That some obscure connection obtained between gout and hepatic disorder has been for long an axiom in high favour, with both clinicians and pathologists. This hypothesis found its chief exponents in Murchison and subsequently Latham, and to discussion of their individual views we now proceed. The first named authority held gout to be either merely a result or a variety of what he termed _lithæmia_. In other words, gout was the outcome of a depraved condition of the blood, due to faulty digestion and functional disturbance of the liver. Now the conditions that lead to functional derangement of the liver are in the main such as favour the development of gout. Nevertheless, such hepatic disturbances do not inevitably culminate in outbreaks of gout, at any rate of classical type; but, unquestionably, such may eventuate in symptoms currently recognised as distinctive of _incomplete_ gout, _e.g._, headache, palpitation, cramps, dizziness, sleeplessness, etc. Moreover, if the faulty habits leading to such hepatic derangement be persisted in, they are but too likely to induce outbreaks of frank gout. “Articular gout,” said Murchison, “is so to speak a local accident which, though sometimes determined by an injury, yet may occur at any time in persons in whom the normal process by which albuminous matter becomes disintegrated in the liver into urea is persistently deranged.” Following such hepatic disturbance, the secretion of bile decreased with resultant abnormal metabolism of proteins, and in this way was produced an _accumulation of uric acid_. This, moreover, according to Murchison, was, especially in the later stages of gout, reinforced by the concurrence of _renal inadequacy_, which he also postulated as a factor in the production of the disorder. The tendency to lithæmia Murchison held to be _hereditary_, and in this was supported by Goodhart, who, discussing its occurrence in young children, was strongly of the opinion that it was due not to dietetic irregularities but to a “constitutional tendency on the part of the individual”; a conclusion, as he thought, strongly supported by the fact that it is more commonly met with in the children or descendants of the “gouty.” But we have to recollect, as Duckworth observes, that lithæmia, “even when persistent and not due to accidental causes, is not by itself gout.” Moreover, gout is not the only morbid condition in which urates are in excess in the blood, for such obtains, _e.g._, in _leukæmia_, pneumonia, anæmia, Bright’s disease, etc. Also, underlying Murchison’s theory is the further unwarrantable assumption, viz., that the “gouty” diathesis is identical with the “uric acid” diathesis.