[Illustration: GOUTY ARTHRITIS.
Note large tuberous swellings on knuckle and metacarpo-phalangeal joints
due to uratic deposits.]
GOUT
BY
LLEWELLYN JONES LLEWELLYN, M.B. Lond.
GOVERNOR AND SENIOR PHYSICIAN, ROYAL MINERAL WATER HOSPITAL,
BATH; FELLOW OF ROYAL SOCIETY OF MEDICINE; AUTHOR OF
“ARTHRITIS DEFORMANS”; CO-AUTHOR OF “FIBROSITIS”; CO-AUTHOR
OF “MALINGERING, OR THE SIMULATION OF DISEASE”; CO-AUTHOR OF
“PENSIONS AND THE PRINCIPLES OF THEIR EVALUATION”; CONTRIBUTOR
TO LATHAM AND ENGLISH’S “SYSTEM OF TREATMENT,” ALSO TO “OXFORD
ENCYCLOPÆDIA OF TREATMENT” AND TO “STUDENT’S TEXT-BOOK OF
SURGERY.”
WITH A SECTION ON
OCULAR DISEASE IN THE GOUTY
BY
W. M. BEAUMONT
CONSULTING OPHTHALMIC SURGEON TO THE SOUTH-WESTERN
REGION OF THE MINISTRY OF PENSIONS; AUTHOR OF “INJURIES
OF THE EYES OF THE UNEMPLOYED, PROBLEMS IN PROGNOSIS,” ETC.
ST. LOUIS
C. V. MOSBY COMPANY
1921
_Printed in Great Britain._
Dedicated
TO
MY WIFE
PREFACE
“A knowledge of the real nature of gout ... is, in my opinion, at the
very foundation of all sound pathology,” wrote Todd many years since;
and the passing years have but invested his reflection with deeper
significance and something of prophetic insight. For who can doubt that
he who would elucidate the pathological groundwork of gout must be at
once a clinical physician, a bio-chemist, a bacteriologist, a morbid
anatomist? and well may we ask, Who is sufficient for all this?
How vivid the light thrown upon the problems of clinical medicine by the
bio-chemists! The story of the fate of protein and purin substances in
the animal body, at one time a medley of guesses and gaps, is gradually
evolving into one of relative certitude and completeness. Revolutionary,
in truth, the change, and many a cherished shibboleth has been ruthlessly
cast aside! With admiration not unmingled with awe we see them laying
well and truly the foundations upon which in the ultimate scientific
medicine must inevitably rest.
Of these the very corner-stones are _chemical physiology_ and _chemical
pathology_, the rapid evolution of which is profoundly altering our
conceptions of health and disease. Those vital processes of the organism
that but yesterday we saw “as through a glass, darkly,” are now in great
part illumined, and the distortions wrought in them by disease made more
manifest.
How pregnant, too, with warning their findings! Processes that to
our untutored minds seem simple are revealed as infinitely complex.
Through what a maze must we thread our way if we would disentangle the
intricacies of metabolism! Intricate enough, forsooth, in health, but how
much more so in disease! For, as Sir Archibald Garrod eloquently phrases
it, “it is becoming evident that special paths of metabolism exist, not
only for proteins, fats, and carbohydrates as such, but that even the
individual primary fractions of the protein molecule follow their several
katabolic paths, and are dealt with in successive stages by series of
enzymes until the final products of katabolism are formed. Any of these
paths may be locked while others remain open.”
It is with chastening reflections such as these that we may best approach
our study of gout, that riddle of the ages upon which so many physicians
from time immemorial have expended their dialectic skill. But, vast
though the increase in our knowledge of the chemical structure of uric
acid and its allies, uncertainty still dogs our steps, and, doubtful of
the pathway to solution of the pathological mystery of gout, we must
perforce approach the problem in a more strictly catholic attitude.
_Uric acid_ has apparently failed us as the _causa causans_. Neither this
substance nor its precursors can be held responsible for the fever, local
inflammation and constitutional disturbances in gout, being, as they are,
practically _non-toxic_. Albeit, though I hold this view, I do not for
one moment suggest that _uric acid_ has nothing whatever to do with gout.
The fact that _tophi_, its pathognomonic stigmata, are compounded of
_biurate of soda_, would _per se_ stamp such an attitude as untenable. On
the other hand, _uric acid_ must be viewed at its proper perspective as a
_concomitant_ or _sequel_ of _gouty inflammation_, the essential cause of
which must be sought elsewhere.
“The old order changeth, giving place to new,” and happily with the
advent of _bacteriology_ our views, or rather our hazards, as to the
nature of joint diseases underwent profound modification. But, strange
to say, though quick to apprehend the significance of infection, its
causal relation to other joint disorders, we still seem unaccountably
loth to discard our timeworn conception of “gouty” arthritis as of purely
_metabolic_ origin. This to my mind is the more remarkable in that the
onset, clinical phenomena, and course of acute gout, and no less the life
history of the disorder as a whole, are emphatically indicative of the
intrusion of an _infective element_ in its genesis.
The extreme frequency with which _infective foci_ are met with in the
victims of gout, the frequency, too, with which exacerbations of the
disorder are presaged by _acute glandular affections_ of undeniably
_infective_ source, is by no means adequately realised. For our
forefathers gout began, and, forsooth, often ended, in the “stomach,” or
it was the “liver” that was impeached. But the portal to the alimentary
canal was for them only a cavity, the contained structures of which,
albeit, to their mind often betrayed evidences of a “gouty diathesis.”
They distinguished “gouty” teeth, “gouty” tonsillitis, “gouty”
pharyngitis, even “gouty” parotitis; but all these they classed as tokens
or sequelæ of gout, not possible causes or _excitants_ thereof.
Now as to the true significance of these acute glandular affections
held by clinicians of repute to be of “gouty” origin. What of “gouty”
tonsillitis, pharyngitis, parotitis? Still more, what of our deductions
regarding the relationship of these same when met with in association
with _non-gouty_ forms of arthritis? Do we not hold them each and all as
evidences of _infection_? and, we may well ask, why not in gout?
The marvel then is that even to-day many still hold that the tonsillitis,
pharyngitis, even the gingivitis, like the subsequent articular lesions,
are one and all attributable to the underlying _gout_. We certainly
should not do so in the case of any arthritis other than “gouty,” and to
my mind the time is ripe for a change of attitude.
The “gouty” throats, like the “gouty” teeth, should be regarded not as
symptomatic of gout, but _etiologically_ related thereto. We should cease
to talk of “gouty” throats, teeth, etc., should renounce the prefix,
for there is nothing _specific_ of _gout_ either in the tonsillar,
pharyngeal, or dental lesions. We should instead view these various local
disorders in their true perspective as _foci_ of _infection, causally_
related to the subsequent and _secondary_ “gouty” arthritis.
