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At least 19 recordsLinked to original sources
PubMed1995

Body iron stores, dietary iron intake and coronary heart disease mortality.

OBJECTIVES: To assess whether increased body iron stores and dietary iron intake are associated with an increased risk of coronary heart disease mortality. DESIGN: A prospective population study with a mean mortality follow-up time of 14 years. SETTING: Participants attending a health screening examination carried out in several localities in Finland. SUBJECTS: All 6086 men and 6102 women aged from 45 to 64 years at the baseline examination without known heart disease, who had had serum iron and total iron binding capacity (TIBC) assessed. In a random fifth of these people, dietary iron intake was assessed by a dietary history. INTERVENTIONS: The study was observational without any interventions. MAIN OUTCOME MEASURES: Mortality from coronary heart disease. RESULTS: Altogether, 739 of the men and 245 of the women died from coronary heart disease. No relationship between TIBC and coronary mortality was observed in the men; in the women, an inverse although not significant association was found. Transferrin saturation was inversely but not significantly associated with coronary mortality in men; in women, the relationship was U-formed with a higher mortality at both the lower and higher ends of the distribution. Adjustment for other risk factors did not alter the results. No association was found with dietary iron intake and coronary mortality. CONCLUSIONS: The results do not corroborate earlier findings that excess body iron stores and increased iron intake are associated with an elevated risk of coronary heart disease.

Coronary Disease↗
PubMed1996

Relationship among reduced level of stored iron and dietary iron in trained women.

The aim of the study was to assess the relationship between dietary iron intake (both haeme- and non-haeme-iron) and its status in trained female subjects. Forty female athletes and forty non-trained women of the same age participated in this study. Blood samples were taken to assess haematological (red blood cell count-Er, haemoglobin concentration-Hb, packed cell volume-PCV) and iron related parameters (serum ferritin concentration-SF, serum iron concentration-SI, total iron binding capacity-TIBC). A self questionnaire was used to record food intake for seven days and diets were analyzed on the basis of mean daily nutrient intake, energy values, iron intake and sources of dietary iron. According to established clinical criteria for iron deficiency some athletes and control subjects shown iron depletion (20% and 10%, respectively), iron deficiency erythropoiesis (10% and 7.5%, respectively) and iron-deficient anaemia (10% and 7.5%, respectively). There was no difference in the mean total dietary iron intake between the two female groups, while the mean intake of haeme-iron was significantly lower in the control group. The findings in the present study are: (1) the significant relation exists between serum ferritin level and quantity of haeme-iron intake (but not with total iron intake), and (2) 10% of female athletes have iron deficiency.

Adolescent↗
PubMed2005

Hemochromatosis gene mutations, body iron stores, dietary iron, and risk of colorectal adenoma in women.

BACKGROUND: Some experimental evidence suggests that iron may play a role in colorectal carcinogenesis, but human data for this role have been conflicting, possibly because of problems related to study design or measurement of iron exposure. We assessed dietary iron intake and genetic and biochemical markers of iron status in a prospective, nested case-control study of women enrolled in the Nurses' Health Study. METHODS: Among 32 826 women who provided a blood specimen, we identified 527 women with colorectal adenoma and 527 matched control subjects who underwent endoscopy but were not diagnosed with adenoma after blood collection. We assessed iron intake, mutations in the HFE gene that are associated with hereditary hemochromatosis (i.e., H63D and C282Y), and plasma biochemical measures of total body iron, including transferrin saturation and the ratio of the concentrations of transferrin receptors to ferritin. Logistic regression models were used to estimate relative risks (RR) and 95% confidence intervals (CI). All statistical tests were two-sided. RESULTS: Women with any HFE gene mutation had higher total body iron stores, as reflected by higher transferrin saturations (P < .001) and lower levels of the ratio of transferrin receptors to ferritin (P = .02), than women with no HFE gene mutation. However, HFE gene mutations were not associated with risk of adenoma (multivariable RR = 1.08, 95% CI = 0.83 to 1.39; P = .58). Moreover, comparison of extreme categories showed no associations between adenoma and the extent of transferrin saturation (multivariable RR = 0.96, 95% CI = 0.63 to 1.47; Ptrend = .66), the ratio of transferrin receptors to ferritin (multivariable RR = 0.98, 95% CI, 0.60 to 1.60; Ptrend = .99), or dietary iron intake (multivariable RR = 1.04, 95% CI = 0.68 to 1.57; Ptrend = .94). CONCLUSIONS: Although our study used several distinct measures of iron status (i.e., genetic mutations, biochemical markers, and dietary intake) and a nested case-control design, we did not observe a role for iron in the pathogenesis of colorectal neoplasia in women.

