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nevertheless, I do agree with previous correspondents thatthere is enough known to warrant further investigation bythe means now available. I should be glad to hear fromanyone interested in any aspect of this problem.Physiology Department,

University College,P.O. Box 78,

Cardiff CF1 XL. V. R. PICKLES.

HERPES SIMPLEX AND HERPES ZOSTER INNEOPLASIA

SIR,-I noted with interest the letter from Dr Ross andDr Tyrrell (May 4, p. 871) since I have carried out asimilar survey of viral infections of the skin in neoplasticdisorders. My survey, however, included not only patientswith carcinoma but also patients with a number of neo-plastic disorders commonly associated with immunologicaldeficiencies. The survey comprised patients with multiplemyeloma (78), Hodgkin’s disease (159), malignant lym-phoma (109), chronic lymphatic leukaemia (51) andcarcinoma-sarcomas (156). In addition, 348 subjectsattending a casualty department were examined as controls.They were all interviewed by me, using a questionnairesimilar to that of Dr Ross and Dr Tyrrell. The resultsare in the accompanying table.

PERCENTAGE OF PATIENTS WITH NEOPLASIA GIVING A HISTORY OF

RECURRENT HERPES SIMPLEX AND HERPES ZOSTER

As in the previous report, recurrent herpes simplex wasmuch less common in the carcinoma-sarcoma group thanin the controls. Patients with multiple myeloma also havea low incidence. However, patients with Hodgkin’s disease,malignant lymphoma, and chronic lymphatic leukaemiahave much the same incidence as the control group. Incontrast, the incidence of herpes zoster in the Hodgkin’s/lymphoma/C.L.L. group is strikingly increased comparedwith controls and patients with myeloma or carcinoma-sarcoma.

These results suggest that herpes zoster infection maywell be related to incompetence of cell-mediated immuneresponses, since zoster is a feature of Hodgkin’s diseaseand perhaps also of the lymphomas and C.L.L. If theoccurrence of herpes simplex was determined by immuno-logical factors then patients with defective cell-mediatedimmunity (Hodgkin’s disease) and/or patients with defec-tive humoral immunity (myeloma) would be expected toshow an increased incidence. Clearly this is not so in

my survey, and therefore there is no evidence from theresults to suggest that simplex infection is related to

immune function. Two previous surveys in immuno-suppressed renal-transplant patients also failed to show anincrease in the incidence of simplex infection,.1,2 Thatpatients with carcinoma-sarcoma and multiple myelomahave a lowered incidence of herpes simplex is intriguing,but there is so far little support for an immunologicalexplanation.

St. John’s Hospital forDiseases of the Skin,

Lisle Street,London WC2. WARWICK L. MORISON.

1. Spencer, E. S., Anderson, H. K. Br. Med. J. 1970, iii, 251.2. Rifkind, D. Experience in Renal Transplantation (edited by T. E.

Starzl); p. 213. Philadelphia, 1964.

HL-A TYPING AND CADAVERRENAL TRANSPLANTATION

Sm,—At the risk of feeding the controversy about therole of HL-A histocompatibility in cadaveric kidney-graftsurvival, I beg to present a national survey carried out inBelgium, which yielded results similar to those of Belzeret al.1 but different from those of Dausset et al .2 z

HL-A histocompatibility was estimated by the number ofantigenic identities or incompatibilities, observed or calcu-lated according to the method of Hors et al.,3 for 235 firstcadaver-kidney transplants performed in Brussels, Ghent,Liege, and Louvain from 1970 to 1972, excluding technicalfailures only. Cross-reactions between antigens on thefirst and second loci were taken into account in the estima-tions. In more than 85% of lymphocytotoxicity typingdeterminations, using the method of Kissmeyer-Nielsen,4 4at least 7 antigens on the first locus and 10 antigens on thesecond locus were screened. In 33% of the cases, the 4antigens of the HL-A system were detected in the donorand/or in the recipient of the graft, leading to the