Similarly, when we come to analyse the component elements of an acute
paroxysm of gout, how strongly indicative of the intrusion of an
_infective_ element the following features: the onset, temperature curve,
character of local articular changes of the disorder, the presence of
_leucocytosis_, with secondary anæmia and enlargement of the lymphatic
glands! Again, how suggestive the occasional complication of acute
gout by _lymphangitis_ and _phlebitis_! Of like significance, too, the
paroxysmal nature and periodicity of the disorder, and the compatibility
of the morbid anatomical changes and the cytological content of the
aspirated joint fluid with their genesis by _infection_.
As to correlation of the metabolic phenomena of gout with the postulated
infective element, I would suggest that, although abnormalities of
metabolism form an integral part of gout, they are of themselves
inadequate to achieve its efflorescence. As we shall see when we come to
consider those elemental manifestations of gout, _i.e._, uratic deposits,
or _tophi_, neither the purely physical nor the purely chemical theory
of their origin will suffice, nor, for that matter, can any solution of
their formation be gleaned from even a blend of the twain. In short, such
hypotheses are too _mechanical_.
The intrusion of some other factor, “something vital, something
biological,” seems essential for the elucidation of _uratosis_,
_i.e._, uratic deposition. For this, _not uricæmia_, is the specific
characteristic phenomenon of gout. If we cannot explain uratosis on
physical or chemical grounds, then how much less, in view of the
_non-toxicity_ of _uric acid_, can we on this basis account for the
_inflammatory_ phenomena of the disorder!
Now _inflammatory reaction_ is, I hold, an invariable _antecedent_ in all
gouty processes, whether of _articular_ or _ab-articular_ site. Granted
that inflammatory reaction is a necessary prelude, the specificity
of gout is attested by the fact that the same is followed by local
deposition of urates. But while this sequential uratic deposition invests
all forms of “gouty” inflammation with a specific character unshared by
any other disease, it follows that the cause of the said inflammation
must, if possible, be ascertained.
Now, as I believe, “gouty” subjects are _ab initio_ victimised by innate
tissue peculiarities, doubtless reflected in corresponding obliquities of
tissue function and metamorphosis, and through their medium the general
resistance of the body to invasion by _infections_ is lowered; in other
words, under the influence of these morbific agencies the latent morbid
potentialities of the gouty become overt and manifest. For in the gouty,
as Walker Hall observes, “a slight injury or indiscretion of diet, an
overloaded intestine, or increased toxicity of the intestinal flora, may
be followed by a disturbance of the general nuclein metabolism and a
local reaction in certain tissues.”
Enough has been said to disclose the dominant trend of this work, and
although there are many aspects of the subject in regard to which I hold
somewhat iconoclastic views, yet exigencies of space forbid me even to
allude to them in this foreword. I hasten therefore to discharge the
pleasing duty of acknowledging my great indebtedness to the acumen and
discrimination which has been brought to bear on this subject by a long
succession of eminent physicians, in proof of which I need only adduce
the names of those giants of the past the illustrious Sydenham, Sir
Thomas Watson, Sir Charles Scudamore, Jonathan Hutchinson, not to mention
Trousseau, Charcot, Lecorche, and Rendu. But I should fail in my duty did
I not in a special sense express my deep indebtedness to the classic and
epoch-making work of Sir Alfred Garrod. For the rest, too, I have derived
much enlightenment from Sir Dyce Duckworth’s treatise and the various
works on the subject by Luff, Lindsay, and others.
From the bio-chemical aspect I owe much to the researches of Walker Hall,
and to those of our American _confrères_ Folin, Denis, Benedict, Pratt,
McLeod, Walker Jones, Gideon Wells, etc.
Reverting to my own colleagues at the Royal Mineral Water Hospital,
Bath, I would tender my deep thanks to the Honorary Physicians, Drs.
Waterhouse, Thomson, Lindsay, and King Martyn, for the uniformly generous
manner in which they afforded me opportunities for studying cases under
their care.
To Dr. Munro, our senior pathologist, I am especially beholden for
invaluable, nay indispensable, help in the matter of blood examinations,
the cytological study of joint fluids, and the microscopic verifications
of tophi. To Dr. MacKay also my cordial thanks are due for the
skiagraphs contained in this work.
For the section dealing with the ocular disorders met with in the gouty
my most sincere thanks are due to Mr. W. M. Beaumont, of Bath, whose
singularly wide experience in this sphere renders him unusually equipped
to deal with this highly controversial aspect of gout. To Drs. Cave and
Gordon, of Bath, also I am indebted for many valuable suggestions kindly
afforded me while writing this volume. To my brother Dr. Bassett Jones I
am under deep obligation for unwearying assistance in our joint endeavour
to ascertain the exact relationship of gout to lumbago, sciatica, and
other types of fibrositis.
For the preparation of the index of this work I would proffer my grateful
thanks to Mr. Charles Hewitt and to Miss Donnan and Miss Crosse for
having undertaken the arduous task of typing the manuscript thereof.
Lastly, I would express my thanks to my publisher, Mr. Heinemann, for
much consideration and many courtesies.
LL. J. LL.
31, UPPER BROOK STREET, W. 1.
TABLE OF CONTENTS
CHAPTER I
HISTORICAL AND INTRODUCTORY
The Antiquity of Gout. Prevalence of Gout in the Anglo-Saxon
Period. Views of the Humoralist. The Aphorisms of Hippocrates.
Introduction of the Word Gout. Early Views as to the Nature of
Tophi. The “Honour of the Gout.” That Gout confers Immunity
from other Disorders. Growing Infrequency and Attenuation of
Gout _pp._ 1-13
CHAPTER II
THE PEDIGREE OF GOUT
Tardy Dissociation of Chronic Gout. Identification of Muscular
Rheumatism. Differentiation of Chronic Gout from Arthritis
Deformans. Cleavage of Arthritis Deformans into Two Types.
Elimination of the Infective Arthritides _pp._ 14-20
CHAPTER III
EARLIER THEORIES OF PATHOGENESIS
Garrod’s Theory. Antagonistic Views. Histogenous Theories.
Antecedent Structural Changes. Hepatic Inadequacy.
Hyperpyræmia. Nervous Theories. Growing Scepticism as to
Garrod’s Pathogeny of Gout _pp._ 21-34
CHAPTER IV
DEFINITION, CLASSIFICATION, ETIOLOGY, AND MORBID ANATOMY
Definition. Classification. Suggested Classification
of Articular Gout. Etiology and Morbid Anatomy. Bodily
Conformation and Individual Temperament. Locality, Race,
Climate. Food, Drink, Occupation. Lead Poisoning. Mental and
Physical Over-exertion. Summary. Morbid Anatomy _pp._ 35-58
CHAPTER V
PATHOLOGY OF GOUT-PROTEIN METABOLISM
Revelations of the Bio-chemist. The Formation of Urea. Fate
of the Amino-acids. Seat of Formation of Urea. Amino-acids
in Relation to Gout. The Glycocoll Theory of Gout. Urea
Excretion in Gout. Creatine and Creatinine. Inborn Errors
of Metabolism _pp._ 59-70
CHAPTER VI
NUCLEIN METABOLISM
The Isolation of Nucleic Acid. Researches on Spermatozoa. The
Discovery of Purins. Uric Acid a Derivative of Nucleic Acid.
