1057
technique
are
be responsible. In this investigataken with all the samples and we think that the negative cultures were
held
to
tion great therefore do not chance occurrences. There is evidence that T.F. produced some change in responsiveness in subacute sclerosing panencephalitis,14 but brain damage was not affected. Perhaps the damage was already too severe. Slightly affected c.M.v.-infected infants in whom progressive brain damage might be prevented are more likely to benefit from T.F. treatment. We intend to study viruria and any possible clinical effects during a controlled trial of T.F. treatment in such infants. care was
Results of urine culture for C.M.V. (+=positive culture and 0=negative culture) and 48-hour skin-test response to P.P.D. and candida antigen in three patients given two doses (T.F.1 and T.F.2) of transfer factor. Time in days is shown from the day OFT.F. .1.
real. In patients 2 and 3 there was no consistent in antibody to c.M.v. after treatment.
change
We thank Dr S. Lewis and Dr E. de H. Lobo for referring patients; Dr H. Valdimarsson, Dr T. E. Cleghorn, and Mrs. Lorna Layward for advice and help; Mrs Angela Perry for secretarial assistance; and the Wellcome Trust (W.C.M.) and the Medical Research Council (I.T.T.) for financial support. Requests for reprints should be addressed to J. F. S., Institute of Child Health, 30 Guilford Street, London WC IN 1EH.
REFERENCES
DISCUSSION
reported to be of benefit in mucocutaneous candidiasis" and hepatitis-B-virus carriage,9 it might be expected to be useful in chronic infection by intracellular organisms; however, there is no conclusive controlled evidence on this point. The mechanism for chronicity in congenital virus infections remains uncertain. T.F. had no obvious beneficial action in congenital hepatitis-B-virus infection,9 but our data, which suggest brief suppression of viruria in congenital c.M.v. are encouraging. Any such beneficial effect of T.F. may not work by the antigen-specific mechanism as claimed by Lawrence. Improvement of c.M.v. retinitis after T.F., with fall in titre of urinary virus excretion, in an immunosuppressed adult recipient of a kidney graft12 has also been reported (a similar effect has been reported with interferon ) 13 The kidney-graft recipient and some patients with mucocutaneous candidiasis had apparent exacerbation of their lesions immediately after T.F. injections, before improvement followed, presumably because of delayed hypersensitivity inflammation. We therefore selected patients in whom the evidence of brain damage indicated that the quality of life was unlikely to be good without treatment; patients with severe brain damage Since
T.F.
has been
treated because there was no prospect of benefit from T.F. In all three infants evidence of an in-vivo or in-vitro C.M.!. response to tuberculin and/or candida developed after T.F. We do not have suitable antigens for testing C.M.I. to C.rt.v., but the presence of antibody in the donors suggests that they were sensitised. The development of sensitivity to the other antigens indicates that T.F. was effective in stimulating C.M.I. The infants might have become sensitised to candida as a result of symptomless infection during the study, but this is very unlikely in the case of tuberculin; however, the initial skin test P.P.D. doses might have resulted in sensitisation. We observed no evidence of clinical deterioration or benefit after T.F. Urine virus cultures were negative for only a very short period after T.F. treatment, so it is unlikely that two doses of T.F. would be beneficial. Urine cultures from children with congenital c.M.v. are rarely C.M.v.-negative, and when they are, faults in laboratory
1. Hanshaw, J. B. J. infect. Dis. 1971, 123, 555. 2. Stern, H., Tucker, S. M. Br. med. J. 1973, ii, 268. 3. Hanshaw, J. B., Scheiner, A. P., Moxley, A. W.
et
al. New
Engl. J.
Med.
1976, 295, 468. 4. Reynolds, D. W., Stagno, S., Stubbs, G., Gaev,
B. A., Abel, V., Scheiner, 1974, 290, 297. 5. Stagno, S., Reynolds, D. W., Tsiantos, A., Fucillo, D. A., Long, W., Alford, C. A. J. infect. Dis. 1975, 132, 568. 6. Melish, M. E., Hanshaw, J. B. Am. J. Dis. Child. 1973, 126, 190. 7. McCracken, G. H., Luby, J. P. J. Pediat. 1972, 80, 488. 8. Lawrence, H. S. in Advances in Immunology (edited by F. J. Dixon and H. G. Kunkel) vol. II, p. 195. New York, 1969. 9. Kohler, P. F., Trembath, J., Merrill, D. A., Singleton, J. W., Dubois, R. S.
