761 M (or those of an aspirin-treated normal to convert P.G. G2 to thromboxane A2 were unable but subject) of thromboxane synthetase. Hence, his to a deficiency owing platelets would show diminished aggregation responses to P.G. G2, as well as other aggregating agents. Further studies are in progress to characterise the defect in patients K and M, but these preliminary observations suggest that, in some congenital disorders, the synthesis of thromboxane A2 may be inhibited at a site subsequent to the formation of P.G. G2 (leaving the prostacyclin pathway intact) and that this type of inhibition may be achievable by pharmacological means as well.
platelets of patient
Roosevelt Hospital, New York 10019, U.S.A., and Columbia University, College of Physicians and Surgeons, New York
HARVEY J. WEISS BRUCE A. LAGES
SERUM-HIGH-DENSITY-LIPOPROTEIN AND UNIVERSITY GROUP DIABETES PROGRAM RESULTS
SIR,-The University Group Diabetes Program (U.G.D.P.) concluded that treatment with oral hypoglycaemic agents (tolbutamide or phenformin) led to an excess cardiovascular mortality.’The reason for this is not clear. Lopes-Virella and ColwelP have reported decreased a-lipoprotein and high-density-lipoprotein (H.D.L.) cholesterol levels in diabetics but without reference to age, sex, or type of treatment. We have measured lipoprotein levels in elderly diabetics on insulin or oral therapy. The patients were matched for age and had been CHOLESTEROL, TRIGLYCERIDE, AND LIPOPROTEIN FRACTIONS IN DIABETIC PATIENTS, 12 ON INSULIN AND 11 ON ORAL THERAPY
This work is supported by the United States Israel Bi-national Science Foundation grant no. HANOCH BAR-ON Department of Medicine B,
604.
Hadassah University Hospital, P.O.B. 499, Jerusalem, Israel
DANIELLA LANDAU ELLIOT BERRY
ABO BLOOD-GROUP DISTRIBUTION AND
ISCHÆMIC HEART-DISEASE
SIR,-Professor Mitchell’s paper (Feb. 5, p. 295) will reawaken interest in possible relationship between blood-group distribution and ischaemic heart-disease (I.H.D.). People with blood-group A or AB have a higher serum-cholesterol than those with blood-group 0 or B,1and blood group A is more common than expected in atherosclerosis.3 This difference in serum-cholesterol between the blood-groups is present at birth.4 A large male population survey revealed that pathological Q waves were significantly more frequent in men of blood group A or AB than in men of group B or 0. Men with bloodgroup A or AB also had a significantly higher frequency of a history of parental death before the age of 60 years.2 Within a population the blood-group distribution varies with age, especially above the age of 50,2 so age should be taken into account whenever blood-group distributions are compared. In a follow-up study of 42 804 men we found that the death-rate in those due to I.H.D. was 28% higher than expected (p<0.05) with blood-group A or AB. This evidence points to an effect of blood-group A on cardiovascular mortality and morbidity. There are striking geographical differences in blood-group distribution, with a diminishing frequency of blood-group A from the North of Europe to the South and the Middle East,S roughly parallelling the geographical prevalence of I.H.D. In our opinion blood-group A is a supplementary and independent risk factor for I.H.D. The evidence from our population study strongly supports this contention. H. KESTELOOT L. V. D. LINDEN G. WULLEMAN O. VAN HOUTE
Department of Epidemiology, Military Hospital, 1050 Brussels, Belgium Results as mean±s.E.M.
v.L.D.L.=Very-Iow-density lipoprotein. PICA WITH ZINC DEFICIENCY
treated for more than a year. There were three males and nine females in the insulin-treated group and six males and five females in the orally treated group. Plasma-lipoproteins were isolated by ultracentrifugation. Proteins were measured by a modification of the method of Lowry;4 triglycerides and cholesterol values were determined by the Technicon ’AutoAnalyzer 11’.1 The results are summarised in the table. Patients on oral therapy had significantly lower levels of H.D.L. protein and cholesterol. These differences are probably not related to the sex ratios of the two groups. Above the age of 50 changes in H.D.L. cholesterol between the sexes is far smaller than those observed at younger ages.6 Since a reduction in plasma-H.D.L. may accelerate the development of atherosclerosis and ischaemic heart-disease,’ 8 these results (if confirmed in a larger series) may help to explain the U.G.D.P.
findings. 1. University Group Diabetes Program Diabetes, 1970, 19 suppl. 2, p. 789. 2. University Group Diabetes Program J. Am. med. Ass. 1971, 217, 777. 3 Lopes-Virella M. F., Clowell J. A. Lancet, 1976, i, 1291. 4. Sata T., Havel R. J., Jones A. L. J. Lipid Res. 1972, 13, 757. 5. Manual of Laboratory Operations: Lipid Research Clinics Program, vol. I, lipid and lipoprotein analysis. National Heart and Lung Institute N.I.H. Bethesda, Maryland, 1974. 6 Fredrickson D. S., Levy R. I. in The Metabolic Basis of Inherited Disease (edited by J. B. Stanbury, J. B. Wyngaarden, and D. S. Fredrickson); p. 547. New
York,
1972.
7. Miller G. J., Miller N. E. Lancet, 1975, i, 16. 8. Berg. K, Børresen A.-L, Dahlén, G. ibid. 1976, i, 499.
SIR,-Karayalcin and Lanzkowski’ have described an unusual pica with zinc deficiency in a boy. An association between pica (geophagia) and zinc deficiency was reported in Turkey some years ago.7-BI Iran has been the focus of attention for zinc deficiency. We have found zinc deficiency in association with geophagia in Turkey in girls as well as boys,6aa finding which differed from Prasad’s in Iran.1O Iron, copper and magnesium deficiences have also been reported in Turkish children with geophagia .6Our studies on zinc absorption show that Turkish clay prevented absorption of zinc by the same mechanism as for iron-namely by the high cationexchange capacity previously described by our group."I Department of Pædiatrics,
Hæmatology-Oncology Research Unit, Medical School of Ankara University,
A. (OKÇUOĞLU) A. ARCASOY
Ankara, Turkey
Ş. CIN
ÇAVDAR
1. Flatz, G. Humangenetik, 1970, 10, 318. 2. Van Houte, O., Kesteloot, H. Acta cardiol. 1972, 27, 527. 3. Kingsbury, K. Lancet, 1971, i, 199. 4. Kesteloot, H., Claes, J., Dodion-Fransen, J. Eur. J. Cardiol. 1975, 2, 285. 5. Mourant, A. The Distribution of the Human Blood-groups. Oxford, 1954. 6. Karayalcin, G., Lanzkowsky, P. Lancet, 1976, n, 687. 7. Çavdar (Okçuoğlu) A., Arcasoy, A. Clin. Pediat. 1971, 11, 215. 8. Çavdar (Okçuoğlu) A. Arcasoy, A. Acta med. turc. 1973. 9, 33. 9. Çavdar (Okçuoğlu) A., Arcasoy, A., Cin, Ş. Am. J. clin. Nutr. (in the press). 10. Prasad, A., and others Am. J. Med. 1961. 31, 532. 11. Minnich, V., and others Am. J. clin. Nutr. 1968, 21, 78.