| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-73 |
Sentence |
denotes |
Erythropoietin hyporesponsiveness: from iron deficiency to iron overload. |
| T2 |
74-199 |
Sentence |
denotes |
Iron deficiency is the most frequently encountered cause of suboptimal response to recombinant human erythropoietin (rHuEPO). |
| T3 |
200-327 |
Sentence |
denotes |
Carefully assessing iron status is of paramount importance in chronic renal failure patients prior to or during rHuEPO therapy. |
| T4 |
328-545 |
Sentence |
denotes |
Because there is great need for iron in the EPO-stimulated erythroid progenitors, it is essential that serum ferritin and transferrin saturation levels should be maintained over 300 microg/liter and 30%, respectively. |
| T5 |
546-674 |
Sentence |
denotes |
Investigators have shown that oral iron is unlikely to keep pace with the iron demand for an optimal rHuEPO response in uremics. |
| T6 |
675-761 |
Sentence |
denotes |
Therefore, patients with iron deficiency will always require intravenous iron therapy. |
| T7 |
762-857 |
Sentence |
denotes |
The early and prompt iron supplementation can lead to reductions in rHuEPO dose and hence cost. |
| T8 |
858-1014 |
Sentence |
denotes |
After the iron deficiency has been corrected or excluded, we must remember all of the possible causes of hyporesponsiveness in every rHuEPO-treated patient. |
| T9 |
1015-1110 |
Sentence |
denotes |
As dose requirements vary, it is not clear which dose of rHuEPO causes this hyporesponsiveness. |
| T10 |
1111-1277 |
Sentence |
denotes |
However, if the patient with iron repletion does not respond well after the induction period, the major causes blunting the response to rHuEPO should be investigated. |
| T11 |
1278-1457 |
Sentence |
denotes |
Most factors are reversible and remediable, except resistant anemia associated with hemoglobinopathy or bone marrow fibrosis, which requires a further increase in the rHuEPO dose. |
| T12 |
1458-1585 |
Sentence |
denotes |
By means of early detection and correction of the possible causes, the goal of increasing therapeutic efficacy can be achieved. |
| T13 |
1586-1684 |
Sentence |
denotes |
Iron overload may lead to an enhanced risk for infection, cardiovascular complication, and cancer. |
| T14 |
1685-1857 |
Sentence |
denotes |
Over-treatment with iron should be avoided in dialysis patients, despite the fact that the safe upper limit of serum ferritin to avoid iron overload is not clearly defined. |
| T15 |
1858-1962 |
Sentence |
denotes |
On the other hand, functional iron deficiency may develop even when serum ferritin levels are increased. |
| T16 |
1963-2095 |
Sentence |
denotes |
Controversy remains as to whether intravenous iron therapy can overcome this form of hyporesponsiveness in iron-overloaded patients. |
| T17 |
2096-2244 |
Sentence |
denotes |
Moreover, a treatment option of iron supplementation is not warranted in these patients, as the potential hazards of iron overload will be worsened. |
| T18 |
2245-2504 |
Sentence |
denotes |
We demonstrated that the mean hematocrit significantly increased from 25.1+/-0.9% to 31+/-1.2% after eight weeks of intravenous ascorbate therapy (300 mg three times a week) in 12 hemodialysis patients with serum ferritin levels of more than 500 microg/liter. |
| T19 |
2505-2819 |
Sentence |
denotes |
The enhanced erythropoiesis paralleled with a rise in transferrin saturation (27.8+/-2.5% vs. 44.8+/-9.5%, P < 0.05) and reductions in erythrocyte zinc protoporphyrin (130+/-32 vs. 72+/-19 micromol/mol heme, P < 0.05) and monthly rHuEPO dose (24.2+/-4.5 vs. 16.8+/-3.4 x 10(3) units, P < 0.05) at the end of study. |
| T20 |
2820-3023 |
Sentence |
denotes |
It is speculated that ascorbate supplementation not only facilitates the iron release from storage sites and its delivery to hematopoietic tissues, but also increases iron utilization in erythroid cells. |
| T21 |
3024-3223 |
Sentence |
denotes |
Our study provides a more complete understanding of the pathogenesis of iron overload-related anemia and the development of an adjuvant therapy, intravenous ascorbic acid, to the existing treatments. |
