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PubMed1978

[The treatment of anemia due to iron-deficiency with iron combined with vitamins (author's transl)].

The effect of combined iron-vitamin therapy and iron therapy only was studied in 14 respectively 14 children with hypochromic anemia. Pyridoxalphosphate in serum, activity of red cell glutamic oxaloacetic transaminase and excretion of 4-pyridoxic acid were measured as indices of vitamin B6 nutriture before therapy was started, four and seven days under therapy once more. Erythrocytes, reticulocytes, concentration of hemoglobin were simultaneously counted, whereas serum iron and transferrin have been measured before and after therapy. A group of 22 hematologically healthy children was studied as controls. After iron therapy a decrease of vitamin B6 body pool came off as a consequence of increased requirement of pyridoxalphosphate for heme synthesis. Additional dosage of vitamins compensated the biochemical B6 deficit and had an accelerating effect on heme synthesis.

Anemia, Hypochromic↗
PubMed1991

Red cell lipid peroxidation and antioxidant enzymes in iron deficiency.

Whether iron deficient RBC in humans have a reduced, or an increased, susceptibility to lipid peroxidation was studied in the iron deficiency states of primary proliferative polycythaemia and iron deficiency anaemia and related to changes in the activities of iron-dependent and non-iron dependent antioxidant enzymes. Susceptibility of RBCs to lipid peroxidation was increased when expressed per g Hb. However, this was a result of the low RBC Hb giving an increased membrane lipid: Hb ratio in the incubations. Results were normal when expressed either per cell, or per ml, RBC. Glutathione reductase was normal. Increased RBC superoxide dismutase activity in iron deficiency may be explained by the younger RBC population and reductions in glutathione peroxidase and catalase activities by the microcytic hypochromic changes and the lack of availability of iron, respectively. There is no evidence of an increased susceptibility of RBC to lipid peroxidation in iron deficiency.

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PubMed1979

Catecholamine elevation in iron deficiency.

Iron-deficient rats have increased blood and urinary catecholamines regardless of whether anemia is or is not present. The catecholamine response in both iron-deficient and control animals is largely temperature dependent, showing little difference at the isothermic temperature of 30 degrees C but a two- to threefold increase in iron-deficient animals over controls at lower temperatures. The iron-deficient rat is unable to maintain body temperature at 4 degrees C and this is independent of anemia or of food intake. When animals are run on the treadmill for 4 h, body temperatures increase but the difference observed at 4 degrees C between iron-deficient and control animals persists. The underlying abnormality in temperature regulation and in catecholamine response disappeared after 6 days of iron therapy.

Animals↗
PubMed1994

Central role of zinc protoporphyrin in staging iron deficiency.

In iron deficiency, zinc protoporphyrin (ZPP) is produced instead of heme, and the ZPP concentration in erythrocytes is increased (normal < or = 40 mumol/mol heme). We investigated the relevance of ZPP for staging iron deficiency. ZPP was determined by hematofluorometry in samples from 103 patients. Nineteen patients with iron depletion showed decreased serum ferritin (12.1 +/- 4.4 micrograms/L) with normal ZPP and hemoglobin (Hb). Twelve patients with iron-deficient erythropoiesis had decreased ferritin (10.4 +/- 2.4 micrograms/L), increased ZPP (72 +/- 9 mumol/mol heme), and normal Hb concentrations. In 72 patients with iron-deficiency anemia, ferritin was < 12 micrograms/L. In mild anemia (Hb between 100 and 120 g/L, and normal erythrocyte indices), ZPP was 100 +/- 16 mumol/mol heme. In severe anemia (Hb < 100 g/L, decreased erythrocyte indices), ZPP values were significantly higher (265 +/- 109 mumol/mol heme). We conclude that measurements of ZPP, ferritin, and Hb can reliably be combined to classify the degree of iron deficiency.

Anemia, Hypochromic↗
PubMed1985

Iron absorption in normal and iron-deficient beagle dogs: mucosal iron kinetics.

Absorption of dietary iron requires uptake of iron by the brush border of the intestinal epithelial cells, intracellular transport, and transfer to the systemic circulation. In iron-deficiency anemia, iron absorption is greatly increased, but the individual steps responsible for this increase have not been identified. We have developed a method to evaluate the rate constants for each of these steps, and we report here our results in beagle dogs a) under normal conditions and b) after phlebotomy to produce iron-deficiency anemia. Simultaneous administration of oral 59Fe3+-citrate and intravenous 55Fe-transferrin was used to investigate the kinetics of mucosal iron transport. Plasma levels of both isotopes and the whole-body excretion pattern of 59Fe were monitored sequentially, and the fractional mucosal transport rates were estimated by nonlinear least-squares fit of a physiologically based mathematical model to these data. Under normal conditions the fractional rate of mucosal iron uptake from the intestinal lumen was rate limiting, being less than 1% of the fractional rate of either iron incorporation into the mucosal storage pool or transfer of iron from the mucosa to the plasma. After induction of iron-deficiency anemia, the fractional mucosal iron uptake rate increased sixfold (P less than 0.005), while the rate of incorporation into the mucosal storage pool decreased ninefold (P less than 0.02); in contrast, the fractional rate of iron transfer to the plasma did not change. These results indicate that the enhanced iron absorption in iron-deficiency anemia is attributable to an increase in mucosal iron available for transfer to the plasma, leading in turn to a net increase in iron absorption, despite a normal fractional transfer rate.

