02549nas a2200349 4500000000100000008004100001260001600042653002100058653002400079653002100103653003900124653001200163653001700175653001400192653001100206653001200217653001500229653001400244653002300258653003500281653002600316653001700342100001800359700001300377700001400390700001600404245010100420300001100521490000700532520164600539022001402185 1979 d c1979 Sep 2210aAcid Phosphatase10aAdenosine Deaminase10aAdenylate Kinase10aAfrican Continental Ancestry Group10aAlleles10aErythrocytes10aEsterases10aHumans10aleprosy10aMozambique10aPhenotype10aPhosphoglucomutase10aPhosphogluconate Dehydrogenase10aPolymorphism, Genetic10aSouth Africa1 aHitzeroth H W1 aWalter H1 aHilling M1 aMunderloh W00aGenetic markers and leprosy in South African negroes: Part II. Erythrocyte enzyme polymorphisms. a507-100 v563 a

The phenotype frequencies of the erythrocyte enzyme polymorphisms acid phosphatase (aP), phosphoglucomutase loci 1 and 2 (PGM1 and PGM2), adenylate kinase (AK), adenosine desaminase (ADA), esterase D (EsD) and 6-phosphogluconate dehydrogenase (6-PGD) were determined on a sample of 234-248 South African Negroes with leprosy. These results were compared with data of 841--997 healthy Negro controls of similar geographical and ethnic origin, in order to determine whether or not any association exists between specific phenotypes and the manifestation of leprosy. A part of the data included in the present study were compared with the data of a similar comparative analysis on Mozambican Negroes. With regard to the polymorphisms aP, PGM1 and PGM2, the results derived from South Africa and Mozambique exhibit reverse patterns of deviations from the null hypothesis. From this it does not appear justified to postulate an association between these genetic markers and the occurrence of leprosy. For the enzyme polymorphisms ADA, AK and EsD (data are confined to South African Negroes only) the distribution of phenotypes between patients and controls was very similar. The differences were not statistically significant. However, observations on the 6-PGD polymorphism (data are confined to South African Negroes only) showed an excess of phenotype PGD A among leprosy patients as compared with controls. The difference was statistically highly significant. Further studies based on additional samples are required to substantiate whether or not the statistical outcome reflects a true association between this phenotype and leprosy.

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