The Chemistry of Uric Acid and the Purin Bodies. Chemical
Constitution. Properties of Uric Acid. Uric Acid in the Blood.
Gudzent and Schade’s Theories. Organic Combinations. Complexity
of the Problem _pp._ 71-82
CHAPTER VII
SOURCES OF URIC ACID
Exogenous Purins. Exogenous Uric Acid Excretion. Fate of the
Unexcreted Purins. Endogenous Purins. Source of Endogenous
Purins. Proteins and their Derivatives. Amino-acids and
Dicarboxylic Amino-acids. Endogenous Uric Acid Excretion.
Factors influencing Endogenous Uric Acid Excretion.
Physiological Conditions. Pathological States. Ingestion of
Certain Drugs. Synthetic Formation of Uric Acid _pp._ 83-97
CHAPTER VIII
FORMATION AND DESTRUCTION OF URIC ACID
Distribution of the Enzymes. Stages in Disruption of Nucleic
Acid. Destruction of Uric Acid _pp._ 98-106
CHAPTER IX
URIC ACID IN RELATION TO GOUT
Uric Acid Excretion in Gout. Uric Acid Variations in Acute
Gout. Uric Acid Variations in Chronic Gout. Retarded Exogenous
Uric Acid Output. Lowered Endogenous Uric Acid Output. Other
Anomalies in Excretion in Gout. Purin Metabolism in other
Disorders. Purin Metabolism in Chronic Alcoholism and
Plumbism _pp._ 107-116
CHAPTER X
THE RENAL THEORY OF GOUT
Anomalies in Uric Acid Excretion in Gout. Uricæmia in
Nephritis. The Relationship, if any, between the Amounts of
Uric Acid and of Urea, and Total Non-protein Nitrogen in Human
Blood. Uricæmia not necessarily due to Renal Defect. Uricæmia
not Peculiar to Nephritis. Uricæmia does not necessarily
Portend Gout. To what may be ascribed the Deficient
Eliminating Capacity of the Kidney for Uric Acid. Uratic
Deposits in Nephritis. Differentiation of Uratic Deposits in
Gout and Nephritis. Clinical Associations of Gout and Granular
Kidney _pp._ 117-132
CHAPTER XI
URICÆMIA IN GOUT
Folin and Denis’s Method. Uric Acid a Normal Constituent of
Blood. Effect of Exogenous Purins. Uric Acid Content of Blood
in Gout. Hyperuricæmia in Non-gouty Arthritis. Variations
in Uric Acid Content of Blood independently of Diet. What
Relationship, if any, Exists between the Uric Acid Content of
the Blood and Attacks of Gout. Discussion of the Foregoing
Data. The Significance of Uricæmia. Sources of Fallacy in Uric
Acid Estimation. Disabilities of Modern Tests. Need for further
Investigations _pp._ 133-148
CHAPTER XII
URATOSIS IN RELATION TO GOUT
Constitution of Tophi. Mode of Formation. Localisation of
Uratic Deposits. The Causation of Tophi. Solubilities of Uric
Acid. Tophi in Relation to Uricæmia. Tissue Affinities for Uric
Acid. Retention Capacity of Tissues for Uric Acid. Clinical
Evolution of Tophi. The Cause of the Inflammatory Phenomena.
Non-toxicity of Uric Acid. Are the Precursors of Uric Acid
Toxic? _pp._ 149-170
CHAPTER XIII
THE RISE OF THE INFECTIVE THEORY
Boerhaave’s Forecast of the Infective Theory. Ringrose Gore on
Infective Origin. Leucocytosis in Acute Gouty Polyarthritis.
Chalmers Watson’s Researches on Gout in a Fowl. Trautner’s
Suggestion of a Specific Infection _pp._ 171-176
CHAPTER XIV
GOUT AS AN INFECTION
Local Foci of Infection: Dental, Nasal, Pharyngeal, etc.
Gastro-intestinal Disorders. Variation in Free HCL. Intestinal
Disorders. Infection or Sub—infection _pp._ 177-187
CHAPTER XV
GOUT AS AN INFECTION (_continued_)
Analysis of the Acute Paroxysm. The Evolution and Life History
of Gout. Analogies between Gout and the Specific Infective
Arthritides. Correlation of the Metabolic Phenomena of Gout
with the Postulated Infective Element _pp._ 188-199
CHAPTER XVI
CLINICAL ACCOUNT
Acute Localised Gout. Prodromal Symptoms. Dyspepsia.
Premonitory Symptoms of Tophus Formation. Premonitory Articular
Pains. The Acute Paroxysm. Detailed Consideration of Phenomena.
Mode of Onset. Localisation. Nature of Pain. General Phenomena.
Pyrexia. Changes in the Blood. Uric Acid Excretion. Local
Phenomena. Tophus Formation _pp._ 200-213
CHAPTER XVII
CLINICAL ACCOUNT (_continued_)
Acute Gouty Polyarthritis. Mode of Invasion. Distribution of
Lesions. Local Characters. Constitutional Symptoms. Changes in
the Blood. Leucocytosis. Collateral Phenomena of Gout. Lumbago,
Sciatica, etc. Incidence of Gouty Stigmata in Various Types of
Fibrositis _pp._ 214-224
CHAPTER XVIII
CLINICAL ACCOUNT (_continued_)
Chronic Articular Gout. The Joint Deformities of Chronic Gout.
Tophi: Their Evolution and Distribution. Other Sites of Tophi.
Affinities between Gout and other Diseases. Gout in Relation to
Glycosuria. Gout in Relation to Phlebitis. Cutaneous Disorders.
Gout and Nephritis. Prognosis in Gout _pp._ 225-246
CHAPTER XIX
ETIOLOGICAL AND CLINICAL DIAGNOSIS.
Articular Gout. Etiological Diagnosis. Clinical Diagnosis.
Introductory Remarks. The Diagnostic Status of Tophi. Tophi
in Relation to Arthritis. Frequency of Tophi in True Gouty
Arthritis Underestimated. Difficulty of Detecting Tophi _pp._ 247-257
CHAPTER XX
CLINICAL DIAGNOSIS (_continued_)
Acute Articular Gout. Localised Variety. Differential
Diagnosis. Infections. Acute Gonococcal Arthritis. Traumatic
Lesions. Acute Osteoarthritis. Static Foot Deformities. Hallux
Valgus with Inflamed Bunion. Hallux Rigidus. Metatarsalgia.
