207 EFFECT OF BARIUM SULPHATE ON STRENGTH OF BONE CEMENT

SIR,-While investigating the mechanical properties of bone cement we

became

aware

that surgeons who

use

the

cement

during total hip replacement may have reservations about the addition of barium sulphate (BaS04) as a radto-opaciner on the grounds that this might reduce the cement’s mechanical performance. With CMW bone cement 5 g of barium sulphate can be added to 40 g of poly (methyl methacrylate) powder. The compressive (c.s.) and diametrical tensile (D.T.S.) strengths of cements of varying BaS04 content are in megapascals :

Now that the number of children with Wilms’ tumour who surviving after treatment is increasing rapidly, it is es-

are

pecially important

to

avoid unnecessary

morbidity from

treat-

ment, which in its extreme form may result in the death of the patient. It is also important to be aware of the combined effect

and cytotoxic drugs on normal tissues in the intensive regimens of treatment which are now being used in young children with malignant tumours.

of

radiotherapy

more

for Sick Children, London WC1N 3JH

Hospital

JANE

V. BOND

Mean:’:S.n.

zclw BaS04 on powder 0 10 12.5 15 20

D.T.S. ’MPa;

C.S. (MPa,) 108.5±5.2

344+_2.5 31.3+2.6 32.1+1.8 30.0+4.0 31.4±2.1

103.4±2.9 105.5±2.0 102.4±5.2 107.3+3.2

We conclude that the addition of

BaS04, certainly in the recommended by the manufacturers of CMW bone cement, does not significantly affect the mechanical strength of the set cement, at least in vitro. In the current International Standards Organisation discussions to draw up a specification for bone cement, the minimum acceptable compressive strength for bone cement has tentatively been fixed at 70 MPa. amount

Our research project is Council.

Postgraduate School in Polymer Science,

being

financed

by

the Science Research

of Studies

G. P. PEARSON K. S. LAI D. F. JONES

University of Bradford, Bradford BD7 1DP

RADIATION NEPHROPATHY the damage which may be caused to the kidney by injudicious irradiation cites a 1952 study which suggests that doses greater than 2300 rad in 5 weeks may cause renal damage.’ More recently reports have shown the importance of limiting the dose to the unaffected kidney in children with Wilms’ tumour, many of whom are very young at the time of treatment. In 1969 Mitus et al.2 reviewed the renal function in 108 children who had been irradiated after nephrectomy for Wilms’ tumour in Boston. They concluded that "normal renal function could be preserved in children with unilateral nephrectomy, irradiation and administration of antitumordrugs, provided that irradiation of the normal kidney was kept below 1200 rads." This dose was usually given over 2 weeks from a kilovoltage machine. They reported 3 children who developed acute radiation nephritis after doses of 2400 rad to the unaffected kidney, and drew attention to the risk of late chronic nephritis in children who have received radiotherapy to a normal kidney. D’Angio3 had drawn attention to the radiation potentiating effect of actinomycin as early as 1962. At the time of the Boston study all children were receiving actinomycin as a single agent, either in one postoperative 5-day course, or in repeated courses every 3 months. There was no difference in subsequent renal function between the two groups. The report from Arneil et a1.4 of acute radiation nephritis in 2 children again demonstrates the risks of radiotherapy to normal tissues in young children. One patient with a stage-i Wilms’ tumour received 1500 rad to the unaffected kidney and the other patient with a stage-m Wilms’ tumour received 2000 rad. Both children had one postoperative course of actinomycin and were later given weekly vincristine after completion of

SIR,-Your editorial of July 10 (p. 81)

POVIDONE-IODINE TOXICITY

SIR,-Blanco and Rothwell’ have missed the point of our article.2 We neither stated nor implied that the metabolic acidosis encountered after the use of topical povidone-iodine was the cause of death in our burn patients. We did state, however, that the presence of the acidosis complicated the management of these seriously ill patients. We have not proved that renal impairment is a consequence of the systemic absorption of povidone and iodine. On the other hand, the data presented by Blanco and Rothwell far from prove the converse to be true. In addition, we are not aware of a description of the pathological lesion characteristic of iodine toxicity. Only non-specific changes of congestion and cloudy swelling of the liver and kidney after iodine poisoning in animals and man have been described.34 It is therefore difficult to assess toxicity using routine pathological examination. In conclusion, we do not feel that the use of topical povidone-iodine is indicated in patients with large burns. The absorption of large quantities of povidone and iodine associated with metabolic acidosis in this setting may complicate an already difficult situation.

