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
Perhaps the most cogent evidence of the slight toxic effects of uric
acid or urates is that derived from a study of the _uric acid infarcts_
so frequently noted in infants dying within the first two weeks of
birth. According to Gideon Wells, “little or no change occurs in the
renal tubule as a result of these depositions, except such as can be
attributed to their mechanical effect.” This same observer, discussing
this question of the toxicity of uric acid, observes, “It may be safely
stated that at the present time there exists no good evidence which makes
it probable that uric acid is responsible for any pathological conditions
whatever, except uric acid calculi, uric acid infarcts in the kidneys,
and certain manifestations of gout.” His further conclusion is that uric
acid possesses but a very slight degree of toxicity, and that an actual
intoxication of the organism with this substance probably never occurs.
Again, we have the fact that in instances of _malnutrition in children_
excess of uric acid may occasionally be found in the blood. Yet no
symptoms comparable to _gout_ occur, even though uric acid _calculi_
form. Also, as has been pointed out, showers of uric acid may be present
in their urine, and yet no symptoms arise, save those referable to
_mechanical_ irritation of the renal or vesical tissues.
Turning to experimental researches, the evidence is cumulative as to the
_non-toxicity_ of uric acid. Rabbits and dogs seem quite irresponsive,
either to its ingestion in large quantities in their food, or to repeated
intravenous injections of 1 or 2 grammes thereof, save only that the
urine showed a large increase in uric acid.
Again, Ransom, of New York, found that no systemic disturbance ensued in
two cases of _chronic nephritis_, following the taking by the mouth of
3 grammes of uric acid per diem for three days in succession. All that
resulted was a notable increase in the uric acid output. In one case, he
went further, and on the fourth day administered 6 grammes, but nothing
happened.
Walker Hall, with commendable devotion, took large doses of uric acid
with resultant headache and malaise, which endured for some hours. But
as Luff shrewdly observes, “almost any substance, however (common salt
for example), will produce toxic effects if taken in very excessive
quantities.” Despite his brief indisposition, Walker Hall maintains that
uric acid is rather a symptom of, than the precise _materies morbi_ in
gout.
Nor, apparently, even in gouty subjects can aggravation of the condition
be induced by intravenous injection of uric acid. Bass and Herzberg did
so until the blood content of uric acid reached the high level of 10 mg.,
and yet no joint attack supervened. Neither, for that matter, has it been
possible to establish any relationship between degrees of uricæmia and
the incidence or severity of gouty paroxysms.
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