" full-house " situation.No correlation was observed between the graft survival

and the grade of compatibility whether cross-reactionsbetween antigens were taken into account or not. Overallmean graft survival was 65% at one year and 55% at twoyears. These figures compare favourably with the data ofthe world’s Kidney Transplant Registry. 5 Moreover,no relationship was found between graft survival and thepresence or absence of preformed antibodies or the dura-tion of preoperative dialysis period.Although I am unable to explain the discrepancies in

the literature concerning the role of HL-A histocompati-bility typing, I am struck by the fact that nearly all thedata establishing this role have been issued by typinglaboratories, while most transplant teams, along withTerasaki et al.,6 have reached the opposite conclusion.Much more work will be needed to establish a widelyaccepted policy for selection of recipients when a kidneydonor becomes available.

Department of Internal Medicine,Brugmann Hospital,Brussels, Belgium. P. VEREERSTRAETEN.

FALSE-POSITIVE SCREENING TESTS FOR

INFECTIOUS MONONUCLEOSIS

SIR,—In our experience, on many occasions a blood-filmshowed no morphological evidence of infectious mono-nucleosis (i.M.), but the screening test for i.M. was positive.This made us a bit suspicious about the authenticity ofscreening tests for i.M., so we did a pilot screening test onrandom serum and ’ Sequestrene’ plasma samples fromoutpatients over the age of 60 years, using two differentkits commonly used in the laboratories (’ Monospotand ’ Rythrotex ’).Of 22 cases, we found 5 sequestrene plasmas were positive

by rythrotex. The sera from the same patients collectedat the same time, however, were negative. Using mono-spot on the same sequestrene plasma and serum samples,we found all tests negative. Using known positive serawe found no false-negative results with either kit.

1. Belzer, F. O., Formann, J. L., Salvatierra, O., Perkins, H. A.,Kountz, S. L., Cochrun, K. C., Payne, R. Lancet, April 27,1974, p. 774.

2. Dausset, J., Hors, J., Bresson, M., Festenstein, H., Oliver, R. T. D.,Paris, A. M. I., Sachs, J. A. New Engl. J. Med. 1974, 290, 979.

3. Dausset, J., Feingold, N., Fradelizi, D. Lancet, 1971, i, 609.4. Kissmeyer-Nielsen, F., Kjerbye, K. E. in Histocompatibility

Testing (edited by E. S. Curtoni, P. L. Martin, and R. M. Tosi);p. 381. Copenhagen, 1967.

5. A.C.S./N.I.H. Organ Transplant Registry. Spring Newsletter,1973. Chicago, Illinois.

6. Terasaki, P., Mickey, M. R. Transplant Proc. 1971, 3, 1057.

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Therefore we conclude: (1) there is a high degree ofspecificity with both methods if serum is used, as suggestedin the method provided with the kit; (2) sequestreneplasma should not be used for i.M. screening by rythrotexkit, since we have had a high incidence of false positives(about 20%).Although serum samples should be preferred for I.M.

screening tests, sequestrene plasma may be used with afair degree of accuracy with monospot, which gave con-sistent results with both serum and plasma samples inour study.Department of Hæmtology,

Burton Hospitals,Burton on Trent DE13 0RB. MARGARET E. BUCKLEY.

TRANSIENT OLIGURIA DUE TOPERITONEAL DIALYSIS

SIR,-Transient oliguria follows peritoneal dialysis.11 patients had severe impairment of renal function;

their urea clearances were 0-7-2-5 (mean 2-0, standardderivation 0-84) ml. per minute. One patient had severeurxmia caused by hypotension secondary to dehydrationand recovered quickly. Her urea clearance, measuredsubsequently, was 70 ml. per minute.

