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Query: UNIPROT:P02794 (
ferritin
)
17,525
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Treatment of anemia with human recombinant
erythropoietin
(EPO-R) and its effect on bone marrow was studied in 10 anemic patients on periodic hemodialysis (HD). Blood transfusion was not required once treatment started. Hemoglobin (Hb) levels normalized at six months in all patients (7.2 +/- 0.2 vs 12.4 +/- 3 g/dl, p less than 0.01). Serum
ferritin
levels decreased progressively as Hb increased (r = -0.5609), and six patients needed iron supplement since the third month. Bone marrow iron deposits decreased significantly (p less than 0.001), together with an increase of cellularity and improvement of erythrodysplasia. EPO-R was associated with worsening hypertension in previously hypertensive patients, although it could be controlled with more aggressive treatment. Thrombotic events either systemic or at the vascular access, were not observed. EPO-R corrects the anemia in uremic patients undergoing HD. Iron stores and blood pressure in hypertensive patients on treatment with EPO-R must be monitored regularly.
...
PMID:[Treatment of anemia with recombinant human erythropoietin and the bone marrow response in uremic patients undergoing periodic hemodialysis]. 224 77
In order to clarify possible factors responsible for varying responses in uremic patients treated with recombinant human
erythropoietin
(rHuEPO), we determined the inhibitory effects of ten uremic sera on the erythroid progenitors (CFU-E) and erythroid bursts (BFU-E). We also measured plasma EPO titers, Fe, UIBC,
ferritin
, PTH-C, beta 2-microglobulin, and aluminum in all ten patients. The inhibitor of CFU-E but not BFU-E, was present in the serum of the single anemic patient whose recovery took longer after the administration of rHuEPO. He did not have such conditions as iron deficiency, excess of aluminum, or chronic inflammation. The remaining patients, who had no CFU-E or BFU-E inhibitors, were good responders to rHuEPO. In none of ten patients were there inhibitors of granulocyte-macrophage progenitors (CFU-GM) or any differences in the other parameters. Although the inhibitory factor of CFU-E can be overcome with a larger dose, its prior determination may be useful to set out minimal effective dose of EPO treatment.
...
PMID:The inhibitory factors of hematopoiesis in chronic hemodialysis patients treated with recombinant human erythropoietin. 224 92
Seizures, hypertensive encephalopathy, transient ischemic attacks, and thrombosis of hemodialysis accesses occurred in early clinical trials with recombinant human
erythropoietin
. To determine if these events may be caused by the increased hematocrit value or some direct effect of the recombinant human hormone, 10 transfusion-dependent hemodialysis patients were divided into two groups of five according to their serum
ferritin
concentration: group A. less than 800 microgram/liter, and group B. greater than 800 micrograms/liter. After a month of placebo administration, recombinant human
erythropoietin
was given (150 U/kg intravenously thrice weekly) for four months and then stopped for one month. Hematocrit values were maintained at 0.33 +/- 0.02 (mean +/- SD) by dose adjustment in group A and at 0.26 +/- 0.02 by thrice weekly phlebotomies in group B, who received a constant dose of
erythropoietin
. Viscosity increased from subnormal to normal in group A (P less than 0.02) and cerebral blood flow decreased from above normal to normal (P less than 0.02). In group B minor, statistically insignificant, changes in viscosity and reciprocal changes in cerebral blood flow also occurred. There was no change in either group in transcutaneous oxygen tension. Bleeding time decreased toward normal in both groups during recombinant human
erythropoietin
administration but the changes did not reach statistical significance. Fibrinogen levels were increased in all patients but remained unchanged. No other significant coagulation-related changes were observed. Recombinant
erythropoietin
in the dosage and schedule of administration described in this study did not lead directly or indirectly to changes likely to precipitate seizures or intravascular thrombosis.
...
PMID:Effects of recombinant human erythropoietin on cerebral and cutaneous blood flow and on blood coagulability. 226 76
Thirty six patients with rheumatoid arthritis (RA) (25 with anaemia) were studied to establish the role of iron, vitamin B12, and folic acid deficiency,
erythropoietin
responsiveness, and iron absorption in the diagnosis and pathogenesis of anaemia in RA. Iron deficiency, assessed by stainable bone marrow iron content, occurred in 13/25 (52%), vitamin B12 deficiency in 7/24 (29%), and folic acid deficiency in 5/24 (21%) of the anaemic patients. Only 8/25 (32%) had just one type of anaemia. The iron deficiency of anaemia of chronic disease (ACD) was distinguished by
ferritin
concentration, which was higher in that group. Mean cell volume (MCV) and mean cell haemoglobin (MCH) were lower in both anaemic groups, but most pronounced in iron deficient patients. Folic acid, and especially vitamin B12 deficiency, masked iron deficiency by increasing the MCV and MCH. Iron absorption tended to be highest in iron deficiency and lowest in ACD, suggesting that decreased iron absorption is not a cause of ACD in RA. No specific causes were found for vitamin B12 or folic acid deficiency. Haemoglobin concentration was negatively correlated with erythrocyte sedimentation rate in the group with ACD. Erythropoietin response was lower in ACD than in iron deficient patients. It was concluded that generally more than one type of anaemia is present simultaneously in anaemic patients with RA. The diagnosis of each type may be masked by another. Studies on pathogenesis of the anaemia are difficult as deficiencies generally coexist with ACD. Disease activity and, possibly,
erythropoietin
responsiveness are major factors in ACD pathogenesis.