Adenoma↗
PubMed1978

Estimation of available dietary iron.

Dietary iron requirements are dependent on the amount and availability of food iron ingested. On the basis of recent studies of food iron absorption employing extrinsic tag techniques, the availability of heme iron has been defined and estimates of the availability of nonheme iron based on the amounts of enhancing substances appear possible. A model has been developed whereby the availability of iron in a given meal may be estimated. Calculations are made on a meal basis of 1) the amount of heme iron and its availability, and 2) the amount of nonheme iron and its availability as influenced by the meal's content of enhancing factors. Examples of these calculations are provided.

Absorption↗
PubMed1976

Patterns of iron storage in dietary iron overload and idiopathic hemochromatosis.

Bone marrow iron stores rise in proportion to the total body iron store in dietary iron overload. The situation in the genetic disorder of idiopathic hemochromatosis is not as clear. A method for measuring the storage iron concentration chemically on samples of bone marrow obtained by trephine needle biopsy was therefore developed. Its value as a measure of tissue iron stores was established in a preliminary investigation in which specimens of liver, spleen, and bone marrow were obtained at necropsies on 66 South African Negroes among whom dietary iron overload is common. A wide range of nonheme iron concentrations was found, but in each individual there was a highly significant correlation between the concentrations in the three tissues. Nonheme iron concentrations were then determined on trephine bone marrow biopsy specimens from eight Caucasian patients with untreated idiopathic hemochromatosis, and on percutaneous liver biopsy specimens from four of them. The concentrations in the livers were in the anticipated range of 5,000 mug per gram wet weight (2 per cent dry weight). In contrast the geometric mean value for bone marrow iron concentration was 186 mug per gram wet weight, a figure that fell below the fiftieth percentile for marrow iron concentrations in the South African Negroes, whereas the geometric mean liver iron concentration was above the ninetieth percentile. These findings indicate that subjects with idiopathic hemochromatosis whose liver iron stores are grossly increased do not show a comparable rise in bone marrow iron stores.

Adult↗
PubMed2000

Prediction of dietary iron absorption: an algorithm for calculating absorption and bioavailability of dietary iron.

BACKGROUND: Dietary iron absorption from a meal is determined by iron status, heme- and nonheme-iron contents, and amounts of various dietary factors that influence iron absorption. Limited information is available about the net effect of these factors. OBJECTIVE: The objective was to develop an algorithm for predicting the effects of factors known to influence heme- and nonheme-iron absorption from meals and diets. DESIGN: The basis for the algorithm was the absorption of iron from a wheat roll (22.1 +/- 0.18%) containing no known inhibitors or enhancers of iron absorption and adjusted to a reference dose absorption of 40%. This basal absorption was multiplied by the expected effect of different amounts of dietary factors known to influence iron absorption: phytate, polyphenols, ascorbic acid, meat, fish and seafood, calcium, egg, soy protein, and alcohol. For each factor, an equation describing the dose-effect relation was developed. Special considerations were made for interactions between individual factors. RESULTS: Good agreement was seen when measurements of iron absorption from 24 complete meals were compared with results from use of the algorithm (r(2) = 0.987) and when mean iron absorption in 31 subjects served a varied whole diet labeled with heme- and nonheme-iron tracers over a period of 5 d was compared with the mean total iron absorption calculated by using the algorithm (P = 0.958). CONCLUSIONS: This algorithm has several applications. It can be used to predict iron absorption from various diets, to estimate the effects expected by dietary modification, and to translate physiologic into dietary iron requirements from different types of diets.

Alcohol Drinking↗
PubMed1998

Iron status and dietary iron intake of 6-24-month-old children in Adelaide.

