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DISORDERS OF
Metabolism and Nutrition

A SERIES OF MONOGRAPHS

BY PROF. DR. CARL VON Nooannu

Professor of ”It First Medical Clinic, Vienna
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DISORDERS OF

Respiration and Circulation
svup’romxromcy AND DIAGNOSIS
A SERIES OF MONOGRAI’ES

BY PROF. DR. EDMUND VON Naussnn
Prqfessor of the Second Medical Clinic, V {Erma

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CLINICAL TREATISES

on the

PATHOLOGY and THERAPY
0f DISORDERS 0f
METABOLISM and NUTRITION

PART VIII
G O U T

BY
PROF. DR. H.LSTRAUSS
Prqfeuor of the Third Clinic, Royal Charily Hoxpital, Berlin

Authorized American Edition

TRANSLATED UNDER THE DIRECTION OF NELLIS BARNES FOSTER, M.D.

Auotiata PhyJieian to the New York Hospital,- Auociate
in Biala ital Chemthry, College of Phyxitiam
an Suegeam, Columbia Uni‘venity.

NEW YORK
E. B. TREAT 8; COMPANY
1909

COPYRIGHT, 1909,
BY E. B. TREAT & COMPANY

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PREFACE TO THE AMERICAN EDITION

THE following discussion is a brief résumé of a
contribution on the pathogenesis and therapeutics of
gout, which I published seven years ago in Section 8,
Volume II, of the W uerzburger Abhandlungen. Cor-
responding with the purpose of the “ Abhandlungen,”
my communications were not exhaustive, either from
a scientiﬁc or a practical point of view. They had
no aim but to give, from a practitioner’s standpoint,
a concise picture of the modern conceptions of the
nature and treatment of gout.

At the special request of Messrs. E. B. Treat & Co.,
New York, who have secured the American rights, I
have added a large amount of new material to my
original treatise with the object of explaining such
changes as have developed in the meantime. Here
again I have conﬁned myself to what I consider the
most essential points which have a bearing on practi-
cal treatment.

In a ﬁeld which commands such an abundance of
literature, it is sometimes rather difﬁcult to separate
the more from the less valuable, and I am not sure
whether I have always succeeded in enucleating the
kernel from the shell, and whether many an important

55376010

PREFACE TO THE AMERICAN EDITION

point may not have escaped me. At any rate, I have
endeavored to place more emphasis on those ideas
which are of practical importance than on those which
possess interest only from a theoretical point of view.

H. STRAUSS.
BERLIN, December, 1908.

NOTE BY THE AMERICAN EDITOR

THE amount of literature that has been amassed
in the last decade on the subject of gout presents a
severe task to the clinician who desires to make him-
self familiar with the metabolism of this disease. On
this account a monograph which attempts to separate
the more important results of research from the less,
in the relation to clinical medicine will be of an espe-
cial aid to the practitioner, and will serve also as an
introduction to the present trend of opinion in these
disorders. Professor Strauss is unusually qualiﬁed
to write such a monograph, since as a physician he
is thoroughly conversant with the clinical difﬁculties
that surround gout, and, moreover, as an investigator
he is able to weigh and value accurately the results of
experiments. This is especially notable in Professor
Strauss’ handling of the subject of uricacidemia in
its relation to the deposition of crystalline salts. In
considering the therapeutics of gout, special stress
is placed on the individual demands of the case rather
than a general scheme of conducting all cases, and
here also this point of View is broad and conservative.

NELLIS BARNES FOSTER, M. D.

69 EAST FIFTY-FOURTH STREET, NEW YORK.

"92%)

 

CONTENTS

PAGE

I. DIFFERENTIATION OF GOUT . . . II
II. PATHOGENESIS OF GOUT . . . . 15
PATHOLOGICAL CHEMISTRY OF URIC ACID . I 5
URIC ACID IN THE BLOOD . . . . . 18
CAUSES OF SODIUM URATE DEPOSITS . . 20
ORIGIN OF URIC ACID . . . ‘. . . 21
URIC ACID ELIMINATION . . . . . 23
NEPHRITIS AND GOUT . . . . . . 27
ENDOGENOUS URIC ACID . . . . . . 3O
URIC ACID RETENTION . . . . . . 33

FACTORS IN THE PRECIPITATION 0F URATES 35

III. SYMPTOMS OF URICACIDZEMIA . 43

IV. THERAPY OF GOUT . . . . . . 45
DIETETICS IN GOUT . . . . . . . 45
BEVERAGES . . . . . . . . . . 53
QUANTITY OF FOOD . . . . . . . 54
ANIMAL COMPARED WITH VEGETABLE PRO-

TEINS . . . . . . . . . . . 56
WATER “ CURES” . . . . . . . . 6O
DRUGS . . . . . . . . . . . 63
TREATMENT OF ACUTE ATTACKS . . . 65
PHYSICAL METHODS . . . . . . . 66

HYGIENE..........69

 

 

I.—DIFFERENTIATION OF GOUT

‘AN exhaustive treatise on our present knowledge
of gout, the nature of its clinical manifestations and
its treatment, cannot be conﬁned to a short space;
hence a brief exposition must forego ampliﬁcation and
touch only on those facts in the pathology of gout
which are either of practical signiﬁcance, or, because
they possess an especial interest, are weighty factors
in our conception of the nature of the disease. Fur-
thermore, it is the object of this discussion to review
carefully the changes which have been brought about
during the last ten years in our ideas of theory and
practice, and above all the questions of pathogenesis
and therapy must be considered, for we believe it is
in these, as we review the chapter of the diagnostic
problems of gout, that there have been the most
radical changes—and yet, in spite of this, more prog-
ress is to be desired even here. It is ﬁrst important
to deﬁne the exact limits of the term gout; for after
reading many articles on the subject, the impression
gained is that its clinical boundaries differ widely
with various authors. To do this is a task at once
pleasing and perplexing. The chief clinical difﬁcul-
ties in many cases consist in the determination of
what is the sequel of gout and what is the sequel of

a simultaneously existing arterio—sclcrosis or chronic
II

12 DISORDERS 0F METABOLISM AND NUTRITION

interstitial nephritis—a point to which I shall return
later on. In gout we must make a sharp and careful
distinction between an acute attack, or an acute gen-
eral gouty manifestion and a chronic state of gouty
diathesis. The latter is characterized by an increase
of uric acid in the blood serum, and should not be mis-
taken for diathesis uritica. Clinically it is very easy
to demonstrate a large increase in the quantity of
uric acid in the blood, but the clinical signs of gouty
diathesis are often unreliable. Without going into
an exhaustive discussion of the boundaries of this
condition, we will consider it suﬂicient for the identi-
ﬁcation of doubtful cases to name those criteria which
possess the signiﬁcance of stigmata. The experiment
of Garrod, which unfortunately cannot be car-
ried out on every borderline case,* possesses high

*The thread test as described by Garrod (Gout and Rheu-
matic Gout, p. 86, London, 1876) is as follows: “ Take from one
to two ﬂuid drams of the serum of blood and put into a ﬂat-
tened glass dish ;—and to this add ordinary strong acetic acid,
in the proportion of six minims to each ﬂuid—dram of serum,
which causes the evolution of a few bubbles of gas. When the
ﬂuids are well mixed introduce one or two ultimate ﬁbers, about
an inch in length, from a piece of unwashed huckaback or other
linen fabric.” After standing from thirty-six to sixty hours the
uric acid crystals may be seen by means of a microscope or
strong hand glass. This test has fallen out of use, probably
because it, along with the literature of gout of that period, has
been superseded in a large degree by later research. This test,
however, offers a ready and quick method of detecting an excess
of uric acid in the blood, where the exact quantitative estima-
tions demand laboratory equipment only at the command of the
specialist. The necessary blood serum is most easily secured by

GOUT I 3

clinical value, and there is identiﬁcation by the
tophi. To these the testimony of a typical case-his-
tory of gout adds its weight for the establishment
of a diagnosis. Less important, but at times sugges-
tive, is the gouty ﬁnger, which is a symptom of secon-
dary importance, as is also the acne rosacea of the
gouty patient. Furthermore, the association of gas-
tro—intestinal or cardiac symptoms with a neuralgic
or rheumatoid condition, in stout muscular, large-
framed individuals of irritable temperament is very
frequently signiﬁcant. The demonstration of symp-
toms of chronic nephritis is an observation which is
often valuable, especially when lead poisoning or al-
cholism, or both, are found in the history. Reale
has lately shown that if the patient be gouty the in-
dican test made with Obermayer’s reagent gives a
weaker reaction after boiling than before. For two
cases of chronic gout we are able to conﬁrm these
results, but for all others our researches have shown
this test to be in no way speciﬁc for gout. In our
earlier investigations we were impressed with the
parallel existence in the urine of a reducing, laevo-
rotary, non-fermentable substance, together with a
large amount of indican. From a recent inspection
of our case-records we ﬁnd among our observations

means of small cantharides plasters. Excluding interstitial
nephritis and the lucaemias where there is an increase of uric
acid in the blood, this test has a great value in the diagnosis of
those cases of gout that present no characteristic symptoms
such as tophi. [EDITOR]

I4 DISORDERS OF METABOLISM AND NUTRITION

on this laevo-rotary substance three cases of arthritis
uritica———a considerable percentage of the total num-
ber of those showing laevo-rotation without fermen-
tation. The symptoms of gouty diathesis here men-
tioned are certainly not present in every case; in still
fewer is the gouty character of the trouble revealed
by an acute paroxysm or by a chronic manifestation
of gout. Nor does the increase in indican bear any
essential relation to gout, since Grossman has shown
by quantitative experiments conducted at my instiga-
tion, that after an abundant milk diet indican is
promptly reduced to a minimum. Thus it is appar-
ent that search must be made for each and every
symptom which will betray the presence of gout. In
a doubtful case of inﬂammation of the joints we were
once able to make a diagnosis by the puncture test,
recognizing in the ﬂuid obtained crystals of acid so-
dium urate which demonstrated the gouty character
of the arthritis.