B. A.
10. 11.
Clin. Immun. Immunopath. 1974, 2, 465. Espanol, T., Todd, G. B., Soothill, J. F. Clin. exp. Immun. 1974, 18, 73. Valdimarsson, H., Wood, C. B., Hobbs, J. R., Holt, P. J. L. ibid. 1972, 11,
151.
Rytel, M. W., Aaberg, T. M., Dee, T. H., Heim, L. H. Cell Immun. 1975, 19, 8. 13. O’Reilly, R. J., Everson, L. K., Emodi, G., Hansew, J., Smithwick, E. M., Grimes, E., Pahwa, S., Pahwa, R., Schwartz, S., Armstrong, D., Siegal, F. P., Gupta, S., Dupont, B., Good, R. A. Clin. Immun. Immunopath. 1976, 6, 51. 14. Valdimarrson, H. in Progress in Immunology II (edited by L. Brent and J. Holborow); vol. 5, p. 377. Amsterdam, 1974. 12.
EFFECT OF ZINC ON THYMUS OF RECENTLY MALNOURISHED CHILDREN
were not
MICHAEL H. N. GOLDEN’ ALAN A. BARBARA E. GOLDEN
JACKSON
Tropical Metabolism Research Unit, University of the Indies, Kingston 7, Jamaica
West
Zinc-deficient animals and children have thymic atrophy and an increased susceptibility to infections. Children with protein-energy malnutrition similarly have thymic atrophy, zinc deficiency, and increased susceptibility to infections. 8 children, recently malnourished, who were supplemented with zinc, showed an increase in thymic size as judged radiographically. It is suggested that zinc deficiency may play a part in the thymic atrophy and infections associated with malnutrition.
Summary
*On secondment from the Department of Nutrition, London School of Hygiene and Tropical Medicine.
1058 INTRODUCTION
THE thymus gland is reduced in size more than any other organ in zinc-deficient animals.1,2 Children with acrodermatitis enteropathica have thymic atrophy,3.4 and a lethal trait of Black Pied Danish cattle is also characterised by thymic atrophy. In each of these conditions the thymic atrophy, related defects in cellmediated immunity, and severe infections respond dramatically to zinc therapy. Children with protein-energy malnutrition (P.E.M.) also have thymic atrophy,6-1O an impaired response to infection," and zinc deficiency.12-14 In a study of recently malnourished children we noted an apparent increase in thymic size after dietary zinc supplementation. The present investigation was carried out to see if zinc supplementation could stimulate thymic growth in these children and whether zinc deficiency might be the cause of
thymic atrophy OFP.E.M.
radiographs of patients 1 and 2 before and after supplementation with zinc.
Chest
PATIENTS AND METHODS
8 children who had recently recovered from severe and had reached the expected weight for their heightls were studied (see table). For at least 4 wk before and throughout the study the children received a highenergy diet16 which supplied 4.2 mg zinc per litre. A supplement, of zinc of 2 mg/kg body-weight/day was given for 10 days as zinc acetate. None of the children had clinical infections during the study, but all had had a chest infection during their episode of severe P.E.M. A chest radiograph was taken before zinc supplementation and repeated 10 days later. P.E.M.
The assessment of thymic size from a chest radiograph is notoriously unreliable;17 therefore two independent observers were asked to assess the films blindly in four, different ways. Each observer (1) measured the upper-mediastinal-diameter/chest-diameter ratio; (2) assessed the thymus on a scale of small, medium, or large; and (3) ranked the sixteen films in order of increasing thymic size. After these assessments had been made the films were paired for each subject, and the observers then (4) assessed each pair for the larger thymus. The four sets of data were analysed by the paired
CLINICAL CHARACTERISTICS,
t-test, the Walsh test, the
Mann-Whitney
u
test, and the
sign test respectively 18 RESULTS
The results of the blind assessments are shown in the table. The radiographs of 2 patients are presented in the figure. Analysis of the data showed that the thymus was significantly larger in the children after they had received zinc supplementation, by each of the four methods of analysis. DISCUSSION
Atrophy of the thymus has been associated with zinc deficiency,l,2 pyridoxine deficiency, 19 and a wide variety of acute and chronic illnesses.2° The thymic atrophy of stress is thought to be mediated by corticosteroids21indeed thymic atrophy has been used as a bioassay for steroids.22 The thymic atrophy seen in P.E.M. could be due to a combination of high levels of circulating steroids,23 zinc deficiency, or pyridoxine deficiency. Acute and chronic illness24 and high levels of circulating ster-
AND THYMIC ASSESSMENT BEFORE AND AFTER SUPPLEMENTATION OF RECENTLY MALNOURISHED CHILDREN WITH ZINC ACETATE
PLASMA-ZINC,
*U.M.D.=upper mediastinal diameter, c.D.=chest diameter. t s=small, M=medium, L=large. :I: -=smaller thymus, +=larger thymus.