Gout in the Instep. Gonococcal Arthritis. Tuberculosis and
Syphilitic Disease of the Tarsal Joints or the Related Joints.
Pes Planus. Gout in the Heel. Referred Pain. Local Sources
of Fallacy. Post-calcaneal Bursitis. Synovitis of the Tendo
Achillis. Gout in the Sole. Plantar Neuralgia. Erythromelalgia.
Anomalous Sites for Initial Outbreaks _pp._ 258-267
CHAPTER XXI
CLINICAL DIAGNOSIS (_continued_)
Acute Gouty Polyarthritis. Differential Diagnosis. Acute
Articular Rheumatism. Acute Gonococcal Arthritis. Etiology.
Onset. General Symptoms. Distribution of Lesions. Local
Characters. Associated Phenomena. Secondary Syphilitic
Arthritis. Acute Rheumatoid or Atrophic Arthritis. Age and
Sex. Onset. General Symptoms. Distribution of Lesions. Local
Characters. Associated Phenomena. Infective Arthritis of
Undifferentiated Type _pp._ 268-274
CHAPTER XXII
CLINICAL DIAGNOSIS (_continued_)
Chronic Articular Gout. Chronic Monarticular Gout. Monarticular
Gout in Large Articulation a Rarity. Chronic Gout of
Oligo-articular Distribution. Its Confusion with Chronic
Villous Synovitis. Villous Synovitis Static and Non-gouty in
Origin. Clinical Symptoms of Villous Synovitis. Bilateral
Hydrarthrosis. Peri-synovial and Peri-bursal Gummata. Chronic
Gout of Polyarticular Distribution. Differential Diagnosis.
Osteoarthritis. Local Characters of Joint Swellings. Rheumatoid
Arthritis. Local Characters of Joint Swellings. Nerve
Arthropathies. Hæmophilic Arthritis _pp._ 275-285
CHAPTER XXIII
CLINICAL DIAGNOSIS (_continued_)
Skiagraphy. Significance of Local Areas of Rarefaction. The
Radiographic Types of Gouty Arthritis. Differential Diagnosis.
Infective Arthritis. Hypertrophic or Osteoarthritis. Rheumatoid
or Atrophic Arthritis _pp._ 286-292
CHAPTER XXIV
IRREGULAR GOUT
Historical Account. Murchison’s Views. Retrocedent Gout. Gout
in the Stomach. Cardiac and Cerebral Forms. Other Irregular
Manifestations. Conclusions. Infantile Gout _pp._ 293-307
CHAPTER XXV
OCULAR DISEASE IN THE GOUTY
Evidence of Gout in the Eye. Deposition of Urates. Gouty
Diathesis. Significance and Location of Tophi. Relative
Incidence of Iritis. Metastasis. Arthritic Iritis. Gouty Iritis
not a Clinical Entity. Ocular Symptoms in Hyperuricæmia.
False Gout. Retinal Hæmorrhage. Neuro-retinitis. Glaucoma.
Conclusions _pp._ 308-326
CHAPTER XXVI
TREATMENT OF GOUT
Radical Treatment of Local Foci of Infection or Toxic
Absorption. Diet in Acute and Chronic Gout. The Fallacy of
Fixed Dietaries. Thorough Physical Examination a necessary
Prelude to Dieting. Need for Collaboration of Clinician and
Bio-chemist _pp._ 327-341
CHAPTER XXVII
TREATMENT OF GOUT (_continued_)
Regulation of Diet in the Gouty. The Individual Foodstuffs,
Proteins, Carbohydrates, Fats, Vegetables, Fruits, Condiments.
Special Dietaries. Amylaceous Dyspepsia. Hyperchlorhydria _pp._ 342-371
CHAPTER XXVIII
MEDICINAL AND OTHER MODES OF THERAPY—ACUTE GOUT
Initial Purgation. Colchicum in Acute Gout. Method of
Administration. Preparations and Dosage. Colchicine, Salicylate
of Colchicine. Atophan. Alternative Remedies in Acute Gout.
Salicylates. Alkalies. Quinine. Thyminic Acid. Anodynes in
Acute Gout. Local Measures. Analgesics. Liniments, etc.
Ionisation. Massage. Surgical Methods _pp._ 372-388
CHAPTER XXIX
MEDICINAL AND OTHER MODES OF THERAPY
(_continued_)—INTER-PAROXYSMAL PERIOD
Prophylactic Measures. Treatment of Atonic Dyspepsia.
Hyperacidity due to Organic Acids. Treatment of
Hypochlorhydria. Alkalies, Atophan, and Colchicum as
Prophylactics _pp._ 389-396
CHAPTER XXX
MEDICINAL AND OTHER MODES OF THERAPY (_continued_)—CHRONIC
ARTICULAR GOUT AND ASSOCIATED MORBID CONDITIONS
Alkalies. Contrasts between Salts of Sodium and Potash.
Differential Indications for their Usage. Alternatives.
Salicylates. Benzoates. Hexamine. Iodides. Iodine. Albumen
Compounds. Collosol Preparations of Iodine. Guaiacum. Local
Measures in Chronic Articular Gout. Treatment of Tophi.
Ionisation. Surgical Measures. Treatment of Associated
Morbid Conditions. Fibrositis. Lumbago. Sciatica. Acute
Brachial Fibrositis. Local Massage. Oxaluria. Glycosuria.
Hyperchlorhydria. Gouty Phlebitis. Gouty Eczema. Gouty
Nephritis _pp._ 397-417
CHAPTER XXXI
CLIMATO-THERAPY, HYDRO-THERAPY, ETC.
Climate. Choice of Residence. Clothing. Exercise. Massage.
General Hydro-therapy. Importance of thorough Physical
Examination. Individual Reactive Peculiarities. Prophylactic
Measures. Contra-indications and Untoward Complications.
Methods of Application of General Hydro-therapy. Immersion
Baths. Aix and Vichy Massage. Vapour Baths. Indications for
Sub-thermal Baths. Local Hydro-therapy. Varieties of Douche.
Treatment by Hyperæmia _pp._ 418-430
CHAPTER XXXII
MINERAL SPRINGS AND CHOICE OF SPA
Difficulties of Definition and Classification. Radio-activity.
General Principles of Spa Treatment. Physiological Action
of Radium Emanation. Activation of Body Ferments. Influence
of Uric Acid Metabolism. Increased Excretion of Uric Acid.
Subjective Phenomena of Gout in Relation to Blood Content and
Excretion of Uric Acid. Therapeutic Action and Application.
Alimentary Disorders. Glycosuria. Raised Blood Pressure. Choice
of Spa. The Spare and the Obese. Waters Suitable for Various
Types of Dyspepsia. Bickel’s Experiments. Mineral Waters in
Associated Morbid Conditions. Glycosuria. Oxaluria. Phlebitis.
