Establishment of a simple test for iron absorption from the gastrointestinal tract

Kobune, Masayoshi; Miyanishi, Koji; Takada, Kohichi; Kawano, Yutaka; Nagashima, Hiroyuki; Kikuchi, Shohei; Murase, Kazuyuki; Iyama, Satoshi; Sato, Tsutomu; Sato, Yasushi; Takimoto, Rishu; Kato, Junji

doi:10.1007/s12185-011-0878-8

Cited by 20 publications

(25 citation statements)

References 13 publications

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“…We believe that the transient increases in transferrin saturation reflect the fact that the blood draws were not timed relative to drug intake. As described by Kobune et al, 29 transferrin saturation can rise to .60% within 2-3 hours after intake of an oral iron dose. In future studies, it will be important to specify that laboratory draws for transferrin saturation be obtained before daily dosing.…”

Section: Discussionmentioning

confidence: 78%

Effects of Ferric Citrate in Patients with Nondialysis-Dependent CKD and Iron Deficiency Anemia

Fishbane

Block

Loram

et al. 2017

JASN

131

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Iron deficiency anemia is common and consequential in nondialysis-dependent CKD (NDD-CKD). Efficacy and tolerability of conventional oral iron supplements are mixed; intravenous iron administration associates with finite but important risks. We conducted a randomized double-blind clinical trial in adults with NDD-CKD and iron deficiency anemia to compare the safety and efficacy of oral ferric citrate (n=117) and placebo (n=115). The primary end point was the proportion of patients who achieved a $1.0 g/dl increase in hemoglobin at any time during a 16-week randomized period. Patients who completed the 16-week period could also participate in an 8-week open-label extension period. Significantly more patients randomized to ferric citrate achieved the primary end point (61 [52.1%] versus 22 [19.1%] with placebo; P,0.001). All secondary end points reached statistical significance in the ferric citrate group, including the mean relative change in hemoglobin (0.84 g/dl; 95% confidence interval, 0.58 to 1.10 g/dl; P,0.001) and the proportion of patients who achieved a sustained increase in hemoglobin ($0.75 g/dl over any 4-week period during the randomized trial; 57 [48.7%] versus 17 [14.8%] with placebo; P,0.001). Rates of serious adverse events were similar in the ferric citrate (12.0%) and placebo groups (11.2%). Gastrointestinal disorders were the most common adverse events, with diarrhea reported in 24 (20.5%) and 19 (16.4%) and constipation in 22 (18.8%) and 15 (12.9%) patients treated with ferric citrate and placebo, respectively. Overall, in patients with NDD-CKD, we found oral ferric citrate to be a safe and efficacious treatment for iron deficiency anemia.

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Section: Discussionmentioning

confidence: 78%

Effects of Ferric Citrate in Patients with Nondialysis-Dependent CKD and Iron Deficiency Anemia

Fishbane

Block

Loram

et al. 2017

JASN

131

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“…Iron absorption from the GI tract was measured using the iron absorption test established in our laboratory, as described previously . In brief, the test was started at 9 am after an overnight fast.…”

Section: Methodsmentioning

confidence: 99%

Increased duodenal iron absorption through up‐regulation of divalent metal transporter 1 from enhancement of iron regulatory protein 1 activity in patients with nonalcoholic steatohepatitis