II.——PATHOGENESIS OF GOUT

Pathological Chemistry of Uric Acid.——In so far as
the chemistry of gout is considered, the main part of
the discussion must be concerned with two condi-
tionsz—I. The existence of a crystalline separation
of acid sodium urate in portions of necrotic tissue.
2. The existence of an increased uric acid content
of the blood. Von Wollaston had noted, as early as
the end of the eighteenth century, the occurrence of
a crystalline separation of acid sodium urate (sodium
biurate, Roberts; mononatrium urate, Tollens).
This condition is so closely associated with gout that
it and the so—called “ gout necrosis,” which has been
found characteristic in all histological investigations
of gouty changes, must be considered together. And
this state remains peculiar to gout, in spite of the fact
that even without any clinical history of gout, there
is at times demonstrable at autopsy a precipitate of
urates in the enlarged joints of sufferers from atro-
phic kidney, especially of those who have also had
chronic lead poisoning. And further, it is peculiar
in spite of the fact, to which we can testify, that at
times it has been impossible to ﬁnd the chalky de-
posit on which the essential existence of gOut depends
at autopsy of persons who, during life, have suffered

I5

I6 DISORDERS OF METABOLISM AND NUTRITION

constantly from gout. The urate deposits* are by
no means limited to typically enlarged joints, but ap-
pear also in other joints, in the tendon sheaths, in the
ear (as in the well-known tophi), and Ebstein has
even mentioned the bone marrow as an occasional lo-
cation. The question of the source of the urate de-
posits has given rise to many theories, which
we may examine to better advantage after we have
made ourselves more familiar with the causes of
the supersaturation of the blood of gouty patients
with uric acid. This state? of saturation was as-
serted by Garrod, and has since been demonstrated
by the quantitative determination of the uric acid, as
well as by the “thread” experiment. While the
blood serum of a healthy person or of a fever patient
contains only minute traces of uric acid,——according
to our investigations from 1.5 mg. to 2.0 mg. at the
most in 200 cc. of blood serum—in the blood of a
gouty individual we meet with a marked increase
(as much as 17.5 mg, Weintraud). Besides, Wein—
traud, Klemperer and Magnus-Levy, especially, have
shown an increase of uric acid in the blood of those
suffering from gout; and we have observed in many
cases of gout an increase of the total nitrogen re-
tention which, as shown by us in another article (H.
Strauss: Die chronischen Nierenentziindungen in

*Deposits of urates have been detected in almost all the
structures of the body, even in the meninges. In a suspected
case of gout, I once found a tophus in the external auditory
canal—the only deposit to be found. [EDITOR]

GOUT I7

ihren Einwirkungen auf die Blutﬂiissigkeit. Berlin,
Hirschwald, 1902), is coincident with an increase of
uric acid in the blood serum. In the ascitic ﬂuid of a
gouty patient, who was also suffering from atrophic
kidney and cirrhosis of the liver, twelve days before
a typical attack of gout we found 2.6 mg. of uric
acid nitrogen, which is equivalent to 7.8 mg. of uric
acid per 100 cc. of ﬂuid. The total nitrogen, exclud—
ing the nitrogen of the albumen, amounted to 45. mg.
and the ammonia nitrogen to 4.0 mg. These values
for the uric acid and the ammonia are signiﬁcantly
higher than for the normal. At another time we
found in the ascitic ﬂuid of this case 5.2 mg. of uric
acid nitrogen, equivalent to 15.6 mg. of uric acid.
Although there is, so frequently, an increase of uric
acid in the blood serum in gout, yet this condition
does not offer an exclusive diagnostic peculiarity;
for, as it has been shown, there is also an increase of
uric acid in the blood in pneumonia (Salomon, von
Jaksch, Petren), in nephritis (von Jaksch, Klemperer,
Magnus—Levy, and numerous other observers,) and
also in leukemia (Klemperer, Magnus-Levy and oth-
ers) and, further, the body ﬂuids show an increase of
uric acid under the inﬂuence of X-ray treatment. In
contracted kidney with uraemia, values for uric acid
as high as 16.05 mg. in 100 cc. of blood have been ob—
tained, and in leukemia as high as 22.6 mg. in 100
cc. of blood. In thirty-seven cases of chronic nephri-
tis we have found a minimum value of 1.1 mg. and
a maximum value of 10.5 mg. uric acid in IOO cc. Qf

.18 DISORDERS 0F METABOLISM AND NUTRITION

blood serum. The increase of uric acid in the blood
may therefore be due to various causes, and is of in—
terest for our purpose only in so far as the actual ef-
fects are concerned, and not as the consequence, of
one cause more than another.

Uric Acid in the Blood.———Since the method of
Garrod gives no numerical values, we have employed
for the determination of uric acid an iodine method
which has lately been published by Ruhemann, and
we have also used the iodine solution of Ruhemann
ten times diluted. Dr. Hanson has, at our suggestion,
studied a great number of blood sera which were
obtained by means of the cupping glass, and he was
able to attain his object in the majority of cases
with a quantity of from 6 to 8 cc. of blood. This
amount was obtained by a single cupping. The values
of the uric acid were also relatively high in nephritis
and approached those which we had obtained: by
means of the method of Ludwig-Salkowski from
transudates of nephritics. These estimations indicate
that Ruhemann’s method suffers from some imper—
fections (we mention, for example, the dependence of
the results on the length of time and the intensity of
the shaking, and also on the presence or absence of
other iodine combining substances), so that in our
experience the values obtained are, unfortunately, to
be employed only with a certain reserve. It has long
been believed that a connection must exist between the
increase of uric acid in the blood and the appearance
of the crystalline urates in the necrotic tissue, al-

GOUT 19

though various conclusions have resulted from the
studies of the two manifestations. Garrod believed
the direct origin of the crystalline separation was to
to be found in the saturation of the blood with uric
acid in connection with certain inﬂuences in which a
weak alkalescence would cause the precipitation of the
uric acid already present in excess. Ebstein defends
the conclusion that the necrotic tissue is primary; an
original inﬂammation develops into necrosis, which
gives rise to a consequent condition favorable for the
supersaturation of the ﬂuids with uric acid. The acid
reaction shown by the necrotic tissue facilitates the
conditions for the precipitation of the uric acid, and
under this inﬂuence an immediate deposition of the
acid urates is brought about. Von Noorden ignores en—
tirely the question of the cause of the separation of
the crystalline precipitate from the blood in the
presence of uric acid and considers it as a local by-
product resulting from the solution of the necrotic
constituents of the broken-down protein material;
moreover, the necrosis itself is regarded by this author
as the sequence of a local inﬂammation of the tissues,
whose ﬁrst cause is unknown. With the exception of
the von Noorden theory, the preceding conclusions all
deal with the fact of an increase of the uric acid con-
tent of the blood, while they also comprehend the sig-
niﬁcance of this manifestation in the pathogenesis
of various attacks of gout. The experiments of
Kionka, which have already been mentioned, add
weight to the opinion that a supersaturation of the

20 DISORDERS OF METABOLISM AND NUTRITION

blood with uric acid plays an especial role in the origin
of the crystalline separation. In these experiments,
after feeding hens for a long time on meat, crystal—
line deposits could be demonstrated in the joints and
tendon sheaths. The researches of Reihl, His and
Freudweiler have proved further, that, by the injec- ‘
tion of a suspension of acid sodium urate a tissue
lesion is produced, which at every stage exactly simu-
lates a gouty deposit; there is ﬁrst the deposition of
crystals in sound tissue which results in a beginning
of necrosis, followed by an inflammatory reaction in
the surrounding tissues, and later, the formation of a
focus enclosed by a capsule of connective tissue. Tak-
ing similar experiments with the injection of calcium
carbonate as a basis for comparison, these investiga-
tors came to the conclusion that the consecutive tis-
sue changes are not to be attributed purely to the
reaction set up by the presence of a foreign body, but
to the chemical action of the precipitated sodium
biurate as a speciﬁc toxin.

Causes of Sodium Urate Deposits—His and
Freudweiler have produced later evidence, that an
inﬂammatory process, similar to the one we observe
in gout, can be produced by a crystalline deposition
of sodium biurate; and Kionka has shown by animal
experiments that a long—continued increase of the ali-
mentary uric acid content of the blood leads—at least
in certain places—to a precipitation of uric acid crys-
tals. The concurring views of numerous authors,
that a primary overloading of the blood with uric

GOUT 2 I

acid plays an important role in bringing about a con-
dition favorable for the urate deposit, meet with no
serious controversy. The questions, however, still re—
main to be studied z—I. Why in cases of leukemia,
pneumonia, and of chronic nephritis, in which there
is likewise a noticeable overloading of the blood serum
with uric acid, there seldom or never results a condi-
tion similar to the one observed in gout; and 2. Why
the deposits are always formed in certain pre-deter-
mined places in the body. In regard to the ﬁrst point,
the combination of gout and leukemia has been de-
scribed by Duckworth, Pribram, and Ebstein, but such
cases are very rare; however, in later discussions we
shall refer to the fact that the coincidence of gout and
nephritis is not infrequent. There are several ques-
tions in this important connection which demand
special attention: what is the source of the urate de-
posit; what is our knowledge concerning the origin
of the uric acid in the blood; and what is the manner
and means by which it disappears.

Origin of Uric Acid—While uric acid was earlier
regarded as an incomplete oxidation product of albu—
men, later researches, especially those of Posse] and
his pupil, have shown that uric acid in man and mam-
mals is the end-product of nuclear decomposition, that
is to say, the purin bases are the ﬁnal cleavage pro—
ducts. To account for the presence of uric acid in
the organism, we must therefore make a distinction
between two sources: I. The uric acid arising
through the disintegration of the nuclein containing

22 DISORDERS OF METABOLISM AND NUTRITION

substances of the body, and, 2. The uric acid arising
from the disintegration of nuclein containing sub-
stances in the food. Fasting human beings produce
a considerable amount of uric acid; and likewise those
on a full diet of nuclein containing substances and
those on an almost nuclein free diet. Since these
latter amounts are less than when a mixed diet is
used (G. Rosenfeld, Schreiber and Waldvogel, and
others) Burian and Schur distinguished an exogen-
ous and an endogenous production of uric acid, and
from this they deduce the theory that the endogenous
purin bodies of the urine constitute an individual con—
stant. This theory is opposed to that of O. Loewy,
who makes the gross output of uric acid depend on
diet only. In adults, the quantity of uric acid ex-
creted in twenty-four hours varies with the :indi-
vidual; from 0.3 to 0.6 grams.* A synthetic forma-
tion of uric acid such as takes place in the organism
of birds, appears to occur in the mammal organism
in only a relatively moderate extent. On this account
researches have been made on birds, in the hope of
obtaining an explanation of the uric acid metabolism
of man, but they are capable of a clinical interpreta-
tion only under the greatest limitations and in wholly
restricted directions.

Concerning the organs which are capable of trans-
forming xanthin bases into uric acid, we know

*A synthesis of uric acid has been demonstrated in birds.

The evidence for such a. synthesis in man and other mammals is
not beyond dispute. [EDITOR]

GOUT 23

through the investigations of Spitzer and Wiener,
that the liver and spleen are preéminently the glands
which, after removal from the body, contain enzymes
capable of transforming the purin—base radicle of
nucleins into uric acid, and this transformation can
be effected to a conspicuous degree.

