If we consider aU sorts of conditions, presenting more or less resemblance
to gout, as phases of this disease we have a sort of anchorage, but one which
permits of much deviation. If we examine the various statements made as
to the disease we may find the following fairly representative. "In gout
we have a disease which may give rise to almost any symptom or affect almost
any organ or function." If we start with the patient the following has been
presented: The gouty individual is one whose general metabolism is unstable
and this instability may be present in one or more of the great physiologic
systems (digestive, circulatory, nervous, etc.). If these statements represented
the actual state of our knowledge, one might readily assume that we had
abandoned our anchorage and were adrift. Recently, Woods Hutchinson
has offered the foUowing statement as a solution of the difficulties which
beset us, defining gout as " a disturbance of health associated with the presence
of excessive amounts of urates in the urine." The merit of this definition lies
in its presenting a material point from which we may start. It fails to state
what the corpus deliciti is, although deductively it is not uric acid. It fails
because it does not embrace within its limits those instances of undoubted
goutiness in which "the presence of excessive amounts of urates in the urine"
is inconstant, and it proves too much, because leucocythaemia and the renal
infarcts of the newlyborn are included by the definition, but are admittedly
not involved in the question, so far as the symptomatology is concerned.
However, as a starting point this statement is useful and an effort will be made
to find a working hypothesis upon which we may base a plan for relief of
svmptoms and disabilities consequent upon disturbed metabolism.
Uric acid for over a century has at once been the base and capstone of all
pathologic theory with regard to gout. At present we are in better position
to reach a practical working basis for therapeusis.
1. We are reasonably certain that uric acid, as such, is not toxic. This
fact is now almost universally conceded.
2. The presence of a lu-ic acid sediment in the urine does not of necessity
indicate a gouty tendency, for the power to hold uric acid in solution in the
urine depends largely upon the amount of pigment and the percentage of
salts contained in that excretion.
3. A nitrogen-free diet does not cause an abolition of uric acid excretion.
4. The excretion of uric and phosphoric acid goes on hand in hand â€” at
least during attacks.
Examining these propositions seriatim we see that while uric acid per se
is not toxic it is quite possible that earlier and less oxidized bodies are probably
so. Therefore the increased excretion of uric acid, signifying the increased
or complete oxydation of uric acid antecedents and their ehmination as uric
acid, should be accompanied by a relief of symptoms referable to the presence
of these antecedent bodies in the organism. In practice this is found to be
Next, the observation of coincidence of marked symptoms and diminished
uric acid excretion with periods of relief and increased iiric acid excretion
points out that delayed or imperfect excretion of uric acid is concomitant
with exaggerated pathologic conditions. Since, as has just been stated, uric
acid is not in itself toxic, its forbears must be responsible for the symptoms.
As a nitrogen-free diet is not followed by an absence of uric acid from the
urine, the formation of uric acid in the body from substances contained therein
must be conceded. This uric acid is very properly termed endogenous uric
acid and is independent of the character of the food ingested. It is the exoge-
nous uric acid, the amount varying with the food and modified by various
factors which act on digestion and absorption, when the patient is on ordinary
diet, that completes the other portion of the total uric acid excretion.
As uric and phosphoric acid excretion bear a fairly constant relation to
one another, the clue is at once given as to the probable source of endogenous
uric acid. This source is the cell nuclei and the products of their destruction
are both uric and phosphoric acids as they appear in the urine. Therefore
the breaking up of these nuclei gives rise to the appearance of uric acid and
the xanthin bases, which, as a group, constituting the alloxur bodies are
termed purins because they all contain the radical C5 H4.
248 CONSTITUTIONAL DISEASES.
Since the phosphoric goes hand in hand with the uric acid excretion, it
would be as logical to direct therapeutic attention to the former as to the
latter. So far as the endogenous uric acid is concerned we may define gout
as a toxaemia of varying causation, accompanied by the formation of an
excess of urates, this excess being due to the breaking down of the leucocytes
and fixed cells in the attempt to neutralize the poison.
Now as to exogenous uric acid; obviously this comes from without and
constitutes the source of the smaller moiety of the total output of uric acid.
