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IRON DEFICIENCY IN PULMONARY " EMPHYSEMA "
418
reduce acid and pepsin secretion in the stomach-and there is no need to do so. There is no good reason to expect late metabolic effects from selective vagotomy. Mr. Williams is, in effect, saying that vagotomy and pyloroplasty should be used in all cases of duodenal ulceration in need of surgical treatment. Nevertheless, he believes that surgeons already skilled in gastrectomy should not use vagotomy because they may, from incomplete section, obtain poor results. The simple electrical stimulation test will allow all surgeons to achieve complete nerve section. Is there a nroblem ? West London Hospital, Hammersmith, London, W.6.
HAROLD BURGE.
IRON DEFICIENCY IN PULMONARY " EMPHYSEMA "
SiR,ŁThe findings of Dr. Fielding and Dr. Zorab (Aug. 8) seem to differ from those of Simpson and myself1 only in degree. Thus we found frank evidence of iron deficiency in approximately half of a group of 33 chronically hypoxic patients with pulmonary " emphysema ". The plasma-iron was rather lower in our patients than in those studied by Fielding and Zorab, and in 5 out of 11 of our patients the total iron-binding capacity of the plasma was above the normal range, whereas Fielding and Zorab obtained virtually normal values. Unfortunately, Fielding the arterial oxygen saturation of pulmonary " emphysema ". It seems their patients had less evidence of that possible, however, iron deficiency because they were less hypoxic and had a smaller increase in red-cell volume than ours. The cause of the iron deficiency remains obscure; certainly hypoxia alone cannot be responsible since the serum-iron is normal 2 or even increased in residents at high altitude.
and Zorab do hot their patients with
state
Dunchideock, Exeter, Devon.
D. B. SHAW.
near
GRANULOCYTIC
LEUKÆMIA, PHILADELPHIA
CHROMOSOME, AND LEUCOCYTE ALKALINE PHOSPHATASE
SIR,-King et a1.3 discussed the possible role of human pair 21 in the production of leucocyte alkaline phosphatase (L.A.P.). They followed the stimulating suggestions of Trubowitz and others4 that, since L.A.P. was elevated in trisomy 21 (characteristic of most mongols) and lowered in partial deletion (Philadelphia chromosome of chronic granulocytic leukxmia), the gene for L.A.P. might well be placed on this chromosome. The studies of King and her colleagues indicated, however, that a more complex interpretation was necessary-first, because in their investigation the expected 3:2 ratio of L.A.P. levels between mongolism and normals did not hold, and, secondly, because in the acute transformation of chronic granulocytic leukxmia, the Philadelphia chromosome persisted but the L.A.P. might become markedly chromosome
Fig. 1-Metaphase plate.
173,700 per c.mm. with a differential of 71 segmented cells, 3 band forms, 5 myelocytes, 4 promyelocytes, 3 metamyelocytes, 7 lymphocyfes, 5 basophils, 2 monocytes, and was
1 normoblast. Platelets numbered 1 x 106 per c.mm. The bone-marrow findings were also consistent with a diagnosis of chronic granulocytic leukaemia, and therapy with busulphan was begun. When, however, L.A.P. levels were found elevated (130-175 by the technique of Kaplow 5) treatment was halted after two days. Further investigation showed that the patient had ulcerative colitis with five stools daily, four almost completely pus. Though he received neither cortisone nor additional busulphan, his leucocyte-count fluctuated between 82,000 and 30,000 per c.mm. Nevertheless, the L.A.P. continued to be high for several months. In April, 1964, a bone-marrow aspirate was treated by a modification of the direct method of Sandberg et al .6 More than 55 well-spread metaphase plates showed the presence of a minute (Ph1) chromosome (figs. 1 and 2). No metaphase plate was assuredly without it. With medical treatment and gradual improvement (clinical and biopsy) of his ulcerative colitis, the L.A.P. level dropped progressively to the lower limits of normal (scores of 30-40), where it has remained.
Heath and Moloneyhave described a case similarly combining chronic granulocytic leukaemia with chronic infection. The L.A.P. was elevated, and cytogenetic studies 5. 6. 7.
Kaplow, L. S. Blood, 1959, 14, 975. Sandberg, A. A., Koepf, G. F., Crosswhite, L. H., Hauschka, T. S. Amer. J. Hum. Genet. 1960, 12, 231. Heath, C. W., Jr., Moloney, W. C. Hum. Chromosome Newsletter, 1964, 12, 14.
elevated. of evidence regarding the relationbetween chromosome 21 and L.A.P. would be the ship coincidence of normal or increased L.A.P. in the presence of chronic granulocytic leukaemia with the Philadelphia chromosome. Such a case is reported here. A 16-year-old Caucasian male was admitted to the City of A
significant piece
Hope Medical Center in December, 1963, with the diagnosis of chronic granulocytic leukaemia. A typical leucocyte-count 1. Shaw, D. B., Simpson, T. Quart. J. Med. 1961, 30, 135. 2. Treger, A., Grover, R. F., Shaw, D. B., Blount, S. G. To be published. 3. 4.
King, M. J., Gillis, E. M., Baikie, A. G. Lancet, 1962, ii, 1302. Trubowitz, S., Kirman, D., Masek, B. ibid. p. 486.
