SummaryA case of poisoning as a result of the ingestion of an alcoholic podophyllum extract is described.The resulting toxic effects comprised an initial severe disturbance of consciousness followed by a state of confusion, and a fairly severe type of peripheral neuropathy.A substantial amount of recovery of function had occurred at the end of six months after ingestion of the podophyllin, but a residual neurological deficit was still evident at the end of 16 months.The mode of action and probable effects of the podophyllum extract are discussed briefly. GroupThis paper describes six cases in which ankylosing spondylitis was associated with chronic non-specific inflammatory lesions of the intestines. Four of these cases had chronic ulcerative colitis, one had Crohn's disease, and one had ulcerative colitis and Crohn's disease. The aetiology of ulcerative colitis and Crohn's disease is uncertain. Although it seems unlikely that they represent different man-ifestations of the same diseases, nevertheless there appears to be enough similarity between them to make differentiation difficult at times (Butler, 1953 ; Crohn, Garlock, and Yarnis, 1947), and we may be justified in considering them together. The diagnosis of Crohn's disease was made at operation in both our cases, while radiology with a barium-filled colon was relied on for the diagnosis of ulcerative colitis.The English literature has few references to the association of ankylosing spondylitis and ulcerative colitis. West (1949) (Marche, 1950; Ford, 1953 and for several years he had little trouble. In 1954 he complained of pain in the right knee, followed by pain in the back. Examination showed rigidity of the thoracic and lumbar spines, and limitation of movement of the cervical spine. There was an effusion in the right knee. X-ray examination showed typical changes of ankylosing spondylitis, with obliteration of the sacro-iliac joints and calcification of the spinal ligaments. Erythrocyte sedimentation rate was 20 mm. in one hour. He was treated by physical methods, with improvement. One month before this was written he had a further relapse of diarrhoea, with blood, and a barium enema showed a loss of haustration involving the descending and pelvic colon. For some years this man had had diffuse psoriasis.Case 3.-A man aged 48 complained in 1937 of diarrhoea and bloody stools. He was admitted to hospital, and ulcerative colitis was diagnosed. In 1942, while in hospital with a further attack, he first noted stiffness of his spine. Since then he has had intermittent attacks of ulcerative colitis. He also found that his neck was bending forward, and that he was unable to look up. In 1949 a diagnosis of ankylosing spondylitis was made. He was treated with deep x-ray therapy. Following this he developed his first attack of iridocyclitis, affecting the left eye. In 1950 he experienced a severe attack, affecting the right eye. X-ray examination revealed obliteration of both sacro-iliac joints, typical of ankylosing spondylitis. 1158 Nov. 16, 1957 ANKYLOSING...
PHENYLBUTAZONE AND URIC ACID METABOLISM BEDI late from plasma uric acid readings before and after treatment the total loss of body uric acid and to correlate this calculation with the actual excess observed in the urine. Such a calculation is shown in Table VI. Case 4 is excluded, as measurements of actual body weight were not taken.Where more than one estimation of circulating uric acid was made before treatment the mean has been taken. Such calculations require certain assumptions which need not be discussed here. Nevertheless, if the falls in plasma levels were greater than could be accounted for by the excess excretion, clearly a consistent discrepancy would appear. In Cases 2 and 5 the discrepancy is small, and in Case 3 slightly more uric acid was excreted than can be accounted for by the fall in plasma levels.Only in Case 1 is there the sort of discrepancy which would be required to claim that the fall in plasma levels is greater than can be accounted for by the excess excretion. It was in this case, however, that an acute attack developed during the control period, with a rapid rise in blood levels. The excess excretion of uric acid during this period is more than enough to account for the change in total blood uric acid. Calculating the plasma volume as 0.051 body weight, and assuming that the fall is due to clearance by the kidneys, it would require an excess excretion of 243 mg. to reduce the level from 9.4 to 3 mg. per 100 ml. In the event 483 mg. was excreted in excess during the relevant period. ConclusionsThere are thus two possible effects exerted by phenylbutazone and influencing uric acid estimations: (1) uricosuric-while this is no more than a mild effect it is nevertheless sufficient to account for the observed fall in circulating urate levels; and (2) water retaining-this was sufficient to precipitate congestive heart failure in the one case in which a uricosuric effect was not observed.It is suggested that the variable preponderance of uricosuric and water-retaining effects would account for the variable findings. Much further evidence is required to establish still a third effect, on uric acid metabolism itself; and the fact that uric acid excretion may be increased when phenylbutazone is administered is against such a possibility. SummaryFour cases of gout and one control case were treated with phenylbutazone and the changes in plasma uric acid and urinary uric acid levels were studied.The findings suggest that phenylbutazone has no more than a slight uricosuric effect. This may be neutralized if considerable water retention occurs at the same time.No evidence was found that phenylbutazone has any direct effect on uric acid metabolism. Toxic effects of phenylbutazone have been described by a number of authors, and death has been ascribed mainly to agranulocytosis and to intestinal haemorrhage or perforation. A case is recorded in which death is attributed to a hypersensitivity reaction (in the course of phenylbutazone therapy). Case ReportThe patient was a man aged 73. Five years ago he b...
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