REAPPEARANCE OF TABOPARESIS

REAPPEARANCE OF TABOPARESIS

374 The size of iron ance in the production of iron deficiency. What are the morphological and biochemical characters stores is also relevant, and the...

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374 The size of iron ance in the production of iron deficiency. What are the morphological and biochemical characters stores is also relevant, and the exhaustion of these reserves; of anaemia induced by hookworm? Hookworm produces a we agree the first step in the development of anaemia is obviously more typical iron-deficiency anæmia. In this conclusion with all who have studied the disease in Italy 15—19 or in other easily accomplished in patients with initially low reserves. countries (Jugoslavia,2O France,21 Portugal,22 Egypt,23 GuadaIt is usually a combination of these factors, and not lupe,24 Japan,25 Brazil.4 2.6 Of course when other factors are one alone, that explains the development of anaemia in present-either internal (deficiency in production of intrinsic ancylostomiasis. We conclude that hookworm anaemia factor, changes in intestinal bacterial flora, production of is a real well-defined clinical entity due to iron deficiency infection or infestation, hepatosplenic abnormalities, &c.) or induced worm infestation. by external (deficiencies in B12 and folic acid in the diet)-the PAOLO LARIZZA Department of Medical Pathology, anaemia may differ from pure iron-deficiency anaemia. Though University of Cagliari, SANDRO VENTURA. such associations are common in tropical countries, they are Italy. exceptional in Europe where ancylostome anaemia is usually of classical iron-deficiency type. SHOULD BIBLIOGRAPHIES GIVE TITLES OF Our study of more than 100 anaemic patients brought out PAPERS? theRe features of hookworm anæmia:

(1) Microcytic hypochromic anaemia with red hyperplasia of the bone-marrow caused by inhibition of maturation in the erythropoietic tissue.12 14 (2) Hyposideræmia (serum-iron under 50 ttg. per 100 ml.) 12 13 (plasma-transferrin above 350 pg. per hypertransferrinxmia 100 ml. 13 27), and hyperprotoporphyrinoglobulia (free-erythrocyteprotoporphyrin-9 above 100 pg. per 100 ml).13 28 29 (3) Intravenous 59Fe is distributed in the typical iron-deficiency pattern." 14 30 (4) Constant and quick response to iron therapy.12 14 "

SIR Mr. Patey (July 19) has expressed what is

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the wilfulness of British publishers growing in not allowing their contributors to provide the title of papers in their references. In your own case, the argument is perfectly valid-they would replace a short article. In other journals, and in many English books, the same practice prevails even when half a page is left blank at the end of an article or a chapter. " Now that " the English literature enjoys a prestige as great as that of Eng. Lit." it is surely mandatory that it should be given a final veneer of completeness. I suggest, therefore, that The Lancet makes the gesturehow I cannot suggest. Pressed as you are for space, it is a question of quality versus quantity. concern at

