1293
nevertheless, I do
agree with previous correspondents that there is enough known to warrant further investigation by the means now available. I should be glad to hear from anyone 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 IN NEOPLASIA SIR,-I noted with interest the letter from Dr Ross and Dr Tyrrell (May 4, p. 871) since I have carried out a similar survey of viral infections of the skin in neoplastic disorders. My survey, however, included not only patients with carcinoma but also patients with a number of neoplastic disorders commonly associated with immunological deficiencies. The survey comprised patients with multiple myeloma (78), Hodgkin’s disease (159), malignant lymphoma (109), chronic lymphatic leukaemia (51) and
(156). In addition, 348 subjects attending a casualty department were examined as controls. They were all interviewed by me, using a questionnaire similar to that of Dr Ross and Dr Tyrrell. The results are in the accompanying table. carcinoma-sarcomas
PERCENTAGE OF PATIENTS WITH NEOPLASIA GIVING A HISTORY OF RECURRENT HERPES SIMPLEX AND HERPES ZOSTER
As in the previous report, recurrent herpes simplex was much less common in the carcinoma-sarcoma group than in the controls. Patients with multiple myeloma also have a low incidence. However, patients with Hodgkin’s disease, malignant lymphoma, and chronic lymphatic leukaemia have much the same incidence as the control group. In contrast, the incidence of herpes zoster in the Hodgkin’s/ lymphoma/C.L.L. group is strikingly increased compared with controls and patients with myeloma or carcinomasarcoma.
These results suggest that herpes zoster infection may well be related to incompetence of cell-mediated immune responses, since zoster is a feature of Hodgkin’s disease and perhaps also of the lymphomas and C.L.L. If the occurrence of herpes simplex was determined by immunological factors then patients with defective cell-mediated immunity (Hodgkin’s disease) and/or patients with defective humoral immunity (myeloma) would be expected to show an increased incidence. Clearly this is not so in my survey, and therefore there is no evidence from the results to suggest that simplex infection is related to immune function. Two previous surveys in immunosuppressed renal-transplant patients also failed to show an increase in the incidence of simplex infection,.1,2 That patients with carcinoma-sarcoma and multiple myeloma have a lowered incidence of herpes simplex is intriguing, but there is so far little support for an immunological
explanation. St. John’s Hospital for Diseases of the Skin, Lisle Street, London WC2. 1. 2.
WARWICK L. MORISON.
Spencer, E. S., Anderson, H. K. Br. Med. J. 1970, iii, 251. Rifkind, D. Experience in Renal Transplantation (edited by Starzl); p. 213. Philadelphia, 1964.
T. E.
HL-A TYPING AND CADAVER RENAL TRANSPLANTATION
Sm,—At the risk of feeding the controversy about the role of HL-A histocompatibility in cadaveric kidney-graft survival, I beg to present a national survey carried out in Belgium, which yielded results similar to those of Belzer et al.1 but different from those of Dausset et al .2z HL-A histocompatibility was estimated by the number of antigenic identities or incompatibilities, observed or calculated according to the method of Hors et al.,3 for 235 first cadaver-kidney transplants performed in Brussels, Ghent, Liege, and Louvain from 1970 to 1972, excluding technical failures only. Cross-reactions between antigens on the first and second loci were taken into account in the estimations. In more than 85% of lymphocytotoxicity typing determinations, using the method of Kissmeyer-Nielsen,44 at least 7 antigens on the first locus and 10 antigens on the second locus were screened. In 33% of the cases, the 4 antigens of the HL-A system were detected in the "donor and/or in the recipient of the graft, leading to the fullhouse " situation. No correlation was observed between the graft survival and the grade of compatibility whether cross-reactions between antigens were taken into account or not. Overall mean graft survival was 65% at one year and 55% at two years. These figures compare favourably with the data of the world’s Kidney Transplant Registry.5 Moreover, no relationship was found between graft survival and the presence or absence of preformed antibodies or the duration of preoperative dialysis period. Although I am unable to explain the discrepancies in the literature concerning the role of HL-A histocompatibility typing, I am struck by the fact that nearly all the data establishing this role have been issued by typing laboratories, while most transplant teams, along with Terasaki et al.,6 have reached the opposite conclusion. Much more work will be needed to establish a widely accepted policy for selection of recipients when a kidney donor 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-film showed no morphological evidence of infectious mononucleosis (i.M.), but the screening test for i.M. was positive. This made us a bit suspicious about the authenticity of screening tests for i.M., so we did a pilot screening test on random serum and ’Sequestrene’ plasma samples from outpatients over the age of 60 years, using two different kits commonly used in the laboratories (’ Monospot and ’Rythrotex ’). Of 22 cases, we found 5 sequestrene plasmas were positive by rythrotex. The sera from the same patients collected at the same time, however, were negative. Using monospot on the same sequestrene plasma and serum samples, we found all tests negative. Using known positive sera we found no false-negative results with either kit. 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. 1.