OBJECTIVE: Chronic iron deficiency in children is associated with anaemia and impaired mental and psychomotor development. The aim of this study was to assess the iron status and dietary intake of 6-24-month-old Caucasian and Asian children living in metropolitan Adelaide. METHOD: A total of 234 healthy children (82% Caucasian and 18% Asian) aged 6-24 months were studied. Dietary iron intake of children was estimated from semiquantitative diet recall questionnaire administered to their parents. Blood samples for full blood count, serum ferritin (SF), serum iron (SI) and transferrin (TF) level estimations were obtained by venesection. Based on the laboratory test results, infants were classified as iron sufficient (IS) if the haemoglobin (Hb) concentration was > 110 g L(-1), SF > or = 15 microg L(-1), TF2 3.0 g L(-1), SI > or = 8 micromol L(-1) and iron saturation (ISAT) > or = 12%; or nonanaemic iron deficiency (NAID) if the Hb concentration was > 110 g L(-1) and SF < 15 microg L(-1) or SI < 8 micromol L(-1), TF > 3.0 g L(-1), and ISAT < 12%; or as iron deficiency anaemia (IDA) if the Hb concentration was < 110 g L(-1) in association with SF < 15 microg L(-1) or with SI < 8 micromol L(-1), TF > 3.0 g L(-1) and ISAT < 12%. RESULTS: Sixty-nine per cent of Caucasian children were classified IS, 25% as NAID and 6% were IDA; while 72% of Asian children were classified IS, 14% as NAID and 14% were IDA. Multivariate analysis demonstrated that factors associated with iron deficiency (SF </5 microg L(-1)) included age, duration of breast-feeding and cows' milk intake. CONCLUSION: Iron deficiency is common in our young population. Additional strategies to prevent IDA need be developed and evaluated in Australian infants.

Anemia, Iron-Deficiency↗
PubMed1996

Deliberations and evaluations of the approaches, endpoints and paradigms for iron dietary recommendations.

Iron deficiency severe enough to cause anemia is associated with significant morbidity while uncontrolled iron absorption which occurs in disorders such as hereditary hemochromatosis causes multiorgan failure and early death. Preliminary data from the Third National Health and Nutrition Examination Survey demonstrate that the prevalence of iron deficiency anemia in the United States is now very low. This implies that the current iron consumption is adequate for most individuals. An important unresolved question relates to the necessity for further reducing the prevalence of iron deficiency without anemia. More information is required to determine whether this lesser degree of iron deficiency is harmful. Recent survey data indicate that concomitantly with the reduced prevalence of iron deficiency there has been a rise in serum ferritin concentrations in American men and postmenopausal women. These findings have led to concern about the effectiveness of the physiological mechanisms for limiting storage accumulation in normal individuals and carriers of the hemochromatosis gene when dietary iron content is high. Furthermore, recent epidemiological observations suggest that a modest increase in iron stores (in a range previously considered safe) is a possible risk factor for ischemic heart disease and cancer; however, a causal relationship remains to be proven. Nonetheless, because there is no known benefit of high iron storage status, it seems prudent to avoid further increases in and possibly to reduce the dietary iron intake of men and postmenopausal women. Mean intake in these groups exceeds the current RDA by a significant margin. Therefore, the sources of dietary iron as well as other factors contributing to high serum ferritin values have to be defined. Also, efforts should be made to increase the awareness of professionals and the public about the possible risks of excessive dietary iron. The complexity of the Western diet and an incomplete understanding of all of the factors affecting serum ferritin concentrations make it very difficult to specify a safe upper range for daily iron intake at the present time.

Adolescent↗
PubMed2004

Iron status and dietary iron intake of adolescents from a rural community in Sabah, Malaysia.

Iron deficiency anaemia (IDA) is the most prevalent micronutrient deficiency in the world affecting the general health and wellbeing of millions. In Malaysia, moderately high prevalences of anaemia have been reported amongst infants, young children and women of childbearing age. Data is scant for the adolescents. This study was undertaken to assess the iron status and dietary intake of 165 adolescents, comprising 74 male and 91 female subjects, aged 12 to 19 years, from the rural communities in Tuaran District of Sabah, Malaysia. Convenience sampling was used for the selection of study subjects. Multiple iron status indicators namely, serum ferritin (SF), transferrin saturation (TS), mean corpuscular volume (MCV) and haemoglobin (Hb) were determined for the study. The mean age of the subjects was 15.2 +/-2.1 years. While the majority of the subjects (77.6%) had normal body mass index (BMI) values, 17.6% were underweight and 4.8% overweight. About 35% to 40% of the subjects showed deficient values for haematocrit, serum ferritin, serum iron, mean corpuscular haemoglobin (MCH), mean corpuscular volume (MCV) and transferrin saturation (TS), and 20% were anaemic (Hb <12 g/L). Using the multiple criteria of iron status indicators, the prevalence of iron depletion, iron deficiency and IDA in the male and female adolescents were 5.4% vs. 6.6%, 18.9% vs. 26.4% and 5.4% vs. 26.4%, respectively. Iron deficiency anaemia (85.0%) contributed largely to the prevalence of anaemia. The dietary iron intake of the adolescents was unsatisfactory, with approximately 98% of subjects failing to meet the Malaysian RDA level. Almost all the female subjects (91%) had dietary iron intake below two-thirds of the RDA level compared with a much smaller proportion for the male adolescents (68%). The prevalence of IDA in the present study population, especially in the female adolescents, appears to be a significant public health problem. Priority should therefore be given to the eradication of iron deficiency in adolescents from low-income areas by dietary modification and micronutrient supplementation amongst female adolescents.