Here the ingestion of food, either purin free or of small purin content, must
be considered. Obviously, were the attempt made to regulate the diet accord-
ing to the amount of purin nitrogen found in food, various articles of food
would be permitted which experience has shown to be detrimental to the
patient. And after all, the patient must not be disregarded, for the metabolic
reactions of the gouty are indubitably abnormal. From this it is clear that
an attempt to regulate the output of exogenous uric acid by altering the
intake of purin containing substances must be futile when we consider that
there are factors influencing metabolism in the gouty which are important.
Recently there has been a tendency on the part of some observers to return
to the mechanical theory of gout. This theory advances the idea that the
urates deposited in the joints and the ligamentous structures about them act
as foreign bodies, obstruct the lymph vessels, cause irritation, and exert
pressure upon the articular and periarticular tissues and interfere with their
nutrition, thus explaining the pain, redness and swelling and accounting
for the degenerative manifestations which result later. Old deposits of the
biurates are not of necessity painful but it is the opinion of most observers
that fresh deposits of these substances are always accompanied by painful
Pathology. While there are few organs or tissues which may not be the
subject of gouty changes, the characteristic manifestation of the disease
is in the acutely inflamed great toe, the swollen and reddened appearance
of which has but to be but once seen to be always remembered. Less usual
is a like condition of the thumb.
The manifestations of chronic gout are less typical and may be difficult of
differentiation from those of chronic rheumatism. Deposits of the urates,
however, are pathognomonic of gout. These occur with greatest frequency
in and around the joints, involving the cartilages, ligaments, tendons, biirsse
and last of all the skin and connective tissue. Often we find the tophi about
the finger joints or in the aural cartilages. Upon microscopic examination
the cartilages are seen to be infiltrated with sodium biurate crystals. The
tophi may ulcerate through the skin of the knuckle joints and they are
frequently accompanied by a tendency of the fingers to be drawn to the ulnar
side and of the toes toward the outer side of the foot; this latter being a late
manifestation and frequent, as well, in arthritis deformans and a result of the
fact that the abductor muscles are more powerful than their antagonists.
The tophi should not be mistaken for Heberden's nodes which are of different
origin and occur in arthritis deformans. These are, however, more prom-
inent and painful in gouty subjects. Various exostoses and enchondromata
or "lippings" from the cartilage covering the articular extremities of the
bones, especially of those of the fingers and toes, may be observed but should
not be confounded with true tophi.
The kidney of gout is the granular or cirrhotic kidney and is not in any
respect different from the ordinary kidney of so-called chronic interstitial
The heart is often the seat of an hypertrophy, especially of the left ventricle,
and its valves may show deposits of urates upon their edges. The arteries
are usually sclerosed, which fact is due to the toxic influence of the xanthin
Sjrmptonis. Patients in whom attacks of gout are frequent, often are able
to foretell a coming attack, learning from experience that certain symptoms,
which differ in different individuals, are premonitory; headache, neuralgic
pains, disordered digestion, cardiac irregularity or palpitation, a tense pulse,
a feeling of weariness, depression, etc., may be mentioned in this connection.
Any circumstance which tends to lower vitality or intemperance in eating
or drinking may bring on an attack.
Usually the first symptom noted by the patient is a pain in a joint, usually
in the metatarso-phalangeal articulation of the great toe. Its onset is sudden
and its character is sharp and stabbing. A chill may usher in the attack.
Accompanying the pain are the symptoms of local inflammation; heat, red-
ness, swelling and tenderness, although there may be pain without these
manifestations, or there may be local signs without discomfort. The attack
usually begins at night and, if the first, it may not be typical and therefore
remain undiagnosticated. As morning comes on the pain becomes less,
perhaps to recur during the night following, and for from four days to a week
the cycle continues â€” ^worse at night, better during the day. With the attack
there is commonly a moderate rise of temperature (100Â° to 102Â° F. â€” 37.8Â°
to 38.4Â° C), which may continue, with morning remissions as long as the
acuity of the symptoms persists. After a few days the pain and other symp-
toms subside and the skin of the affected part desquamates.
