Gout, with a section on ocular disease in the gouty — John Shaqi
Gout, with a section on ocular disease in the goutyLlewellyn, Llewellyn J. (Llewellyn Jones)
Science
Gout, with a section on ocular disease in the gouty
Llewellyn, Llewellyn J. (Llewellyn Jones)
Eye -- Diseases; Gout
His own view was that the _primary change lay in the blood corpuscles_,
this being induced by the serial ingress of “gout producing elements”
into the blood stream. As to the retention of uric acid, he deemed it not
the cause, but merely a _symptom_, a consequence of gout. Thus he says,
“The good living and the stimulants do not simply cause an excess of uric
acid to form, but they end by causing some more permanent change, and
probably one affecting the blood globules, which reacts on the kidney,
putting a stop to the excretion of uric acid, and causing its retention
in the serum, where, passing in the round of the circulation, it is very
apt to become deposited as urate of soda.” Moreover, his observations of
the effect of colchicum in checking a gouty paroxysm, seem to indicate,
“that there is a disease to which the name ‘gout’ is applied, distinct
from the excess of uric acid in the blood serum which attends its
progress.”
The imaginative insight of Barclay is very remarkable. If we substitute
the _white_ for the red corpuscles we see how closely his views accord
with those prevalent at the present time, when so important a _rôle_ in
the genesis of gout is attributed to the _leucocytes_. Moreover, as Ewart
observed, the views of Barclay and Parkes approximate in principle to
those afterwards propounded by Ord and Ebstein, that the bodily tissues
“take an active share in determining the deposition of uric acid.”
It is, however, but fair to note that, long prior (1854) to Barclay,
Gairdner held that “the disappearance of urea and uric acid in the urine
and their accumulation in the blood” was but _symptomatic_ and not
causative of gout, coupling with it the suggestion that there was some
antecedent _nerve_ influence at work.
Laycock, too, it may be noted, considered Garrod’s theory inadequate,
adding that “Gout is characterised not by urates in the blood but by the
genesis of uric acid _in the tissues_, and its action thereon, and is
especially characterised by _peculiar changes in the innervation of the
individual_.”
ANTECEDENT STRUCTURAL CHANGES
In 1872 Ord took up the novel standpoint that there was an inborn
tendency in the fibroid tissues of gouty subjects to undergo a special
type of _degeneration_, which same might be inherited or acquired. Also
that this innate peculiarity was attended by excessive formation of
urate of soda in these tissues, and which subsequently gaining entry
therefrom into the blood, was deposited promiscuously in the body with a
predilection for relatively non-vascular structures, viz., _cartilages_.
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