Abstract
A total of 203 couples with unexplained habitual abortions and 364 consecutive normal puerperae along with their live-born babies were studied. The analysis of wife-husband joint ABO blood group distribution in couples with habitual abortion showed an excess of A incompatible mating type and a defect of B incompatible type as compared with expected proportions assuming random mating. The joint wife-husband ABO blood group distribution was further analysed in relation to the adenosine deaminase (ADA) genotype. A defect of O-A and A-O couples when the wife carries the ADA*1/*1 genotype and the husband carries the ADA*2 allele, and a defect of O-O and A-A when the wife carries the ADA*2 allele were observed. In the sample of normal puerperae, analysis of the joint mother-newborn ABO distribution in relation to the ADA genotype showed a pattern similar to that observed in couples with habitual abortion, i.e. there is a defect of O-A and A-O when the mother carries the ADA*1/*1 genotype and the newborn carries the ADA*2 allele and a defect of O-O and A-A types when the mother carries the ADA*2 allele. Altogether the data suggest an early loss of O-A and A-O zygotes when they carry the ADA*2 allele and an early loss of O-O and A-A zygotes when the mother carries the ADA*2 allele resulting in a deficit of these zygotic classes among both spontaneously aborted fetuses and live-born infants. The pattern of association observed in the mother-fetus type O-A (incompatible according to conventional terminology) appears similar to that observed for the reciprocal A-O type (compatible according to conventional terminolgy). Therefore strictly conventional immunological mechanisms cannot explain the whole pattern of associations. Cell to cell interactions involving ABO antigens may have an important role at implantation: ADA, through the control of local adenosine concentration, could modulate these interactions influencing the probability of successful implantation.
Similar content being viewed by others
References
Abramson FD (1974) Spontaneous fetal death in man. Soc Biol 20:375–403
Arch JRS, Newsholme EA (1978) The control of the metabolism and the hormonal role of adenosine. Essays Biochem 14:82–183
Battistuzzi G, Scozzari R, Santolamazza P, Terrenato L, Modiano G (1974) Comparative activity of red cell adenosine deaminase allelic forms. Nature 251:711–712
Bottini E (1985) Interaction between adenosine deaminase and ABO system polymorphisms: effects on intrauterine survival and reproduction. Exp Clin Immunogenet 2:70–76
Bottini E, Carapella E, Cataldi L, Nicotra M, Lucarelli P, Lucarini N, Pascone R, Gloria Bottini F (1981) Adenosine deaminase polymorphism. Associations at clinical level suggest a role in cell functions and immune reactions. J Med Genet 18:331–334
Brown CM, Collis MG (1982) Evidence for an A2/R4 adenosine receptor in the guinea pig trachea. Br J Clin Pharmacol 76:381–387
Cohen BH (1970) ABO and Rh incompatibility. I. Fetal and neonatal mortality with ABO and Rh incompatibility: Some new interpretations. Am J Hum Genet 22:412–440
Diamond JM (1987) Causes of death before birth. Nature 329:487–488
Donofrio J, Coleman MS, Hutton JJ, Daoud A, Lapkin B, Dymin-ski J (1978) Overproduction of adenine deoxynucleosides and deoxynucleotides in adenosine deaminase deficiency with severe combined immunodeficiency disease. J Clin Invest 62:884–887
Dronamraiu KR, Wakin HG, Smith DJ, Bixler D (1984) Fetal mortality in oral cleft families (IX): Factors relating to the occurrence of sporadic clefts. Clin Genet 26:322–330
Editorial (1976) ADA deficiency. Lancet i: 895–896
Glass RH, Golbus MS (1978) Habitual abortion. Fertil Steril 29:257–265
Grubb R, Sjöstedt S (1955) Blood groups in abortion and sterility. Ann Hum Genet 19:183–194
