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Background and Aims: We analyzed iron deficiency and the therapeutic response following intravenous ferric carboxymaltose in a large single-center inflammatory bowel disease (IBD) cohort., Methods: 250 IBD patients were retrospectively analyzed for iron deficiency and iron deficiency anemia. A subgroup was analyzed regarding efficacy and side effects of iron supplementation with ferric carboxymaltose., Results: In the cohort (n = 250), 54.4% of the patients had serum iron levels ≤60 μg/dl, 81.2% had ferritin ≤100 ng/ml, and 25.6% had hemoglobin (Hb) of ≤12 g/dl (females) or ≤13 g/dl (males). In the treatment subcohort (n = 80), 83.1% of the patients had iron ≤60 μg/dl, 90.4% had ferritin ≤100 ng/ml, and 66.7% had Hb ≤12/13 g/dl before ferric carboxymaltose treatment. After a median dose of 500 mg ferric carboxymaltose, 74.7% of the patients reached iron >60 μg/dl, 61.6% had ferritin >100 ng/ml, and 90.7% reached Hb >12/13 g/dl at follow-up (p < 0.0001 for all parameters vs. pretreatment values). The most frequent adverse event was a transient increase of liver enzymes with male gender as risk factor (p = 0.008, OR 8.62, 95% CI 1.74-41.66)., Conclusions: Iron deficiency and anemia are frequent in IBD patients. Treatment with ferric carboxymaltose is efficious, safe and well tolerated in iron-deficient IBD patients., (Copyright © 2011 S. Karger AG, Basel.)

Background: The use of intravenous iron to correct anemia in end-stage renal diseases (ESRD) has been suspected of catalyzing the production of activated oxygen species and promoting oxidative damage. We investigated the pro-oxidative potential of injected iron in hemodialysis patients., Methods: In study A, 65 patients with ESRD were studied. 20 patients received weekly infusions of iron polymaltose (maltofer), whereas 45 patients had been off iron therapy for more than 2 months. In study B, 12 patients were investigated during two consecutive hemodialysis sessions, one session without and one session with infusion of 100 mg of maltofer over 4 h. Serum iron status, non-transferrin-bound iron (NTBI) and markers of oxidative stress were studied in blood samples from these patients., Results: In study A, NTBI was detected in 41% of the patients and the proportion of NTBI-positive patients was the same whether or not they received iron therapy. In study B, the serum iron and transferrin saturation index increased during iron infusion and NTBI transiently appeared in some patients but markers of oxidative stress were not significantly affected., Conclusion: Although ESRD patients have a high prevalence of NTBI in their serum, no correlation could be established between the presence of NTBI and an increased oxidative stress. The slow infusion of maltofer does not promote a significant increase in the plasma concentration of oxidative stress markers. It may therefore be considered as a safe complement to erythropoietin therapy.

Background: Many studies of anaemia in patients on chronic haemodialysis have noted a high prevalence of iron deficiency despite oral iron supplementation. Our study examined the effect of intravenous iron given as bolus replacement. As the majority of these patients were not receiving concurrent recombinant human erythropoietin (rhEPO) it allowed an analysis of the safety and efficacy of intravenous iron as a single agent., Methods: All patients with a haemoglobin level of less than 10 g/dl and considered iron deficient by the finding of a percentage transferrin saturation of less than 20% were given intravenous iron in the form of iron polymaltose (dextrin) by total dose infusion (TDI). The dose was calculated from tables supplied by the manufacturers. Patients with serum ferritin levels in excess of 225 ng/ml were excluded., Results: In our unit, 62 out of 80 (77%) patients were considered iron deficient and received IV iron. Ten (10%) were considered to be in iron balance and 8 (10%) had biochemistry suggesting iron overload. None of the patients receiving iron experienced any adverse reactions. At three months a rise in haemoglobin level of at least 1 g/dl was noted in 53% of patients. The response was less in the remainder, but only 2 showed no response., Conclusions: Low levels of iron deficiency are often unrecognized in chronic haemodialysis patients on conventional therapy including oral iron supplementation. In such patients, the use of total dose infusion of iron polymaltose (dextrin) is a safe and effective method of raising haemoglobin levels. Substantial improvements may be achieved without the concurrent use of rhEPO., (Copyright 2002 S. Karger AG, Basel)