1059 values. mediator for the thymic atrophy seen in the various conditions. We have observed (unpublished) that many Jamaican children who have recovered from P.E.M. and have no clinical infection do not have a demonstrable thymic shadow on chest X-ray. At this time, their circulating corticosteroids have returned to normal values and their major nutritional deficiencies have been corrected; this failure of regrowth of the thymus is therefore not due to stress. However, plasma-zinc values remain low when the children are still taking a high-energy diet after reco-
oids2S in themselves lead
to a
fall in
Thus, insufficient zinc may be
plasma-zinc
Reviews of Books
a common
Cross-sectional Anatomy
Computed Tomography and Ultrasound Correlation. BARBARA L. CARTER, JAMES MOREHEAD, SAMUEL M. WOLPERT, STEVEN B. HAMMERSCHLAG, HARRY J. GRIFFITHS, and PAUL C. KAHN. Hemel Hempstead: Prentice-Hall International. New York: Appleton-Century Crofts. 1977. Pp. 206. £34,$54.
Computerized Axial Tomography An Anatomic Atlas
of Serial Sections of the Human Body. JOSEPH GAMBARELLI, GERARD GUÉRINEL, LAURENT CHEVROT,
very.26 Our investigation shows that modest zinc supplementation can cause thymic growth in children who have been recently malnourished. This suggests that zinc deficiency be the cause of the thymic atrophy seen in P.E.M.
Among the serious complications of P.E.M. are severe infections. Because cell-mediated and humoral immunity are defective in P.E.M.," these infections are often caused by organisms of relatively low pathogenicity. Similar infections are a feature of impaired immunity iu.x_.aç[QçJ.er.ma.ti.tis uoenteropathica77 and zinc deficiency. Zinc stimulates both lymphocyte function28 and cell-mediated immunity. 29 Thus, the frequent severe infections and the thymic atrophy may both be related to the zinc deficiency found in P.E.M. We acknowledge the support of the Research Corporation of America. M. H. N. G. thanks the Wellcome Trust for a fellowship. We also thank the nursing staff of T.M.R.U. and Mrs L. Charley for technical assistance.
Requests for reprints should be addressed to M. H. N. G. REFERENCES Trace Element Metabolism in
J. Animals; vol. II, p. 742. Baltimore, 1974. 2. Miller, E. R., Lueck, E., Ullrey, D. E., Baltzer, B. V., Bradley, B. L., Hoefer, 1. Quarterman,
J. A. J. Nutr. 1968, 95, 278. 3. Rodin, A. E., Goldman, A. S. Am.
J. clin. Path. 1969, 51, 315. 4. Julius, R., Schulkind, M., Sprinkle, T., Rennert, O. J. Pediat. 1973, 83, 1007. 5. Brummerstedt, E., Flagstad, T., Basse, A., biol. scand. 1971, 79, 686. 6. Vint, F. W. E. Afr. med. J. 1937, 13, 332. 7. Hutt, M. S. R. J. trop. Pediat. 1969, 15, 153.
Andresen, E. Acta path. micro-
8. Watts, T ibid. p. 155. P. M., Schonland, M. M., Brereton-Stiles, G. G., et al. Lancet, 1971, ii, 939. 10. Magerwa, J. W. J. Path. 1971, 105, 105. 11. Suskind, R. M. Malnutrition and the Immune Response; pp. 99, 185. New York, 1977. 12. Cheek, D. B., Hill, D. E., Cordano, A., Graham, G. G. Pediat. Res. 1970, 4,135. 13. Warren, P. J., Hansen, J. D. L., Lenman, B. H. Proc. Nutr. Soc. 1969, 28,
9. Smythe,
6A
Shukry, A. J., Prasad, A. J., Gabr, M. K., Elhifney, E. E., Mokhatar, N., Darby, W. J. Am. J. clin. Nutr. 1965, 17, 15. 15. Nelson, W. E., Vaughan, V. C., McKay, R. J. Textbook of Pediatrics; p. 42.