Fig. 2-Ideogram made from metaphase plate. Arrows point to the PhI chromosome. .
reduce acid and pepsin secretion in the stomach-and there is no need to do so. There is no good reason to expect late metabolic effects from selective vagotomy. Mr. Williams is, in effect, saying that vagotomy and pyloroplasty should be used in all cases of duodenal ulceration in need of surgical treatment. Nevertheless, he believes that surgeons already skilled in gastrectomy should not use vagotomy because they may, from incomplete section, obtain poor results. The simple electrical stimulation test will allow all surgeons to achieve complete nerve section. Is there a nroblem ? West London Hospital, Hammersmith, London, W.6.
HAROLD BURGE.
IRON DEFICIENCY IN PULMONARY " EMPHYSEMA "
SiR,ŁThe findings of Dr. Fielding and Dr. Zorab (Aug. 8) seem to differ from those of Simpson and myself1 only in degree. Thus we found frank evidence of iron deficiency in approximately half of a group of 33 chronically hypoxic patients with pulmonary " emphysema ". The plasma-iron was rather lower in our patients than in those studied by Fielding and Zorab, and in 5 out of 11 of our patients the total iron-binding capacity of the plasma was above the normal range, whereas Fielding and Zorab obtained virtually normal values. Unfortunately, Fielding the arterial oxygen saturation of pulmonary " emphysema ". It seems their patients had less evidence of that possible, however, iron deficiency because they were less hypoxic and had a smaller increase in red-cell volume than ours. The cause of the iron deficiency remains obscure; certainly hypoxia alone cannot be responsible since the serum-iron is normal 2 or even increased in residents at high altitude.
and Zorab do hot their patients with
state
Dunchideock, Exeter, Devon.
D. B. SHAW.
near
GRANULOCYTIC
LEUKÆMIA, PHILADELPHIA
CHROMOSOME, AND LEUCOCYTE ALKALINE PHOSPHATASE
SIR,-King et a1.3 discussed the possible role of human pair 21 in the production of leucocyte alkaline phosphatase (L.A.P.). They followed the stimulating suggestions of Trubowitz and others4 that, since L.A.P. was elevated in trisomy 21 (characteristic of most mongols) and lowered in partial deletion (Philadelphia chromosome of chronic granulocytic leukxmia), the gene for L.A.P. might well be placed on this chromosome. The studies of King and her colleagues indicated, however, that a more complex interpretation was necessary-first, because in their investigation the expected 3:2 ratio of L.A.P. levels between mongolism and normals did not hold, and, secondly, because in the acute transformation of chronic granulocytic leukxmia, the Philadelphia chromosome persisted but the L.A.P. might become markedly chromosome
Fig. 1-Metaphase plate.
173,700 per c.mm. with a differential of 71 segmented cells, 3 band forms, 5 myelocytes, 4 promyelocytes, 3 metamyelocytes, 7 lymphocyfes, 5 basophils, 2 monocytes, and was
1 normoblast. Platelets numbered 1 x 106 per c.mm. The bone-marrow findings were also consistent with a diagnosis of chronic granulocytic leukaemia, and therapy with busulphan was begun. When, however, L.A.P. levels were found elevated (130-175 by the technique of Kaplow 5) treatment was halted after two days. Further investigation showed that the patient had ulcerative colitis with five stools daily, four almost completely pus. Though he received neither cortisone nor additional busulphan, his leucocyte-count fluctuated between 82,000 and 30,000 per c.mm. Nevertheless, the L.A.P. continued to be high for several months. In April, 1964, a bone-marrow aspirate was treated by a modification of the direct method of Sandberg et al .6 More than 55 well-spread metaphase plates showed the presence of a minute (Ph1) chromosome (figs. 1 and 2). No metaphase plate was assuredly without it. With medical treatment and gradual improvement (clinical and biopsy) of his ulcerative colitis, the L.A.P. level dropped progressively to the lower limits of normal (scores of 30-40), where it has remained.
Heath and Moloneyhave described a case similarly combining chronic granulocytic leukaemia with chronic infection. The L.A.P. was elevated, and cytogenetic studies 5. 6. 7.
Kaplow, L. S. Blood, 1959, 14, 975. Sandberg, A. A., Koepf, G. F., Crosswhite, L. H., Hauschka, T. S. Amer. J. Hum. Genet. 1960, 12, 231. Heath, C. W., Jr., Moloney, W. C. Hum. Chromosome Newsletter, 1964, 12, 14.
elevated. of evidence regarding the relationbetween chromosome 21 and L.A.P. would be the ship coincidence of normal or increased L.A.P. in the presence of chronic granulocytic leukaemia with the Philadelphia chromosome. Such a case is reported here. A 16-year-old Caucasian male was admitted to the City of A
significant piece
Hope Medical Center in December, 1963, with the diagnosis of chronic granulocytic leukaemia. A typical leucocyte-count 1. Shaw, D. B., Simpson, T. Quart. J. Med. 1961, 30, 135. 2. Treger, A., Grover, R. F., Shaw, D. B., Blount, S. G. To be published. 3. 4.
King, M. J., Gillis, E. M., Baikie, A. G. Lancet, 1962, ii, 1302. Trubowitz, S., Kirman, D., Masek, B. ibid. p. 486.
Fig. 2-Ideogram made from metaphase plate. Arrows point to the PhI chromosome. .