778

cryoglobulins. To prevent the formation of new immunoglobulins and antibodies low-dose corticosteroid therapy was started. 2 weeks later the patient left hospital with her S.L.E. in stable remission, clinically and on laboratory findings; bodies

or

her cold rash life.

was

in clinical

remission, for the first time in her

not

be recommended

B. K. SHURKALIN S. L. AGEYEV V. A. PITENOV R. M. BALABANOVA Z. S. ALEKBEROVA

Department of Hæmosorption, 2nd Moscow Medical Institute, Moscow, U.S.S.R.

PEPTIC ULCER AFTER RENAL TRANSPLANTATION

SIR,-In discussing peptic ulcer after renal transplantation (Feb. 17, p. 366) you omit important facts and make some

questionable recommendations. There is evidence that high frequency and mortality from upper gastrointestinal complications after transplantation is associated with high dose maintenance prednisolone (50-400 mg) in the early postoperative period.’ The simple measure of adopting a low dosage prednisolone regimen (20 mg) from the first day after operation is likely to greatly reduce this problem, and is an effective means of immunosuppression.2 We feel this point deserves greater emphasis. With regard to pre-transplant gastric assessment, it is true that dyspeptic symptoms, pentagastrin tests, and barium meal examinations are of limited value. However, the combined use of endoscopic and radiological investigation before operation showed ulcer craters or scars in 34 of 131 (26%) patients accepted for the Belfast transplant programme.’ While the influence of post-transplant corticosteroids may add some de novo ulceration, the size of this contribution is likely to be small as judged from the figures given by Conn and Blitzer.3 Most "acute" ulcers after renal transplantation are therefore likely to represent steroid-induced exacerbations of pre-existing disease. Screening of the transplant candidate thus will identify the majority of at-risk patients likely to benefit from prophylactic treatment. Some ursemic patients with ulcer have acid hypersecretion and plasma gastrin levels in the ZollingerEllison range, and in such patients ulcer disease may run a severe clinical course;4 there is, however, little use for routine measurement of gastric acid or plasma gastrin. Gastric acid output may show minor short-term fluctuations after transplantation,5 but in the long-term the peak acid output shows a significant tendency to decline.6 This latter observation further strengthens arguments’ against prophylactic ulcer surgery before transplantation, but we do not believe that the correct alternative instead is to give prophylactic cimetidine to all patients, as you suggest. Prevention of upper gastrointestinal complications in renal

transplant patients can be more logically achieved by pretransplant gastric assessment, administration of prophylactic cimetidine to those who have peptic ulcer, and use of a low

dosage prednisolone regimen. Cimetidine is not free from sideeffects, should only be given for specific indications, and can1.

Doherty, C. C., McGeown, 15, 361.

M. G. Proc. Eur.

Dialy. Transpl. Assoc. 1978,

2. McGeown, M. G. Lancet, 1973, i, 310. 3. Conn, H. O., Blitzer, B. L. New Engl. J. Med. 1976, 294, 473. 4. Doherty, C. C. M. D. thesis. 1978, Queen’s University of Belfast. 5. Chisholm, G. D., and others Br. med. J. 1977, i, 1630. 6. Doherty, C. C. Irish J. med Sc. 1978, 147, 376. 7. Doherty, C. C., O’Connor, F. A., Buchanan, K. D., Sloan, McGeown, M. G. Proc. Eur. Dialy. Transpl. Assoc. 1977, 14,

J., Ardill, J., 386.

routine third

drug for

renal

trans-

plant patients. Renal Unit, Belfast City Hospital, Belfast BT9 7AB

Plasmaperfusion through charcoal may make it possible to avoid the undesirable consequences of long-term corticosteroid therapy in such patients. Y. M. LOPUKHIN M. N. MOLODENKOV N. G. EVSEYEV

as a

CIARAN C. DOHERTY MARY G. MCGEOWN

RENAL TRANSPLANTATION IN DIABETICS

SIR,—Dr Deppermann and Professor Ritz (Jan. 6, p. 41) that the initial impressionl.2 that diabetes mellitus represented a specific indication for renal transplantation was not supported by a recent Scandinavian series3 and that the view of the Scandinavian workers is supported by recent reports from other transplant centres.4-6 Among the three literature

state

sources

cited, two were from this institution.4,6 interpretation of Deppermann and

I do not agree with the

Ritz of their results or with the conclusions they draw from our reported results. Workers here still believe that diabetes mellitus represents a specific indication for renal transplantation and that transplantation is superior to chronic hasmodialysis. Three-year patient survival is 85%, 74%, and 52% when sibling donors, parent or offspring donors, and cadaveric donors, respectively, are used.’ These results are similar to those reported by the Human Renal Transplant Registry for non-diabetic patients and comparable to those reported by the European Dialysis and Transplant Association for patients on hxmodialysis. Furthermore, the diabetic patient with a functioning graft has a greater chance for rehabilitation than has the patient on ha’modialysis. Thus, since survival-rates of diabetic patients on hæmodialysis remain dismal, renal transplantation of the diabetic patient with kidneys from living related or cadaveric sources remains the treatment of choice.6-8 Mayo Clinic,

Rochester,

Minnesota 55901, U.S.A.