14. Sandsted, H. H.,
Philadelphia, 1969. 16. Ashworth, A. Br. J. Nutr 1969, 23, 835. 17 Caffey, J. P. Pediatric X-ray Diagnosis; p. 443. Chicago, 1972. 18 Siegel, S. Nonparametric Statistics; pp. 68, 83, 116. New York, 1956. 19 Robson, L. C., Schwarz, M. R Cell Immun. 1975, 16, 145. 20. Boyd, E. Am. J. Dis. Child. 1932, 43, 1162. 21. Selye, H. Nature, 1936, 138, 32 22. Ringler, I., West, K., Dulin, W. E., Boland, E. W. Metabolism, 1964, 13, 37. 23
Schonland, M. M., Shanley, B. C., Loening, W. E. K., Parent, M. A., Coovadia, H. M. Lancet, 1972, ii, 435. 24. Halsted, J. A., Smith, J. C. ibid. 1970, i, 322. 25. Falchuk, K. H. New Engl. J. Med. 1977, 296, 1129. 26 Golden, B. E., Golden, M. H. N. Unpublished. 27. Endre, L., Katona, Z., Gyurkovits, K. Lancet, 1975, i, 1196. 28 Williams, R. O., Loeb, L. A. J. cell. Biol. 1973, 58, 594. 29. Pekarek, R. S., Powandea, M. C., Hoagland, A. M. Fedn Proc. 1976, 35, 360 abstr.
and MATHIEU MATTEL Berlin and New York:
Springer.
1977.
Pp.
286.$105.60.
CROSS-SECTIONAL anatomy used to be looked upon almost as professional perversion of anatomists. The scanner has changed all this, and this aspect of basic medical science has become all-important to those who examine scanning films, be they radiologists, surgeons, gastroenterologists, or rheumatologists. The whole concept of clinical anatomy has been given a new impetus, and its relevance to modern medicine is clearly demonstrated by these two works both of which have been produced by teams of radiologists and anatomists. The first book draws heavily on the pioneering work of Eycleshymer and Schoemaker who published A Cross-Section Anatomy in 1911. It is an atlas prepared essentially for clinicians to use as a reference to the normal when studying computerised tomography (c.T.) scans and echograms of the head, trunk, and limbs. There is a brief introductory text describing the material and the methodology of producing c.T. scans and echograms. All illustrations are in black-and-white and correlate tone drawings of anatomical, embalmed specimens with scans and ultrasonograms. The pages in this book are not numbered which makes using the index laborious. The second work is more ambitious. It is based principally on the analysis of axial transverse sections (and frontal sections of the head) made serially at centimetre intervals on frozen corpses. Each section was photographed in colour, radiographed, drawn in black-andwhite and compared with the scanner image at the corresponding level. The chapter presenting axial tomography from a theoretical and practical point of view provides a most useful introduction to the subject and the 46 references cited provide good guides to further reading. Both sets of authors have used the accepted international anatomical terminology. These works will be of interest to anatomists who wish to keep abreast of clinical developments and will be most valuable to clinicians who need to interpret scanner sections. Radiologists who are users, or potential users, of scanning equipment will find the topographical information invaluable. a
Biochemical Diagnosis of the Elderly H. M. HODKINSON. Andover:
Chapman and Hall.
1977.
Pp.
111.
£ 5.50. earlier assumptions, clinicians are becoming that human physiology and pathology do increasingly not remain virtually unchanged throughout adult life, but that many age-related changes occur. Several authoritative monographs on different aspects of the medicine of old age have appeared highlighting these changes, and Dr Hodkinson’s book is a most welcome addition. It is essentially practical, almost bedside, in nature, and it brings together in a very small compass a great deal of relevant, but hitherto scattered, information. It is based largely on Dr Hodkinson’s own experience in the geriatric department at Northwick Park Hospital, but there is also wide reference to other work. Chapters 1-3 deal with the basic principles and interpretation of biochemical tests, while chapters 4-9 examine in more detail groups of tests (e.g., electrolytes and renal function, plasma-proteins, thyroid
CONTRARY
to
aware
technique
are
be responsible. In this investigataken with all the samples and we think that the negative cultures were
held
to
tion great therefore do not chance occurrences. There is evidence that T.F. produced some change in responsiveness in subacute sclerosing panencephalitis,14 but brain damage was not affected. Perhaps the damage was already too severe. Slightly affected c.M.v.-infected infants in whom progressive brain damage might be prevented are more likely to benefit from T.F. treatment. We intend to study viruria and any possible clinical effects during a controlled trial of T.F. treatment in such infants. care was
Results of urine culture for C.M.V. (+=positive culture and 0=negative culture) and 48-hour skin-test response to P.P.D. and candida antigen in three patients given two doses (T.F.1 and T.F.2) of transfer factor. Time in days is shown from the day OFT.F. .1.