on

radiotherapy. 1. Kunkler, P B., Farr, R. F., Luxton, R. W. Br J. Radiol. 1952, 25, 190 2 Mitus, A., Tefft, M., Fellers, F. X. Pediatrics, 1969, 44, 912. 3 D’Angio.G J. Am. J. Rœntgenol. 1962, 87, 106. 4. Arneil, G. C., Emmanuel, I. C., Flatman, G. E., Harris, F., Young, D. G., Zachary, R. B. Lancet, 1974, i, 960.

Royal Victoria Hospital, Montreal, Quebec, Canada H3A 1AI

JONATHAN L. MEAKINS JOHN B. PIETSCH

FACTOR VIII INHIBITOR BYPASSING ACTIVITY

SIR,-Dr Pollock and Dr Lewis (July 3, p.43) have raised number of points concerning our report on the use of F.E.I.B.A. in a haemophiliac with inhibitors.5

a

We stated that there were no side-effects due to F.E.I.B.A. in patient, and we would like to clarify this. The plateletcount was low before the start of F.E.I.B.A. treatment and, though remaining low for the first five days of F.E.I.B.A. therapy at a time of heavy bleeding, it rose rapidly to normal

our

levels when bleeding stopped and remained normal despite continuation of F.E.I.B.A. The thrombin clotting-time was normal throughout and the serum fibrinogen/fibrin degradation product level showed only a transient rise during the period of heavy bleeding. We conclude that there was no evidence of disseminated intravascular coagulation due to F.E.I.B.A. We do not dispute that transhexanamic acid, a potent antifibrinolytic agent, may have contributed to cessation of bleeding from the abdominal drain sites; the liver is rich in fibrinolytic activator which may have contributed to failure of local hxmostasis, in the presence of devitalised liver tissue.67 However, once heavy bleeding had ceased the laparotomy wound and multiple deep lacerations and abrasions healed completely and uneventfully. During this period the only therapeutic 1. Blanco, C., Rothwell, K. G. Lancet, 1976, i, 911. 2. Pietsch, J., Meakins, J. L. ibid. p. 280 3. Finkelstein, R., Jacobi, M. Ann. intern. Med. 1937, 10, 1283. 4. Webster, S. H., Rice, M. E., Highman, B., Von Oettingen, W. F. J. Pharmac. exp. Ther. 1957, 120, 171. English, P J, Sheppard, E. M., Wensley, R. T. Lancet, 1976, i, 1299. Sandberg, H., Rezai, M., Bangayan, T., Bellet, S., Feinberg, L., Hunter, S. J. Lab Clin. Med. 1963, 61, 592. Longmire, W. P. Jr., Cleveland, R. J. Surg. Clins. N. Am. 1972, 52, 687.

5. 6.

208 agents used were transhexanamic acid and F.E.i.B.A. We do not believe that this striking demonstration of normal healing in our patient could be ascribed to transhexanamic acid alone. Pollock and Lewis in their patient were unable to demonstrate either in-vitro correction of abnormal clotting tests or clinical haemostasis after using F.E.I.B.A. In contrast, we obtained near complete correction of in-vitro clotting tests associated with an eventual satisfactory outcome, in an injury known to carry a high mortality in patients with normal haemostasis. We have since used F.E.I.B.A. in another patient where we have been able to demonstrate near complete correction of abnormal clotting tests in association with a useful clinical effect. From our two patients it might appear that correction of abnormal clotting tests is prerequisite for the successful clinical use of F.E.i.B.A. Department of