et al. 2015

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Increased hepatic iron accumulation is thought to be involved in the pathogenesis of nonalcoholic steatohepatitis (NASH). Hepatic iron accumulation, as well as oxidative DNA damage, is significantly increased in NASH livers. However, the precise mechanism of iron accumulation in the NASH liver remains unclear. In this study, 40 cases with a diagnosis of NASH (n 5 25) or simple steatosis (SS; n 5 15) by liver biopsy were enrolled. An oral iron absorption test (OIAT) was used, in which 100 mg of sodium ferrous citrate was administered to each individual. The OIAT showed that absorption of iron from the gastrointestinal (GI) tract was increased significantly in NASH patients, compared to SS and control subjects. Iron reduction therapy was effective in patients with NASH, who exhibited iron deposition in the liver and no alanine aminotransferase improvement after other therapies (n 5 9). Serum hepcidin concentration and messenger RNA (mRNA) levels of divalent metal transporter 1 (DMT1) also were significantly elevated in patients with NASH. OIAT results were correlated with grade of liver iron accumulation and DMT1 mRNA levels. Then, we demonstrated that DMT1 mRNA levels increased significantly in Caco-2/TC7 cell monolayers cultured in transwells with serum from NASH patients. An electrophoresis mobility shift assay showed activation of iron regulatory protein (IRP) in those cells, and IRP1 small interfering RNA clearly inhibited the increase of DMT1 mRNA levels. Conclusion: In spite of elevation of serum hepcidin, iron absorption from the GI tract increased through up-regulation of DMT1 by IRP1 activation by humoral factor(s) in sera of patients with NASH. (HEPATOLOGY 2015;62:751-761)

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“…None of the patients showed a positive finding to suggest any of the above mentioned conditions It was, therefore, suspected that our patients suffered from some defect in intestinal iron absorption. To ascertain this, they were subjected to low dose iron tolerance test [3][4][5] with 10 mg of oral ferrous sulphate (Fer-in-sol in 30 ml of de-ionized iron free water), given on empty stomach followed by one hourly estimation of serum iron for 4 hours and then after 24 hours. The results are shown in Figure 2.…”

Section: Journal Of Hematology and Thromboembolic Diseasesmentioning

confidence: 99%

“…However, a minority of IDA patients remain unresponsive. Nearly 50 cases have been described in medical literature [2,3]. For the cause of non-responsive IDA (NR-IDA) in such patients, attention is ordinarily drawn to noncompliance, occult blood loss, worm infestations, helicobacter infection, known malabsorption syndromes and paroxysmal nocturnal hemoglobinuria (PNH).…”

Section: Introductionmentioning

confidence: 99%

Isolated Defect of Intestinal Iron Absorption in Siblings of Iron Deficiency Anemia

Varghese¹,

Allumai²,

Tawfik³

2015

J Hematol Thrombo Dis

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Iron deficiency anemia (IDA) is the commonest type of anemia all over the world. It is easily treatable with oral iron therapy, but a minority of patients does remain unresponsive. This may be related to inappropriate compliance, manifest or occult blood loss, worm infestations, helicobacter infection, known malabsorption syndromes or paroxysmal nocturnal hemoglobinuria (PNH). We observed six such patients with non-responsive recurrent classical IDA who did not show any of the above conditions on specific investigations.Iron tolerance test (as an index of oral iron absorption) was performed on these patients. All of them showed negligible or no iron absorption, suggesting a defect in intestinal oral iron absorption as the cause of non-responsive IDA. This contention was supported by a dramatic response to parenteral iron therapy in all of them. Since the tests for known malabsorption syndromes were negative, it would be assumed that these subjects had an isolated defect in oral iron absorption that has been only scantily reported in the literature. Five of the six patients were siblings of two families. This raises the possibility of the defect in iron absorption to have a genetic connotation. Pending the complete work up for genetic studies, including the gene mutation for membrane bound serum protease type 6 (TMPRSS6) in these subjects and their families, this presentation is a short communication to expose and share our small experience of what looks to be an isolated defect in intestinal iron absorption.

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Establishment of a simple test for iron absorption from the gastrointestinal tract

Cited by 20 publications

References 13 publications

Effects of Ferric Citrate in Patients with Nondialysis-Dependent CKD and Iron Deficiency Anemia

Effects of Ferric Citrate in Patients with Nondialysis-Dependent CKD and Iron Deficiency Anemia

Increased duodenal iron absorption through up‐regulation of divalent metal transporter 1 from enhancement of iron regulatory protein 1 activity in patients with nonalcoholic steatohepatitis

Isolated Defect of Intestinal Iron Absorption in Siblings of Iron Deficiency Anemia

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