real. In patients 2 and 3 there was no consistent in antibody to c.M.v. after treatment.
change
We thank Dr S. Lewis and Dr E. de H. Lobo for referring patients; Dr H. Valdimarsson, Dr T. E. Cleghorn, and Mrs. Lorna Layward for advice and help; Mrs Angela Perry for secretarial assistance; and the Wellcome Trust (W.C.M.) and the Medical Research Council (I.T.T.) for financial support. Requests for reprints should be addressed to J. F. S., Institute of Child Health, 30 Guilford Street, London WC IN 1EH.
REFERENCES
DISCUSSION
reported to be of benefit in mucocutaneous candidiasis" and hepatitis-B-virus carriage,9 it might be expected to be useful in chronic infection by intracellular organisms; however, there is no conclusive controlled evidence on this point. The mechanism for chronicity in congenital virus infections remains uncertain. T.F. had no obvious beneficial action in congenital hepatitis-B-virus infection,9 but our data, which suggest brief suppression of viruria in congenital c.M.v. are encouraging. Any such beneficial effect of T.F. may not work by the antigen-specific mechanism as claimed by Lawrence. Improvement of c.M.v. retinitis after T.F., with fall in titre of urinary virus excretion, in an immunosuppressed adult recipient of a kidney graft12 has also been reported (a similar effect has been reported with interferon ) 13 The kidney-graft recipient and some patients with mucocutaneous candidiasis had apparent exacerbation of their lesions immediately after T.F. injections, before improvement followed, presumably because of delayed hypersensitivity inflammation. We therefore selected patients in whom the evidence of brain damage indicated that the quality of life was unlikely to be good without treatment; patients with severe brain damage Since
T.F.
has been
treated because there was no prospect of benefit from T.F. In all three infants evidence of an in-vivo or in-vitro C.M.!. response to tuberculin and/or candida developed after T.F. We do not have suitable antigens for testing C.M.I. to C.rt.v., but the presence of antibody in the donors suggests that they were sensitised. The development of sensitivity to the other antigens indicates that T.F. was effective in stimulating C.M.I. The infants might have become sensitised to candida as a result of symptomless infection during the study, but this is very unlikely in the case of tuberculin; however, the initial skin test P.P.D. doses might have resulted in sensitisation. We observed no evidence of clinical deterioration or benefit after T.F. Urine virus cultures were negative for only a very short period after T.F. treatment, so it is unlikely that two doses of T.F. would be beneficial. Urine cultures from children with congenital c.M.v. are rarely C.M.v.-negative, and when they are, faults in laboratory
1. Hanshaw, J. B. J. infect. Dis. 1971, 123, 555. 2. Stern, H., Tucker, S. M. Br. med. J. 1973, ii, 268. 3. Hanshaw, J. B., Scheiner, A. P., Moxley, A. W.
et
al. New
Engl. J.
Med.
1976, 295, 468. 4. Reynolds, D. W., Stagno, S., Stubbs, G., Gaev,
B. A., Abel, V., Scheiner, 1974, 290, 297. 5. Stagno, S., Reynolds, D. W., Tsiantos, A., Fucillo, D. A., Long, W., Alford, C. A. J. infect. Dis. 1975, 132, 568. 6. Melish, M. E., Hanshaw, J. B. Am. J. Dis. Child. 1973, 126, 190. 7. McCracken, G. H., Luby, J. P. J. Pediat. 1972, 80, 488. 8. Lawrence, H. S. in Advances in Immunology (edited by F. J. Dixon and H. G. Kunkel) vol. II, p. 195. New York, 1969. 9. Kohler, P. F., Trembath, J., Merrill, D. A., Singleton, J. W., Dubois, R. S.