The urine during the attack is scanty, high in color and specific gravity,
may contain a little albumin and if allowed to stand is Hkely to show a sedi-
ment of urates and uric acid. Glucose also may be present. After the
attack the amount of uric acid excreted through the urine may be increased;
before its onset and diiring its acuity this may be diminished.
Gouty pharyngitis may be the only manifestation of an acute attack and
250 CONSTITUTIONAL DISEASES.
is impossible of diSerentiation from other forms of sore throat which show
only redness and slight swelling.
The local symptoms of an attack of acute gout may suddenly disappear
and manifestations due to derangement of the internal organs â€” notably the
stomach, heart, brain or bladder â€” may as suddenly appear. In such cases
the gout is described as " retrocedent " or "metastatic." The symptoms
referable to the heart may be pain, dyspnoea or irregularity of action; those
referable to the stomach, pain, vomiting, or diarrhoea; those referable to the
brain, Various meningeal disturbances; and those referable to the bladder,
those of inflammations of that organ or of the prostate gland. Skin eruptions
(eczemas) have been described in this connection.
Atypical Gout. Certain symptoms not distinctive of gout may appear in
persons of gouty tendency and in such patients are of undoubted gouty origin.
These include almost an3r mentionable symptom; of them the most usual are
various muscular pains, headaches, digestive disorders, burning and tingling
of the palms and soles, digitis mortui.
Certain changes, not characteristic, occur in the organ of vision as a result
of the disease â€” except rarely, in cases where there are deposits of the urates
in various tissues of the eye.
Chronic Gout. When a patient has continued to have numerous attacks of
gout changes take place in his tissues â€” as described in the section on pathology
â€” such as the deposits about the joints and in the cartilages, the deformities of
the extremities and the morbid degenerations of the kidneys and blood-vessels.
Treatment. The treatment of gout resolves it into the management of
the acute attack and that of the gouty tendency.
a. The treatment of the acute attack. When the attack occurs in a healthy
person in whom there exists no reason for limiting oiu: efforts, the indication
is to prescribe the drug or drugs which will most quickly relieve the patient
of his misery. Colchicum will relieve the pain and in the salicylates we
have agents which will hasten the elimination of the purin bodies which are
the causa causans of the attack. The following capsule is recommended:
I^, colchicinas salicylatis gr yiir (0.0006), methylis salicylatis /x vi (0.4);
make one capsule. Signa â€” Take one every hour until pain is relieved.
When the acute symptoms have abated the indication is to relieve the system
of the accumulated purin bodies and to prevent their further retention. (See
treatment of chronic gout and purinsemia, p. 252.)
In patients who have suffered frequent and repeated attacks of gout and
whose heart and arteries are the seat of sclerotic changes, glyceryl nitrate
(nitroglycerine) TTT-51T gr. (0.0006-0.0012) and strychnine -3V to yV gr.
(0.002-0.003) at the intervals required by the severity of the degeneration
should be prescribed to dilate the arteries and to counteract the depressant
effect of the colchicine.
There is no reason why an attack of acute gout should not be cut short
for there is no danger of the disease "going to the heart" unless we fail to
open the arteries and to provide against the myocardial degeneration.
The use of nucleinic acid in the treatment of the uratic deposits has been
suggested and favorable results are reported. Nuclein substances, themselves,
since they contain abundant purin bases are not suitable in this connection.
Base-free thymic acid has been used in attempting to lessen the size of the
tophi, which seem to diminish under its influence, while the excretion of uric
acid is increased.
Quinic acid, particularly quinic acid anhydride may be used in acute
gout in doses of 150 grains (lo.o) per day. It is reported that by its admin-
istration the pains are greatly ameliorated and the local signs about the joints
are lessened. This substance regularly diminishes the output of uric acid.
Certain authorities recommend hypodermatic injections of antipyrine
in the neighborhood of the affected joint, since this drug, in addition to its
analgesic effect is said to have a specific action in gout.
The wine of colchicum seed in beginning dosage of one-half drachm (2.0) in
combination with potassium iodide or sodium salicylate is frequently used
in acute as well as in chronic gout, the dosage of the two last being up to
one drachm (4.0) a day in divided doses.