| T1 |
0-73 |
Sentence |
denotes |
Erythropoietin hyporesponsiveness: from iron deficiency to iron overload. |
| T2 |
74-199 |
Sentence |
denotes |
Iron deficiency is the most frequently encountered cause of suboptimal response to recombinant human erythropoietin (rHuEPO). |
| T3 |
200-327 |
Sentence |
denotes |
Carefully assessing iron status is of paramount importance in chronic renal failure patients prior to or during rHuEPO therapy. |
| T4 |
328-545 |
Sentence |
denotes |
Because there is great need for iron in the EPO-stimulated erythroid progenitors, it is essential that serum ferritin and transferrin saturation levels should be maintained over 300 microg/liter and 30%, respectively. |
| T5 |
546-674 |
Sentence |
denotes |
Investigators have shown that oral iron is unlikely to keep pace with the iron demand for an optimal rHuEPO response in uremics. |
| T6 |
675-761 |
Sentence |
denotes |
Therefore, patients with iron deficiency will always require intravenous iron therapy. |
| T7 |
762-857 |
Sentence |
denotes |
The early and prompt iron supplementation can lead to reductions in rHuEPO dose and hence cost. |
| T8 |
858-1014 |
Sentence |
denotes |
After the iron deficiency has been corrected or excluded, we must remember all of the possible causes of hyporesponsiveness in every rHuEPO-treated patient. |
| T9 |
1015-1110 |
Sentence |
denotes |
As dose requirements vary, it is not clear which dose of rHuEPO causes this hyporesponsiveness. |
| T10 |
1111-1277 |
Sentence |
denotes |
However, if the patient with iron repletion does not respond well after the induction period, the major causes blunting the response to rHuEPO should be investigated. |
| T11 |
1278-1457 |
Sentence |
denotes |
Most factors are reversible and remediable, except resistant anemia associated with hemoglobinopathy or bone marrow fibrosis, which requires a further increase in the rHuEPO dose. |
| T12 |
1458-1585 |
Sentence |
denotes |
By means of early detection and correction of the possible causes, the goal of increasing therapeutic efficacy can be achieved. |
| T13 |
1586-1684 |
Sentence |
denotes |
Iron overload may lead to an enhanced risk for infection, cardiovascular complication, and cancer. |
| T14 |
1685-1857 |
Sentence |
denotes |
Over-treatment with iron should be avoided in dialysis patients, despite the fact that the safe upper limit of serum ferritin to avoid iron overload is not clearly defined. |
| T15 |
1858-1962 |
Sentence |
denotes |
On the other hand, functional iron deficiency may develop even when serum ferritin levels are increased. |
| T16 |
1963-2095 |
Sentence |
denotes |
Controversy remains as to whether intravenous iron therapy can overcome this form of hyporesponsiveness in iron-overloaded patients. |
| T17 |
2096-2244 |
Sentence |
denotes |
Moreover, a treatment option of iron supplementation is not warranted in these patients, as the potential hazards of iron overload will be worsened. |
| T18 |
2245-2504 |
Sentence |
denotes |
We demonstrated that the mean hematocrit significantly increased from 25.1+/-0.9% to 31+/-1.2% after eight weeks of intravenous ascorbate therapy (300 mg three times a week) in 12 hemodialysis patients with serum ferritin levels of more than 500 microg/liter. |
| T19 |
2505-2819 |
Sentence |
denotes |
The enhanced erythropoiesis paralleled with a rise in transferrin saturation (27.8+/-2.5% vs. 44.8+/-9.5%, P < 0.05) and reductions in erythrocyte zinc protoporphyrin (130+/-32 vs. 72+/-19 micromol/mol heme, P < 0.05) and monthly rHuEPO dose (24.2+/-4.5 vs. 16.8+/-3.4 x 10(3) units, P < 0.05) at the end of study. |
| T20 |
2820-3023 |
Sentence |
denotes |
It is speculated that ascorbate supplementation not only facilitates the iron release from storage sites and its delivery to hematopoietic tissues, but also increases iron utilization in erythroid cells. |
| T21 |
3024-3223 |
Sentence |
denotes |
Our study provides a more complete understanding of the pathogenesis of iron overload-related anemia and the development of an adjuvant therapy, intravenous ascorbic acid, to the existing treatments. |