[Heterozygosity in patients with pulmonary tuberculosis showing varying responses to therapy]

The distribution of the levels of heterozygosity was analyzed by 9 loci of genetic markers: PI, TF, PGM1, ACPI, HP, GC, GLO1 C3, and ESD in two groups of patients with pulmonary tuberculosis who had improvements (Group 1, n = 71) and failures (Group 2, n = 35). The heterozygosity observed in the groups was compared with that calculated by the Hardy-Weinberg law by using data on healthy controls (n = 328; the locus ESD was investigated in 78 healthy individuals). The analysis indicated that there were statistically significant deviations of the observed heterozygosities, g1, at 4 loci (GC, PI, C3, and ACPI) from the expected ones; h1 calculated from the data in the control group. The observed heterozygisities were higher than the expected ones at 3 loci (PI, C3, and ACPI), and at the GC locus. the observed heterozygosity being lower than the expected one. Comparing the observed heterozygosities. g1, within the loci, by using Fisher's exact test revealed significant differences between the groups of patients and healthy controls at the same loci, which showed significant differences between the observed and expected heterozygosities. There were no differences between the groups of patients by the observed heterozygosities. The mean expected heterozygosity were h = 0.386 +/- 0.056. The mean observed heterozygosity, were g = 0.415 +/- 0.037, 0.402 +/- 0.061, 0.371 +/- 0.055 in Groups 1 and 2 and in the controls, respectively. There were no differences between the mean expected and obsorved heterozygosities or between the mean observed heterozygosities in the three groups under study. It is proposed that a single locus rather than the mean heterozygosities should be used as a generalized nonspecific measure of genetic control over diseases while the former can show the involvement of a specific marker locus to develop a disease, the latter can simply veil the effects of each of the loci alone. Thus, the findings produce strong evidence for that there is a genetic control in the development of pulmonary tuberculosis.