Adolescent↗
PubMed2000

Iron stores and haemoglobin iron deficits in menstruating women. Calculations based on variations in iron requirements and bioavailability of dietary iron.

BACKGROUND: Iron stores and haemoglobin iron deficits in menstruating women can be calculated from body iron losses and absorption of dietary iron using recently developed methods. OBJECTIVE: To examine iron balance (iron status) expressed as body iron stores or haemoglobin iron deficits in menstruating women from amounts of iron lost (iron requirements) and amounts of dietary iron absorbed. Calculations are made both of stationary states and of the rate of changes in iron stores (iron status) when any of the two main factors determining iron balance are changed. DESIGN: The study is based on (1) previous and new equations describing relationships between iron absorption, iron requirements (losses), iron stores and/or haemoglobin deficits and (2) published data on iron requirements and their variation in menstruating adult women. RESULTS: Both iron stores and haemoglobin iron deficits are strongly related to iron requirements and absorption of dietary iron and follow the same equations during states of iron repletion and iron deficiency. When, for example, increasing or decreasing the bioavailability of the dietary iron, about 90% of the change in iron stores will occur within 1 y. CONCLUSIONS: There are strong relationships between iron requirements, bioavailability of dietary iron and amounts of stored iron. The observations that a reduction in iron stores and a calculated decrease of haemoglobin iron had the same increasing effect on iron absorption suggest that the control of iron absorption is mediated from a common cell, that may register both size of iron stores and hemoglobin iron deficit, eg the hepatocyte. European Journal of Clinical Nutrition (2000) 54, 650-657.

Absorption↗
PubMed1999

Level of dietary iron, not type of dietary fat, is hyperlipidemic in copper-deficient rats.

OBJECTIVE: This study was conducted to determine whether high dietary iron will negate the protective effect of unsaturated fat against hyperlipidemia. METHODS: Forty-eight weanling, male Sprague Dawley rats were randomly assigned to eight dietary groups differing in the levels of copper and iron and type of dietary fat (saturated or unsaturated). The diets were either deficient (0.6 microg Cu/g) or adequate (6.8 microg Cu/g) copper and either adequate (53 microg Fe/g) or high (506 microg Fe/g) iron. All diets contained starch as the sole source of dietary carbohydrate. RESULTS: Regardless of the type of dietary fat, three copper-deficient rats fed the high levels of dietary iron died prematurely due to ruptured hearts. Surviving rats belonging to the copper deficiency and high-dietary iron regimen developed severe anemia, enlarged hearts and livers, and exhibited the highest levels of liver iron. These rats also developed hypercholesterolemia. Triglycerides were elevated by the consumption of high iron diets. CONCLUSION: Data show that levels of dietary iron, not the type of dietary fat, are potential inducers of hypertriglyceridemia. Data also show that the combination of high iron intake and dietary copper deficiency is responsible for elevating blood cholesterol.

Analysis of Variance↗
PubMed1983

Iron requirements and bioavailability of dietary iron.

Over the past few decades so much knowledge has been gained about iron needs, dietary iron availability and adequacy that it is now one of the best defined nutrients in these respects. Development of new, accurate methods for the measurement of both the losses of iron from the body and the absorption of iron from the diet has significantly contributed to this situation. Present knowledge of iron needs is summarized. Specific to iron are the much higher needs in women than in men and the great variation in needs between different women due to a marked physiological variation in menstrual iron losses and to the effects of pregnancies. Iron availability is discussed separately for heme and non-heme iron (the major type of food iron). Heme iron in small amounts is, on average, better absorbed than non-heme iron. The absorption of heme iron is influenced very little by the iron status of the subject and by the other food components in the diet with the exception of meat which stimulates absorption. On the other hand, the absorption of non-heme iron is markedly influenced both by the iron status of the subject and a great number of dietary factors. The absorption of iron from the diet is thus determined more by meal composition than by the amount of iron present in the diet. The great variation in absorption between different meals is illustrated and the importance of various factors influencing non-heme iron absorption is also demonstrated. Whilst the mode of food preparation itself influences iron absorption, meat or fish and ascorbic acid are some principal food constituents that enhance absorption of iron. On the other hand, several factors like tannins, phytates, phosphates, soya protein products and various "dietary" fibres have been reported to inhibit non-heme iron absorption. A consideration of the nutritional adequacy of iron high-lights the importance of methods of evaluation, particularly the usefulness of the "bioavailable nutrient density" (BND) approach for different meals; BND for iron represents the amount of iron absorbed per 1'000 kcal (4'180 kJ). The main problem in iron nutrition in Western countries today is that arising from the combination of a low-energy intake, especially in women having the highest iron needs, with a conservation in the choice of meals/meal composition. Provision of bioavailable dietary iron to meet needs has hence not been adjusted to "modern life".