Uric Acid Elimination—For the excretion of the
already formed uric acid from the blood and ﬂuids
of the tissues, there are two methods: I. the excre-
tion of uric acid as such through the kidneys. 2. the
transformation of the uric acid into other compounds.
Concerning the excretion of the uric acid from the
body through the kidneys, the recent investigations
of Vogel, Schmoll, Magnus—Levy, and others have
shown that in gouty subjects a temporary nitrogen
retention occurs, without increase of body weight,
and that at the time of an attack an increased nitro-
gen excretion occasionally results. Magnus-Levy con-
siders this nitrogen to be retained in the form of
toxins.

rAt the time of an acute gouty attack, as was shown
some time ago by E. Pfeiffer and Magnus-Levy, uric
acid should be excreted in greatly increased amounts;
and indeed, the beginning of an attack is often
marked by this increased uric acid output. His has
also observed an increase during an attack, which had
been preceded by a marked decrease of uric acid
excretion. According to the researches of a large
number of authors (Vogel, Camerer, Schmoll, Rom-
mel, Smith, Jerome and H. Strauss) in the interval

24 DISORDERS 0F METABOLISM AND NUTRITION

which is free from attacks, the uric acid excretion
is generally about normal, although the percentage
tends to be lowered rather than to rise. This is also
true of patients fed on a purin-free diet; but in these
cases the values obtained were found to approach the
lower more frequently than the upper limits of the
normal. In a total of thirty results, compiled from
various authors by Brugsch and Schittenhelm, only
eight exceeded the maximum value of 0.4 gram.
This demands our attention, because in leukemia,
pneumonia, and X—ray treatment, the amount of
endogenous uric acid is increased. Another deviation
from the normal in the excretion of the endogenous
uric acid has been demonstrated by Pfeil, Soetbeer,
Burian and Schur, Kaufman and. Mohr, Brugsch,
Block, Pollack and others, who have shown that when
purin-containing substances are added to a purin—free
diet, the excretion of the exdogenous uric acid is less
and occurs more slowly in gouty individuals than
in healthy ones. The experiments of Brugsch and
Schittenhelm also give evidence that when purin
bodies are added, there is a retardation in their
metabolic change into uric acid. That a transforma-
tion of uric acid in the organism is possible within
wide limits has been indicated by the early researches
of Frerichs—Woehler, and also by the later experi-
ments of ,Weintraud and others, all of which lead
to the conclusion that a considerable fraction of the
uric acid which is formed in the organism, or in-
troduced into it, appears in the urine as urea. In

GOUT 25

dogs, as pointed out by Minkowski and Salkowski,
an increase of uric acid forming substances produces
allantoin instead of urea; both of these latter com-
pounds being much more easily soluble than uric
acid. A means of still further disposal at the com-
mand of the organism, is that a portion of the uric
acid may be changed into glycocoll, which is then
excreted in the form of glycocoll compounds, espe—
cially hippuric acid. Wiener ﬁrst called attention
to this and indicated the kidneys and muscles as pre-
eminently the place for the transformation. A
uricolytic ferment, which is most abundant in the
kidneys, has been demonstrated for the herbivora,
and, according to Pfeiffer, for pigs. Through the
researches of Stockvis, Chassevant, Richet, Ascoli,
Spitzer, Wiener, M. Jacoby and others we arrive
at the conclusion that the destruction of uric acid
is also effected in the liver, as well as in the kidneys
and muscles; and Klemperer has recently shown that
the blood shares this power of acting on the acid
sodium urate by “auto—digestion.” Two questions
arise from the consideration of these observations:
I. Whence comes the increase of the uric acid con-
tent of the blood in gout? 2. What factors cause the
precipitation of the acid sodium urate from the uric
acid contained in the ﬂuids of the tissues? In answer
to the ﬁrst problem, various theories have been ad-
vanced: I. the increase of uric acid in the blood
can come about through its increased formation, 2.
through its abnormal retention, 3. through its de-

26 DISORDERS 0F METABOLISM AND NUTRITION

fective transformation into other compounds, and 4.
through various combinations of these processes. Eb-
stein holds the theory that the formation of uric acid
is increased; but this is extremely difﬁcult to demon-
strate. The possibility of an abnormal retention of
uric acid seems to us undeniable, as in the records of
numerous cases it has been a prominent symptom
manifested by chronic nephritics. This view had the
support of Garrod and has recently been reinforced
by the anatomical studies of Levison, and it is also
readily suggested by the results which have been
obtained in regard to the elimination of both the
exogenous and endogenous uric acid in gouty patients.
Tollens has lately joined the group of those investi-
gators on metabolism who attach great importance to
this explanation. Pollack has compared it directly
with the processes which take place in the kidneys of
alcoholics in which the pathologist often ﬁnds certain
evidence of chronic interstitial nephritis, even when
during life there was no trace of albumen in. the
urine. Some other investigators (Brugsch and Schit-
tenhelm) have considered the increase of uric acid
to be due to a disturbance of the uricolytic power of
the kidneys; others still (Burian and Schur) have
attributed it to a combination of this deﬁciency and
renal detention. So far as we are able to judge from
our own experience the numerous cases of gout which
we have seen have manifested either symptoms of
chronic interstitial nephritis or the function of the
kidney has been suspected to be impaired. To pre-
vent any misunderstanding it should be mentioned

GOUT 27

that in the class of those whose kidney function is
considered suspicious are included chieﬂy those who
suffer from chronic lead poisoning or from a dis-
tinctly marked form of alcoholism; these cases will
be discussed later. As we have already asserted,
the analbuminuric form of chronic interstitial nephritis
is not at all unusual. On two occasions when its ex-
istence had been for a long time assumed, we saw
albumen make its appearance in the urine. In two
other cases our diagnosis of an analbuminuric nephri-
tis, made during life, was veriﬁed at autopsy.

Nephritis and Gout—The number of cases of ne-
phritis among gouty patients would be found much
greater, even when no trace of albumen is discovered
on clinical examination, if the existence of a latent
chronic interstitial nephritis were always suspected
and characteristic symptoms were taken as proof of
the disease. Such indications are: increased pulse
tension (higher sphygmometric readings), signs
of cardiac hypertrophy, changes in the retinal ﬁelds,
or defective kidney function. In this connection may
be cited some very striking observations from our
own experience. In a case of a painter twenty—eight
years of age we found a short time after a typical
attack of gout a blood pressure of 150 mm. of
mercury (Gartner), but no appearance of albumi-
nuria.

In another case——likewise with an etiology of lead
poisoning—we have carried on investigations of the
metabolism during eight days, the onset of the at-
tack being excluded, and found a conspicuous nitro-

28 DISORDERS OF METABOLISM AND NUTRITION

gen retention without increase of body weight. We
have employed the methylene blue test in three cases.
In two of these the beginning of the excretion fol-
lowed ingestion in half an hour, in one case after an
hour. In one case the excretion terminated after
thirty-six -hours, in another after forty hours, and
in the third, after ninety-six hours. In two cases a
retardation of the excretion could be proved. In four
cases we have demonstrated the nitrogen retention,
whose signiﬁcance in, and relation to, chronic nephri-
tis we have stated elsewhere; and at the time of an
attack we obtained values of 35, 64, 66, and 83, mg.

In another case which, to be sure, was complicated
with chronic interstitial nephritis, we found 61 mg.
in the interval between attacks. In two cases we
found the molecular concentration normal during an
attack (A=—-o.54° and —o.56°); on the other hand,
one case showed a most remarkable result, inasmuch
as during an attack when all precautions were taken,
a determination was obtained of A=—o.75°. And
three days later (the attack had already subsided
considerably) a repeated investigation of the blood
serum gave the still remarkable value of A=—o.76°*.

*The above mentioned results have been already published
(Nierenmonographie p. 69), and in spite of the fact that Wald-
vogel has more recently reported a similar observation, we
hesitated at ﬁrst, without the existence of further data, to in-
terpret this ﬁnding in a direct relation to an attack of gout,
because we have found values similar to the foregoing, in two
cases, in which the condition was neither one of gout nor
nephritis, nor urasmia.

GOU’I‘ 29

In the ascitic ﬂuid of the case of gout mentioned,
also suffering from atrophic kidney and cirrhosis of
the liver, and who had a nitrogen retention of 61 mg.,
we found repeatedly A:—o.56°, —057°, —o.58°,

~and once :—o.6o°. If we may venture so far as
to diagnose a latent nephritis by a single symptom,
then we believe that if several of the usual symptoms
of a chronic nephritis occur simultaneously with gout,
in spite of the absence of albumen in the urine, one
cannot exclude the existence of a- chronic nephritis
without farther evidence against it. For the modern
clinician, nephritis should be diagnosed before there
is a demonstrable albuminuria. However, we are
fully alive to the fact that there are functional renal
disturbances which are not manifested by distinct
anatomical lesions. Although we cannot consider.
every case of gouty diathesis as simply the result of
a diseased kidney, we hold—though not so radically
as Levison, for example—that a long-continued dis-
turbance of kidney function is etiologically very im-
portant for many, though not for all cases, and we
will not concede the objectioln to be of value that in
the interval between attacks, the gouty sufferer may
show an undiminished excretion of uric acid. It
is also true in nephritis that uric acid excretion may
be normal, but in spite of the fact, we ﬁnd a very
great increase of uric acid in the blood; which,
as we can prove, exhibits only partially the general
tendency in nephritis toward retention of nitro-
genous metabolism products. This comes about he-

30 DISORDERS OF METABOLISM AND NUTRITION

cause the uric acid value, as we have pointed out,
normally varies in such wide limits that a lack of
100 to 150 mg. in the urine per day is scarcely
noticed. If we consider how little uric acid is neces-
sary in the blood serum in order to produce an in-
crease in the body ﬂuids of from 5 to 10 mg. of uric
acid per 100 cc. of ﬂuid, it will then be understood that
by the process of retention a considerable accumula-
tion of uric acid in the blood serum may occur in a-
comparatively short time, even when the excretion
of uric acid is not appreciably interfered with. But
it cannot be denied that there is, possibly, another l
disturbing factor which plays a role in the increase
of uric acid in the ﬂuids and which tells against the
uricolytic power of the kidneys. More0ver, at all
events, it appears to me that in numerous, but by no
means all, cases of gout we are justiﬁed in assuming a
more or less close relation between a nephrogenous in-
hibition of uric acid excretion and the uric acid in-
crease in the blood serum and the ﬂuids. Although in
chronic nephritis the kidneys are able, to react prompt-
ly to an increased production of uric acid by an in-
creased excretion, there may be, nevertheless, an in-
crease of uric acid in the blood in these cases.
Endogenous Uric Acid—In reference to the en-
dogenous formation of uric acid in gout, we wish to
cite an experiment which was carried out on a pa-
tient in the third medical clinic, who was suffering
from gout in the joints of the ﬁngers and of both
knees. This experiment is of especial interest, be-

GOUT 31

cause, on two days, foods rich in purin were added
to the standard purin free diet, as follows; on the
ﬁrst experimental day 325 grams of sweetbreads were
given along with the regular diet of two liters of
milk, 300 grams of bread, and 40 grams of butter;
and on the second experimental day, 2 grams of pure
caffein (150 grams water and 30 grams Syrup. Cort.
Aur.). During these experiments the patient was
kept in bed. The following table shows the uric
acid excreted by this patient.

