition of misfolded <protein> fibrils.] The old descriptive appearance and the modern chemical explanation must be kept distinct.
In nineteenth-century usage the affected organs could be enlarged, firm and unusually translucent or wax-like on section. The name <amyloid> means starch-like. The historical chemical argument relied on colour reactions with <iodine> and <sulfuric acid>, suggesting affinity with <starch> or <cellulose>. Such a reaction was a clue to recognition, not a modern identification of the deposited substance. <Rudolf Virchow>'s 1856 account explicitly discusses the waxy change of the <spleen>, <liver> and <kidneys>, and its occurrence with longstanding destructive disease.<On the Course of the Amyloid Degeneration by Rudolf Virchow>[1856 English abstract, pp. 380–383, opening account of visceral sites and chronic disease]{ref}
The three principal visceral examples can be described more precisely:
* In the <spleen>, deposits in the <splenic white pulp> may produce translucent granules, the so-called <sago spleen>. More diffuse involvement gives a widespread lardaceous appearance.
* In the <liver>, deposits along the <hepatic sinusoids> can compress adjacent <hepatocytes>; extensive deposition may produce a large firm <liver>.<Hepatic amyloidosis: morphologic differences between systemic AL and AA types>[Abstract, autopsy examination of 286 livers; sinusoidal and portal patterns]{ref}
* In the <kidney>, deposits in <glomeruli>, <blood vessels> and sometimes the interstitium interfere with function. Involvement of the <glomeruli> explains the <albuminuria> of Question 1; it may progress to <nephrotic syndrome> and <kidney failure>.
The distribution is not confined to those three organs. <Amyloidosis> can also affect the <gastrointestinal tract>, <heart>, <blood vessels> and other sites; the pattern depends on the precursor <protein>. Modern examples include <AA amyloidosis> associated with sustained <inflammation>, <AL amyloidosis> involving <immunoglobulin light chains>, and <transthyretin amyloidosis>. This classification is a present-day explanation, not a list of molecular diagnoses asserted for unnamed 1867 patients.<Amyloidosis by Merck Manual Professional Edition>[Introduction; Etiology, systemic types and common sites of deposition]{ref}
Modern confirmation uses <histology> with <Congo red> and examination with a <polarizing microscope>, followed by identification of the deposited <protein>, for example with <mass spectrometry>. The characteristic birefringence supports identification of <amyloid>; typing distinguishes biologically different diseases. These are later laboratory methods, not apparatus available to the candidate in 1867.<Systemic Light Chain Amyloidosis in The EBMT Handbook>[§82.2 Diagnosis, Congo red, polarized light and amyloid subtyping]{ref}
Thus an adequate historical list starts with \b[<spleen>, <liver> and <kidneys>], while the modern explanation is extracellular <protein> deposition rather than conversion of an organ into <starch>.
Back to article page
