Gouty glycosuria is more common in males than females. The subjects are usually robust, middle-aged, and of full habit. Sugar is found intermittently in their urine in small amounts, but no acetone bodies. It is as a rule unaccompanied by thirst or wasting. It quickly responds to dietetic restrictions. As Gull long since observed, gouty glycosuria does not “discover itself,” but is “not uncommonly discovered.” This tersely sums up the clinical difference between this affection and true diabetes, albeit, as in all glycosurias, there is always the risk that carbohydrate excess, mental strain, or other adverse circumstances may aggravate the disorder and the case merge into one of true diabetes.
Following the installation of glycosuria, the tendency to paroxysmal articular outbreaks often ceases. The converse also has been observed, viz., that when, in sequence to dietetic restrictions, the sugar disappears, the articular pains may reappear. The fact that attacks of glycosuria may alternate with attacks of gout led to the assumption that a positive antagonism existed between the two disorders. Hence the phrase “the more sugar the less gout,” and vice versâ. This, however, with reservations, for a fugitive glycosuria has been seen during an acute articular paroxysm, and a classical outbreak in the toe has been known to supervene in the course of a well-established glycosuria.
It is generally held that glycosuria is most commonly associated with irregular forms of gout. But, in view of our ignorance of the intimate nature of even regular gout, I should myself deprecate affixing the prefix “gouty” to any glycosuria other than one that has supervened in sequence to, or alternates with, gouty arthritic seizures. Moreover, the glycosuria of gout is usually the alimentary glycosuria of fat elderly people, in whom the sugar excreted represents the unconsumed surplus of carbohydrate food. But fat elderly people are not necessarily “gouty,” neither is every so-called benign glycosuria inevitably linked on to a gouty diathesis. In fact, the relegation of glycosuria to the gouty category is but too often not a matter of diagnostic certainty, but rather an inference. Hence my plea that the prefix “gouty” would best be restricted to glycosurias occurring in individuals who suffer regular attacks of gout, or those displaying those objective tokens pathognomonic of the disorder, i.e., tophi.
Again, James Taylor has recently reminded us that, if nerve affections are relatively common in true diabetes, the same may be met with in gouty glycosuria, even when of temporary duration. Thus symptoms indicative of peripheral neuritis may occur, i.e., lost knee jerks, paræsthesiæ, and paresis of the lower limbs. Now, as this authority pertinently observes, the subjects of gouty glycosuria are frequently given to alcohol. Consequently the question whether or not the symptoms are due, not to sugar, but to alcohol, arises forthwith.
In some undoubtedly the alcoholic factor plays a rôle, but such symptoms may, on the contrary, arise in very abstemious individuals. This notwithstanding, James Taylor holds that the clinical complex differs substantially from that met with in true alcoholic neuritis. It is slighter in degree, the paresis usually restricted to lower limbs, while the exquisite tenderness to pressure on nerve trunks so typical of alcoholic neuritis is little or not at all in evidence. Nor is there the same tendency to contractures in muscles as met with in the alcoholic variety, and withal there is an absence usually of the mental changes—loss of memory—associated therewith. Accordingly Taylor holds that we must recognise the existence in the gouty of a true glycosuric peripheral neuritis quite independent of alcoholic peripheral neuritis.
Other concomitant nerve troubles noted in this association are severe intercostal neuralgia and, even more commonly, neuralgia of the fifth nerve, and to this may be added migraine and that other neurosis asthma. Intense mental irritability and depression is not an infrequent sequel in gouty glycosuria. According to James Taylor, melancholia even may result, especially if the glycosuria have merged into true diabetes—a sequel, he says, especially prone to occur in Jewish subjects.
Having seen and suffered many painful disillusionments through too flippant relegation of neuralgias or neuritides to diatheses “gouty” or “rheumatic,” I would emphasise the necessity for great caution. In other words, before labelling a neuralgia or neuritis as “gouty,” all possible causes, infective or other, should be excluded, this always, but pre-eminently so in brachialgia, sciatica, and trigeminal neuralgias. Nor even, should there be a history of classic outbreaks or blatant tophi present, should we be less vigilant.
By all means recognise the gouty diathesis. It often avails much in treatment, but not if, e.g., dental caries, antral disease, cervical rib, or pelvic growth be overlooked, not to speak of recent or concurrent sources of infection or toxic absorption.
Lastly, we should always recollect that gouty glycosuria, as Gull said, “does not discover itself”; it is not writ large on the subject like true diabetes. But given the incidence of nerve troubles in a gouty person, i.e., a paræsthesia, itching, neuralgia, etc., we should always suspect its presence.[39] Incidentally our search may reveal not only sugar, but also albumen, and the latter may explain much that appeared inexplicable.