To determine whether increased dietary iron could be a risk factor for active tuberculosis, dietary iron history and human immunodeficiency virus (HIV) status were studied in 98 patients with pulmonary tuberculosis and in 98 control subjects from rural Zimbabwe. Exposure to high levels of dietary iron in the form of traditional beer is associated with increased iron stores in rural Africans. HIV seropositivity was associated with a 17.3-fold increase in the estimated odds of developing active tuberculosis (95% confidence interval [95% CI], 7.4-40.6; P<.001), and increased dietary iron was associated with a 3.5-fold increase (95% CI, 1.4-8.9; P=.009). Among patients treated for tuberculosis, HIV seropositivity was associated with a 3.8-fold increase in the estimated hazard ratio of death (95% CI, 1.0-13.8; P=.046), and increased dietary iron was associated with a 1.3-fold increase (95% CI, 0.4-6.4; P=.2). These findings are consistent with the hypothesis that elevated dietary iron may increase the risk of active pulmonary tuberculosis.
Iron status in man is influenced by environmental and genetic factors. The molecular variation of haptoglobin is one of the genetic factors influencing iron status in Caucasians. Differences in iron metabolism between blacks and whites have been reported. We wanted to investigate the effect of haptoglobin polymorphism on iron status in blacks. We studied 300 African subjects who were apparently healthy with normal erythrocyte sedimentation rate and with no increase in dietary iron because of traditional beer consumption. We determined haptoglobin (Hp) phenotypes using starch gel electrophoresis and measured indirect iron status indices using standard methods. We compared iron status indices according to haptoglobin type. Ninety two individuals (31%) had Hp 1-1, 114 persons (38%) had Hp 2-1, 20 subjects (7%) had Hp 2-1(Modified) and 54 individuals (18%) had Hp 2-2 type. Haptoglobin was not detectable in 19 subjects and Hp 2-1(Johnson) was found in one subject. In both males and females, serum iron concentration, total iron binding capacity, transferrin saturation and ferritin concentration were not different with regard to Hp phenotype. These results suggest that haptoglobin phenotypic variation may not be a factor which influences iron status in black persons.
Background: Genetic variants of human transferrin (TF) have been described, but little is known about their functional differences. We studied iron status according to TF phenotype in a healthy Zimbabwean population and in subjects at risk of African iron overload. Methods: The study population consisted of 483 nondrinkers, 31 drinking spouse pairs, and 5 family pedigrees (n = 88) with index cases of iron overload. TF phenotypes were determined using starch gel electrophoresis. To evaluate iron status, serum iron, total iron-binding capacity (TIBC), ferritin, and soluble TF receptors were measured, and the percentage of saturation and the serum iron:TF ratio were calculated. The binding of the TF variants was studied by equilibrium dialysis. Results: The reference population was characterized by a high TF D allele frequency (0.050) and a complete absence of homozygous TF DD individuals. Similar allele frequencies were observed in subjects at risk of African iron overload. In the reference population, male TF CD heterozygotes had significantly lower (P <0.01) values for serum iron, TIBC, TF saturation, and serum iron:TF ratio than the TF CC homozygotes; in females, only TIBC was significantly different. Overall red blood cell indices did not differ according to TF phenotype. In the population at risk of African iron overload, only serum iron:TF ratio was consistently significantly lower in TF CD phenotypes (P <0.05). After equilibrium dialysis, the amount of iron bound by TF was significantly lower (P <0.01) in TF CD individuals. Conclusions: The present data demonstrate a functional difference between TF phenotypes in blacks.
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