there may be
a
phenylbutazone
future for treatment with full doses of and indomethacin over alternate weeks.
410, Albert Street, East Melbourne, Australia.
MICHAEL KELLY.
URINARY EXCRETION OF UROCANIC ACID AND FIGLU IN NEOPLASTIC DISEASE SIR,-Dr. Rose’s (Aug. 8) findings of low serum-folicacid levels in 9 out of 19 patients with acute or chronic leukaemia or reticulosis accord with the low serum-folate levels found by Kershaw and Girdwood1 in 9 out of 24 patients with leukaemia, reticulosis, or disseminated
malignancy. These workers also measured the urinary output of FIGLU after a histidine load in the same 24 patients. In only 5 was the output abnormal, and these did not include any of the leukxmia group. Rao et awl. also studied serum-folic-acid levels in various neoplastic diseases. They found average serum levels of 3-5 f].g. per ml. in a series of 38 patients with solid tumours as against levels of 5 f].g. per ml. in normal controls. The corresponding figures in lymphoma (8 patients) and leukaemia (9 patients) were 2-4 f].g. per ml. Magnus3 has similarly shown levels below 2-8 f].g. per ml. in 21 out of 28 patients with
disseminated malignancy. There seems little doubt from the above figures that low serum-folate levels are common in malignancy and that they are liable to be found when the disease is disseminated. Hepatic function was, in fact, assessed in my series of 28 patients (July 18). In 18 patients there was no evidence of liver dysfunction but in the remaining 10 patients the findings raised the possibility. The results of the investigation of these 10 patients are shown in the table.
of treatment, such
the
of T.H.A.M.
(tris-hydroxymethyl-aminomethane).5 I believe that ordinarily peritoneal dialysis is the treatment of choice, since it can be easily instituted without the experience required for exchange transfusion, and without the delay entailed in waiting for the blood. In addition, peritoneal dialysis may well carry fewer risks than exchange transfusion. as
use
s
Neurophysiology Department,
The Hospital for Sick Children, Great Ormond Street, London, W.C.1.
J. U. CRICHTON.
THIGH PAIN IN SUBPHRENIC ABSCESS
SIR,-Iwish to draw attention to the importance of increasing pain in the thigh as an early sign of a perinephric abscess. In the past three months several patients with subphrenic abscess were admitted to the department of urology with fever, thigh pain, and hip spasm. Because of the absence of abdominal signs, the original diagnosis was incorrect. The typical signs of fever, pyuria, and loin tenderness and fullness are well known. Zachary Cope has emphasised the importance of referred pain, hypersesthesia, and spasm of the iliopsoas and obdurator muscles in the diagnosis of acute abdominal condition.
When abdominal signs are slight or absent, the presence of increasing pain in the femoral triangle or outer thigh associated with hip spasm, pyuria, and fever should lead the clinician to the diagnosis of perinephric abscess. Department
of
Urology,
Newcastle General Hospital, Newcastle upon Tyne.
R. M.
JAMESON.
NEONATAL BACTERIAL INFECTION
SIR,-Thompson et al.,6I Williams," and we 9 10 have reported that neonatal staphylococcal disease is commoner All 10 patients who showed evidence of hepatic dysfunction excreted abnormal quantities of urocanic acid and formiminoglutamic acid, but 14 patients with similar excretions did not reveal any evidence of liver dysfunction. In a subsequent series of 11 patients, the bromsulphthaleinretention test was carried out as an additional means of assessing hepatic function: 9 of the 11 excreted abnormal quantities of histidine metabolites, but only 3 had any evidence of hepatic dysfunction, and 1 of these had a normal FIGLU test. results suggest that abnormal excretion of urocanic acid and formiminoglutamic acid occurs in most patients with hepatic disease. The high prevalence of an excessive output of these metabolites in patients with malignant disease-many of whom show no evidence of hepatic dysfunction-still awaits adequate explanation.
The
Department of Materia Medica and Therapeutics, University of Glasgow.
in males than females. We are unaware of similar observations concerning the sex-distribution of neonatal bacterial disease other than that caused by the
staphylococcus. Between July, 1957, and June, 1963, cultures were taken from all lesions occurring in the 14,717 infants born in the maternity wing of the Geelong and District Hospital. We have discussed elsewhere the occurrence of staphylococcal disease in these babies." 12 We have assessed the sex distribution of neonatal lesions yielding on culture a pure growth of an organism other than a staphylococcus (lesions yielding a mixture of organisms are not
included). In 402
cases
of
"sticky"
eyes the distribution
was
as
follows&midot;
IAIN W. DYMOCK.
ACUTE SALICYLATE POISONING
In 69
SIR,-Dr. Sweetnam (Aug. 15) may be correct in advocating the use of exchange transfusion in the treatment of salicylate intoxication, but distinction should be drawn between areas of easy communication (and hence rapid access to a skilled transfusion team and to adequate supplies of suitable blood), and areas where these conditions do not prevail. In North America, where salicylate intoxication seems to be a greater problem than in this country, there are more advocates of peritoneal dialysis,4 or newer methods 1. Kershaw, P. W., Girdwood, R. H. Scot. med. J. 1964, 9, 201. 2. Rama Rao, P. B., Lagerlof, B., Einhorn, J., Reizenstein, P. 1963, i, 1192. 3. Magnus, E. M. ibid. 1963, ii, 302. 4. Summitt, R. L., Etteldorf, J. N. J. Pediat. 1964, 64, 803.
Lancet,
cases
of infected umbilical cords the distribution was
as
fft11ftW:’&midot;
This
analysis shows that
an
increased
male/female
ratio
of neonatal bacterial disease is not neculiar to the staohvlo5. Kaplan, S. A. Amer. J. dis. Child. 1962, 103, 1. 6. Thompson, D. J., Gezon, H. M., Hatch, T. F., Rycheck, R. R., Rogers, K. D. New Engl. J. Med. 1963, 269, 337. 7. Thompson, D. J., Gezon, H. M., Hatch, T. F., Rycheck, R. R., Rogers, K. D. J. Pediat. 1963, 63, 869. 8. Williams, R. E. O. Lancet, 1964, i, 274. 9. Plueckhahn, V. D., Banks, J. ibid. p. 1042. 10. Plueckhahn, V. D. New Engl. J. Med. 1964, 270, 1201. 11. 12.
Plueckhahn, V. D. Brit. med. J. 1961, ii, 779. Plueckhahn, V. D., Banks, J. Med. J. Aust. 1963, ii, 519.