As to the usurpation of colchicum by atophan, I do not think it is at all likely, for it does not, I consider, exert the specific effect of the former on the gouty inflammatory process, taking the humbler rôle of obviating the formation or promoting the absorption and elimination of uratic deposits. In other words, colchicum influences the causa causans of gouty inflammation, atophan only the consequences or sequels thereof.
The most favourable juncture at which to prescribe atophan is at the close of a paroxysm. I have myself been much impressed with the manner in which it produces softening and palpable diminution in the size of tophaceous deposits, so much so, indeed, that I feel sure we have in this drug a valuable agent wherewith to prevent the formation of uratic deposits.
A two or three weeks’ course of atophan after an acute attack is, I have found, very advantageous, in doses of 30-45 grains per diem, after meals. It may, for the special reasons given, be well combined with an alkaline stomachic mixture taken half an hour or more before food.
| ℞ | Potassii bicarbonatis | gr. 15 |
| Sodii bicarbonatis | gr. 20 | |
| Spts. ammoniæ aromat. | ♏︎ 20 | |
| Tinct. zingiberis fort. | ♏︎ 5 | |
| Inf. aurantii co. ad unciam. | ||
| Fiat haustus, thrice daily well diluted with water. | ||
To sum up, our medicinal treatment of acute gout consists in initial purgation, followed by maintenance of an adequate daily evacuation; secondly, the exhibition of colchicum or its active principle and continuance of the same in diminishing doses until pain and inflammatory phenomena have departed. With the passing of the paroxysm atophan should be resorted to in combination with an alkaline stomachic mixture. Supervision of the subject should not cease until the digestive and assimilative functions have, as far as possible, attained functional efficiency, for it is certain that this is the most important point in the management of the gouty constitution. Conjoined therewith, the bowels should never be allowed to become constipated, the urine maintained free from acid lithates, and the skin active by regular exercise.
Alternative Remedies in Acute Gout.—Of the various drugs advocated as substitutes for colchicum the salicylate group alone seems to have evoked something like enthusiasm. Thus Germain Sée affirmed that sodium salicylate was the best remedy for gout, whether of acute or chronic type. In this country Haig strongly upheld its claim. On the other hand, Ebstein, when he used this salt in acute gout, found that the inflammation, though it quickly subsided in one joint, immediately reappeared in another, even though the administration of the drug was continued.
Lecorche, again, though he found it useful in acute gout, was equally certain that it was altogether inferior to colchicum. It did lessen the pain and the violence of the paroxysm, but in no way shortened its duration. But, on the other hand, he attached a prophylactic value to it in chronic gout marked by recurring subacute attacks. His method was to give it in the intervals of paroxysms in doses of from 60-80 grains a day, whereby he claimed to abort attacks, prevent ankyloses, and facilitate absorption of uratic deposits.
As to its mode of action, salicylate of soda, both in gouty and healthy subjects, determines an immediate increase in the uric acid excretion, 30-60 per cent. The increase, however, is but ephemeral, the excretion of uric acid sinking gradually to normal in about forty hours, and this whether the drug be persisted with or not. The increase in total nitrogen excretion does not reach 10 per cent.
Discussing this mode of response, MacLeod (who noted the same after citrates) is of opinion that salicylate of soda and citrate act, not by influencing the metabolic processes that originate uric acid, but by promoting the excretion thereof. Walker Hall and Magnus Levy, albeit, suggest that the increase is due to diminution in the normal destruction of purins in the organism, with resulting transmission of the same in larger quantities to the kidneys for excretion. It is possible therefore that in the presence of sodium salicylate there is diminished oxidation of uric acid.