Respiratory Disorders. Fibrositis. Gouty Eczema. Uric Acid
Gravel. Arterio-sclerosis. Chronic Nephritis. Concluding
Remarks on Spa Treatment _pp._ 431-465
INDEX _pp._ 457-469
CHAPTER I
HISTORICAL AND INTRODUCTORY
THE ANTIQUITY OF GOUT
“Teeth, bones, and hair,” quoth the Sage of Norwich, “give the most
lasting defiance to corruption,” and were it not that “Time which
antiquates antiquities and hath an art to make dust of all things hath
yet spared these minor monuments,” it might perhaps have been inferred
that gout was the primordial arthritic disease that afflicted mankind.
That it was the first articular affection to achieve clinical
individuality may be allowed, but, from the aspect of antiquity, gout
is relatively modern—the appanage of civilisation. True, Hippocrates,
discoursing in the famous Asclepion at Cos, enunciated his aphorisms on
gout some 300 years before the Christian Era, the dawn of which moreover
found Cicero in his discussions at Tusculum lamenting its excruciating
tortures “doloribus podagræ cruciari” and the peculiar burning character
of its pains “cum arderet podagræ doloribus.”
But what of that? For did not Flinders Petrie in the hoary tombs of Gurob
(dating back to the 28th Dynasty 1300 B.C.) find in mouldering skeletons
of bygone civilisations unequivocal evidence of _osteoarthritis_.[1] But
despite these sure though silent witnesses of the prevalence of this
disorder among the ancient people of Egypt, yet in contrast with gout, no
hint transpires in the writings of Greek or Roman physicians, nor those
of much later date, that the condition was recognised _clinically_, as a
joint disorder, distinct from others of the same category.
Small call to marvel thereat, for how much more arresting the clinical
_facies_ of gout, with its classic insignia—tumor, robor, calor, et
dolor—than of osteoarthritis, its etiolate tokens indicative rather of
infirmity than of disease. Apart from this, it may well be that the
early Egyptians owed their relative immunity from gout, and alike their
proneness to osteoarthritis, to living hard laborious days, unenervated
by that luxury and sloth, which in the first century A.D. drew upon the
ancient Romans the caustic reproofs of Pliny and Seneca. For the old
philosophers lamented the growing prevalence of the disorder, almost
unknown in the early, more virile days of the Empire, rightly seeing in
it but another harbinger of impending decadence, clearly attributable as
it was to riotous living and debauchery.
Indeed, we have it on the authority of Galen that “In the time of
Hippocrates there were only a few who suffered from podagra, such was the
moderation in living, but in our own times, when sensuality has touched
the highest conceivable point, the number of patients with the gout has
grown to an extent that cannot be estimated.”
Nothing, in truth, seems more clearly established than this, that gout
is the Nemesis that overtakes those addicted to luxurious habits and
dietetic excesses. On the testimony of eminent travellers we are assured
that amongst aborigines the disease is unknown. The indigenous native
tribes of India are immune, but not so the immigrant flesh-loving
Parsees. Strange to relate, Anglo-Indians of gouty habit, while resident
in the Orient, seem exempt, some say, owing to cutaneous activity, but
more probably because _quâ_ Rendu “these are countries in which we cannot
survive unless we are frugal.”
Nations too, like individuals, when fallen on hard times, lose their
gout. Thus the Arabs, at the zenith of their mediæval Empire, were prone
thereto, but in these latter days are almost exempt from its ravages.
But, on the other hand, if we are to believe Professor Cantani, in no
other disorder are the “sins of the fathers visited upon the children”
with such pertinacity, claiming as he does that its marked incidence in
Southern Italians is a direct heritage from the ancient Greeks and Romans.
PREVALENCE OF GOUT IN THE ANGLO-SAXON PERIOD
Reverting to our own country, what evidences as to its antiquity are
forthcoming? This much may at any rate be affirmed, that according to
Mason Good “Gout is one of the maladies which seem to have been common in
England in its earliest ages of barbarism. It is frequently noticed by
the Anglo-Saxon historian, and the name assigned to it is Fot-adl.”
Cockayne, in his “Leechdoms Wortcumming and Starcraft,” of early England,
has it that the word “addle” appears to have been a synonym for ailment,
thus “Shingles was hight circle addle.” That gout should have flourished
so among our Anglo-Saxon forbears is perhaps a matter for regret but not
for astonishment, when we recall their coarse Gargantuan feasts, washed
down with doughty draughts of ale, “sack and the well spic’d hippocras.”
Gout, we see then, even in our own land, is full ancient, and the word,
as Bradley as shown, may be traced in the English tongue right through
the literature of the various periods.[2] This not only in the brochures
of physicians, but also as in the days of Lucian in the works of
historians, and the satires of poets, which indeed abound with allusions
to the disease.
VIEWS OF THE HUMORALISTS
The Greek physicians, quite familiar as they were with the overt
manifestations of gout, did not, as far as its nosology was concerned,
commit themselves to any appellation that might imply their adherence
to any theory as to its causation. They contented themselves with a
mere _topographical_ designation, terming the affection, _podagra_,
_chirargra_, etc., according as foot or hand was the seat of the
disorder, while for polyarticular types the generic term _arthritis_ was
invoked.
Nevertheless the old Greek physicians had their views as to its
pathology. Thus the source of the peccant humours resided for them in the
_brain_, which they had invested with all the functions of an absorbent
and secreting gland. This hypothesis in time was displaced by the true
humoral theory, according to which the bodily fluids, those found in the
alimentary canal, the blood stream, and the glandular organs, were the
primordial agents of disease. No need, albeit, for gibes on our part, for
how true much of their conception of the genesis of disease even to-day.
Indeed, what else than a fusion of the foregoing views? the modern theory
of Sir Dyce Duckworth, who would ascribe gout to the combined influence
of _neural_ and _humoral_ factors. And now to consider briefly the
individual views of the fathers of medicine.
THE APHORISMS OF HIPPOCRATES
In the eyes of the pioneer priest-physician, the disorder was
attributable to a retention of humours, and many of his dicta have stood
the corroding test of time. He noted, like Sydenham, its tendency to
periodicity, its liability to recur at spring and fall. Also that eunuchs
are immune and youths also, _ante usum veneris_, while in females its
incidence is usually delayed until after the menopause.
The curability of the disease in its earlier stages was affirmed, but
that after the deposit of chalk in the joints it proved rebellious to
treatment, which for him resided in purgation and the local application
of cooling agents.
In the first and second centuries Celsus, Galen, and Aretæus the
Cappadocian recounted their views as to its nature and therapy, while the
Augustan poet in his Pontic epistles, like Hippocrates, laments that his
gouty swellings defy the art of medicine.
“Tollere nodosam nescit medicina podogram.”
_Ovid_, _Ep. ex Pont._, I, 3, 23.