22 peritoneal dialyses were performed using a pro-

prietary dialysate solution constituted as follows: sodium

141, chloride 101, calcium 3-5, magnesium 1-5, and lactate45-0 meq. per litre. Potassium was added according to theclinical requirements of the situation, in a concentration of4-0 meq. per litre, or was omitted completely. The solu-tion contained dextrose 15% except in 4 dialyses whereextra dextrose was added, thus raising the concentrationto 7-0%, in order to facilitate the removal of fluid. The

TABLE I-MEAN DAILY URINE OUTPUTS (ml. PER 24 HOURS) INCONTROL SITUATION AND DURING AND AFTER PERITONEAL

DIALYSIS

TABLE II-URINE OUTPUT (ml. PER 24 HOURS) DATA DURINGCONTROL PERIOD AND DURING DIALYSIS

* Difference statistically significant at p < 0-0005. Student’s t test.

TABLE III-RELATIONS BETWEEN BLOOD-UREA AND FALL IN URINE

OUTPUT

mean duration of dialysis was 35 hours. The mean negativefluid balance was 6-1 litres.The results are shown in tables 1-111. The urine output

falls as peritoneal dialysis proceeds. The minimum valuesare approximately one-third of the control values. Thereduction in the urine output was statistically significantat the level P=0.0005. Oliguria developed in all cases.

The urine outputs returned to the control values withinthree days of the end of a peritoneal dialysis. Table Hshows the figures for the whole group of patients. There isconsiderable individual variation, which may reflect lackof clinical uniformity among the cases or in the duration ofdialysis. Table in shows the fall in the blood-urea producedby the dialysis and also the simultaneous fall in the urineoutput. The coefficient of correlation between these twosets of values is r= +0-446 (significant at the level P=0.05).

I suggest that the oliguria during and after peritonealdialysis is due to the dialysis, which by reducing the bloodurea and osmolarity causes a fall in the filtered osmoticload delivered to the renal tubules. If this is true, then thechange in the blood-urea should be related to the change inthe urine output. The observed coefficient of correlationwas r=+0.446 (P=0.05). There was no obvious correla-tion between the degree of oliguria and the urea clearance,the size of the negative fluid balance achieved, or theduration of the dialysis. There was no significant correla-tion at the 5% probability level between the oliguria andthe pre-dialysis blood-urea or the post-dialysis blood-urea.

It is most important that the presence of oliguria duringand after peritoneal dialysis is fully appreciated. In thisphase, unless great care is taken in restricting the patient’sfluid intake, in the expectation of oliguria, considerablefluid retention will occur-possibly to the extent of neces-sitating further dialysis.

I thank Prof. B. Richards (University of Manchester Instituteof Science and Technology) for help in performing statisticalanalyses and for advice; and Dr A. J. Ralston (UniversityHospital of South Manchester) for permission to study hispatients and for help in preparing this communication.

University Hospital ofSouth Manchester. G. M. YUILL.*

*Present address: Crumpsall Hospital, Manchester 8.

MISUSE OF THE CHI-SQUARED TESTSIR ; Adams et al. reported the first placebo-controlled,

cross-over study showing a beneficial effect of pyridoxine(vitamin B6) in super-dietary amounts upon a mood changepresumably induced by oral contraceptives.i We havebeen interested in this subject 2 and would like to commenton the statistical methods used in the report.The table showing clinical response to administration

of pyridoxine or placebo (table vi) presents the data asthough there were two independent samples of 11 womeneach in the vitamin-B6-deficient group (and similarly, twoindependent samples of 11 women each in the non-vitamin-B6-deficient group). If there were really two independentsamples of 11 women in the deficient group, the x2 testwould be appropriate. Adams et al. omitted the continuitycorrection (1/2) which, however, does not significantlychange the p values obtained. However, because of thesmall sample sizes, not all the theoretical values were atleast five. Thus Fisher’s exact test would have been theappropriate analytical method.More importantly, since, according to the experimental

design, there were only 11 women in the vitamin-Be-defi-cient group, each of whom was alternately on pyridoxine1. Adams, P. W., Wynn, V., Rose, D. P., Seed, M., Folkard, J.,

Strong, R. Lancet, 1973, i, 897.2. Luhby, A. L., Brin, M., Gordon. M., Davis, P., Murphy, M.,

Spiegel, H. Am. J. clin. Nutr. 1971, 24, 684.