Clinical

Hæmatology,

Royal Infirmary, Manchester M13 9WL

P. J. ENGLISH E. M. SHEPPARD R. T. WENSLEY

CHILDHOOD SEIZURES

SIR,-In Harrison and Taylor’s follow-up of the social and medical outcome of childhood seizures, the children were originally identified only on the basis of having had "at least one seizure in early childhood". Although one gets the impression that the material covers most of the children with seizures in the Oxford area between 1948 and 1953, it is not clearly stated whether the series is strictly unselected. We have just finished an epidemiological study in Gothenburg on children, born in 1956 and 1957, with seizure disorders. The series was collected through the electroencephalogram (E.E.G.) reports from the only neurophysiological laboratory in Gothenburg, and in the follow-up none was lost. Seizures appearing in the neonatal period only and febrile convulsions before the age of 5 years only were not included because we knew that E.E.G. was not always done in such cases; otherwise the series was complete and unselected. We took one or more seizures at age 1 month to 15 years as the basis for the material. 175 children (40 with one seizure only, 135 with epilepsy) were found, giving a frequency of 14.7per 1000 (3-77 for those with one seizure only, and 11 for those with epilepsy) in the population less than 16 years of age. There are some interesting similarities and differences between Harrison and Taylor’s study and ours. The mortality in their material was 10-1% (29-5% of all deaths were caused by convulsions) while the corresponding figure in our material was only 5-1%, and none died in convulsions. Harrison and Taylor found that 17-5% were "completely or semi-illiterate", a figure identical to our material. Those with continuing epilepsy represented 24.2% of their sample, 24.77% in ours. There are remarkable similarities between Oxford and Gothenburg with regard childhood seizures. We also agree with the Oxford workers’ impression that epilepsy is commonly "regarded as a frightening illness". We did miss, however, a further analysis in Harrison and Taylor’s material. Probably the result would have been the same as in our study and Brorson’s2—namely, that poor prognosis of epilepsy is correlated to the presence of abnormal neurological signs and/or mental retardation. In children with normal intelligence and normal physical examination there is in contrast no reason to be frightened for the prognosis. Furthermore, drug treatment is now more effective. Perhaps Cohen’s statement3 that 80% of people with epilepsy can live normally will soon no longer be in Harrison and Taylor’s words, "an artefact of the viewer’s location". Department of Pædiatrics, Östra Sjukhuset, Gothenburg, Sweden

LEVAMISOLE AND CELL-MEDIATED IMMUNITY AND SERUM-IMMUNOGLOBULINS IN RHEUMATOID ARTHRITIS

far with levamisole in rheumatoid arthritis (R.A.) confusing. Encouraging benefit has been reported;’ -4 but Dinai and Prasin a double-blind controlled trial, observed no improvement and even suggested deleterious effect with levamisole. We treated a selected group of 20 patients (ages 25-76) with severe active R.A. and skin anergy to tuberculin and D.N.C.B. Levamisole (’Decaris,’ Gedeon Richter Ltd, Hungary) was given in a single daily dose of 150 mg over four weeks. Skin tests and serum levels of IgG, IgA, and IgM were compared before and after treatment. After treatment, a definitely positive skin response to tuberculin was restored in 60% of cases. The reversion of skin anergy to D.N.C.B. was less frequent (30%). Initially high mean serum levels of IgG, IgA, and IgM fell during treatment (see accompanying table). The mean decrease in IgG was significant. The accompanying figure shows that most pronounced fall in immunoglobulin was in cases with extremely high pretreatment values. Clinical improvement, evaluated by duration of morning stiffness, degree of joint swelling, and quantity of analgesic drugs needed, was observed in 11 patients and was considerable in 8. No improvement was seen or even some deterioration occurred in 9 patients. Levamisole induced neither side-effects nor changes in blood-cell counts during the period of observation. We conclude that the effects of of levamisole in man are not limited to enhancement of cell-mediated immunity. In R.A.,

SIR,-Results

so

are

Schuermans, Y Lancet, 1975, i, 11 Basch, C. M., Spiter, L. E., Engelman, E. P. Arthr. Rheum 1975, 18, 385 Huskisson, E. C., Scott, J., Balme, H W., Dieppe, P. A , Trapnell, J., Willoughby, D. A Lancet, Feb 21, 1976, p.393 4. Veys, E N., Mielants, H., de Bussere, A., Decrans, L., Gabriel, P. ibid. Apnl 10, 1976. p. 808. 5. Dinai, Y., Pras, D. M. ibid. 1975, n, 556.

1

2. 3.

G. HAGBERG O. HANSSON

1. Harrison, R. M., Taylor, D C Lancet, 1976, i, 948. 2 Brorson, I.. O in T he Care of Epileptics in Swedish). The National Board of Health and Welfare, Stockholm 1970. 3 Cohen. Br med J 1958, ii, 672

Serum-immunoglobulins (Úó levaniisole

treatment.

of

mean

control

value) before and after