495

caused by dialysis, presumably because potassium wasbeing very effectively removed and digitoxin was not.Thus, the use of dialytic procedures for digoxin toxicity

not only seems unwise but also may well be dangerous.

V.A. Hospital,Little Rock,

Arkansas 72206, U.S.A.

JAMES E. DOHERTYGEORGE L. ACKERMAN

J. J. KANE.

REFRACTORY ANÆMIA AND THE" OTHER CELL LINES "

SIR,-Dr Hakim and his associates reported thereduced pyruvate-kinase activity and decreased nitroblue-tetrazolium reduction of polymorphonuclear leucocytes inpatients with refractory anaemia. They do not suggestthat their interesting findings reflect a more fundamentalabnormality of the bone-marrow than is commonly believed.

Various red-cell abnormalities, including enzyme defectsand abnormal heme synthesis, have been emphasised inconnection with refractory anaemia. Amazingly littleattention has been paid to the abnormalities in the othermarrow cell lines in this condition, although neutropenia isoften observed and thrombocytopenia is not rare. 2 Iflooked for, one or several of the following morphologicalabnormalities might be found in the peripheral blood:pelgeroid granulocytes, granulation defects in polymorpho-nuclear leucocytes, occasional immature granulocytes,monocytosis, atypical monocytes, and bizarre platelets.The bone-marrow is often hypercellular with abnormalitiesin erythrocytic, granulocytic, and megakaryocytic celllines. In addition to morphological deviations, function ofgranulocytes and platelets is impaired.3 3

It is well known that a certain proportion of patientswith refractory anasmia will ultimately develop acute

myelomonocytic leukxmia.4 In most cases one can detectthe above abnormalities during the preleukaemic phase.It is, however, unknown how often a refractory anaemiawith similar morphological signs does represent a pre-leukaemic state.

Thus, the term " refractory anaemia " is often somewhat

misleading. Probably a minority of cases represent a truered-cell maturation failure. It is easy to predict thatseveral other white-cell and platelet abnormalities will befound in refractory anxmia. The basic error might inthese instances be in a hypothetical precursor cell which isthe progenitor to red cells, granulocytes, monocytes, andmeMkarvncvtfs

Hatanpaä Hospital,Tampere 10,

Finland. MATTI SAARNI.

COMPLICATIONS OF INTRAVENOUS FEEDING

SIR,-I noted with interest the commentary by Dr Jonesand Dr McIntosh (Jan. 20, p. 156). The description of thesymptoms with progressive lethargy and increasingsevere apncea and metabolic acidosis in the face of negativebacteriological findings is strongly suggestive of hyper-ammonxmia in association with an excessive ammonia loadfrom the protein-hydrolysate or aminoacid mixture used.The hyperammonaemia was previously described 5 in

1. Hakim, J., Boivin, P., Boucherot, J., Troube, H. Lancet, Jan. 61973, p. 37.

2. Dacie, J. V., Smith, M. D., White, J. C., Mollin, D. L. Br. J. Hœmat.1959, 5, 56.

3. Caen, J., Sultan, Y., Dreyfus, B. Nouv. Rev. fr. Hémat. 1969, 9, 123.4. Saarni, M. I., Linman, J. W. Cancer, 1971, 27, 1221.5. Landes, R. D., Avery, G. B., Walker, F. A., Hsia, Y. Pediat. Res.

1972, 6, 394.

association with propionic acidaemia and also noted earlier. 8In our experience, the level of ammonia in protein-

hydrolysate solutions has ranged up to 50 mg. per 100 ml.With the ammonia-free crystalline aminoacid solutions

(’ Fre Amine ’) the syndrome of hyperammonoemia has alsobeen reported in association with hyperalimentation andmay be related to excessive loads of branched-chain amino-acids. It would be of interest to know whether blood-ammonia levels were measured in this patient and whethersimilar symptoms have recurred without catheter block-age when hyperalimentation has been reinstituted.

Children’s PsychiatricResearch Institute,P.O. Box 2460,

London, Ontario N6A 4G6, Canada. FRANK A. WALKER.

CAUSE OF FRICTION BLISTERS

SiR,—I was interested to read the paper by Dr Comaish(Jan. 13, p. 81). It seems unlikely that, under the conditionsof his experiments, " strain hardening " would cause a

rise in friction before the epidermis ruptures. A more

probable explanation is that the increase in friction is dueto a small fluid leak on to the skin surface just beforeobvious epidermal rupture occurs.Dr Comaish used my data in his calculations and was

kind enough to acknowledge this. As a result of the experi-ments which I carried out and described at that time,I wrote:

"Blister formation appears to occur in two independentstages; first, prickle-cell necrosis which causes an intra-epidermalsplit, and second, the filling of this with fluid, probably fromthe dermis. It is the ease with which an intra-epidermal split isformed which is being measured in these experiments.

" The prickle-cell necrosis is unlikely to be due to a localheating effect and there is no evidence that it is enzymicallydetermined; it is not influenced by short-term changes in dermalblood flow or by the intensity of the triple response. It is sug-gested that the prickle-cell necrosis is caused by repeated cellulardistortion which might cause a denaturation of the cellularprotein." "

Skin Department,St. Thomas’ Hospital,London SE1 7EH. P. F. D. NAYLOR.

B CELLS IN LEPROSY

SiR,—The change in cellular response in lepromatousand tuberculoid forms of leprosy is well known, although itis more pronounced in the lepromatous variety. We thoughtthat the alteration might, in some way, be reflected in thepercentage of B cells in peripheral blood. Furthermore,the results might be useful in identifying the clinical formsof leprosy. Similar findings were helpful in the reclassi-fication of other diseases (chronic lymphatic leukxmiaand hypogammaglobulinxmias).9,10Lymphocytes were isolated by the Ficoll-Isopaque

method 11 from 30 patients, some with lepromatous andothers with tuberculoid leprosy. The lymphocytes wereincubated with anti-IgA, anti-IgM, and anti-IgG fluor-escent antisera.12 The percentages of cells with patches offluorescence on their surface were studied under a fluor-

6. Walker, F. A. New Engl. J. Med. 1971, 285, 1324.7. Naylor, P. F. D. Br. J. Derm. 1955, 67, 327.8. Bullock, W. E. Clin. Res. 1968, 16, 328.9. Catovsky, D., Holt, P. J. L. Lancet, 1971, ii, 976.

10. Preud’homme, J. L., Seligmann, M. ibid. 1972, i, 442.11. Thorsby, E., Bratlie, A. in Histocompatibility Testing, 1970; p. 655.

Copenhagen, 1970.12. Papamichail, M., Brown, J. C., Holborow, E. J. Lancet, 1971, ii, 850.