For the pain acetphenetidine (phenacetine), antipyrine salicylate (sali-
pyrine), and saligenin tannate have their advocates. Hypodermatic injec-
tions of morphine will always relieve but these should not be given unless
The insomnia may be controlled by the bromides or chloral.
The diet during the attack should consist entirely of milk and vichy, equal
parts. Of this eight ounces (250.0) should be given every two to four hours.
This tends to act as a diuretic and to cause the colchicum to be absorbed into
the circulation rather than to be excreted through the intestine without accom-
plishing the effect for which it is administered. It is very important that
the patient should drink copiously of water.
Local Treatment. The joint should be protected by a generous swathing
of cotton, and various local applications, warm rather than cold, may be
made, always remembering that it is very important that the skin should
be kept intact. Painting with collodion (not more than two coats) either
with or without the tincture of iodine may afford relief as may also any of the
following applications: Sodium bicarbonate, i to 16 of warm water; equal
parts of guaiacol and glycerin; one part of the extract of belladonna to eight
of glycerin; oil of peppermint; chloroform and olive oil, equal parts; bella-
donna liniment and chloroform, equal parts. Local applications are likely
to afford less relief than in rheumatism and are less effective cold than
warm. At times the tenderness is so marked that not even the bed clothing
252 CONSTITUTIONAL DISEASES.
can be borne upon the afflicted part; in such cases the use of a frame to sup-
port the sheets is advisable.
Synonyms. Lithaemia; Uricacidaemia; UricEemia; American Gout; Gouti-
Definition. A disease of rather indeterminate nature dependent upon the
preseirce in the blood of partially oxydized food elements more especially the
.Etiology. The condition is caused by intemperate eating and the abuse
of alcohol, combined with too little exercise and a sedentary habit of life.
The accumulation of the urates is rather due to their production within the
body as a result of faulty metaboUsm than to a too great ingestion of substances
which contain these bodies.
Symptoms. Various indefinite symptoms characterize this disease. One
of the most constant is digestive disturbance which may be manifested by
intestinal fermentation, constipation, etc.
Headache is frequent and may be accompanied by dizziness, ringing in
the ears, insomnia, numbness and tingling of the hands and feet, neiuralgias
and indefinite pains in various joints and muscles of the body. Neurasthenic
symptoms are common as well as irritability of temper. Dermatoses, such
as eczema, psoriasis and prtuitus ani are often observed. Palpitation, cough
and loss of flesh and strength may be present. The luine usually contains
less lu-ic acid than normal, and there is frequently an excess of indican due
to the digestive derangement. There may be traces of albumin and a few
hyaline casts. Crystals of calcium oxalate are often seen.
Treatment. The keynote of treatment lies in (i) limiting all toxic influ-
ences and formation of toxins, particularly in the alimentary canal, in order to
minimize the retrograde metamorphosis of the body nucleins; (2) preventing
the absorption of all toxic material; and (3) promoting the elimination of toxic
Diet. The diet should consist of purin-free foods in so far as possible; these
are, milk, eggs, butter, cheese, white bread, rice, sago and fruits. Those con-
taining under two-hundredths percent, of purin nitrogen are beer, stout, onions,
asparagus, brown bread. Under three-hundredths percent, oatmeal, lentils,
beans, peas. Under five-hundredths percent, salmon, cod, pike, halibut, mut-
ton, veal, pork, ham, tmrkey, chicken. Under one percent, liver, steaks, soups.
Under four percent, sweetbreads. Obviously were the attempt made to regu-
late the diet according to the amount of purin nitrogen found in food, various
articles would be permitted which would prove detrimental; also the patient
must not be disregarded, for the metabolic reactions in this gouty condition
are indubitably abnormal. Hence it is clear that any attempt to regulate the
output of uric acid formed in the body by altering the intake of purin con-
taining substances must be futile when we consider that there are factors
influencing metabolism in our patients which are important. Finally the
clinical observation that the appearance of an excess of uric acid and urates
in the urine is generally coincident with the diminution or disappearance of
the symptoms leads to the conclusion that the elimination of bodies antece-
dent to uric acid by agents which increase the uric acid output as uric acid
is also not to be forgotten.