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Our investigations into other possible ways in which ansemia could be produced, such as excess haemolysis, or bone-marrow inhibition by hookworm toxins, have clearly shown that hookworm ansemia 12 14 is not determined in any of these ways. The correction of the anaemia by the simple administration Department of Pathology, Jackson Memorial Hospital, of iron, while infestation is still present, is the chief evidence MAX MILLARD. Miami, Florida. that the anaemia depends exclusively on iron deficiency. The most important question is how the hookworm induces REAPPEARANCE OF TABOPARESIS iron deficiency. Hookworm may impair the normal gastroduodenal processes by which food iron is dissolved and SIR,—Ihave just returned from a two months’ guest ionised. 14 30 It may also interfere with iron absorption by lectureship in Munich, and I can confirm Dr. Noel the duodenal and jejunal mucosa.14 30 A. duodenale also Harris’ remarks (Aug. 9) from my observations at the increases the elimination of iron from the gut by bleeding Universitaets-Nervenklinik. At least four recent cases from mucosal lesions. Basing our opinion on our experience of general paresis of the insane were admitted during with the radioactive method of Gerritsen et al. 31 we believe that, though haemorrhage, and consequent loss of iron is very my presence. Syphilis of the central nervous system had important in the genesis of the sideropenia, haemorrhage apparently not become as rare in the large German cities as it was here, but the recent increase in patients suffering cannot by itself explain all the anaemias in those infested by parasites. Severe ansemia may develop in patients with slight from taboparesis has been noticeable. It was thought blood-loss, and some men with ancylostomiasis may lose about to be due to the turmoil and strife of populations in Europe 10-20 ml. of blood a day without becoming anæmic. after the late war when treatment of venereal disease was The effect of hookworm may be enhanced by a diet extremely inadequate or lacking. poor in iron or by a diet abnormal in calcium and phosphorus Department of Experimental Psychiatry The Medical School, content. Such an alimentary factor is of very little significance W. MAYER-GROSS. Birmingham. in Italy and probably in other European countries. In other parts of the world, however, 432 it is of fundamental importNEUROLOGICAL COMPLICATIONS OF 15. Benetazzo, B., Gambini, C. Arch. ital. Sci. med. trop. Parass. 1950, ASIAN INLUENZA 31, 442. Cannavo, L., Caruselli, M. L’anchilostomiasi. I Congr. Studio Mal. Inf. Parass. Rome, 1949. 17. Del Zoppo, R. Ann. Ig. 1952, 3, 24. 18. Giromini, M., Granati, A. Anchilostomiasi ed idatidosi nei lavoratori agricoli, XIX Congr. Med. Lavoro. Rome, 1953. 19. De Maria, B., Rossi-Espagnet, A. Rass. Fisiopat. clin. terap. 1957, 29, 923. 20. Nikolic, J., Weiser, J. Arch. za Higijenu Rada, 1950, 1, 25. 21. Bonnin, H., Moretti, G. F. Pr. Méd. 1950, 58, 158. 22. Trincao, C., Parreira, F., Gouveia, E., Franco, A. Rev. Hémat. 1952, 7, 575, 580. 23. McFadzean, A. J. S., Wong, C. C. Trans. R. Soc. trop. Med. Hyg. 1952, 46, 674. 24. Languillon, J., Mauzè, J. Sang, 1950, 21, 652. 25. Baba, T., Nagata, K., Aizawa, T. Gunma J. med. Sci. 1956, 5, 281. 26. Cruz, W. O., De Mollo, R. P. Blood, 1948, 3, 456. 27. Ventura, S. Hœmatologica, 1954, 38, 227. 28. Ventura, S., Meduri, D., Dori, A., Filipazi, A. Hœmatologica, 1954, 38, 747. 29. Larizza, P., Ventura, S. Sang, 1956, 27, 610. 30. Ventura, S., Marinoni, U., Puricelli, G., Suardi, L., Matioli, G Hœmatologica, 1957, 42, 563. 31. Gerritsen, T., Heinz, H. J., Stafford, G. H. Science, 1954, 119, 412 32. Smillie, W. G. Mon. Rockefeller Inst. med. Res. 1922, 17, 73.

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SIR,-In your issue of July 5 you published four interesting papers dealing with the neuropsychiatr complications of Asian influenza. In your accompanying annotation you state that psychotic outbursts related to influenza " are a symptom of encephalitis and do nc: represent a latent psychosis which has been revealed by a generalised infection ". Following the epidemic of Asian influenza in Israel during November and December, 1957, 4 patients who developpsychotic manifestations during the course of the influence illness

were admitted to Talbieh Psychiatric Hospi:. Jerusalem. The psychosis appeared in 3 of the cases wit three days of the onset of the influenza. The correlation betW;’.: the development of the psychosis and recent infection ascertained by a progressive rise in titre of the hæmoagglu tion inhibition for the Asian virus variety during the psych outburst. (A detailed report of our cases was recently p lished in Dapim Refuim, Israel, 1958.)