To Celsus, venesection at the onset of an attack seemed both curative and
prophylactic. Corpulence of habit a state to be avoided, and conformably
he prescribed frugality of fare and adequate exercise. Galen (130-200),
more venturesome than his contemporaries, voiced his belief that tophi
were compact of phlegm, blood, or bile, singly or in combination. For
the rest, he enjoined bleeding and purgation and local applications,
contravening, by the bye, Hippocrates’ claim as to the immunity of
eunuchs in that in his (Galen’s) day their sloth and intemperance were
such as readily begat the disorder.
About this period Lucian of Saramosta enumerated the various anti-gout
nostrums vaunted as specifics in his day. Though in his comic poems, the
Trago-podagra and Ocypus he rightly holds up to scorn the charlatanism
rampant at the time, still it is quite clear that he possessed no mean
knowledge of the clinical vagaries of gout and was quite alive to the
mischief of too meddlesome treatment thereof.
Said the hero of the Trago-podagra:
“Irritantibus me
Soleo occupere multo iracundior
His vero qui cogitant nihil adversum mihi
Benignam adhibeo mentem, facilisque fio.”
Again, Seneca, in a jeremiad on the decadent habits of Roman ladies of
the patrician order, observes: “The nature of women is not altered but
their manner of living, for while they rival the men in every kind of
licentiousness, they equal them too in their very bodily disorders. Why
need we then be surprised at seeing so many of the female sex afflicted
with gout.” That the old philosopher’s misgivings were but too well
founded is obvious when we recall that so widespread were the ravages of
gout among the Romans in the third century that Diocletian, by an edict,
exempted from the public burdens those severely crippled thereby, in
sooth a blatant illustration of political pandering to national vice.
But to return to the researches of physicians, those of Aretæus seem
to have been the most enlightened of his time. A succinct account of
the mode of invasion of gout and its centripetal spread in later stages
to the larger joints is followed by enumeration of the exciting causes
of outbreaks. Anent these, he quaintly notes the reluctance which the
victims display to assigning the malady to its true cause—their own
excesses—preferring to attribute it to a new shoe, a long walk, or an
injury. Noting that men are more liable than women, he tells us, too,
that between the gouty attacks the subject has even carried off the palm
in the Olympic games. The white hellebore, to his mind, at any rate in
early attacks, was the remedy _par excellence_. But, for the true nature
of the disease, he, with humility and piety, avows that its secret origin
is known only to the gods.
Not so his successor Cælius Aurelianus, who affirmed it to be not
only hereditary but due to indigestion, over-drinking, debauchery,
and exposure. Under their maleficent influence morbid humours were
generated which sooner or later found a vent in one or other foot, with
a predilection for tendons and ligaments; these structures he averred
being the locus morbi. An abstemious dietary with exercise was his sheet
anchor in therapy, with local scarification in preference to cupping and
leeching, but violent purging and emetics he decried, and drugs to him
made little appeal.
More ambitious than his predecessors, Alexander of Tralles, in the
sixth century, held that there were many varieties of gout, some due
to intra-articular effusions of blood, reminding us of Rieken’s view
(1829) that hæmophilia is an anomalous variant of gout. Other cases,
Alexander averred, were the outcome of extravasation of bile or other
peccant fluids between tendons and ligaments. Abstinence, especially
from wine and blood-forming foods, was enjoined and a plentiful use of
drastic purgatives, elaterium, etc., with local sinapisms and blisters.
For the absorption of chalk stones he commended unguents containing oil,
turpentine, ammoniacum, dragon’s blood, and litharge.
Aetius, a contemporary, is noteworthy in that during the intervals of
attacks he highly eulogised the use of friction while, like Alexander
of Tralles, he seems to have been much impressed with the virtues
of colchicum, of which he says, “Hermodactylon confestim minuit
dolores.” Planchon, in 1855, in his treatise, “De hermodactes au point
de vue botanique et pharmaceutique,” claims to have proved that the
hermodactylon of the ancients was _Colchicum variegatum_, of similar
properties to the _Colchicum autumnale_.
Paulus Ægineta, like most of his _confrères_, regarded gout and
rheumatism as the same disorder, differing only in their location. He
subscribed whole heartedly to the prevailing humoral theory, but inclined
to think the site of the discharged humours was influenced by weakness or
injury of the parts. He noted, too, that mental states, sorrow, anxiety,
etc., might act as determining causes.
Nor will any historical _résumé_ rest complete without a reference to the
numerous works of the Arabian physicians—Avicenna, Rhazes, Serapion, and
Haly Abbas—who one or other all maintained gout to be hereditary, rare in
women and due to peccant humours, developed in the train of depletions,
debaucheries, and the like.
INTRODUCTION OF THE WORD “GOUT”
In the thirteenth century the Greek terms “podagra,” “chirargra,” etc.,
were to a large extent abandoned, and following Radulfe’s lead gave way
to the use of the generic term “gout,” derived from the Latin “gutta.”
Its adoption was doubtless traceable to the prevailing humoral views
of the origin of the disorder, as due to some morbid matter exuding by
“drops” into the joint cavities. Indeed, according to Johnson, the word
“gut” was used as a synonym for “drop” by Scottish physicians even in his
day.
In any case, the term found little difficulty in installing itself among
all nations, taking in French the form “goutte,” in German “gicht,” in
Spanish “gota,” etc. Trousseau thought it “an admirable name, because in
whatever sense it may have been originally employed by those by whom it
was invented, it is not now given to anything else than that to which
it is applied.” In contrast therewith, that trenchant critic Pye-Smith
complained of the laxity with which the Germans invoked the word “gicht.”
He says it is popularly credited with all the pains which are called
“rheumatics” in England. “Sometimes ‘gicht’ is nothing but bad corns and
is rarely true gout.” Albeit, Pye-Smith did not, as we shall see later,
hold even his English _confrères_ in this respect void of offence.
From these remote times onwards through the Middle Ages to the present
day, an almost continuous series of historical records testify that not
only has gout always been with us, but that its clinical characters
throughout the ages have remained unaltered, conforming ever to the
primitive type. During the seventeenth and eighteenth centuries many
physicians, both British and continental, ventilated their views as to
the nature of gout, all swearing allegiance to the old humoral pathology,
notably Sydenham, Boerhaave, Van Swieten, Hoffmann, Cadogan, etc.
The English Hippocrates, as Trousseau christened the illustrious
Sydenham, displayed his catholic outlook by the pregnant words: “No very
limited theory and no one particular hypothesis can be found applicable
to explain the whole nature of gout.” A live-long martyr himself thereto,
he brought all the strength of his dominating intellect to bear upon its
elucidation. As to its causation, he held it to be due to a “morbific
matter,” the outcome of imperfect “coctions” in the _primæ viæ_ and in
the secondary assimilating organs. He refrained from speculating as to
the constitution of the _materia peccans_, but as Trousseau observes, “he
made his _morbi seminium_ play the part which modern chemistry attributes
to the products it has discovered. Take it all in all,” he says, “the
theory of the great English physician is much more medical than the
theories of modern chemists.”