B. A.
10. 11.
Clin. Immun. Immunopath. 1974, 2, 465. Espanol, T., Todd, G. B., Soothill, J. F. Clin. exp. Immun. 1974, 18, 73. Valdimarsson, H., Wood, C. B., Hobbs, J. R., Holt, P. J. L. ibid. 1972, 11,
151.
Rytel, M. W., Aaberg, T. M., Dee, T. H., Heim, L. H. Cell Immun. 1975, 19, 8. 13. O’Reilly, R. J., Everson, L. K., Emodi, G., Hansew, J., Smithwick, E. M., Grimes, E., Pahwa, S., Pahwa, R., Schwartz, S., Armstrong, D., Siegal, F. P., Gupta, S., Dupont, B., Good, R. A. Clin. Immun. Immunopath. 1976, 6, 51. 14. Valdimarrson, H. in Progress in Immunology II (edited by L. Brent and J. Holborow); vol. 5, p. 377. Amsterdam, 1974. 12.
EFFECT OF ZINC ON THYMUS OF RECENTLY MALNOURISHED CHILDREN
were not
MICHAEL H. N. GOLDEN’ ALAN A. BARBARA E. GOLDEN
JACKSON
Tropical Metabolism Research Unit, University of the Indies, Kingston 7, Jamaica
West
Zinc-deficient animals and children have thymic atrophy and an increased susceptibility to infections. Children with protein-energy malnutrition similarly have thymic atrophy, zinc deficiency, and increased susceptibility to infections. 8 children, recently malnourished, who were supplemented with zinc, showed an increase in thymic size as judged radiographically. It is suggested that zinc deficiency may play a part in the thymic atrophy and infections associated with malnutrition.
Summary
*On secondment from the Department of Nutrition, London School of Hygiene and Tropical Medicine.
1058 INTRODUCTION
THE thymus gland is reduced in size more than any other organ in zinc-deficient animals.1,2 Children with acrodermatitis enteropathica have thymic atrophy,3.4 and a lethal trait of Black Pied Danish cattle is also characterised by thymic atrophy. In each of these conditions the thymic atrophy, related defects in cellmediated immunity, and severe infections respond dramatically to zinc therapy. Children with protein-energy malnutrition (P.E.M.) also have thymic atrophy,6-1O an impaired response to infection," and zinc deficiency.12-14 In a study of recently malnourished children we noted an apparent increase in thymic size after dietary zinc supplementation. The present investigation was carried out to see if zinc supplementation could stimulate thymic growth in these children and whether zinc deficiency might be the cause of
thymic atrophy OFP.E.M.
radiographs of patients 1 and 2 before and after supplementation with zinc.
Chest
PATIENTS AND METHODS
8 children who had recently recovered from severe and had reached the expected weight for their heightls were studied (see table). For at least 4 wk before and throughout the study the children received a highenergy diet16 which supplied 4.2 mg zinc per litre. A supplement, of zinc of 2 mg/kg body-weight/day was given for 10 days as zinc acetate. None of the children had clinical infections during the study, but all had had a chest infection during their episode of severe P.E.M. A chest radiograph was taken before zinc supplementation and repeated 10 days later. P.E.M.
The assessment of thymic size from a chest radiograph is notoriously unreliable;17 therefore two independent observers were asked to assess the films blindly in four, different ways. Each observer (1) measured the upper-mediastinal-diameter/chest-diameter ratio; (2) assessed the thymus on a scale of small, medium, or large; and (3) ranked the sixteen films in order of increasing thymic size. After these assessments had been made the films were paired for each subject, and the observers then (4) assessed each pair for the larger thymus. The four sets of data were analysed by the paired
CLINICAL CHARACTERISTICS,
t-test, the Walsh test, the
Mann-Whitney
u
test, and the
sign test respectively 18 RESULTS
The results of the blind assessments are shown in the table. The radiographs of 2 patients are presented in the figure. Analysis of the data showed that the thymus was significantly larger in the children after they had received zinc supplementation, by each of the four methods of analysis. DISCUSSION
Atrophy of the thymus has been associated with zinc deficiency,l,2 pyridoxine deficiency, 19 and a wide variety of acute and chronic illnesses.2° The thymic atrophy of stress is thought to be mediated by corticosteroids21indeed thymic atrophy has been used as a bioassay for steroids.22 The thymic atrophy seen in P.E.M. could be due to a combination of high levels of circulating steroids,23 zinc deficiency, or pyridoxine deficiency. Acute and chronic illness24 and high levels of circulating ster-
AND THYMIC ASSESSMENT BEFORE AND AFTER SUPPLEMENTATION OF RECENTLY MALNOURISHED CHILDREN WITH ZINC ACETATE
PLASMA-ZINC,
*U.M.D.=upper mediastinal diameter, c.D.=chest diameter. t s=small, M=medium, L=large. :I: -=smaller thymus, +=larger thymus.
