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
Reverting now to Latham’s views as to the _hepatic_ origin of gout, we
find them very similar to those formulated by Murchison. He held that
the defective transmutation of glycocine into urea was responsible for
the occurrence of uric acid in the urine. These chemical irregularities
were attributed by him to functional disturbance or partial suspension of
the normal hepatic metabolism. This, again, was referred back by him to
some obscure change in the central system, viz., that part of the medulla
oblongata from which the vagus takes origin.
HYPERPYRÆMIA
Excess of carbonaceous materials in the blood was considered by Hare to
be an essential, though by no means the sole factor in the genesis of
gout. This same “hyperpyræmia,” as he terms it, was also, he believed,
responsible for migraine, asthma, epilepsy, and other paroxysmal
neuroses. For the alternation of attacks of acute articular gout with
paroxysms of migraine, asthma, and epilepsy, seemed to him to indicate a
kindred origin. The same inference, also, he deemed might be drawn from
the well-ascertained fact that the temporary or even permanent cessation
of long standing asthma, migraine, and epilepsy, might exactly coincide
with the onset of acute gout.
These alternations and substitutions seem to suggest that the preceding
alterations in metabolism are similar in nature, finding expression
indifferently in gout, asthma, epilepsy, etc. Carbon foods, he
considered, are much more likely to accumulate in the blood than the
nitrogenous. Ingestion of the latter is swiftly reflected in increased
elimination of nitrogenous excreta. On the other hand, following the
intake of carbonaceous foodstuffs, no such rapid and proportionate
increase in the excretion of carbonic acid ensues. In other words, the
capacity of the organism to deal with or katabolise in response to the
absorption of excess of carbon foods, is strictly limited. Muscular
exercise and exposure to cold, factors which but slightly influence
protein katabolism, are largely responsible for adequate carbon
katabolism. Accordingly, given deficient exercise, excess of carbonaceous
food and a warm temperature, an accumulation of the carbon content of the
blood is favoured.
Hare considered that present day habits of warm clothing, warm rooms
combined with excessive intake of starch and sugar, are precisely the
favourable conditions for producing a state of hyperpyræmia. Increased
fat formation would of course tend to diminish such a tendency to carbon
accumulation, but this capacity in many subjects is conspicuously
lacking, and may already have attained its limit.
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