EARLY VIEWS AS TO THE NATURE OF TOPHI
“Et tophus scaber, et nigris exesa chelydris Creta.”
_Georg._, ii., 214.
The word “tophus” or “tofus,” the Greek τοφος, seems to have been applied
to rough crumbling rock, the disintegrated volcanic tufa. As to its
constitution it is clear from the above quotation that Virgil evidently
associated it with chalk, a shrewder guess than the fanciful hypothesis
of Galen, though the views of Paracelsus (1493-1541) enunciated some
centuries subsequently, were even more grotesque, a “mucous essence,” a
“Tartarus” burning “like hell fire.”
Nevertheless, our contempt need be chastened when we recollect that, up
to the latter half of the eighteenth century, equally weird assumptions
found acceptance. By some “various excrementitial humours,” by others
“checked and decomposing sweat” were deemed the basis of tophi.
A mucilaginous extract, derived from the solid and liquid intake,
appealed to some as an explanation of their formation, while to others,
tophi were compounds of subtle and penetrating salts.
But the later view, doubtless the reflex of _etiological_ hypotheses,
was that tophi were of _tartareous_ nature, closely similar to that
encrusting the interior of wine casks. Hoffmann declared that the
_materies morbi_ actually was a salt of tartar circulating in the blood.
His investigations of tophi and also of the stools, saliva, and urine of
gouty subjects, convinced him that the peccant matter was tartar of wine.
Hoffmann’s views, however, were laughed to scorn by M. Coste as being
obviously absurd, inasmuch as gout was not uncommon amongst those who
had never partaken of wine, _ergo_, never of tartar. How infinitely
more physicianly the inference of Sydenham, who, like some of the older
humoralists held the tophus to be “undigested gouty matter thrown out
around the joints in a liquid form and afterwards becoming hardened.”
So it went on until, alchemy being displaced by chemistry, uric acid was
in 1775 discovered by Scheele, and in 1787 Wollaston established its
existence in tophi, and to the further elaboration of our knowledge of
this substance we shall allude later. Here we would only observe that
Wollaston’s researches marked the coming substitution of the humoral and
solidist theories by a chemical hypothesis as to the etiology of gout.
THE “HONOUR OF THE GOUT”
The absurd delusion, not wholly dissipated even to-day, that to have the
gout, “Morbus Dominorum,” was highly creditable, a mark of good breeding,
was firmly ingrained in our forefathers. We all recall the story of the
old Scottish gentlewoman who would never allow that any but people of
family could have _bonâ fide_ gout. Let but the _roturier_ aspire to this
privilege, and she scouted the very idea—“Na, na, it is only my father
and Lord Gallowa’ that have the regular gout.” As to the origin of this
mistaken ambition, it most probably was the outcome of the fact that it
was peculiarly an appanage of the great, the wealthy, and alas! those of
intellectual distinction!
Statesmen, warriors, literary men and poets loom large amongst its
victims. Lord Burleigh suffered greatly therefrom, and good Queen Bess
on that account always bid him sit in her presence, and was wont to say,
“My Lord, we make much of you, not for your bad legs, but for your good
head!” With more humour, Horace Walpole complained, “If either my father
or mother had had it I should not dislike it so much! I am herald enough
to approve it, if descended genealogically, but it is an absolute upstart
in me, and what is more provoking, I had trusted in my great abstinence
for keeping it from me, but thus it is!”[3]
Of warriors, Lord Howe, Marshal Saxe, Wallenstein, and Condé were among
its victims; while of literary men and poets thus afflicted may be
mentioned Milton, Dryden, Congreve, Linnæus, Newton, and Fielding. Of
physicians, the great Harvey was a martyr to gout, and was wont to treat
it after the following heroic fashion. Sitting, in the coldest weather,
with bare legs on the leads of Cockaine House, he would immerse them in
a pail of water until he nearly collapsed from cold. Mrs. Hunter, wife
of John Hunter, in a letter to Edward Jenner about her distinguished
husband, dated Bath, September 18th, 1785, laments that “He has been
tormented with the flying gout since last March!” In short, the disorder,
with a notable frequency, figures in the life history of some of the
ablest men in all ages, hence the complacency with which lesser men,
often without good reason, affect to have the gout.
“But nothing,” as Sir Thomas Watson says, “can show more strongly the
power of fashion than this desire to be thought to possess, not only
the tone and manners of the higher orders of society, not their follies
merely and pleasant vices, but their very pains and aches, their bodily
imperfections and infirmities. All this is more than sufficiently
ludicrous and lamentable, but so it is. Even the philosophic Sydenham
consoled himself under the sufferings of the gout with the reflection
that it destroys more rich men than poor, more wise men than fools.”
“At vero (quod mihi aliisque licet, tam fortunæ quam Ingenii
dotibus mediocriter instructis, hoc morbo laborantibus solatio
esse possit) ita vixerunt atque ita tandem mortem obierunt
magni Reges, Dynastæ, exercituum classiumque Duces, Philosophi,
aliique his similes haud pauci.
“Verbo dicam, articularis hicce morbus (quod vix de quovis alio
adfirmaveris) divites plures interemit quam pauperes, plures
sapientes quam fatuos.”
The Scotch at one time regarded gout as fit and meet punishment for the
luxurious living of the English. But, as was pointed out, the cogency of
the moral was somewhat spoilt by the fact that the disorder was found
to exist even among the poor and temperate Faroe Islanders. In truth,
although “the taint may be hereditary, it may be generated by a low diet
and abstinence carried to extremes.”
THAT GOUT CONFERS IMMUNITY FROM OTHER DISORDERS
The fallacy that longevity and freedom from other maladies was ensured
by gout was prevalent among our forefathers. In satire of this, one
Philander Misaurus issued a brochure entitled “The Honour of the Gout,”
and purporting to be writ, “Right in the Heat of a violent Paroxysm; and
now publish’d for the common Good” (1735). “Bless us,” says he, “that any
man should wish to be rid of the Gout; for want of which he may become
obnoxious to fevers and headache, be blinded in his understanding, loose
the best of his Health and the Security of his Life”; and forthwith in
his zeal for the common good gives us the following invocation:—
“Blessed Gout, most desirable Gout, Sovereign Antidote
Of murdering Maladies; powerful corrector of Intemperance;
Deign to visit me with thy purging Fires, and throw off the
Tophous Injury which I may have suffer’d by Wine and Wit,
Too hard for the Virtue of a Devotee upon a Holy Festival.
But fail not thy humble Supplicant, who needs thy
Friendly Help, to keep his tottering Tenement in
Order: Fail him not, every Vernal and Autumnal
Æquinox.”