Ascorbic Acid↗
PubMed1998

Increases in the concentrations of available iron in response to dietary iron supplementation are associated with changes in crypt cell proliferation in rat large intestine.

High concentrations of iron in the diet have been shown to increase chemically induced colorectal tumors in rats. It is therefore important to understand the influence of dietary iron on the concentration of unabsorbed iron in the large intestine and its distribution between soluble and insoluble pools in the luminal compartment. We sought to investigate this issue and to establish whether iron modifies mucosal cell proliferation, which is thought to influence initiation and progression through the adenoma carcinoma sequence. In the first experiment, four groups of seven rats were fed diets at two concentrations of iron, 29 and 102 mg/kg, with or without the addition of 2.5 g phytic acid/kg. The concentrations of iron in the contents of the large bowel extractable with water ("free iron") or a buffered EDTA solution ("exchangeable iron") were determined. The concentration of freely soluble iron increased approximately 100% with iron supplementation in both the cecum and the colon, and there was an approximately five- to sixfold increase in exchangeable iron at both sites (P < 0. 05). In a second experiment with identical feeding conditions, there was a significantly greater number of cell divisions per crypt in the colon of the high iron group and a significantly greater number of cell divisions in the upper part of the crypt in the cecum. The concentrations of free and exchangeable iron observed in colonic contents in this study are consistent with those reported by others to increase free radical production in fecal material. Further studies are required to determine whether the small changes in crypt cytokinetics are a consequence of oxidative mucosal damage.

Animals↗
PubMed2005

Ferroportin (Q248H) mutations in African families with dietary iron overload.

BACKGROUND: Dietary iron overload found in sub-Saharan Africa might be caused by an interaction between dietary iron and an iron-loading gene. Caucasian people with ferroportin gene mutations have iron overload histologically similar to that found in African patients with iron overload. Ferroportin is also implicated in the hypoferremic response to inflammation. The prevalence of the ferroportin Q248H mutation, unique to African people, and its association with dietary iron overload, mean cell volume (MCV) and C-reactive protein (CRP) were examined in 19 southern African families. METHODS: Polymerase chain reaction (PCR) and restriction enzyme digestion were used to identify the Q248H mutation. Statistical analysis was carried out to correlate the presence of the mutation with markers of iron overload and inflammation. RESULTS: We identified three (1.4%) Q248H homozygotes and 53 (24.1%) heterozygotes in the families examined in the present study. There was no increased prevalence of the mutation in index subjects or their families. Logistic regression showed significantly higher serum ferritin concentrations with the mutation. The mean cell volume (MCV) was significantly lower, and the serum CRP significantly higher in subjects who carried the mutation. CONCLUSIONS: The present study of 19 families with African iron overload failed to show evidence that the ferroportin (Q248H) mutation is responsible for the condition. Logistic regression, correcting for factors influencing iron status, did show increased ferritin levels in individuals with the mutation. The strong association with low MCV suggests the possibility that the ferroportin (Q248H) mutation might interfere with iron supply, whereas the elevated serum CRP might indicate that the ferroportin mutation influences the inflammatory response in African populations.

Biomarkers↗
PubMed1996

Effect of high levels of dietary iron, iron injection, and dietary vitamin E on the oxidative stability of turkey meat during storage.

