1419
parts of Africa would not consider letting their children be admitted at all unless they could accompany them. The
suggested " emphasis ...
on
much
improved outpatient
services " is unrealistic unless the home conditions able and the mother is
capable
of
carrying
out
are favourthe necessary
nursing procedures. Halesowen, Worcestershire.
J. TWOMEY.
DELAYED HYPERSENSITIVITY IN LEPROSY SIR,-The article by Dr. Waldorf and his associates (Oct. 8; p. 773) provides partial confirmation of the previous observation1 of the U.S. Naval Medical Research Unit no. 2, Taipei, Taiwan, that the capacity to manifest contact allergy to a haptenic substance is impaired in persons with leprosy. Unfortunately, they are not correct in asserting that our study failed to establish the incidence of sensitivity to hapten (picryl chloride) and other antigens " in a comparable control population ". As specifically stated in the abstract, a non-leprous control group of 30 volunteers was tested with all antigens used in a group of 107 leprosy patients. That the incidence of sensitivity to these antigens must have been determined in the normal control group was implicit in the use of tests of statistical significance for validation of group comparisons. Dr. Waldorf and his associates emphasise an apparent difference in reactivity to 2,4-dinitrochlorobenzene (D.N.C.B.) detected between 17 lepromatous patients without erythema nodosum leprosum (E.N.L.) and 7 with E.N.L. In our study of 54 lepromatous patients, 36 were without E.N.L. and 13 of these developed sensitivity to picryl chloride; 10 of 18 patients with E.N.L. became sensitised. Differences between the two groups in the proportion of individuals sensitised were not significant on X2 analysis. Both groups differed significantly (P<0-01) from the normal control group wherein 28 of 30 individuals became sensitised. In view of these findings further studies will be necessary before the capacity to manifest contact-type allergy can be assessed as a possible immunological marker for those with E.N.L. Although many consider E.N.L. to be a form of hypersensitivity reaction, there is, as yet, no solid evidence to support the concept that immunological responsiveness is fundamentally different between those who do or do not happen to have E.N.L. Lacking tuberculoid patients for study, Dr. Waldorf and his associates have overextended their data in order to make the assumption that patients with pure tuberculoid leprosy would also react normally to contact allergens. The finding of positive skin tests to D.N.C.B. in 4 patients with dimorphous leprosy said only to be clinically closer " to tuberculoid leprosy provides little support for such a supposition. Again, in work with picryl chloride, I noted the incidence of reactivity to this hapten to be significantly less in 53 tuberculoid patients than in normal controls. Other studies of delayed hypersensitivity to purified protein derivative of tuberculin and antigens of Candida albicans 23 also provide evidence for a relative impairment of the delayed hypersensitivity response in tuberculoid "
Dr. Bullock states in his letter, 30 volunteers were studied as a " non-leprous control group". Although our findings are generally in agreement with those of Dr. Bullock, there are some areas where our results differ, perhaps owing to use of different antigens, testing techniques, patient-population, or kind of patient-classification. We wish to compliment Dr. Bullock on his extensive investigations and we are confident he would agree that more intensive exploration in this area is necessary. Department of Dermatology, New York University School of Medicine, DONALD S. WALDORF. New York. National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. JOHN N. SHEAGREN. United States Public Health Service San Francisco, California.
Hospital,
United States Public Health Service
Hospital,
Baltimore, Maryland.
JOHN R. TRAUTMAN. JEROME B. BLOCK.
VITAMIN-B12 DEFICIENCY IN PSYCHIATRY
SIR,-We were interested in the article by Dr. Henderson and his colleagues (Oct. 15, p. 809), and in the ensuing letters from Mr. Hansen and his co-authors (Oct. 19, p. 965) and Dr. Reynolds and Dr. Matthews (Nov. 5, p. 1024). The objection raised by Dr. Reynolds and Dr. Matthews, that the antigastricantibody (A.G.A.) test is an inadequate screening test of all causes of vitamin-B12 deficiency, is extremely pertinent. They mention anticonvulsant-drug-induced disturbances of folate and vitamin-B12 metabolism. A further cause is vitamin-B,2 deficiency occurring as a long-term complication of partial gastrectomy.l2 This may result in neurological sequelae such as subacute combined degeneration of the cord 34 and confusional states.5 It might be expected therefore that some of these postpartial-gastrectomy patients are now being referred to psychiatric hospitals. In a survey over the past year of patients admitted to St. Patrick’s Psychiatric Hospital, Dublin, with confusional and depressive symptoms, one of us (M. G. T. W.) has found serum-vitamin-B12 deficiency in 13 out of 50 patients assessed. We have investigated these 13 patients by determining the acid and intrinsic-factor secretion during the augmented histamine test and by estimation ofvitamin-B12 absorption by the Schilling method. 8 of these patients had malabsorption of vitamin B12 associated with achlorhydria and intrinsic-factor secretion of less than 200 ng. vitamin-Bl2 units.2 of these patients had had a partial gastrectomy eight and ten years previously; in neither of these patients would the A.G.A. screening-test have been positive. We consider that any patient admitted to a psychiatric hospital who has previously had a partial gastrectomy should have the serum-vitamin-B12 level estimated. Department of Clinical Medicine, D. G. WEIR. Trinity College, Dublin. St. Patrick’s Hospital, Dublin.
M. G. T. WEBB.
leprosy. University of Rochester School of Medicine and Dentistry, 260 Crittenden Boulevard, New York 14620.
WARD E. BULLOCK, Jr.
*** This letter has been shown to Dr. Waldorf and his co-authors, whose reply follows.-ED. L.
SIR, We wish to thank Dr. Bullock for his comments on our paper and also for providing details of his work not reported in his original abstract. Our statement, made in reference to this abstract, that " the incidence of sensitivity ... in a comparable control population was not determined ..." is incorrect, for, as 1. Bullock, W. E., Jr. Clin. Res. 1966, 14, 337. 2. 3.
Guinto, R. S., Mabalay, M. C. Int. J. Lep. 1962, 30, 278. Buck, A. A., Hasenclever, H. F. Am. J. Hyg. 1963, 77, 305.
MEASUREMENT OF GASTRIC ACIDITY SIR,-Professor Lubran (Nov. 12, p. 1070) recommends titrating aspirated gastric juice to pH 3-5 in order to measure " strong acid ". As far as I know, the measurement of " strong acid " is notionally impossible and in any case presupposes a relation to parietal-cell function which is certainly not proven. When we titrate gastric juice to an end-point of pH 7 or 7-4, we assume that all the excess hydrogen ions are derived from the parietal cells. While this may not be true, and while acids such as the bound aminoacids and sialic acid may be secreted 1. 2.
3. 4. 5. 6.
Deller, D. J., Witts, L. J. Q. Jl Med. 1962, 31, 71. Weir, D. G., Temperley, I. J., Gatenby, P. B. B. Ir. J. med. Sci. 1966, p. 97. Weir, D. G., Gatenby, P. B. B. Br. med. J. 1963, ii, 1175. Williams, J. A. The Small Intestine; p. 42. Oxford, 1965. Olivarius, B. de F., Roos, D. Lancet, 1965, ii, 1298. Webb, M. G. T., Weir, D. G. Unpublished.