1059 values. mediator for the thymic atrophy seen in the various conditions. We have observed (unpublished) that many Jamaican children who have recovered from P.E.M. and have no clinical infection do not have a demonstrable thymic shadow on chest X-ray. At this time, their circulating corticosteroids have returned to normal values and their major nutritional deficiencies have been corrected; this failure of regrowth of the thymus is therefore not due to stress. However, plasma-zinc values remain low when the children are still taking a high-energy diet after reco-
oids2S in themselves lead
to a
fall in
Thus, insufficient zinc may be
plasma-zinc
Reviews of Books
a common
Cross-sectional Anatomy
Computed Tomography and Ultrasound Correlation. BARBARA L. CARTER, JAMES MOREHEAD, SAMUEL M. WOLPERT, STEVEN B. HAMMERSCHLAG, HARRY J. GRIFFITHS, and PAUL C. KAHN. Hemel Hempstead: Prentice-Hall International. New York: Appleton-Century Crofts. 1977. Pp. 206. £34,$54.
Computerized Axial Tomography An Anatomic Atlas
of Serial Sections of the Human Body. JOSEPH GAMBARELLI, GERARD GUÉRINEL, LAURENT CHEVROT,
very.26 Our investigation shows that modest zinc supplementation can cause thymic growth in children who have been recently malnourished. This suggests that zinc deficiency be the cause of the thymic atrophy seen in P.E.M.
Among the serious complications of P.E.M. are severe infections. Because cell-mediated and humoral immunity are defective in P.E.M.," these infections are often caused by organisms of relatively low pathogenicity. Similar infections are a feature of impaired immunity iu.x_.aç[QçJ.er.ma.ti.tis uoenteropathica77 and zinc deficiency. Zinc stimulates both lymphocyte function28 and cell-mediated immunity. 29 Thus, the frequent severe infections and the thymic atrophy may both be related to the zinc deficiency found in P.E.M. We acknowledge the support of the Research Corporation of America. M. H. N. G. thanks the Wellcome Trust for a fellowship. We also thank the nursing staff of T.M.R.U. and Mrs L. Charley for technical assistance.
Requests for reprints should be addressed to M. H. N. G. REFERENCES Trace Element Metabolism in
J. Animals; vol. II, p. 742. Baltimore, 1974. 2. Miller, E. R., Lueck, E., Ullrey, D. E., Baltzer, B. V., Bradley, B. L., Hoefer, 1. Quarterman,
J. A. J. Nutr. 1968, 95, 278. 3. Rodin, A. E., Goldman, A. S. Am.
J. clin. Path. 1969, 51, 315. 4. Julius, R., Schulkind, M., Sprinkle, T., Rennert, O. J. Pediat. 1973, 83, 1007. 5. Brummerstedt, E., Flagstad, T., Basse, A., biol. scand. 1971, 79, 686. 6. Vint, F. W. E. Afr. med. J. 1937, 13, 332. 7. Hutt, M. S. R. J. trop. Pediat. 1969, 15, 153.
Andresen, E. Acta path. micro-
8. Watts, T ibid. p. 155. P. M., Schonland, M. M., Brereton-Stiles, G. G., et al. Lancet, 1971, ii, 939. 10. Magerwa, J. W. J. Path. 1971, 105, 105. 11. Suskind, R. M. Malnutrition and the Immune Response; pp. 99, 185. New York, 1977. 12. Cheek, D. B., Hill, D. E., Cordano, A., Graham, G. G. Pediat. Res. 1970, 4,135. 13. Warren, P. J., Hansen, J. D. L., Lenman, B. H. Proc. Nutr. Soc. 1969, 28,
9. Smythe,
6A
Shukry, A. J., Prasad, A. J., Gabr, M. K., Elhifney, E. E., Mokhatar, N., Darby, W. J. Am. J. clin. Nutr. 1965, 17, 15. 15. Nelson, W. E., Vaughan, V. C., McKay, R. J. Textbook of Pediatrics; p. 42.