.-
‘5 E
g "a 5 . U.
*5 1: ....
ﬁg gt}; '2'“: 1% § 1.:
a) ~H .44 -~ 4)
a E‘ in :2 :3 a
1 1450/1012 1005 g. 0.386 g. Standard diet.
2 1465/1009 8.07 g. 0.315 g. Standard diet.
3 2070/1013 15.50 g. 0.337 g. Standard diet.
4 1400/1011 8.72 g. 0.257 g. Standard diet.
5 1500/1012 11.03 g. 0.386 g. Standard diet.
6 1650/1013 14.09 g. 0.493 g. Standard diet.
7 1680/1013 11.40 g. 0.626 g. Standard diet, 325
g. sweetbread added.
8 1560/1015 16.77 g. 0.531 g. Standard diet.
9 1775/1014 13.54 g. 0.319 g. Standard diet.
10 1440/1014 10.58 g. 0.339 g. Standard diet.

H
H

1850/1012 13.98 g. 0.621 g. Standard diet, 2 g.
caffein added.

12 1050/1016 10.36 g. 0.347 g. Standard diet.

13 1535/1017 13.70 g. 0.410 g. Standard diet, 200

g. meat and 250 g.

vegetables added.

32 DISORDERS 0F METABOLISM AND NUTRITION

The values found in this experiment for the en-
dogenous uric acid, while the patient remained on
the standard diet, were considerably less than those
obtained by Burian and Schur; but the amount of
excreted uric acid was noticeably greater upon the ad-
ministration of uric acid forming substances (calves’
sweetbread and a large quantity of caffein). Since
the values for the endogenous uric acid are relatively
small in our experiment—and, as the table shows,
are absolutely independent of the amounts of total
nitrogen—the question is raised, whether we do not
have to deal with a diminished excretion of the uric
acid. This question will be left open in consideration
of the obvious fact that on the days of the employ-
ment of the thymus and also of the caffein contain-
ing materials, the patient was able to excrete a large
amount of uric acid. To determine what was due to
the inﬂuence of the caffein two further experiments
were conducted with the regular diet to which two
eggs had been added. This resulted in a slight in-
crease of uric acid output, a rise of from 390 mg.
(average for two days) to 496 mg., and of from
285 mg. (average of six days) to 486 mg. In the
meantime Grossman (Berliner Klinische ,Wochen-
schrift, 1903) has made three furtherexperiments at
my instigation, and has been able to establish low
values for the endogenous uric acid as soon as the
patients had become accustomed to the prescribed diet.
Therefore, my owln previous results fully agree with
the ﬁndings of later investigators.

GOUT 33

Uric 'Acid Reten-tion.—While we should not ven-
ture so far as to ascribe to uric acid retention the ori-
gin of every case of gout, we are not prepared to
deny the possibility of such a process for many cases.
At the same time a deﬁcient destruction of uric acid
may lead to its increase in the blood. If we have
dwelt somewhat at length upon diminished excretion
as a factor in the increase of uric acid in the blood,
it is because we consider it much more important in a

\large number of cases than others seem willing to
concede. The fact that even in this connection we lay
stress upon the importance of the uricolytic func-
tion of the kidneys, to which Brugsch and Schitten-
helm particularly refer, seems to us necessary for
the following reason: Even though we attribute much
importance to the retention phenomena in many cases,
the question always arises why in these cases the
organism should not be capable of compensating for
the deﬁcient secretion in some way or other. How—
ever, the organism is still in a condition to contend
with a surplus of retained uric acid. This is shown,
not only in the fact mentioned that the administra-
tion of a large amount of uric acid caused no t0xic
symptoms, and also that while in leukemia there is
a great overproduction of uric acid, a certain
amount present in the blood is never exceeded. Also
i Weintraud saw an increase of only 5 mg. in 100 cc.
of blood after feeding thymus, and we have observed
approximately the same value in the cases of gout
which we have had the opportunity to study. That

34 DISORDERS OF METABOLISM AND NUTRITION

other factors than the retention are also responsible
for the increase of uric acid in the blood of gouty
patients is suggested by the fact that gout is closely
related to a whole sequence of metabolism diseases,
especially to obesity and diabetes, maladies which we
can perhaps assign to an insufﬁciency of the kata-
bolic powers of the organism. During the course
of the so—called metabolism diseases, changes are
many times found in the liver, which is concerned‘

’/

with sugar metabolism (in connection with diabetes, =

these changes are not so far reaching as was earlier 1'

believed), and, on the other hand, as we have seen, also
shares in uric acid metabolism. These hepatic changes,
according to Ebstein, appear most often in the form of
hypertrophic cirrhosis. In this connection may be men-
tioned a case that we had under our observation sev-
eral years ago, a patient, who suffered simultaneously
from obesity, gout, hypertrophic cirrhosis, and
bronzed diabetes. The clinical history of the pa-
tient in so far as it deals with his residence in
the third medical clinic has already been given
brieﬂy in the article published by Raphael at our sug-
gestion (Researches on alimentary glycosuria, Zeit—
schr. f. klin. Med. Bd. 37). As the patient was seen
many times in the ensuing three years, the history
of the further course of the disease is now possible.
The case also possesses especial interest because it
belongs to the slow and relatively mild form of bronzed
diabetes, to which special attention has recently been
called by Murri. The patient suffered from no in-

GOUT 3 5

herited disease. He was sixty years of age, a master
tailor. Ten years ago he repeatedly had typical at—
tacks of gout, and at present still complains of acute
pain in his left shoulder. He was a man of average
size, strongly built, with well—developed muscles and
fairly thick panniculus. The skin showed a decidedly
brown coloration, which had not been present in early
life and which persisted during the three years of
observation. The body was well rounded, the sub-
cutaneous fat being normal. The liver was markedly
enlarged, smooth, and blunt edged; the spleen was
likewise considerably enlarged and hardened. The
stools were bile colored. In amount the urine varied
from two to three liters per day; it was clear and,
considering the quantity, had a slight excess of
urobilin. There was no albumen present. In the
course of the three years repeated urine examinations
showed at times a total absence of sugar, but it was
usually present in small amounts, which scarcely ever
exceeded a total of from IO to 40 grams per day.
Since the patient complained of itching of the skin,
polydipsia and polyuria, and also at times became
greatly emaciated, ,there remained scarcely a doubt
that we had to deal with a case of true diabetes in a
gouty subject, accompanying hypertrophic cirrhosis
of the liver, and brown pigmentation of the skin.
Factors in the Precipitation of Urates.-——In gout
the overloading of the blood serum and the tissue
ﬂuid with uric acid, which has been the subject of
so many discussions, is not, however, a necessary

36 DISORDERS 0F METABOLISM AND NUTRITION

condition for the precipitation of the crystalline de-
posit of acid sodium urate. And also, the fact that
this crystalline precipitation does not take place in
all tissues, but only in certain deﬁnite locations, shows
that the purely chemical process caused by a super-
abundance of uric acid in the plasma cannot be the
decisive factor. The consideration must be added,
to which attention has already been called, that a simi-
lar increase is possible in the blood of those who are
not gouty. It is desirable on this account to discuss
the question—without taking into consideration the
place of the precipitation—of what peculiar forces
may act to cause the precipitation of urates from a
solution which contains large amounts of uric acid,
but is not saturated. This shows the direction for
an investigation of the relation between alkalescence
and acidity of the blood. Researches on these lines
have been conducted by Klemperer (by the determina-
tion of the CO2 content of the blood), by ourselves
(Zeitschr. f. klim‘ch. Med., Bd. 30), and by Magnus-
Levy according to the titration procedure of Loewy.
In the meantime we have made two further investi—
gations on patients during attacks of gout; but none
of the results obtained by the above—mentioned investi-
gators has brought to light any reduction in the alka-
lescence of the blood. Luff has also had the same
experience in the use of Wright’s method. Since we
have shown by numerous single determinations with
what extraordinary tenacity the human organism holds

GOUT 37

to a blood alkalescence within a certain limited range
(300-350 mg. NaOH to 100 cc. blood) the inﬂuence
of the alkalis introduced into the body does not seem
of the highest importance in the solution and hence ex-
cretion of uric acid. However, it may be mentioned
that E. Pfeiffer has succeeded, by the introduction of
alkali during a gouty attack, in diminishing the
amount of the uric acid deposited from solution;
and that, on the other hand, the addition of an acid
reacting compound to a solution containing uric
acid, or its salts, does not under all circumstances
cause the precipitation of uric acid. However, uric
acid can be retained in solution, as has been shown
by Minsowski and contemporaneously by Goto, a
pupil of Kossel, by means of a chemically pure
nucleic acid, namely, thymic acid. These a priori
conﬂicting reactions can be explained by the fact that
uric acid has been wrongly classiﬁed as an acid while
the other members of the xanthin group are regarded
as bases. Uric acid is, however, only a more com-
plete oxidation product of purin, since trioyxpurin
is differentiated only gradually from xa'nthin
(=dioxypurin) and from hypoxanthin (=oxypurin)
in its relation to acids and alkalis. Since in the dietetic
treatment of gout we shall be obliged to return again
to these facts, it is perhaps well to show here in a
schematic manner the relations of the various bodies
to each other as they have been elucidated by the
studies of E. Fischer, Kossel and others.

38 DISORDERS OF METABOLISM AND NUTRITION

I. Nucleoproteid
l

Albumen Nuclein

l

Albumen Nucleic acid

Nuclein bases Phosphoric acids

 

 

II. Nuclein bases = Xanthin bodies 2 Alloxuric
bodies = Purin derivatives.

Purin C45 H 44N Xanthin C5 H N440

Guanian H: N, O Uric acidC5 H4 N4 03

Theobromin = Dimethylxanthin C7 H8N402

Caffein = Trimethylxanthin C 8 H 10 N4 02

The nuclein is broken up by the action of the fer-
ments, nuclease, disamidase, xanthin-oxydase and
uricolytic ferment.

