This section is from the book "Materia Medica: Pharmacology: Therapeutics Prescription Writing For Students and Practitioners", by Walter A. Bastedo. Also available from Amazon: Materia Medica: Pharmacology: Therapeutics: Prescription Writing for Students and Practitioners.
Since the lithium salts of uric acid are more soluble than the corresponding sodium salts, lithium has been favored as the alkali in gout and the uric-acid diathesis. But the quadriurate, which seems to be the responsible irritant in attacks of gout, is not rendered soluble by any lithium salt except in concentrated solution; and is not prevented by lithium, so far as known, from forming in gouty subjects. Daniels obtained no effect from lithium citrate alone in a case of gout, but got a greater excretion of uric acid from atophan when lithium citrate was given with it. She attributed a mobilizing effect on deposited urates to the lithium, though it had no power of itself to increase the elimination. The lithia waters on the market are chiefly remarkable for the minuteness of the amount of lithia present, several gallons, as a rule, containing not more than a single therapeutic dose.
Cleaveland (1913) reports lithium poisoning in himself on two occasions. The first time he took 120 grains (8 gm.) of lithium chloride in twenty-eight hours. The symptoms began after the first dose of 2 grams. There were fulness in the head, dizziness, ringing in the ears, and blurring of the vision, followed by tremors and marked prostration. The second time, several months later, he took 60 grains (4 gm.) and the symptoms were repeated. He felt as if he had taken a large dose of quinine. There were no gastro-intestinal symptoms. C. A. Good (1903), in experiments on cats and dogs, found that 60 mg. per kilo daily invariably caused death sooner or later from gastro-enteritis.