In considering endogenous uric acid, unquestionably methods whereby
the toxaemia which results in nuclear destruction is obviated should be con-
sidered. Metabolism, in character at least, is profoundly altered by the
ingestion of various substances such as lead. Waters containing lime and
iron are well known to be harmful. Indirect poisons are also potent as well
as direct. The effect of alcohol in purinsemic subjects is not wholly due to the
alcohol per se, but more probably to some of the more readily fermentable
carbohydrates, as the aethers, esters or acetone groups which are found in the
sweeter or more fruity wines used by the rich, or accessory products found
in the malted beverages drunk by those in moderate circumstances. The
logical inference is that substances capable of producing intestinal putre-
faction, and consequent autointoxication, should be prohibited.
If the endogenous uric acid is restrained as to its amount by preventing
unnecessary w^aste from autointoxication, exogenous uric acid can be readily
controlled. Evidently a prohibition of red meat, as has been the custom,
should diminish the excretion of exogenous uric acid, but we are confronted
by the fact that the ingestion of nitrogen is essential to the existence of the
organism and so far we cannot make use of that contained in the atmosphere.
The distinction between animal and vegetable foods is more apparent than
real, for the glutens (vegetable albumins) at least, are assimilated with more
difficiilty than animal albumins, and the excess of carbohydrates leads to
intestinal fermentation and putrefaction. Clinically the prohibition of red
meat has not been a success, and modern research tells us why this is so.
To make a positive statement, it can be safely said that animal food in moder-
ation is advisable. Pickled, salted and fried meats are forbidden. Fish is
excellent, even oysters and lobsters are permissible if fresh. All vegetables
and raw fruit, if apart from meals, are allowable. Tea, coft'ee and cocoa
in moderation are permitted. Alcohol in excess and inferior wines are
injurious. Malt beverages should be supplanted by cider, in quantity not
exceeding a pint each day. As has been pointed out, the quantity, rather
than the variety of the food, is to be limited. AU rich, highly-seasoned, greasy
and twice-cooked foods, strong soups, cooked tomatoes, rhubarb, sweet
cooked foods are to be avoided. Large mixed meals of animal and farina-
254 CONSTITUTIONAL DISEASES.
ceous foods with fruit and wine, especially if the latter be sweet or fruity
provoke the disease. Plainly cooked animal food, preferably roasted
or grilled, and limited to the quantity necessary for nutrition, is eminently
satisfactory. Two ounces (60.0) per day of good whiskey, well diluted,
will satisfy those habituated to alcohol. Excess of water should be taken only
apart from meals. Sedentary habits interfere with digestion and assimila-
tion and lead to the ingestion of more food than the muscles and liver can
burn up. Consequently an out-of-door life with such exercise as moderate
bicycling, golf and the like is to be recommended. In fact, excessive food,
improper forms and amounts of alcohol, and lack of exercise are factors which
lead to gout and the purinsemic conditions which are earned rather than
inherited. The last therapeutic fact which calls for comment is the method
by which an excess of uric acid, and especially its forbears, is removed
from the tissues. The alkalies and salicylates are our chief reliance in
that they not only make these products more soluble, but also because they
favor their elimination. The prolonged use of alkalies is obviously disad-
vantageous so that we must rely chiefly upon the saUcylates. One of the
most excellent and useful of the forms of these salts is saligenin tannate,
a substance obtained from several species of Salix and Populus (nat. ord.
SalicacecB). It is a decomposition product of the glucoside salicin saligenin
in chemical combination with castaneotannic acid. Over salicylic acid it
presents the advantage that, while equally efi&cacious, it does not disorder the
digestion nor cause untoward symptoms. It is preferable to the salicylates
in that it is antiseptic, while the latter are not, and it easily splits up. Over
both it offers the advantage of larger dose and longer period of administration.
The dose is 1 5 grains (i .0) in powder twice or three times daily after meals. The
bowels should be kept open by means of sodium phosphate, cascara, podo-
Piperazine water will be found useful in certain cases but the administra-
tion of lithium in tablet form or otherwise is likely to peld little or no result;
the bitter tonics such as mix vomica , gentian or cinchona are often useful.
The headaches and other pains may be controlled by antipyrine salicylate