He quaintly suggests that Paracelsus, if he would ensure men against
death, had but to inoculate them with gout. Gout, indeed, was held to
be a jealous disorder, intolerant of usurpation by any other disease,
recalling the remark of Posthumus to his gaolers:—
“Yet am I better
Than one that’s sick o’ the Gout: since he had rather
Groan so in perpetuity, than be cur’d
By the sure physician, death: who is the key
To unbar these locks.”
_Cymbeline._
Still the fallacy that gout was salutary died hard, and although it seems
incredible, yet, Archbishop Sheldon is said not only to have longed for
gout but actually to have offered £1,000 to any one who would procure him
this blessing; for he regarded gout as “the only remedy for the distress
in his head.” How ingrained the notion may be gathered from the fact that
in the early part of the last century, M. Coste in his “Traité Pratique
de la Goutte,” observed: “A popular error, which I wish to expose in a
few words, is this prejudice, which has already lasted more than two
thousand years, and which has reached even the thrones of princes,
where the disease commonly shows itself, viz., that gout prolongs life
(_que la goutte prolonge la vie_). This error,” says he, “has taken the
surest method of introducing itself, by making flattering promises, by
persuading its victims that there is a singular advantage in having gout,
and that the malady drives away all other evils, and that it ensures long
life to those whom it attacks.”
In like refrain, our own countryman Heberden deplores that people “are
neither ashamed nor afraid of it; but solace themselves with the hope
that they shall one day have the gout; or, if they have already suffered
it, impute all their other ails, not to having had too much of that
disease, but to wanting more. The gout, far from being blamed as the
cause, is looked up to as the expected deliverer from these evils.” Such
deluded views being prevalent, it is hardly a matter for surprise that
misguided persons deliberately courted a “fit of the gout” by resorting
to excess and intemperance.
But alas, while the initial visitations of gout, after their passing, may
leave behind them a renewed sense of well-being, it is no less certain
that, when once installed, the intervals of respite grow shorter and
shorter. Crippledom grows apace, the general health breaks and untimely
senescence overtakes the worn-out victim, and, as Heberden puts it, “that
gout causes premature death, when all the comforts of life ...
‘Multæ formæ infortunatorum,
Meditatio pœnæ, et consuetudo,
Podagros miseros consolentur.’
_Lucian._
are destroyed, and the physical powers either insensibly undermined or
suddenly crushed by an attack of paralysis or apoplexy, should hardly be
reckoned among the misfortunes attending the disease.”
But for our encouragement it may be observed that not always does gout
carry with it such a terrible Nemesis. “Gout is the disease of those
who _will_ have it,” said a wise physician, and though the inbred gouty
tendency may be so strong as to cast defiance at abstinence, yet it is
by no means always so. A man may inherit gout, but he need not foster
it by self-indulgence. Much less need he, as so often happens, acquire
it by depraved habits of life. In no disease do sobriety and virtuous
living ensure so great a reward. As Sir Thomas Watson long since said
to those inheriting this unwelcome legacy: “Let the son of a rich and
gouty nobleman change places with the son of a farm servant, and earn his
temperate meal by the daily sweat of his brow, and the chance of his
being visited with gout will be very small.”
“O fortunatos nimium, sua si bona norint
Agricolas!”
_Georg._, ii., 458.
GROWING INFREQUENCY AND ATTENUATION OF GOUT
So accurate and graphic were the clinical pictures of gout depicted by
the ancient physicians that there is no doubt the gout of to-day conforms
to the primitive type as met with among the Greeks and Romans. This
certainly as regards the _arthritic_ phenomena of the disease; for in
those remote ages little or no account seems to have been taken of its
_irregular_ or _ab-articular_ manifestations. While disregard of the
latter group renders more credible their claims as to the widespread
prevalence of the affection, nevertheless, I think there can be no doubt
that the frequency of _gout_ amongst the ancient Greeks and Romans was
probably over-estimated.
Can it be questioned that a large percentage of the cases of gout in
those bygone times consisted of undifferentiated _infective_ forms of
_arthritis_. _Syphilis_ and _gonorrhœa_ must have existed then as now,
and their _specific_ forms of _arthritis_, how easily confused with “rich
man’s gout!” Surely too, they, like ourselves, must have suffered with
states of _oral sepsis_, _pyorrhœa alveolaris_, etc., not to speak of
_infective disorders_, with their correlated _arthritides_. In short, the
_differentiation_ of arthritic disorders was then hardly in its infancy,
and it is in light of this disability that we must appraise their clearly
extravagant assertions as to the widespread ravages of gout in their day.
But passing to more recent times, there is little doubt that the
classical type of _podagra_ is very much rarer to-day than, say, in the
time of Sydenham. Indeed, it may be said to be becoming progressively
infrequent. Thus, writing in 1890, Sir Dyce Duckworth tells us that some
twenty-six years prior to that date, Sir George Burrows informed him
that “he then saw fewer cases of acute gout than he was accustomed to
see in his earlier practice.” It may be recalled, too, that Sir Charles
Scudamore, in retrospect of his own experience, of still earlier date,
was led to much the same conclusion. Moreover, not only is the disorder
less frequent, but its virulence seems to have suffered attenuation, and
this to a marked degree.
Again, Ewart, writing in 1896, observed that “goutiness” is becoming
relatively more common than declared gout. This, he thought, by reason
of the increasing attenuation in transmission of the “gouty” taint.
In this, as well as the more mitigated character of the arthritic
manifestations, he saw hope of “an ultimate extinction of the bias in
‘gouty’ families.” For, as he rightly says, side by side with “the
tendency to a reproduction of morbid parental peculiarities, there is a
yet stronger tendency in Nature to reproduce the healthy type of the race
in each successive generation.”
But while there is a general consensus of opinion as to the growing
rarity of acute regular gout, on the other hand, many, as if loth to part
with the disorder, claim that _pari passu_ with the decline of regular
types the incidence of _irregular_ manifestations grew proportionately.
In my experience the incidence of _regular_ gout has appreciably
diminished during the past twenty years. Moreover, such examples as
one has met with incline much more in character to the _asthenic_ than
to the sthenic variety of _podagra_. But, in contrast to many, I have
observed no increase in the _irregular_ manifestations of gout. On the
contrary, a steady diminution in the nebulous content of this category,
but to this vexed subject we shall recur in a subsequent chapter dealing
with the propriety or not of retaining this ill-defined term in medical
nomenclature.
My conclusion, then, is that not only is arthritic gout becoming
less prevalent, but that the type of the disease also has suffered
attenuation. Probably this dual change is the outcome of many factors,
not the least of these an increase in national sobriety. For as Sir
Alfred Garrod long since observed, “There is no truth in medicine better
established than the fact that the use of fermented liquors is the most
powerful of all the predisposing causes of gout; nay, so powerful, that
it may be a question whether gout would ever have been known to mankind
had such beverages not being indulged in.
“Αυσιμελου Βάκχου, και λυσιμελους Αφοδίτης,
Γένναται θυχατηρ, λυσιμελὴς, Ποδὰγρα.”