With the exception of the reaction of the solvent,
the relative amount of the individual salts held in
solution 1s of next importance in the question of the
precipitation of the uric acid, that is to say, these
compounds of uric acid which are more difﬁcult of
. solution. Researches on urine have been undertaken
along these lines and it has been found that the re-
lationship of monosodium phosphate to disodium
phosphate has a very important bearing on the ques-
tion of the solution of uric acid, and on the condi-
tions of the solution of its salts 1n the urine (Ritter,

 

GOUT 39

J. Strauss, and others). We must also assume for
the blood and other ﬂuids that the proportionate
amounts of the individual salts are not responsible for
the question of the solution, or of the precipitation
of the uric acid. As it is expressed in common
phraseology, when various salts are present in a solu-
tion, those which are more easily soluble form com-
pounds; those less easily soluble, if their amount is
not so great as to saturate the solution, can be pre-
cipitated. To this point Senator was one of the
earliest to call attention. His, in his investigations
in the domain of physical chemistry, has shown its
signiﬁcance in the question under discussion,
and, more recently, Freudweiler has taken it: into
consideration. We hold it to be extraordinarily im-
portant in this connection and believe an especial re-
view of the collected results to be demanded in order
to explain the existence of a crystalline separation.
If it is considered that in those places where the
blood supply is meager (cartilages, tendon sheaths,
etc.), diffusion must result much more slowly than
in those parts which are very vascular, it will be
seen without further explanation that the intermix-
ture of the substances dissolved in the blood and the
ﬂuids with the local metabolism products and the
uric acid, must be retarded also. This is not less
true of the consequent molecular exchange. The ex-
perience that the deposition of uric acid when experi-
mentally brought about by the damming back of the
kidney secretion according to Zalesky and Chrzons-

4O DISORDERS OF METABOLISM AND NUTRITION

zewsky takes place ﬁrst in the lymphatics and is
greatest there, thereby makes the hypothesis especially
acceptable that aside from the vessels, the cartilages
or fascia are the most favorable places for such a
salt concentration or chemical interchange. In these
mentioned locations a precipitation of uric acid can
result more easily than the formation of one of its
compounds, when the blood serum is overladen but
not saturated.* Kionka also observed this preference
of uric acid for the cartilages in his experiments in
feeding hens; and, furthermore, Almagia has estab-
lished the fact that the cartilage possesses a special
afﬁnity for uric acid even under normal conditions.

The importance attributed to the products of local
processes in the precipitation of uric acid is not de—
tracted from by the results of more recent animal
experiments made by van Loghem, Silbergleit and
others, who found that in animals the introduction of
alkali favors the formation of urate deposits, while
the introduction of acids inhibits it. This can only
be explained by the assumption of local metabolic dis-
turbances or changes. This shows that the precipi-
tation of uric acid from a blood serum in which it
is contained in excess, demands a local cause. Due
consideration has been given this point on many sides,

*At present we are unable to solve the question whether it
is uric acid or its compounds which are actually present in the
blood of gouty subjects; nor has it been settled for healthy
individuals, in spite of the interesting researches which were
made on urine by E. Pfeiffer with Heintz’s method.

 

 

com 41

by Ebstein especially. The peculiar relation of the
supply of the lymphatics causes it to appear easily
comprehensible that here (cartilages), as Ebstein men-
tioned, a local retardation of the circulation would gen-
erate a condition of ﬂuids overladen with uric acid. In
these special localities there may be certain factors
which excite the production of uric acid precipitating
substance. Fagge has designated trauma as the cause
of acute attacks of gout. Freudweiler thinks it to be a
local inﬂammatory process; Scudamore blames a con-
dition of plethora; Gairdner, a venous congestion.*
A clear conception is extremely hard to gain from
such varying opinions. All that is certain is that the
entire process is exceedingly complex. Personally
we attribute the establishment of a gouty attack to
the heaping up of certain products of metabolism,
which may be designated as factor X, in localities
where there is already an abundance of uric acid,
which is consequently precipitated. This results in
inﬂammatory processes and in severe cases leads to
necrosis. This outcome is especially favored by the
fact that the uric acid in the blood predisposes the
tissues to the irritation of a precipitate. And the
poor circulation through these tissues which experience

* We have lately seen a case of acute gout affecting the right
index ﬁnger. The patient had already suffered for a month
from stasis of the lower extremities which had induced a. sec-
ondary scleroderma. While in previous years the arthritis had
involved the large joints, the gouty symptoms of this patient had
remitted for two years until the time of the above mentioned
attack in the ﬁnger.

42 DISORDERS OF METABOLISM AND NUTRITION

has shown to be most often subjected to gouty
changes leaves them less able to withstand an ap-
proaching necrosis. In our opinion the last word on
this question has not yet been spoken. At present we
do not consider it advisable for us to make any deﬁ-
nite statement concerning this complicated question,
or to indicate with certainty any particular substance
[chondroit'in sulphuric acid or its salts (Minkow-
ski), sulphuric acid (Gemmel), glycocoll (Kionka)]
as the means of precipitation. The question of what
special conditions cause the increase of the uric acid in
the blood of gouty patients, does not, at the present
time, lend itself to a general reply, and it can only
be said that the attack of gout is occasioned by the
co-operation of two factors, one known and the other
unknown. The known factor is supplied by the in-
crease of uric acid in the blood serum and in the
ﬂuids; this increase may be the result of various
causes, the most frequent of which is probably renal.
The second, or unknown factor, X, causes the pro-
duction of a substance which will precipitate the in-
creased uric acid at certain places (cartilages, ten-
don sheaths, connective tissue, etc.). The presence
of both factors is necessary for the occurrence of
an attack of gout.

III. SYMPTOMS OF URICACIDXEMIA

PAIN is not an invariable accompaniment of gout,
the urate deposits being occasionally found without any
history of a previous attack. Pain is felt if the process
is very acute, or if the precipitated uric acid causes
very great inﬂammatory irritation. But even with-
out the precipitation of uric acid the subject of a
gouty diathesis will be liable to various complaints.
If we deﬁne gout as uricacidaemia, we shall not err
in associating with it a series of disturbances, such
as headache, neuralgia, rheumatic conditions, etc., as
has been done for some time in uricacidaemia etio-
logically dependent on chronic interstitial nephritis.
However, this is not the place to decide whether
uricacidaemia pure and simple causes these disorders
in nephritic patients, or whether the blood is charged
with foreign substances, which under normal condi—
tions would be excreted. At any rate, it would seem
that Haig goes considerably too far in his valua-
tion of the nosological importance of an excess of
uric acid in the blood,* and in our opinion among

*The diagnosis of uricacidaemia cannot be made on the evi-
dences of a urine analysis, as maintained by Haig. The methods
of analysis which he employed are worthless, but with suitable
methods the ratios of uric acid to urea are not constant even in
health, depending as they do on the amount and character of

the food ingested. It should also be recalled that the percentage
43

44 DISORDERS 0F METABOLISM AND NUTRITION

the pathological cases he would have included, there
would probably be not a few which we would desig-
nate as analbuminuric nephritis or renal sclerosis.
These statements, however, do not prevent us from
expressing deﬁnite views on the therapy of gout.

of total nitrogen excreted as urea falls as the total nitrogen is
diminished. It cannot be stated too emphatically that any of
these ratios that are in common clinical use are absolutely with-
out value unless the patient is under the rigid supervision in his
diet which characterizes a metabolism research. [EDITOR]

IV. THERAPY OF GOUT

Dietetics in Gout—On the ground that our present
knowledge of the pathology of gout—in spite of the
fact that we are still far from the goal—is not to
be despised, these opinions are valuable in the treat-
ment of gouty diatheses as well as in the treatment of
gouty attacks.

The treatment of gouty diathesis is essentially one
of diet and hygiene, and it is from this point of view
that it has always been regarded by physicians. If
it were a task worth undertaking to make a compila-
tion of the diet lists of the various authors who have
devoted themselves to the treatment of gout, a com-
posite would sketch rougly, but within close limits,
our present position, which is based on the most mod-
ern conceptions of gout. Three main questions arise
concerning this point of view: First, how can we
fortify and strengthen our gouty patient so that he will
be more capable of withstanding the impending at-
tack? Second, what means do we possess for
diminishing the uric acid content of the blood?
Third, is it possible to abort an attack, and if so by
what means is this result to be attained? A far-
reaching discussion of the ﬁrst question does not seem
necessary, as the methods which we would use to
strengthen the gouty individual differ very little from
those we would use for the invigoration of any pa-
tient, and, as we shall return later with special em-

45

46 DISORDERS 0F METABOLISM AND NUTRITION

phasis to the subject of the avoidance of certain
predisposing factors, the alcohol intake, for example,
we will concern ourselves here with the second and
third questions.

Theoretically we can effect a decrease in the amount
of the uric acid in the blood either through a lessen-
ing in its formation or through an increase in its
excretion. In the former case we know too little of
the transformation power of uric acid to depend on
it as a starting point for conscious therapeutic effort.
The excretion of uric acid we are able to effect by ex-
citing diuresis. There has been too little investiga-
tion of the endogenous formation of uric acid for
us to be able to apprehend it either as a therapeutic
or as a prophylactic measure. We possess the means
of inﬂuencing only the exogenous, that is, the alimen—
tary, formation of uric acid. It is on this point, then,
that the essential portion of the treatment of uric
acid diathesis rests; and so we must devote to it a
detailed discussion. As has been especially brought
to notice, the uric acid in the ﬂuids arises essentially
from the destruction of the cell nucleii. Therefore
all food materials which contain a large amount of
cell nucleii, the so-called purin bodies, must be allowed
either under great restriction or entirely forbidden.
The best examples of such food materials are sweet-
breads, liver, spleen, kidneys, and brains; and also
the young, germinating parts of plants, especially of
asparagus, as these portions are always rich in cell
nucleii. Eggs and milk which contain paranuclein
instead of the uric acid forming nuclein are allowed.

GOUT 47

Neither is there anything to prohibit in simple cheeses
or the various cheese preparations; however, opinions
differ concerning the suitability for gouty subjects
of the more piquant cheeses. In reference to the
quantity of meat, we take the position that the aver-
age amount, up to a half pound, may be allowed; be-
cause meat when it has been cooked, and if it has
not been allowed to become gamey, is not abnormally
rich in extractives. However, an excess in the use of
meat is everywhere bound up with the pathogenesis
of gout,* and it is notable that gout is extremely fre-
quent among foresters, who consume large amounts
of game. This is especially true in England and in
the rural districts of Germany. It appears to us after
some investigations which we have published else-
where (Berl. klin. Wochenschr. 1896, No. 23) that
the difﬁculty in the meat problem lies not so much in
the amount of the albumen, as in the amount of the
purin or extractive substances which the meat con-
tains. [We are reinforced in this opinion by more
recent investigations conducted on patients suffering
from renal calculi and atrophic kidney: among these
we have more than doubled the output of uric acid
by the administration of 30 g. per day of meat ex-
tract. In contrast with meat extract appears “ Siris,”

* It is notable in this connection that gout is not found among
the natives in India and that Europeans who have suﬁered from
gout enjoy an immunity in India, but only so long as they ob-
serve dietary precautions. The Parsees, who like the Europeans
are a race imported to India, are large meat eaters, and among
them gout is common. [EDITOR]

48 DISORDERS OF METABOLISM AND NUTRITION

which is recommended as a substitute for it, and which
after identical investigations covering two or three
days, a dose of 20 g. per day was followed by a
notably small increase in the uric acid excretion.
These investigations were conducted with the hearty
co-operation of Dr. Wolff. In our experiments the
amounts of uric acid after the administration of the
“ Siris ” did not go above those of the control period
more than from 6% to 27%.