A study was carried out to evaluate the combined effect of excess Fe, supplied either in the diets (Experiments 1, 2, and 3) or by injection (Experiment 4), and various levels of dietary vitamin E on the oxidative stability of the thigh muscle of turkeys stored at -18 C for various periods. Iron was added to a commercial diet that already contained 20 mg/kg supplemental Fe, at concentrations of 0, 100, 250, and 500 mg/kg as ferrous sulfate or injected as Fe-dextran to the left drumstick muscle (total amount of 1.2 g per turkey). Vitamin E was added to the experimental diets not already supplemented with this vitamin, at levels of 0, 28, and 150 mg/kg. Thiobarbituric acid reactive substances (TBARS) values of the meat gradually increased as its storage duration increased from about 15 to 120 d. Increasing dietary Fe supplementation from 0 to 500 mg/kg tended to decrease TBARS values in one experiment only; otherwise, this variable was not affected by dietary Fe level. Injection of Fe significantly (P < 0.05) increased TBARS values, only in meat from the injected side. The TBARS values of the meat up to about 30 d of storage were significantly lower due to the supplementation of the diet with vitamin E at a level of 28 mg/kg in one out of three experiments and at a level of 150 mg/kg in two out of two experiments. The protective effect of the higher level of vitamin E remained evident after about 108 d of storage. No interaction was observed between Fe and vitamin E treatments in their effect on TBARS values. Blood hemoglobin concentrations were significantly increased by the supplementation of the diet with the high levels of Fe, in one experiment only. This variable was consistently and significantly increased from about 10 to 23 wk of age. The results show that high levels of dietary Fe do not adversely affect the oxidative stability of thigh meat of turkey; however, stability might be reduced by injected Fe. Dietary vitamin E, at a level of 150 mg/kg, consistently increased this stability.

Aging↗
PubMed2004

Duodenal HFE expression and hepcidin levels determine body iron homeostasis: modulation by genetic diversity and dietary iron availability.

HFE affects the interaction of transferrin bound iron with transferrin receptors (TfR) thereby modulating iron uptake. To study genetically determined differences in HFE expression we examined individual HFE levels in C57BL/Sv129 mice and assessed their relationship to the regulation of iron homeostasis in the duodenum and the liver, and their regulation by diet. We found an up to 14-fold variation in inter-individual expression of HFE mRNA in the duodenum. Mice with high duodenal HFE mRNA expression presented with significantly higher levels of TfR and DMT-1 mRNAs and an increased IRP-1 binding affinity as compared to mice with low HFE levels. Duodenal HFE expression was positively associated with serum iron and liver HFE levels. Dietary iron supplementation decreased HFE in the duodenum but not in the liver. This was paralleled by reduced amounts of DMT-1 and FP-1 in the duodenum while the expression of DMT-1, FP-1, and hepcidin in the liver were increased with dietary iron overload. Duodenal and liver HFE levels are regulated by divergent penetration of as yet unelucidated modifier genes and to a much lesser extent by dietary iron. These measures control duodenal iron transport and liver iron homeostasis by modulating HFE expression either directly or via stimulation of iron sensitive regulatory molecules, such as hepcidin, which then exert their effects on body iron homeostasis.

Animals↗
PubMed1999

Non-transferrin-bound iron and hepatic dysfunction in African dietary iron overload.

BACKGROUND: Circulating iron is normally bound to transferrin. Non-transferrin-bound iron (NTBI) has been described in most forms of iron overload, but has not been studied in African dietary iron overload. This abnormal iron fraction is probably toxic, but this has not been demonstrated. METHODS: High-pressure liquid chromatography was used to assay serum NTBI in 25 black African subjects with iron overload documented by liver biopsy and in 170 relatives and neighbours. Levels of NTBI were correlated with indirect measures of iron status and conventional liver function tests. RESULTS: Non-transferrin-bound iron (> 2 micromol/L) was present in 43 people, 22 of patients of whom underwent liver biopsy and 21 relatives and neighbours. All but four of these had evidence of iron overload on the basis of either liver biopsy or elevated transferrin and serum ferritin concentrations. Among all 195 subjects, the presence of NTBI in serum was independently related to elevations in alanine and aspartate aminotransferase activity and bilirubin concentration. This relationship between serum NTBI and hepatic dysfunction was confirmed in the subgroup of 25 subjects with iron overload documented by liver biopsy. Non-transferrin-bound iron correlated significantly with elevations in alanine and aspartate aminotransferase activities after adjustment for hepatic iron grades, inflammation and diet. CONCLUSIONS: Non-transferrin-bound iron was found to be commonly present in African patients with dietary iron overload and to correlate with transferrin saturation and serum ferritin concentration. The independent relationship between NTBI and elevated liver function tests suggests that it may be part of a pathway leading to hepatic injury.

Aspartate Aminotransferases↗
PubMed2001

Association of pulmonary tuberculosis with increased dietary iron.

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.

Adult↗