Parenteral iron therapy in obstetrics: 8 years experience with iron-sucrose complex

Fe is an essential component of haem in myoglobin and accounts for 70 % of haemoglobin. The balance of Fe, unlike that of other metals such as Na or Ca, is regulated solely by gastrointestinal absorption, which itself depends on the bioavailability of Fe in food, i.e. the chemical Fe species. Factors that maintain Fe homeostasis by modulating Fe transfer through the intestinal mucosa are found at the luminal, mucosal and systemic levels. Fe deficiency and its consequence, Fe-deficiency anaemia, form the commonest nutritional pathology in pregnant women. The current gold standard to detect Fe deficiency remains the serum ferritin value. Previously there was general consensus against parenteral Fe administration, i.e. parenteral Fe was only recommended for special conditions such as unresponsiveness to oral Fe, intolerance to oral Fe, severe anaemia, lack of time for therapy etc. However, especially in hospital settings, clinicians regularly face these conditions but are still worried about reactions that were described using Fe preparations such as Fe-dextrans. A widely used and safe alternative is the Fe-sucrose complex, which has become of major interest to prevent functional Fe deficiency after use of recombinant erythropoietin Numerous reports show the effectiveness and safety of the Fe-sucrose complex. Good tolerance to this Fe formulation is partly due to the low allergenic effect of the sucrose complex, partly due to slow release of elementary Fe from the complex. Accumulation of Fe-sucrose in parenchyma of organs is low compared with Fe-dextrans or Fe-gluconate, while incorporation into the bone marrow for erythropoiesis is considerably faster. Oral Fe is only started if haemoglobin levels are below 110 g/l. If levels fall below 100 g/l or are below 100 g/l at time of diagnosis, parenteral Fe-sucrose is used primarily. In cases of severe anaemia (haemoglobin <90 g/l) or non-response to parenteral Fe after 2 weeks, recombinant erythropoietin is considered in combination. By using parenteral Fe-sucrose in cases of severe Fe deficiency, anaemia during pregnancy is treated efficiently and safely according to our results and rate of blood transfusion could be reduced considerably to below 1 % of patients per yea

Parenteral iron therapy in obstetrics: 8 years experience with iron–sucrose complex

Fe is an essential component of haem in myoglobin and accounts for 70 % of haemoglobin. The balance of Fe, unlike that of other metals such as Na or Ca, is regulated solely by gastrointestinal absorption, which itself depends on the bioavailability of Fe in food, i.e. the chemical Fe species. Factors that maintain Fe homeostasis by modulating Fe transfer through the intestinal mucosa are found at the luminal, mucosal and systemic levels. Fe deficiency and its consequence, Fe-deficiency anaemia, form the commonest nutritional pathology in pregnant women. The current gold standard to detect Fe deficiency remains the serum ferritin value. Previously there was general consensus against parenteral Fe administration, i.e. parenteral Fe was only recommended for special conditions such as unresponsiveness to oral Fe, intolerance to oral Fe, severe anaemia, lack of time for therapy etc. However, especially in hospital settings, clinicians regularly face these conditions but are still worried about reactions that were described using Fe preparations such as Fe-dextrans. A widely used and safe alternative is the Fe-sucrose complex, which has become of major interest to prevent functional Fe deficiency after use of recombinant erythropoietin Numerous reports show the effectiveness and safety of the Fe-sucrose complex. Good tolerance to this Fe formulation is partly due to the low allergenic effect of the sucrose complex, partly due to slow release of elementary Fe from the complex. Accumulation of Fe-sucrose in parenchyma of organs is low compared with Fe-dextrans or Fe-gluconate, while incorporation into the bone marrow for erythropoiesis is considerably faster. Oral Fe is only started if haemoglobin levels are below 110 g/l. If levels fall below 100 g/l or are below 100 g/l at time of diagnosis, parenteral Fe-sucrose is used primarily. In cases of severe anaemia (haemoglobin <90 g/l) or non-response to parenteral Fe after 2 weeks, recombinant erythropoietin is considered in combination. By using parenteral Fe-sucrose in cases of severe Fe deficiency, anaemia during pregnancy is treated efficiently and safely according to our results and rate of blood transfusion could be reduced considerably to below 1 % of patients per yea

Dexamethasone-induced enhancement of resistance to ionizing radiation and chemotherapeutic agents in human tumor cells.

BACKGROUND: Dexamethasone-induced changes in radioresistance have previously been observed by several authors. Here, we examined effects of dexamethasone on resistance to ionizing radiation in 10 additional human cell lines and strains, and on resistance to carboplatin and paclitaxel in 13 fresh tumor samples. MATERIAL AND METHODS: Eight human carcinoma cell lines, a glioblastoma cell line and a strain of normal human diploid fibroblasts were arbitrarily chosen for these in-vitro studies. Effects on radiosensitivity were assessed using a conventional colony formation assay. Effects on resistance to the drugs were investigated prospectively (ATP cell viability assay) using 13 fresh tumor samples from consecutive patients operated for ovarian cancer within the context of a Swiss nation-wide randomized prospective clinical trial (SAKK 45/94). RESULTS: Dexamethasone promoted proliferation of 1 of the cell lines without affecting radiosensitivity, while it completely inhibited proliferation of another cell line (effects on radiosensitivity could thus not be examined). Furthermore, dexamethasone induced enhanced radioresistance in 1 of the 8 carcinoma cell lines examined. In the glioblastoma cell line, there was no effect on growth or radioresistance, nor in the fibroblasts. Treatment with dexamethasone enhanced resistance of the malignant cells to carboplatin in 4 of the 13 fresh tumor samples examined, while no enhancement in resistance to paclitaxel was observed. CONCLUSIONS: In agreement with previous reports, we found that dexamethasone may induce radioresistance in human carcinoma cells. Including the published data from the literature, dexamethasone induced enhancement in radioresistance in 4 of 12 carcinoma cell lines (33%), but not in 3 glioblastoma cell lines, nor in 3 fibroblast strains. Dexamethasone also induced enhanced resistance to carboplatin with a similar probability in fresh samples of ovarian cancer evaluated prospectively (in 4 of 13 samples; 31%). We worry that induction of resistance by corticosteroids given to patients undergoing either radiotherapy or chemotherapy with agents causing DNA damage might be associated with a reduced clinical responsiveness in a significant fraction of patients with a carcinoma