In three series of experiments in which we gave
an equal quantity of metabolic nitrogen in the form
of scraped beef and “Tropon” there was only twice
during the scraped beef period a somewhat greater
increase of the uric acid excretion than in the
“Tropon” period (the rise was in one case over
half). We must, however, take into account that
a duration of such a diet extending over a month
or a year is probably much more harmful than] is
a single dose: and also that the amount of ex-
tractive material at 'the conclusion of this cumu-
lative process can lead to an increase of uric acid
in the blood. For this reason, the gouty patient
should be advised to take meat with the least possi-
ble amount of extractive material, ﬁsh, tame fowl,
or meat prepared in such a way that it has been de-
prived of a portion of its nitrogen extractives. Boiled
meat on this account is to be preferred to roasted
meat, and the especial avoidance of the so-called
“English beefsteak,”* and also of the use of rich

*Opinion relative to the use of beefsteak and rare cooked

GOUT 49

sauces and rich meat broths is advised. The following
table, taken from my lecture on “Dietary Treatment
of Internal Diseases,” contains the amounts of the ex-
tractive substances in various kinds of meat, based on
the results obtained by the investigations of Rosenq-
vist and Offer.

EXTRACTIVE SUBSTANCES IN VARIOUS MEATS

100 g. meat Extractive I00 g. meat Purins
Average Average

I Scraped beef ........ 0.610 1 Scraped beef .0071
2 Pike ................ 0.601 2 Raw ham ...........0.052
3 Raw ham ...........0.560 3 Soup meat (beef)....0.o46
4 Cooked ham ........ 0.534 4 Chicken (leg). .. .0.039
5 Cod ................ 0.531 5 Veal ................ 0.037
6 Perch ............... 0.526 6 Filet of beef. .. .. . . . .0036
x7 Dried beef .......... 0.479 7 Mutton ............. 0.035
8 Roast beef .......... 0.475 8 Roast beef .......... 0.034
9 Veal ................ 0.437 9 Dried beef .......... 0.033
10 Venison .............o.429 10 Pork ............... 0.032
II Chicken (leg) . . . . .0428 II Chicken (breast). .. .0032
12 Fowl (breast) ....... 0.4.25 12 Fowl (leg) .......... 0.030
13 Soup meat (beef)....o.420 I3 Cooked ham ......... 0.029
14 Mutton ............. 0.417 14 Fowl (breast) ....... 0.021
15 Chicken (breast).... .0416 15 Pike ................ 0.021
16 Pork ................ 0.405 16 Cod ................. 0.016
17 Fowl (leg) .......... 0.380 17 Venison ............. 0.011
18 Filet of beef ......... 0.338 18 Perch ............... 0.008

meats is not concordant. It is claimed that by cooking the pre—
cursors of thymic acid are destroyed, and there is some evidence
in support of the theory that uric acid is rendered more soluble
by this same thymic acid; the rare cooked meats are in this
respect more desirable. In broiling and roasting meat, however,
the extractive substances and purin bases are retained within
the meat. It is readily seen that the question is not easy of
solution and the safe way in therapeutics lies in experiment
with the individual cases. [12011012.]

50 DISORDERS OF METABOLISM AND NUTRITION

Whether crabs and lobsters are harmful through
their indigestibility depends on the individual case.
Since we possess nitrogen containing food material
in milk and eggs, as originally recommended by
Sydenham, and later by Kolish, Klemperer, Laquer,
Umber, and others, and in the artiﬁcial preparations
casein, tropon, roborat, etc., which contribute in only
a very small amount to the uric acid formation, we
are in the position to supply the gouty subject, in the
majority of cases, with such a quantity of nitrogen
that he will not lose strength and at the same time
will not receive too great an amount of uric acid
forming material. Fish roe, and this also includes
caviar, does not raise the uric acid content of the urine,

PURIN CONTENT OF COMMON FOODS*
Average Per Cent. of Purins. Grams

Cereals Purin Nitrogen per kilo
Bread, white .................. None None
Oatmeal ...................... 0.0212. 0530
Rice .......................... None None

Pulses
Peameal ...................... 0.0156 0.390
Beans (Haricot) . . . . . . . . . . .0.0250 0.638
Lentils ........................0.0250 0.637
Lentils (malted) .............. 0.0150 0.3755

Roots and Tuber:

Potatoes ...................... 0.0008 0.0200
Onions ....................... 0.0031 0.090
Tapioca ...................... None None
Green V egetable:
Cabbage ...................... None None
Lettuce ....................... None None
Cauliﬂowers .................. None None
Asparagus (cooked) .......... 0.0086 0.2150

*From Hall’s “Purin Bodies!’

GOUT 51

Per cent. of Purin Grams
Beers Nitrogen per litre
Lager Beer ................... 0.0050 0.1250
Pale Ale ...................... 0.0059 0.1450
Porter ........................ 0.0060 0.1550
Wines
Claret ........................ No trace
Volnay ....................... No trace
Sherry ....................... N0 trace
Port .......................... N0 trace
Methyl Per
Tea, etc. Purins Tea Cup
Ceylon ....................... 0.0164 0.0805
Indian ........................ 0.0147 0.0700
China ........................ 0.0107 0.0460
Coffee ........................ 0.0294 0.1100
Fish
Cod .......................... 0.0233 0.582
Plaice ........................ 0.0318 0.795
Halibut ....................... 0.0408 1.020
Salmon ....................... 0.0466 1.165
Average Per Cent. of Purins. Grams
Meats Purin Nitrogen per kilo
Tripe ........................ 0.0229 0.572
Mutton, Australian ............ 0.0386 0.965
Veal, loin ..................... 0.0465 1.162
Pork, loin .................... 0.0485 1.212
Pork, neck .................... 0.0227 0.567
Ham ......................... 0.0462 1.555
Beef, ribs ..................... 0.0455 1.137
Beef, sirloin ................... 0.0522 1.305
Beek, steak ................... 0.0826 2.066
Liver ......................... 0.1101 2.752
Sweetbread, thymus ........... 0.4025 10.063
Chicken ....................... 0.0518 1.295
Turkey ....................... 0.0504 1.260
Rabbit ........................ 0.0380 0.970

52 DISORDERS OF METABOLISM AND NUTRITION

according to the researches of Jerome; on the other
hand, “ ﬁsh milt” is rich in nuclein bases which can
be transformed into uric acid (Minkowski).

Concerning the fats and carbohydrates, many series
of observations have been published. We have con-
ducted investigations for the purpose of determining
their inﬂuence on the uric acid output in patients
suffering from renal calculus. The method of the
experiment was the substituting of carbohydrate or fat
for a portion of hashed meat; that is, by the addition
of I00 g. of butter to the standard diet. The uric acid
excretion showed quite as little gross difference as in
the experiments of Herrmann, Horbaczewski, Kan-
era, and others, who also found that during a car-
bohydrate and butter period the amount of uric acid
excreted was somewhat less than during a meat period.
The intake of carbohydrate and of fat may therefore
be allowed—at least so far as the question of uric acid
comes into consideration—to adjust itself according
to the demands of the individual case. At times,
occasion may arise for taking especial measures rela-
tive to the carbohydrate and fat intake.*

*The condition which indicates a limitation of carbohydrate
is primarily, glycosuria. In the gastro-intestinal disorders to
which gouty patients are particularly prone, a strict limitation
of fats is ﬁrst demanded; if this does not suﬂice to amend the
condition, the protein food should be decreased or allowed only
in the most digestible forms. Carbohydrate in the form of
starch is the least likely of all the food factors to occasion
gastro-intestinal disorders, provided the starches are properly
cooked. [EDITOR]

GOUT 5 3

Beverages.—In reference to beverages, a supply of
ﬂuid, copious rather than sparing, seems proper, care
being observed, however, not to overtax the heart.
It is preferable that the daily quantity of urine be
two, rather than one and one-half liters; and the
amount of ﬂuid absorbed should be regular and dis-
tributed through the day in uniform portions. A
direct decrease of ﬂuids may be recommended in those
cases in which there is special indication in the
heart’s action. More minute details will be given in
the description of the so-called “ drink cure.” Vari-
ous investigators share the opinion that tea, coffee,
‘ and cocoa are harmful. That these substances (theo-
brominzdimethylxanthin, caffein=trimethylxanthin)
can increase the uric acid output of gouty patients,
has been shown by Hess and Schmoll, and our ex-
periments with caffein corroborate theirs. Minkow-
ski, on the other hand, regards the danger of in-
jury as not very great, since the reports of the in-
vestigations of Rost, Bondzynski and Gottlieb, and
even of Albanese, show that theobromin and caﬂfein
are only partially decomposed in the body, and that
the amount assimilated is really very small. Since,
however, these substances excite the activity ofwthe
heart and are detrimental if a predisposition to ar-
terio-sclerosis is already present, in order to promote
a good general condition, we would recommend either
a. deﬁnite restriction or a complete prohibition of them
in the diet of a gouty patient. On the same ground
the avoidance of alcohol is advisable in all cases where

54 DISORDERS OF METABOLISM AND NUTRITION

it is not necessary as a medicine. We assert that in
gout, alcohol is injurious to all of the most impor-
tant organs, such as the kidneys, heart and digestive
tract. This is not the place to take up the discussion
of the numerous other effects of alcohol in gout, par-
ticularly the one which it exerts on the precipitation of
the uric acid; because in the question of the dietetic
treatment of gout, however important the inﬂuence
of any single material for food or nourishment may
be, it is never the only one to be considered. More—
over, it is not only essential to remove those factors
which produce an increase of uric acid in the blood,
but, in addition, to eliminate those which, according to
general experience, are able to act injuriously in any
way on the co-related organs. Especially to be men-
tioned is the fact that, among these organs, the kid-
neys, heart, and. digestive tract deserve our greatest
solicitude. The preservation of the heart enjoins on
every sufferer from gout abstinence from gluttony,
intemperance, and incontinence, and a carefully ar-
ranged and regulated manner of life.