14. Sandsted, H. H.,
Philadelphia, 1969. 16. Ashworth, A. Br. J. Nutr 1969, 23, 835. 17 Caffey, J. P. Pediatric X-ray Diagnosis; p. 443. Chicago, 1972. 18 Siegel, S. Nonparametric Statistics; pp. 68, 83, 116. New York, 1956. 19 Robson, L. C., Schwarz, M. R Cell Immun. 1975, 16, 145. 20. Boyd, E. Am. J. Dis. Child. 1932, 43, 1162. 21. Selye, H. Nature, 1936, 138, 32 22. Ringler, I., West, K., Dulin, W. E., Boland, E. W. Metabolism, 1964, 13, 37. 23
Schonland, M. M., Shanley, B. C., Loening, W. E. K., Parent, M. A., Coovadia, H. M. Lancet, 1972, ii, 435. 24. Halsted, J. A., Smith, J. C. ibid. 1970, i, 322. 25. Falchuk, K. H. New Engl. J. Med. 1977, 296, 1129. 26 Golden, B. E., Golden, M. H. N. Unpublished. 27. Endre, L., Katona, Z., Gyurkovits, K. Lancet, 1975, i, 1196. 28 Williams, R. O., Loeb, L. A. J. cell. Biol. 1973, 58, 594. 29. Pekarek, R. S., Powandea, M. C., Hoagland, A. M. Fedn Proc. 1976, 35, 360 abstr.
and MATHIEU MATTEL Berlin and New York:
Springer.
1977.
Pp.
286.$105.60.
CROSS-SECTIONAL anatomy used to be looked upon almost as professional perversion of anatomists. The scanner has changed all this, and this aspect of basic medical science has become all-important to those who examine scanning films, be they radiologists, surgeons, gastroenterologists, or rheumatologists. The whole concept of clinical anatomy has been given a new impetus, and its relevance to modern medicine is clearly demonstrated by these two works both of which have been produced by teams of radiologists and anatomists. The first book draws heavily on the pioneering work of Eycleshymer and Schoemaker who published A Cross-Section Anatomy in 1911. It is an atlas prepared essentially for clinicians to use as a reference to the normal when studying computerised tomography (c.T.) scans and echograms of the head, trunk, and limbs. There is a brief introductory text describing the material and the methodology of producing c.T. scans and echograms. All illustrations are in black-and-white and correlate tone drawings of anatomical, embalmed specimens with scans and ultrasonograms. The pages in this book are not numbered which makes using the index laborious. The second work is more ambitious. It is based principally on the analysis of axial transverse sections (and frontal sections of the head) made serially at centimetre intervals on frozen corpses. Each section was photographed in colour, radiographed, drawn in black-andwhite and compared with the scanner image at the corresponding level. The chapter presenting axial tomography from a theoretical and practical point of view provides a most useful introduction to the subject and the 46 references cited provide good guides to further reading. Both sets of authors have used the accepted international anatomical terminology. These works will be of interest to anatomists who wish to keep abreast of clinical developments and will be most valuable to clinicians who need to interpret scanner sections. Radiologists who are users, or potential users, of scanning equipment will find the topographical information invaluable. a
Biochemical Diagnosis of the Elderly H. M. HODKINSON. Andover:
Chapman and Hall.
1977.
Pp.
111.
£ 5.50. earlier assumptions, clinicians are becoming that human physiology and pathology do increasingly not remain virtually unchanged throughout adult life, but that many age-related changes occur. Several authoritative monographs on different aspects of the medicine of old age have appeared highlighting these changes, and Dr Hodkinson’s book is a most welcome addition. It is essentially practical, almost bedside, in nature, and it brings together in a very small compass a great deal of relevant, but hitherto scattered, information. It is based largely on Dr Hodkinson’s own experience in the geriatric department at Northwick Park Hospital, but there is also wide reference to other work. Chapters 1-3 deal with the basic principles and interpretation of biochemical tests, while chapters 4-9 examine in more detail groups of tests (e.g., electrolytes and renal function, plasma-proteins, thyroid
CONTRARY
to
aware
