MitiletL JouvxAtj Lmuwx 3o,.-'~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ cirrhosis in post-natal life consists in the further changein the large bile ducts and gall bladder. An attempt to explain this additional lesion may be made as follows: The bile ducts are extremely'small at birth,'and any inflammatory change will, from the small size of the lumen, produce stenosis much mnore readily than later in life. An analogous effect is seen in the fact that laryngeal obstruction in diphtheria is more frequent in young subjects than in older patients, quite apart from the much greater frequency of the disease in the young. The opposed inflamed surfaces of the bile ducts will also come in contact more readily, and, as in catarrhal appendicitis, obliteration might result. The following considerations bear on the hypothesis that the disease is primarily a congenital cirrhosis. I. The almost constant occurrence of cirrhosis in these cases of bile duct obstruction in infants as compared with the infrequency and irregularity with which cirrhosis follows obstruction'of the larger bile ducts in later life. The mixed character of the cirrhosis explains the discrepancy in the recorded cases, some authors speaking of biliary, others of multilobular, cirrhosis. 2. The large size ofthe liver-this resembles hypertrophic biliary cirrhosis. In simple obstruction of the larger bile ducts in adults, the liver, though swollen from retained bile in the early stages, is usually small after death. 3. The large size of the spleen-aphenomenon not met with in uncomplicated biliary obstruction. The large size of the spleen is best explained as the result of toxic bodies reaching the organ by the splenic artery. In hereditary tsyphilis, where it is probable that the poison reaches the liver by the umbilical vein and is derived from the maternal circulation rather than that the ovum is infected by a syphi-litic spermatozoon, there is a similar splenic enlargement. In both conditions there is cirrhosis due to poisons arriving by the umbilical vein; the difference between the pericellular cirrhosis of hereditary syphilis and the mixed (monolobular and multilobular) cirrhosis of so-called congenital obliteration of the bile ducts must depend on a difference in the poisons in the two diseases. This is at one withThomson's statistical proof that syphilis plays no part in the antecedents of so-called congenital obliteration of the bile ducts.'4. The fact that in some instances several cases of this rare disease have eccurred in the same family. Hypertrophic biliary cirrhosis not infrequently occurs in several members of the same family, and has been thought by Boixto be a waterborne disease. Against the view that so-called con-genital obliteration of the bile ducts is in reality a form of congenital cirrhosis, it might withreason be objected that the poison that sets up the change must pass through the mother, and that she should show evidence of its influence. It must be admitted that there are at present no data to provide a satisfactory answer to this argument. As bearing on this point, however, it may be mentioned that the extremely fatal biliary cirrhosis in Brahmin infants around Calcutta, which is also a family disease, has been thought to depend on the mother's milk. The mothers restrict themselves to a dry diet and take a decoction of black pepper. If this is the causal factor, it evidently affects the nurslings more than the nurses, and might justify the suggestibn that in fcetal life the infant's livermay be more susceptible thanthe mother to poisons tending to produce cirrhosis; while again the effects of syphilis may be, and usually are, much more manifest in the infant than in the syphilised mother. To sum up, it seems reasonable to believe that the disease is primarily started by …