HORST ZINCKE

STREPTOCOCCUS FÆCALIS URINARY-TRACT INFECTION AND RENAL-ALLOGRAFT REJECTION

SIR,-We were intrigued by the report of Byrd et a1.9 of an association between Streptococcus fcecalis urinary infection and graft rejection in kidney transplantation. This prompted us to look at our own data-the records of 140 patients receiving primary cadaver kidneys between 1971 and 1975. Complete data could not be obtained in 3 patients only, leaving 137 for analysis. We arbitrarily defined Strep. fcecalis urinary infection as >105 organisms/ml in at least one midstream urine specimen. 19 patients had Strep. fcecalis urinary infection in the first month after transplantation. 8 further patients had infections in months 2-12. 110 patients did not have a Strep. fcecalis infection in the first year after transplantation. Of those graft recipients with proven Strep. fa-calis urinary infection in the first postoperative month, 7/19 (37%) had 1.

Kjellstrand, C. M., Simmons, R. L., Goetz, F. C., Buselmeier, T. J., Shideman, J. R., Hartitzsch, V. B., Najarian, J. S. Lancet, 1973, ii, 4. 2. Kjellstrand, C. M., Shideman, J. R., Simmons, R. L., Buselmeter, T. J., Hartitzsch, V. V., Goetz, F. C., Najarian, J. S. Kidney Int. 1974, 6, suppl. p. 15. 3. Joint Scandinavian Report Lancet, 1978, ii, 915 4. Mitchell, J. C. Mayo Clinic Proc. 1977, 52, 281. 5. Totten, M. A., Izenstein, B., Gleason, R. E., Kassissieh, S. D, Libertino, J. A., D’Elia, J. A. Kidney Int. 1977, 12, 492. 6. Zincke, H., Woods, J. E., Palumbo, P. J., Leary, F. J., Johnson, W. J. J. Am med. Ass. 1977, 237, 1101. 7. Zincke, H., Woods, J. E., Sterioff, S., Johnson, W. J., Palumbo, P. J, Mitchell, J. C., Frohnert, P. P., Anderson, C. F., Service, F. J., Leary, F J Transplantation Proc. (in the press). 8. Woods, J. E., and others. Lancet, 1972, ii, 795. 9. Byrd, L. H., Cheigh, J. S., Stenzel, K. H., Tapia, L., Aronian, J, Rubin, A. L. Lancet, 1978, ii, 1167.

779

graft failure in the first year compared with 35/110 (32%) with no Strep. fcccalis urinary infection, graft-loss rates due to rejection being 5/19 (26%) and 22/110 (20%), respectively. These differences are not significant. Our analysis is, of course, open to many criticisms-many of which could also be applied to the study of Byrd and coworkers. Both studies are retrospective, the analysis of the significance of urinary infection in the first year is limited to urinary infections in the first month only, and, perhaps most importantly, the definitions of urinary-tract infection in both studies are arbitrary. This interesting question will only be answered, we believe, by prospective studies where the presence or absence of Strep. fœcalis urinary infection in doubtful cases is confirmed or excluded by suprapubic bladder aspiration. Department of Nephrology, Royal Melbourne Hospital, Parkville, 3050 Victoria, Australia

JUDITH A. WHITWORTH A. J. F. D’APICE PRISCILLA KINCAID-SMITH

PREVENTION OF ANTIBLASTIC NEUTROPENIA WITH LITHIUM CARBONATE et al.1 have described the use of lithium in of granulocytopenia caused by antiblastic treatment for acute myeloid leukaemia (A.M.L.) and Gupta et al .2 gave oral lithium salts to stimulate granulocytopoiesis in patients with Felty’s syndrome. We have used lithium to prevent or treat the neutropenia caused by antiblastic chemotherapy in patients with solid tumours and lymphoma. So far we have treated fifty patients with daily doses of 900 mg/day of lithium carbonate, divided in three doses, and have checked the serum lithium levels once or twice a week in the first three weeks to

(sumarised in the table) wasçèvaluated by comseverity of the neutropenia in tlie two lithium and control groups before and after the first cycle of chemotherapy. In the nine lithium-treated patients the white-blood-cell count (by 17.3%) and the neutrophil-count (by 29.6%) both rose after chemotherapy, while in the nine controls both the whiteblood-cell count (by 25.3%) and the neutrophil-count (by 20-3%) fell, the differences between the two groups being significant (P

Streptococcus faecalis urinary-tract infection and renal-allograft rejection.

778 cryoglobulins. To prevent the formation of new immunoglobulins and antibodies low-dose corticosteroid therapy was started. 2 weeks later the pati...
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