Anemia, Hypochromic↗
PubMed1990

Retention of cadmium in cadmium-naive normal and iron-deficient rats as well as in cadmium-induced iron-deficient animals.

The retention of cadmium was investigated in cadmium-naive normal and iron-deficient rats in comparison to rats with cadmium-induced iron deficiency. Rats subchronically (4 weeks) exposed to dietary cadmium (28, 56, 112 ppm Cd and 28 ppm Fe) received a radioactively labeled dose of 2 mumol Cd/kg body wt; acutely (no cadmium exposure with diet) treated rats received doses between 1 and 8 mumol Cd/kg body wt. Two animals of each group received iron (1 mumol/kg as 59FeSO4 in order to monitor iron absorption in parallel. After a period of 4 weeks of feeding a cadmium-fortified diet, the test dose was administered and after a 2-weeks period 109Cd and of 59Fe retention was determined. The results showed in part an unexpected pattern of cadmium retention: subchronic feeding of cadmium induced iron deficiency. This implies an immediate interaction between the two metals with regard to intestinal transfer of iron. The retention of iron was increased in the Cd-induced anemia to the same extent as that in iron deficiency induced by iron restriction. Cadmium retention in iron deficiency induced by iron withdrawal also showed a marked increase, which implies that iron deficiency stimulates the intestinal transfer system for both metals in a similar way. Contrary to this effect, the cadmium retention in cadmium-induced iron deficiency was reduced to about 30% of control values. A self-induced aggravation of the body cadmium burden, as a consequence of the iron deficiency which is known to result from subchronic exposure to feeding of dietary cadmium, was thus excluded.

Anemia, Hypochromic↗
PubMed1998

Plasma thyroid hormone kinetics are altered in iron-deficient rats.

Iron deficiency anemia is associated with lower plasma thyroid hormone concentrations in rodents and, in some studies, in humans. The objective of this project was to determine if plasma triiodothyronine (T3) and thyroxine (T4) kinetics were affected by iron deficiency. Studies were done at a near-thermoneutral temperature (30 degrees C), and a cool environmental temperature (15 degrees C), to determine plasma T3 and T4 kinetics as a function of dietary iron intake and environmental need for the hormones. Weanling male Sprague-Dawley rats were fed either a low Fe diet [iron-deficient group (ID), <5 microg/g Fe] or a control diet [control group (CN), 35 microg/g Fe] at each temperature for 7 wk before the tracer kinetic studies. An additional ID group receiving exogenous thyroid hormone replacement was also used at the cooler temperature. For T4, the disposal rate was >60% lower (89 +/- 6 vs. 256 +/- 53 pmol/h, P < 0.001) in ID rats than in controls at 30 degrees C, and approximately 40% lower (192 +/- 27 vs. 372 +/- 26 pmol/h, P < 0.01) in ID rats at 15 degrees C. Exogenous T4 replacement in a cohort of ID rats at 15 degrees C normalized the T4 concentration and the disposal rate. For T3, the disposal rate was significantly lower in ID rats in a cool environment (92 +/- 11 vs. 129 +/- 11 pmol/h, P < 0.01); thyroxine replacement again normalized the T3 disposal rate (126 +/- 12 pmol/h). Neither liver nor brown fat thyroxine 5'-deiodinase activities were sufficiently different to explain the lower T3 disposal rates in iron deficiency. Thus, plasma thyroid hormone kinetics in iron deficiency anemia are corrected by simply providing more thyroxine. This suggests a central regulatory defect as the primary lesion and not peripheral alterations.

Anemia, Iron-Deficiency↗
PubMed1999

Upper and lower gastrointestinal evaluation of elderly inpatients who are iron deficient.

PURPOSE: Iron deficiency anemia is commonly caused by chronic gastrointestinal blood loss, and a thorough examination of the gastrointestinal tract has become standard practice. In contrast, iron deficiency without anemia has hardly been studied, and its causes are less certain. The aim of the present study was to determine the diagnostic value of upper and lower gastrointestinal evaluation in elderly hospitalized patients with iron deficiency, irrespective of the hemoglobin level. PATIENTS AND METHODS: In a prospective study, 151 consecutive elderly patients with iron deficiency (serum ferritin level < 50 microg/L at two separate occasions) were investigated using esophagogastroduodenoscopy with colonoscopy (n = 90) or barium enema (n = 61). RESULTS: A potential upper gastrointestinal tract lesion was found in 47 (49%) of the 96 anemic patients and in 31 (56%) of the 55 nonanemic patients (P = 0.38). Nonanemic patients had a greater prevalence of erosive gastritis or duodenitis. Anemic patients (72%) were more frequently investigated with a colonoscopy than nonanemic patients (38%, P = 0.001), and a lower gastrointestinal lesion was found in 32% of the anemic patients and 16% of the nonanemic patients (P = 0.03). Cancer was the most common lesion in the colon; 11 of the 18 patients were asymptomatic. Site-specific symptoms, fecal occult blood loss, and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) were not associated with the detection of gastrointestinal lesions. In 9.5% of the patients with a benign upper gastrointestinal lesion, a synchronous colonic tumor was found. CONCLUSION: Elderly patients with iron deficiency should undergo endoscopic examination, irrespective of the hemoglobin level. The presence of gastrointestinal symptoms, a positive fecal occult blood test, and the use of NSAIDs are of limited value in guiding the diagnostic procedure.

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