Apart from its intrinsic fascination, the tracing out of analogies, clinical or pathological, between diseases apparently diverse has often proved a fruitful source of enlightenment, for the natural history of disease is such that one disorder trenches upon the clinical territory of another, symptoms overlap and similarity if not community of origin is revealed. Few will gainsay that gouty individuals are the victims of some inborn defect or eccentricity of metabolism, and instinctively the thought arises, are there no other disorders of like character? Immediately we bethink ourselves of alkaptonuria, cystinuria and pentosuria. Sir Archibald Garrod, as we know, classed these disorders as “chemical malformation” of hereditary origin. In other words, all are the outcome of an abnormality in intermediary metabolism. In alkaptonuria the metabolic warp concerns the _aromatic_ groups, in cystinuria the sulphur-containing radicles of the _protein_ molecule. On the other hand, in pentosuria the origin of the endogenous pentose is variously ascribed to the _nucleo-protein_ of the cell nuclei or to galactose. Lastly, in gout it is in the metabolism of _nucleo-protein_, or rather of the _nucleic acids_ of the cell nuclei that the flaw resides. We see, therefore, that Langdon Brown, discussing gout, is well justified in observing that, “We may look upon a person who is readily poisoned by purins in the same light as the person who has cystinuria, alkaptonuria, or pentosuria, _i.e._, they all lack a link in the chain of protein katabolism, so that intermediate products appear in the urine instead of the usual end-products.” In other words, they all display a pathological kinship, viz., in that they are all due to inborn errors of metabolism. Certain broad clinical resemblances also obtain. All members of the group, including gout, display _hereditary_ tendencies. All occur much more often in _males_ than in females. They all alike tend to persist through life. Lastly, their distinctive chemical products, including uric acid, are all apparently of _low toxicity_. But when we pass to the realm of their symptomatology, resemblance, if it does not cease, becomes relatively obscured. Cystinuria and pentosuria appear to be “harmless anomalies,” and the same is true of alkaptonuria. The cystinuric, albeit, does suffer with _urinary_ concretions, and we may recall that some authorities hold that gout and uric acid _calculi_ are not unrelated. As to alkaptonuria, it has this attenuated link with gout that in its later stages the victims thereof tend to develop a degenerative type of _arthritis_, while the frequently associated pigmentary change, _ochronosis_, has a predilection for deposition in the cartilages of the ears and _joints_. But how colourless the clinical features of alkaptonuria, etc., as contrasted with the vivid arresting phenomena of gout! how remote the latter disorder from these “harmless anomalies”!