Unfortunately for the cogency of the argument, there is no proof that such visceral inflammations as do occur in the “gouty” are of gouty origin. Unfortunately, too, the microbic agent that we postulate as responsible for “gouty” arthritis is as yet unisolated. If this disability be removed, it might be found that the said organism was capable of originating, not only the arthritic, but the alleged visceral, forms of gout. But pending such discovery I am of opinion that the term “visceral” gout should be abandoned, in other words that we should cease to talk of, e.g., bronchitis, dyspepsia, etc., as “gouty,” and should talk of them as bronchitis or dyspepsia occurring in the gouty. In this way we may escape, or, better, render uncalled for, the scathing criticism of Pye Smith:—“It has become common to ascribe bronchitis, dyspepsia, gastralgia, iritis, gravel, cystitis, and even psoriasis to the ‘gouty’ diathesis; but the evidence is very slight, and the ‘gout’ to which such evidence as there is applies is the distillation of morbid humours which belong to a bygone pathology.... There is no reason to believe that gout ever flies to the stomach, but over-indulgence at the table may produce acute dyspepsia as well as inflammation of the great toe. Elderly people are liable to gravel, gout and cough; and while lead and drink may lead to gout and chronic Bright’s disease, cirrhotic kidneys favour an attack of gout.”
Infantile Gout
While subjects of gout have told me that they had had an attack in their teens, I have never myself seen an instance. Still less can I claim to have seen what I felt justified in calling “gout” in children. On the other hand, if, as one authority states, “tonsillitis (quinsy), enlarged tonsils, granular states of the pharynx, and catarrhal conditions of the throat and respiratory mucous membranes are not infrequent expressions of gouty inheritance in children,” then, of course, all of us must be quite familiar with “infantile gout.”
But even this formidable list of legacies from gouty parents is eclipsed by a more recent writer, J. Comby (1902), who, discussing “infantile arthritism,” divides children coming of gouty stock into two types: the “lymphatic” and “nervous.” The children of the former class suffer from fleeting swelling of the lymphatic glands, rhino-pharyngitis, tonsillitis, and, if they be girls, from chlorosis. Also they are given markedly to tachycardia, bradycardia, and vasomotor ataxia. They are also especially liable to asthma and the crises of dyspnœa, and pulmonary congestion may alternate with urticarial and eczematous eruptions. Truly, their lot is hard, for they fall a ready prey to colic, constipation, all varieties of dyspepsia, not to mention nocturnal and diurnal enuresis!
Comby also claims that these gouty children are especially liable to recurrent or cyclical vomiting. In this matter he is confirmed by J. Thomson, who noted that these children not infrequently give a history of having had asthma, urticaria, eczema, stammering, and other nervous complaints, also that in many instances uric acid crystals or a copious deposit of urates have been noted in their urine.
As to the “nervous” type, they labour with insomnia, night terrors, convulsions, and when older with migraine. To these liabilities must be added undue proneness to acne, seborrhœa, psoriasis, chilblains, angio-neurotic œdema, urticaria, etc., not to mention muscular and joint aches and pains.
Whether this medley of distempers can with any pretensions to scientific reason be affiliated to a gouty heritage, or whether they can be regarded as expressions of a budding “gouty diathesis,” is, I submit, of the nature of pure speculation. That the child who suffers with cyclical vomiting may show uric acid crystals or urates in his urine is certainly no proof that he has inherited gout, much less that he is actually “gouty.” In uro-lithiasis the uric acid is precipitated in the urinary passages, viz., strictly speaking, outside the body, whereas in gout the pathological error originates within the organism. More apposite is Uffenheimer’s observation, previously noted, that children of this type suffer the same disturbances of purin metabolism as are met with in adult gouty subjects.
If the fact is confirmed that the output of exogenous purin in such children is diminished or retarded, it would certainly be a most interesting finding, possibly with a now unguessed-at significance. But we should recall that even in the subjects of regular gout such is not invariable, and, moreover, occurs in diseases other than gout. Pending further exact investigations I think it would be wiser not to indulge in such vast generalisations, mindful of the sentiments expressed by the illustrious Sydenham in his letter to Dr. Gould:—
“I have bin very careful to write nothing but what was the product of careful observation. So when the scandall of my person shall be layd aside in my grave it will appear that I neither suffered myselfe to be deceived by indulging in idle speculations nor have deceived others by obtruding anything to them but downright matter of fact.”