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411likely that inadequate control of renal failure was responsible for the deterioration in nerve conduction.Anorexia at the onset of hepatitis was a feature in all patients. An adequate caloric intake was maintained, however, and vitamin supplements were continued. Half the patients had no overt protein imbalance and in the others protein loss was of a minor degree. It is therefore unlikely that protein loss or malnutrition was responsible for changes in nerve conduction.Drug absorption and metabolism are impaired in both renal and hepatic failure. No patient received any preparation known to be neurotoxic when given to people with normal renal and hepatic function.Previous reports of hepatitis in dialysis units have not mentioned impaired peripheral nerve function (Jones et al., 1967;Eastwood et al., 1968;London et al., 1969), but our results suggest that the two are closely linked.Klippel and Lhermitte (1908) noted that "catarrhal infective jaundice can be complicated by a more or less generalized polyneuritis." They thought that the polyneuritis was due to the infective agent responsible for the jaundice and was not dependent on hepatic insufficiency. Lelong and Bernard (1935) reported the case of a 14-year-old girl who developed hepatitis and a predominantly motor neuropathy which improved after two months. Peripheral neuropathy has also been described in the accounts of hepatitis occurring during the second world war (Brain, 1942-3;Lescher, 1944;Byrne and Taylor, 1945;Lovell, 1945 It is possible that an immunological response to a viral infection could give rise to segmental demyelination of the peripheral nerves. The reduction in nerve conduction velocities in our study was not as pronounced as is usually found associated with widespread segmental demyelination (Gilliatt, 1966). However, the improvement after recovery from hepatitis suggests that demyelination, with subsequent remyelination, may be partly responsible for the neural changes.Hepatic parenchymal insufficiency could damage peripheral nerves by producing unfavourable metabolic disturbances. Dayan and Williams (1967) suggested that the predominantly demyelinating peripheral neuropathy associated with chronic hepatic failure might be related to disordered insulin metabolism. Profound hypoglycaemia, though known to occur in acute hepatic necrosis, was not observed in our patients. Alterations of insulin metabolism or other metabolic pathways remain possible factors in the aetiology of the impaired neural conduction.The interpretation of the changes in nerve conduction velocity is complicated by the pre-existing impairment of conduction associated with chronic renal failure. Our observations show a deterioration in neural conduction in patients suffering from serum hepatitis but the pathogenesis of this change is not clear.

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is about 3000. Among children aged under 5 cryptosporidiosis may be found more commonly than salmonella infection.4 Detailed follow up study of cases diagnosed by the laboratory commonly shows other cases among contacts,' including adults, and the number of cases reported clearly represents only a proportion of the actual incidence.

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