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
------------------+--------------+--------------+--------------
| | Uric acid. | Amount of
Time. | Urea. Grams. | Milligrams. | urine. C.C.
------------------+--------------+--------------+--------------
10-11 | 1·07 | 26 | 175
11-12 | 1·13 | 27 | 118
12-1 p.m. | 1·07 | 24 | 164
1-2 (meal). | 0·64 | 21 | 60
2-3 | 1·12 | 22 | 43
3-4 | 1·16 | 38 | 41
4-5 | 0·84 | 40 | 53
5-6 | 1·16 | 56 | 59
6-7 | 1·20 | 39 | 56
7-8 | 1·37 | 30 | 95
8-9 | 1·47 | 33 | 183
9-10 | 1·33 | 24 | 155
10-11 | 1·33 | 23 | 180
------------------+--------------+--------------+--------------
It is clear from the results obtained that a very definite increase of
endogenous purin excretion ensued, and that the said increase occurred
sooner as regards _uric acid_ than urea. This bears out what Mares
demonstrated many years ago, viz., that the greatest increase in uric
acid excretion occurs in a few hours after a meal, whereas the increase
in the case of urea comes more tardily, not reaching its maximum until
some hours after.
Horbaczewski referred such increase in uric acid excretion to a digestive
_leucocytosis_; in other words, that the uric acid was the outcome of
destruction of the leucocytes, and consequent formation of purin from the
released nucleic acid. Unfortunately for this theory, the period of most
marked augmentation in uric acid excretion ensues when the leucocytes are
most in evidence in the blood-stream, not _after_ they have disappeared,
as would be the case if uric acid was derived from the purin product of
the nucleic acid liberated by leucocytic destruction. We have a parallel
instance in the case of _pneumonia_, in which it has been shown that
the elimination of uric acid and other purins is at its acme when the
leucocytes are most abundant; in other words, the highest uric acid
output coincides with the period of most marked leucocytosis, whereas
during the post-critical stage, viz., when leucocytes are being destroyed
in great numbers, the output of uric acid is very markedly lowered.
Discussing Horbaczewski’s theory in light of the above criticisms,
MacLeod suggests, “that the facts appear to indicate that the purin
substance is a metabolic product of the living leucocytes,” and not, so
to speak, the chemical outcast of their disruption and death.
Public-domain text, read in full here on John Shaqi.
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