Quantity of F 00d.—Tl1e meals of the gouty subject
should be small in bulk and low in nourishment. The
stimulation of his appetite should be avoided in every
way, and he should not use highly flavored sauces,
or potted meats and sausages, because these either
predispose the intestine to injury by means of irri-
tating materials, such as pepper, paprika, mustard,
onions, or because they contain substances harmful
to the kidneys, as, for example, cloves, caraway, gar-

GOUT 5 5

lie, leeks etc. We repeat only the admonitions of the
numerous authors who have written on gout, and we
wish to emphasize the importance of sparing the heart,
kidneys and digestivetract; this principle, remaining
the same whether the physician believes in the re-
tention theory, or whether his object is to strengthen
the kidneys for the purpose of effecting an improve-
ment in their uricolytic power. A condition of un—
dernourishment is above all to be desired when we
have to treat a combination of gout and obesity, or
when the condition of the heart demands it.* Other-
wise the quantitative measure of the diet should be
so regulated that the caloric intake will be held just
below the normal limit. To gouty subjects who are
cachectic abundant nourishment must naturally be
given; on the other hand strong, full-blooded indi—
viduals, especially those with a tendency to obesity,
should be placed on a diet of relatively low caloric
value. In the opinion of William Temple, the most

*In cases of obesity where there are signs of embarrassed
heart function a restricted milk diet as originally devised by
Karell is of the greatest importance. The method prescribed is
to give the patient 200 cc. of milk at 8 A. M., 12 M., 4 and 8
P. M. for six days. No other food or ﬂuid is allowed. For the
next two to six days in addition to the milk, an egg is given in
the morning, and in the evening a little zwieback. Then two
eggs are added and the amount of food is gradually increased
until by the ﬁfteenth or sixteenth day a full diet is resumed
Under this regimen, which is equivalent to partial starvation,
there is a gradual and constant loss of weight and the ﬂuids of
the body are reduced as in the case of “ dry diets.” The useful-
ness of this diet is limited neither to gout nor obesity. [EDITOR]

56 DISORDERS OF METABOLISM AND NUTRITION

suitable diet is one which is simple, which is adapted
to the digestive peculiarities of the patient, and which
supplies so far as possible his daily needs. The views
of Sydenham were that the amount of food should be
no greater than the stomach can easily digest, and
it should be so proportioned that it will be sufﬁ-
cient to maintain the strength of the body but not
enough to cause still further weakness by too great
abundance.

Animal Compared with Vegetable Proteins.—The
mixture of various food materials should be also sub-
ject to the restrictions already mentioned; the quality
of the resulting combination should be about normal.
The amount of albumen (as free as possible from
nuclein) especially, should not be allowed to drop
below 60 to 80 grams per day. In reference to the
amount of carbohydrate, as has already been pointed
out, there may be an especial indication, either a pres-
ent or a threatening digestive disturbance, or the
combination with obesity or diabetes. Ebstein be-
lieves that a vegetable diet containing the necessary
amount of plant albumen is to be recommended; and
the opinion is more and more accepted that the diet
in gout should be arranged so far as possible for the
exclusion of nuclein and for the prevention of any
disturbance of the heart, kidney or digestive func-
tions. So if we consider the old controversy silenced
as to whether the gouty patient gains more on a
vegetable than on an animal diet, we must devote an
especial discussion to the question of the amount of

GOUT 57

the nitrogen-free portion of the food. Beginning with
fats, the fact is to be emphasized that the more easily
digested milk fats, butter, and cream, are to be pre-
ferred to other kinds. Fat meats, bacon, and also
fat ﬁsh are suitable only for those patients whose
digestive powers are known to be excellent. In refer-
ence to carbohydrates various opinions are held by
different physicians. Personally we believe that in
those cases in which there is no good reason for ab-
staining from carbohydrates, they should be per-
mitted; the choice of the kind and the manner of
preparation being regulated according to the digestive
capacity of the individual. Gouty patients with nor-
mal digestions have no need for the precautions which
are necessary for those who are prone to gastro-in—
testinal disturbances.

Lately there have been advanced some new points
of View in regard to suitability, volume, and method
of administration of vegetable food. Falkenstein,
who has recommended the treatment of gouty
diathesis with hydrochloric acid, now explains the
effect of this procedure, on the basis of the results
obtained by the investigations of van Loghem and
Silbergleit, by assuming that the ingestion of
the hydrochloric acid withdraws circulating alkali.
This elimination of alkali is supposed to reduce its
quantity in the ﬂuids and circulation to such an ex-
tent that the remaining amount is less than necessary
for the formation of the easily precipitated sodium biu-
rate. In pursuance of this opinion, Falkenstein ad-

58 DISORDERS OF METABOLISM AND NUTRITION

vises against the administration of large quantities of
alkalis combined with vegetable acids, which are found
principally in fruit and vegetables. Brugsch and
Schittenhelm have adopted this theory, while Klem-
perer does not yet consider it justiﬁed. Personally I
do not think this question sufﬁciently matured, and
although I certainly recommend the avoidance of an
excess of alkali, I am in favor of following methods
which have stood the test of many years’ experience.
However, we would repeat that the young germinat-
ing portions of plants (especially of asparagus) should
be allowed only in the smallest possible amounts in
the diet of gouty patients; since the investigations of
Schultze and Booshard have shown that various
sprouting plants contain large amounts of allantoin
and the xanthin bases, and in numerous instances
Schultze and von Planta have also found vernin which
can be split into guanin by the action of hydrochloric
acid. Of individual foods Minkowski advises against
cakes, confectionery and sweets; also roots, various
sorts of cabbage, cucumbers, sorrel, and tomatoes.
Pfeiffer excludes sweets, potatoes, chestnuts, farina-
ceous foods; and Duckworth holds sweet tarts and
fruits injurious, and forbids, except in small amounts,
rhubarb, tomatoes, asparagus, sorrel, salted or pickled
mushrooms, sweet grapes, peaches, candied fruit, etc.
In reference to the preparation of individual car-
bohydrates Garrod recommends that all fruits with
stones, and apples and pears, should be eaten only
when stewed. The entire problem appears very fre-

GOUT 59

quently to demand essentially the same treatment as
diseaSe of the stomach or intestine, in which the
right way is often shown by the experience of the
patient himself in regard to his tolerance for certain
foods. Surely without hesitation one may permit the
majority of patients to eat white bread, rice, maize,
farinaceous foods, tender vegetables, such as spinach,
cauliﬂower, green peas, carrots, etc., and easily di-
gested fruits may also be given. In constipation espe-
cially selection should be made of the amount, kind,
and form of the administration of the carbohydrates,
as also for those who are inclined to diarrhoea. A
diet of a predominating vegetable character should
be assigned to those patients who have a highly irri—
table nervous system. The much recommended fruit
cures (strawberry, lemon, and cherry cures) are in
the main particularily good in combating the constipa-
tion, because in that condition there is special indica-
tion for taking a large amount of fruit. A particular
result of the fruit cure on the alkalinity of the ﬂuids
has been observed (Leber, Bendix, and others) which
accords with the result of our investigations. In the
light of a more recent opinion the increased alkalinity
of the ﬂuids, even could we attain it, would not be
desirable. In whatever way the previous diet of the
gouty patient may be changed, it must always be re-
membered that an abrupt alteration of the manner of
living frequently results in extremely bad effects on
these patients. The change from the old to the new
regimen should be made only gradually, and it should

t

60 DISORDERS OF METABOLISM AND NUTRITION

never be forgotten that besides the diet treatment, it
is most desirable to bring about a comprehensive regu-
lation of the manner of life, and to introduce in almost
every case the use of physical methods of healing. It
is desirable when one is not dealing with a debilitated
person, that abundant exercise in the fresh air should
be prescribed and overseen by the physician, such as
walking, riding, rowing, hunting, tennis playing,
bicycling, or if these are not possible, indoor gymnas-
tics, bowling, billiards, fencing, etc., adjusted in every
case to the individual needs. The control of the
physician is necessary for the reason already men-
tioned by Sydenham, that an immoderate amount of
exercise can precipitate an attack of gout. Also cer-
tain hydro— and balneo-therapeutic procedures serve
the object of stimulating the whole metabolism, and
improving the systemic circulation, if caution is ob-
served in the treatment of certain conditions of the
heart and too strenuous measures are not employed.
(Cave cold baths.) Physical measures are indicated
in the full—blooded subjects and in those who are fre-
quent sufferers from constipation.

Water “Cures.”—The results of 'a medical treat-
ment of a gouty diathesis are hard to control, because
in a given individual the return of the attack of gout
is very probable and frequent ﬂuctuations are inevit-
able; and because the premises on which any method
of treatment is based are very uncertain. As yet we
know little as to what way and how far we are able to
inﬂuence the uric acid content of the blood by thera-
peutic procedures for its transformation. On the

GOUT Or

other hand, however, we do know that our inﬂuence
on the puriﬁcation of the blood from its superabund-
ance of uric acid by the stimulation of diuresis is very
limited. The mineral water cures always seem suitable
for the latter object, either carried out at home or,
better still, at some designated water cure. From this
point of view, ﬁrst of all a thorough washing out of
the organism is to be recommended, and we consider
mineral water particularily good for this object in
uncomplicated cases. The water should be of a low
molecular concentration in order that—if taken warm
enough—it may pass quickly from the stomach into
the blood and thence into the urine. According to
examinations which were conducted by von Kost—
kewicz at our suggestion several years ago, the
waters which were best for our purpose,—that is
those which lie in the lower half of the zone of
“ gastro-isotonicity,”—were especially: Assmann-
shauser, Wildunger, Neuenahrer, Obersalzbrunner,
Fachinger, Emser Kesselbrunnen and Emser Kriihn-
Chen, Tarasp—Schulser Bonifaciusquelle, Sodener
Milchbrunnen, Vichy, Homburger Luisenquelle,
Offenbacher Kaiser Friedrichsquelle, Karlsba'd
waters, and others.* Other excellent waters for

* The American springs that are best suited to gouty patients
are Hot Springs, Ark., Hot Springs, Va., White Sulphur
Springs, W. Va., Bedford, Va. We have obtained best results
from Hot Springs, Ark.

Of waters for table use, it is our opinion that any pleasant
table water is adapted to cases of this disease, but if a special
water is desired, Salvatorquelle or Vals may be recommended.