Harris H, Hopkinson DA (1976) Handbook of enzyme electrophoresis in human genetics. North Holland, Amsterdam
Hershfield MS (1979) Apparent suicide inactivation of human lymphoblast S-adenosylhomocysteine hydrolase by 2′-deoxyadenosine and adenine arabinoside: a basis for direct toxic effects of analogs of adenosine. J Biol Chem 254:22–25
Hicks JB (1987) Mechanism of differentiation. Nature 326:444–445
Hiraizumi Y, Spradlin CT, Ito R, Anderson SA (1973) Frequency of prenatal deaths and its relationship to the ABO blood groups in man. Am J Hum Genet 25:362–371
Hirschhorn R (1977) Adenosine deaminase deficiency and immunodeficiencies. Fed Proc 36:2166–2170
Hirszfeld L, Zborowski H (1925) Gruppenspezifische Beziehungen zwischen Mutter und Frucht und elektive Durchlässigkeit der Placenta. Klin Wochenschr 4:1152–1157
Holgate ST, Mann JS, Cushley MJ (1984) Adenosine as a bronchoconstrictor mediator in asthma and its antagonism by methylxanthines. J Allergy Clin Immunol 74:302–306
Lauritsen JG (1977) Genetic aspects of spontaneous abortion. Thesis, University of Aarhus
Lauritsen JG, Jorgensen J, Kissmeyer-Nielsen F (1976) Significance of HLA and blood-group incompatibility in spontaneous abortion. Clin Genet 9:575–582
Lepore A, Lucarini N, Evangelista MA, Palombaro G, Londrillo A, Ballarini P; Borgiani P, Bottini GF, Bottini E (1989) Enzyme variability and neonatal jaundice. The role of adenosine deaminase and acid phosphatase. J Perinat Med 17:195–201
Levene H, Rosenfield RE (1961) ABO incompatibility. In: Steinberg AG (ed) Progress in medical genetics 1. Grune & Stratton, New York and London
Levine P (1943) Serological factors as possible causes in spontaneous abortions. J Hered 34:71–80
Londos C, Wolff J (1977) Two distinct adenosine-sensitive sites on adenylate cyclase. Proc Natl Acad Sci USA 74:5482–5486
Matsunaga E, Itoh S (1958) Blood groups and fertility in a Japanese population, with special reference to intrauterine selection due to maternal-foetal incompatibility. Ann Hum Genet 22:111–131
Mitchell BS, Mejias E, Daddona PE, Kelley WN (1978) Purinogenic immunodeficiency diseases: selective toxicity of deoxyribonucleosides for T cells. Proc Natl Acad Sci USA 75:5011–5014
Morton NE, Krieger H (1966) Natural selection on polymorphisms in northeastern Brazil. Am J Hum Genet 18:153–171
Nie NH, Hull CH, Jenkins JG, Steinbrenner K, Bent DH (1975) Statistical package for the social sciences. McGraw Hill, New York
Rosen FS (1978) Enzyme defects and immune dysfunction. Nature 276:559–560
Sjöstedt, S, Grubb R, Linell F (1951) Blood group incompatibility in abortion and sterility. Acta Pathol Microbiol Scand 28:375–387
Sokal RR, Rohlf FJ (1981) Biometry. WH Freeman, New York
Spencer N, Hopkinson DA, Harris H (1968) Adenosine deaminase polymorphism in man. Ann Hum Genet 32:9–14
Takano K, Miller JR (1972) ABO incompatibility as a cause of spontaneous abortion. Evidence from abortuses. J Med Genet 9:144–150
Vogel F, Motulsky AG (1986) Human genetics, 2nd end. Springer, Berlin Heidelberg New York
Wadheim CM, Rotter JI, Maclaren NK, Riley WJ, Anderson C (1986) Preferential transmission of diabetic alleles within the HLA gene complex. New Engl J Med 315:1314–1318
Wilson JM, Mitchell BS, Daddona PE, Kelley WN (1979) Purinogenic immunodeficiency disease. Differential effects of deoxyadenosine and deoxyguanosine on DNA synthesis in human T lymphoblasts. J Clin Invest 64:1475–1484
Winston RML, Handyside AH (1993) New challenges in human in vitro fertilization. Science 260:932–936
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Lucarini, N., Nicotra, M., Gloria-Bottini, F. et al. Interaction between ABO blood groups and ADA genetic polymorphism during intrauterine life. Hum Genet 96, 527–531 (1995). https://doi.org/10.1007/BF00197406
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1007/BF00197406