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
In summarising the doctrines of Ord and Ebstein, it may be observed that
if the latter’s contentions have been disproved, Ord’s claim that the
tissues of gouty subjects exhibit a specific tendency to _degeneration_
has also as yet not been substantiated. Albeit, we must not forget that
in 1883 Ralfe subscribed to Ord’s views as to the tendency to _textural
degenerations_ in gouty subjects, either through heredity or acquirement.
For this observer, however, the basal factor in the production of the
disease was a diminished _alkalinity of the blood_, due to a surcharging
of it with acid and acid salts. Disagreeing with Garrod’s assumption
that _deficient renal elimination_ was the prime cause of the retention
of uric acid, he was of opinion that “the first step in the process lies
in the failure of the _tissues_ to reduce the acid, as it occurs in
health.”... “In the large glands or where the current of the circulation
is free, the uric acid is carried into the blood and gradually reduced to
urea; in tissues outside the current of the circulation, the insoluble
uric acid is not so readily carried off, and so on the slightest
disturbance is deposited, as is the case in cartilages of the joint, the
ear, etc.” As to the determining cause of the gouty attack, he invokes
the agency of the _nervous_ system to explain its incidence, for he held
it probable that the primitive failure of the tissues to reduce uric
acid eventually led to derangement of some special nerve centre, which
disturbance occasioned the gouty outbreak, with resultant “accumulation
of uric acid in the blood and deposition of urate of soda in the tissues.”
In 1895 Berkart propounded a mode of genesis which may be regarded as
a variant of Ord’s theory. The severity of the symptoms of acute gout
were such as he deemed incompatible with their production as a result of
simple mechanical irritation by crystals of biurate of soda. Uric acid,
he held, must be afforded a humbler _rôle_ than that of a proximate
cause. It was, for him, but an _epi-phenomenon_, the accompaniment of a
_panarthritis_, the origin of which was as follows:—
While not postulating the identity of rheumatoid arthritis in gout, he
yet held that both disorders originated in some obscure form of _atrophy_
of the bone substance, and that the degenerative change also overtook the
cartilages and fibrous tissues of the joints. Subsequently, there ensued
a _necrosis_ in the tissues in and around the joint. The degeneration
and subsequent necrosis, he held, were the outcome of a profound “vice
of nutrition.” The pain, inflammatory reaction, œdema, and cuticular
desquamation were the direct result, he thought, of the necrosis. The
excess of uric acid in the blood he referred to _leucocytosis_, and in
part to disintegration of the tissues.
HEPATIC INADEQUACY
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