[EDITOR]

62 DISORDERS 0F METABOLISM AND NUTRITION

the treatment of a uric acid diathesis showing a
higher molecular concentration are: Tarasper
Luciusquelle, Salzschlirfer Bonifaciusquelle, Sode-
ner, Wiesenbrunnen, and the Homburger Elizabeth-
quelle; Weisbadener Kochbrunnen, Kissinger Rak-
oczy and Pandur and likewise at Marienbad, Fer-
dinands- and Kreutzbrunnen approach the upper boun—
dary of the “ gastro-isotonicity.” It is not necessary
to give in numerical form the amount of ﬂuid intake,
but a gouty patient should excrete daily not less than
15 50-1800 cc. urine. Since the gouty subject should
avoid as much as possible both soups rich in extrac-
tives and alcohol, the need of ﬂuid must be supplied
ﬁrst of all by milk, lemonade, pure water, or such
mineral waters as contain a low molecular concentra-
tion, especially lithia. A regard for the heart and kid-
neys demands a frequent administration of small
amounts of ﬂuid distributed over the day, and this
seems to us advisable rather than the occasional in-
take of large portions. The ﬂuid enters the blood
with much greater case if taken in small portions than
in large ones. The rule given by some authors to
drink a fourth of a liter of lukewarm water at night,
just before going to bed, serves the purpose admir-
ably, as does also the rule that the evening meal
should be frugal and non—irritating, because the acute
attacks occur most frequently in the hours of darkness.
Since the time has not yet come for the cures resulting
from the use of mineral water to be explained on a
strictly scientiﬁc basis, the advances of physical chem-

GOUT 63

istry may be employed only for the gross questions of
the differentiation of Physiology and Pathology, and
to amplify our outlook, until now relatively narrow,
into the complicated mechanism underlying the con-
tinual alteration in the relationship of the ﬂuids. We
may seek in these provinces the results of a pure em-
piricism, which give preference to alkaline, and above
all to lithia containing water. We shall not discuss
how far this idea may be correct; in practice these
waters are believed in for every case. However, those
who concur with the opinion of Falkenstein and van
Loghem will prescribe carbonic acid waters instead
of alkaline waters. There are above all certain con-
ditions which are in part complications, in part
sequelae, of gout, such as obesity, diabetes, hepatic in-
farct, stomach and intestinal disturbances, etc., in
which certain springs would appear to be distinctly pro-
hibited, as they would aggravate, not only the gout,
but also the other symptoms. However, we will return
later to the properties of the springs which may be
made use of in certain forms of and at certain stages
of gout. The excellence of treatment in a “cure”
frequently shows its effects, because at a “cure”
many factors for healing are at work at the same time,
and also because the physicians are specially trained
for a deﬁnite class of patients.

Drugs.—The pharmacopoeia of gout has, in the last
ten years, been remarkably enriched by the zeal of an
energetic industry. Unfortunately this is more in the
nature of a quantitative than a qualitative character,

h

64 DISORDERS OF METABOLISM AND NUTRITION

and the majority of these remedies are justly vouch-
safed only a more or less ephemeral existence, so that
to-day we are obliged as much as formerly to mention
colchicum and its preparations ﬁrst among the numer-
our remedies which have been recommended for the
attacks of gout or gouty diathesis; and also the num-
erous lithium preparations, the organic bases piperazin,
lysidin, urotropin, quinic acid and its compounds,
urosin, sidonal, chinatropin, etc. Since these display
the best means of combating the gouty attack, lengthy
discussion of any one preparation seems scarcely re-
quired, and on this account it will be sufﬁcient merely
to mention that the colchicum preparations in all cases
are assisted in their results by the sodium salicylates,
salipyrin, aspirin, antipyrin, phenacetin, citrophen, and
'similar means; but there is no substitute for the col-
chicum. For protracted attacks potassium iodide is
recommended, and for the prevention of the return
of the attack, Garrod praises guaiacum resin. It is
not necessary to discuss here in detail the advantages
and disadvantages in the effects produced by any one
drug, nor the special indications for its use, nor deﬁ-
nite forms for its prescription; but we will reiterate
that emphatic hopes placed in any speciﬁc cure for
gout have all too little warrant, and that, in general,
it is well to try, after colchicum, the salicylic prepara-
tions, and urotropin, and later in all cases quinic acid.
This, at least, is the standpoint of empiricism. As al-
ready mentioned, Falkenstein has lately recommended
the administration of hydrochloric acid as a prophy-

GOUT 65

lactic for the attack. Although this kind of medication
may be advisable in cases where there is evidence of
sub-acidity of the gastric secretion, it is exceedingly
difﬁcult to deﬁne with mathematical and scientiﬁc
exactitude the therapeutic value of this remedy in
other cases of gouty affections.

Treatment of Acute Attacks—The administration
of colchicum or of the salicylic preparations is not,
however, alone sufﬁcient for the treatment of the at-
tack; numerous general and local conditions require
attention. If we know of no special diet ‘which for
this or that particular reason is suitable for a certain
case, then we believe that in the beginning one that
is bland and non-irritating to be indicated, whose
quality is about that required for a fever patient, and
whose quantity should be held throughout to a basis
of undernourishment, following in general the lines
demanded for the treatment of a feverish condition.
We are justiﬁed in repeating that here, as in fevers,
there is a demand for an abundant intake of ﬂuids.
The requirement for food of a non—irritating character
appears to us especially important, because of the num-
erous gouty patients who, during an attack, either
show symptoms of dyspepsia or at least impaired di—
gestive functions. Experience teaches that it is well
to rule out all such irritating materials as alcohol,
spices, etc., unless the condition of the heart demands
some form of stimulation. Even if we do not expect
an abortion of the attack from the calomel cure, we
consider that measures taken to promote a regular

66 DISORDERS OF METABOLISM AND NUTRITION

movement of the bowels in constipation, and a mild
purging at the onset of an attack are important. To
move the patient to a recumbent position either on the
bed or on a sofa is, in the majority of cases, scarcely
necessary, because as a rule the patient will, of his
own initiative, care for the afﬂicted extremities in a
resting position. However, there are still special ar-
rangements by which the physician can contribute to
an alleviation of the attack. The feeling of tension
and of pain of which the patient complains in the parts
affected may be greatly relieved through the gentle
application of cooling salve (zinc or menthol) and a
very loosely wound bandage of cotton batting, which
is not allowed to press upon the inﬂamed parts. Most
patients ﬁnd great relief in a surrounding hoop of
metal, which prevents the pressure of the bed clothes;
and also in the elevation of the limb to diminish the
ﬂow of blood through the part. In some cases direct
mitigation is gained by a narcotic. There are some
patients who are beneﬁted by a poultice of spiritous
liquors or applications of chloroform liniment,
veratrin salve, or similar substances.

Physical Methods.—The principles of treatment
employed in the ﬁrst half of the attack seem to us very
important, as then caution should dominate all pro-
ceedings; but the prescribed methods must not be
continued too long, for they differ essentially from
those required in the second half of the attack, that
is from the time when spontaneous pain ceases. We
follow to-day the thermal and mechanical methods

GOUT 67

which have been handed down from earliest times, ﬁrst
in the form of local baths of lukewarm water, later
in the form of local hot air baths. Besides these when
cautiously carried out, passive movements and mas-
sage in the vicinity of the affected joints are of great
beneﬁt. In the beginning these are given only as “ in-
duction massage,” with the exclusion of the affected
part—that is a centripetal massage of the parts situ-
ated near the joints involved. We do not now hesi-
tate so long as formerly before beginning active
movements, and unless they have been already at-
tempted by the patient, “resistance movements” are
ﬁrst employed (“resistance movement” gymnas-
tics). These passive movements should be ﬁrst used
either in a local or complete warm bath which miti-
gates the patient’s sensation of pain and may be later
abandoned.

Since the periarticular swelling and the restoration
of the function of the joint is sometimes abnormally
delayed, especial attention should be given to massage
and to local therapy in the form of hot air treatment,
—the Fango- and Moor—applications, local sand baths,
etc. The thermotherapy in connection with massage
and motion therapy, however, do not merely constitute
an integral part in the treatment of acute attacks
of gout, but are of the utmost importance for
every chronic stiffness of the joints, which we so of-
ten meet with at the close of an acute attack, or as
the manifestation of a condition of chronic gout.
These conditions are not infrequently inﬂuenced by

68 DISORDERS 0F METABOLISM AND NUTRITION

the so-called akrotothermal waters (Teplitz, Gastein,
Wildbad, Baden-Baden, VVildbad-Plaffers, Ragaz,
etc), also by the sulphur thermal springs (for instance,
Burtscheid, Aachen, Herkulesbad, P‘istyan, some of
the Buda-Pest springs, Aix-les-Bains, Schinznach,
baths near Vienna, baths in Argau, etc.) and also
Peat baths (Franzenbad, Marienbad, etc.) and also
by the sulphur mud baths (Nenndorf, Pistyan, Aix-
les-Bains, etc.). The greatest results, however, are
to be expected in those cases in which there is a cor-
rectly chosen combination of several methods of phy-
sical healing, which have been thoroughly studied.
Only the strongest individualization can lead to the
goal, and every scheme occasionally fails. The prin-
ciples of the treatment of gout are various, depend-
ing on whether one is dealing with a patient of
cachectic or of plethoric habitus. And frequently the
sufferer from gout discovers only after long experi-
menting the modus vivendi which is precisely adapted
to his needs; this when found should be reviewed in
its therapeutic aspect. Duckworth was entirely cor—
rect when he said that a doctrinaire was as dangerous
3 man in medicine as in politics or other realms. An-
other reason why the treatment of gouty patients
should be individualized is that they frequently pre-
sent manifestations which on superﬁcial examination
may be taken for sequelae of gout, while a more‘care—
ful analysis will prove them to be the effects of arterio-
sclerosis, chronic nephritis, obesity or diabetes. In
cases of this description the object of the therapy in—

GOUT 69

stituted will be to include not only the gout, but
also all other possible affections, within the broadest
limits.

Hygiene—It is clear, without further explanation,
that while we should seek to place at the disposal of
our patients all of those factors which are available,
either from common acceptance or personal experience
in treating an attack of gout, we must also avoid as
much as possible errors in diet, colds, or sudden
changes to unaccustomed ways of living—for ex-
ample, one of our patients feared any illness which
might conﬁne him to bed for a few days, as the en-
forced inactivity was frequently followed by a severe
attack of gout. It is certain that much can be ac-
complished through a carefully conducted prophylaxis
even after symptoms of a threatening attack are al-
ready noticeable. Ebstein asserts that at such a time
patients should be allowed on their feet as much as
possible, because in this way attacks have often been
aborted. And he further advises a careful massage-
ing of the affected parts, with the exclusion of the
joints involved. Duckworth is opposed to any strin-
gent attempt to suppress the attack. If the limited
space at our disposal did not prevent us from further
discussion we would go more deeply into the details of
the question, and in our exposition of the more un-
usual manifestations of gout or of its less frequent
complications, we would point out that while the last
ten years have somewhat broadened our knowledge
and powers, there are, unfortunately, many of the

70 DISORDERS OF METABOLISM AND NUTRITION

principal points of this equally involved and interest-
ing dominion which are yet shrouded in darkness.
May the time be not far distant in which these also
may be illumined through the light of scientiﬁc knowl-
edge, when not only the theoretical hypothesis of
the pathogenesis of gout, but also the reasons for our
therapeutic and prophylactic treatment of this disease,
will be placed on a ﬁrm and exact basis.

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