Our earlier work demonstrated that the sweetener sucralose, C12 H19 CI3 O8, mixed with water had no effect on intraoral plaque pH. The current study compared the effect on resting plaque pH of sucralose to sucrose when these sweeteners were used in hot coffee at equivalent sweetness levels. Twelve subjects with an identified acidogenic plaque were tested at dicrete sessions, using coffee as vehicle with: (1) sucrose; (2) sucralose; (3) sucralose plus maltodextrin (SM); (4) sucralose plus dextrose and maltodextrin (SMD), and (5) no additional sweetener. Each subject rinsed for 1 min with the test rinse, expectorated, and plaque pH was measured at six dental sites for 60 min using an antimony touch electrode method. Data were summarized for baseline pH, delta pH (baseline pH minus lowest pH attained), minimum pH, and area under the pH curve (AUC). Baseline pH was not different throughout all tests. Quantification of AUC in the various groups showed that sucralose with coffee had no statistically significant impact on plaque acidogenesis. AUC, minimum pH and delta pH were least changed by coffee and sucralose, while the SM and SMD combinations generally led to intermediate changes as compared with coffee sweetened with sucrose or sucralose. Because of its acidic nature, unsweetened coffee led to a modest pH depression, the effect of which appears to be blunted by sucralose. This study confirms that sucralose is non-acidogenic and indicates that sucralose may reduce the acidogenic potential of coffee.

A requirement-adapted peripheral-venous parenteral nutrition was developed by exchanging the conventional carbohydrates like glucose, etc., for disaccharide maltose in combination with a fat emulsion (650 mosm/l; 2,000 kcal). In a clinical randomised study, we compared this nutrition regimen with a common requirement-adapted parenteral nutrition regimen, which was applicated by central-venous catheter (2,000 mosm/l; 2,000 kcal). All results, including the results of tracer-investigations with the strable isotope 13C-leucine, showed no metabolic difference between these two nutrition regimens.

40 healthy men received an infusion solution of low molecular dextran with either 0%, 5%, 10% or 20% Maltose over a 60 min period. The combination of LMWD with 10% maltose solution showed a significant increase of urine excretion from 132 ml/h to 315 ml/h at the end of the infusion. The overall excretion rate in 3 h was 683 ml, 185 ml more than infused. The increase in urine excretion from 53.0 ml/h to 173.5 ml/h after the application of 5% maltose/dextran 40 solution was only due to a water diuresis. The maltose concentration was not high enough to induce a visible osmotic diuresis. The application of 20% maltose/dextran 40 solution showed a clear osmotic effect. Nevertheless, there was no significant increase in the urinary excretion rate compared to the LMWD solution without any maltose. The high oncotic and osmotic pressure of this combination activated mechanisms, which were opposed to the induced osmotic diuresis.

The suitability of maltose for parenteral nutrition was investigated in metabolically healthy volunteers. A solution containing 20% of maltose was infused intravenously for four hours using three different doses (0.125 g/kg; 0.25 g/kg; 0.5 g/kg BW/h). Following cessation of the infusions the laboratory controls were carried on for four more hours. The infusions of maltose were tolerated without any complications. However, only when using the lowest dosage a steady state in blood concentration of maltose was reached, i.e. in the case of 0.125 g/kg BW/h. The results show that in humans the metabolic capacity for maltose is limited. The glucose concentration in blood remained almost unaltered during maltose infusion, while the serum insulin concentration was slightly elevated. A further sign for metabolism of maltose was the decrease in free fatty acid concentration. Because of the low metabolic capacity for maltose the urinary loss (in the form of maltose and glucose) is high with greater infusion rates and amounts to 20-30% of the intravenous load. A greater part of the sugar excreted in the urine consists of glucose, despite an almost normal blood glucose concentration. Considering the results of the experiments with volunteers it is concluded that maltose is not suited for intravenous therapy. Because of the low metabolic capacity of the human organism the renal losses are too great.

Male rats were starved and refed diets containing 40% disaccharides (maltose, trehalose, sucrose, turanose), trisaccharide (melezitose), starch, or the monosaccharide equivalents. Responses of hepatic glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME), fatty acid synthetase (FAS), and total liver lipid (TLL) or changes in concentration of portal blood total carbohydrate and fructose were determined following refeeding of the different carbohydrate diets. Maltose, trehalose, sucrose, and turanose refeeding resulted in G6PD and ME responses which were higher than the responses to their component monosaccharides (disaccharide effect). Starch refeeding decreased the responses of G6PD, ME, and FAS when compared to refeeding of glucose. Refeeding diets containing fructose (sucrose, turanose, melezitose, and monosaccharide equivalents containing fructose) increased the responses of G6PD, ME, FAS, and TLL. No correlation between portal blood carbohydrate concentration and hepatic enzyme levels could be demonstrated. It is concluded that readily digestible disaccharides produce an effect which is greater than the effect produced by their monosaccharide equivalents. If these disaccharide configurations are fed as part of a trisaccharide or polysaccharide, the disaccharide effect is no longer discernible.

The effects of conventional food and of formula diet on gut microflora were tested in six healthy persons. In comparison with conventional food, the total gut microflora concentrations slightly increased during formula diet with oligosaccharides. During the periods of formula diet rich in sucrose of maltose, total flora concentrations declined. These changes of total gut microflora were especially caused by the increase and decrease of the enterococci and enterobacteria, the bacteroides showing rather small changes. The concentrations of lactobacteria, sporeforming bacilli and yeasts decreased rapidly with formula diet and did not increase again until normal food was supplied.