...
PMID:Anaemia in rheumatoid arthritis: the role of iron, vitamin B12, and folic acid deficiency, and erythropoietin responsiveness. 231 22
Five percutaneous biopsy and 17 necropsy liver specimens were analysed histologically and chemically for iron content in 22 patients receiving dialysis for chronic renal failure, 13 of whom were given intravenous iron-dextran. Brissot scores for assessing histological hepatic iron deposition and chemically measured liver iron concentrations correlated closely. Both variables depended on total cumulative dose of iron, and to a lesser extent, on time since the last dose. Fibrosis (seen in five patients) was minimal and non-specific. Electron microscopic examination showed that there was no generalised damage and confirmed the presence of iron in the hepatocytes in the form of
ferritin
. High liver iron concentrations, in excess of 1000 micrograms/100 mg dry weight, were seen in two patients. Four others given comparable cumulated amounts (18-23 g iron) did not have such high concentrations. Plasma
ferritin
concentrations were high in eight patients, some with and some without fibrosis. The risk of temporarily high iron deposition in the liver causing damage seemed to be minimal when weighed against the benefit of increased haemoglobin in most of the patients. Intravenous iron treatment merits further evaluation, particularly with the advent of
erythropoietin
treatment, which requires continuously available iron.
...
PMID:Hepatic iron in dialysed patients given intravenous iron dextran. 231 87
The achievement of recombinant human
erythropoietin
(r-HuEpo) supposed an important advance in the treatment of the anaemia of chronic renal failure. The results achieved with r-HuEpo in seven patients with chronic renal failure subjected to haemodialysis who required repeated blood transfusions are reported. The duration of treatment was 12 weeks at an initial doses of 50 U/Kg. A significant increase of haematocrit, red-cell count, haemoglobin, reticulocytes and platelets was attained. The decrease of serum iron, transferrin saturation index and
ferritin
in spite of oral iron therapy was striking. None of the patients required blood transfusion during the period of study, and all but one referred subjective improvement. No severe adverse effects were observed, except for one case of thrombosis of arteriovenous fistula, whose relation with this treatment is dubious. Although this is a short-term preliminary study, it can be inferred that r-HuEpo treatment is effective and free of major risks for the anaemia of chronic renal failure.
...
PMID:[Initial response to treatment with erythropoietin in anemia caused by chronic renal insufficiency]. 233 85
Anemia is a common complication of multiple myeloma. It resolves early in the disease if chemotherapy induces a complete remission, but persists if the disease progresses, causing disabling symptoms and often requiring blood transfusions. We treated 13 patients with myeloma-associated anemia by administering recombinant human
erythropoietin
three times a week for six months. Eleven patients (85 percent) had steady increases in hemoglobin levels and eventual correction of the anemia. Their symptoms of anemia subsided, and they reported a heightened sense of well-being. No patient had any adverse side effects, particularly episodes of hypertension. Monitoring of the serum M component showed a predominantly stable tumor load without apparent interaction between the underlying disease and the response to
erythropoietin
therapy. The number of erythroid burst-forming units in the bone marrow and peripheral blood and the level of erythropoiesis in bone marrow smears increased significantly during therapy. Pretreatment serum levels of
erythropoietin
were higher in the patients who did not respond and in those who required more than two months of treatment before they responded. Serum iron,
ferritin
, and transferrin concentrations reflected responses to treatment. We conclude that recombinant human
erythropoietin
is a promising therapeutic tool for treating myeloma-associated anemia.
...
PMID:Erythropoietin treatment of anemia associated with multiple myeloma. 198 68
Therapy with recombinant human
erythropoietin
(rEPO) can correct anemia in RDT patients. However, iron deficiency can develop making treatment unsuccessful. Eighteen non-transfused RDT patients with hematocrit less than 26% were treated with rEPO to raise the HCT to 30-35%; then the dose was individually adjusted to maintain the HCT. The mean HCT rose from 22.3% to 31.5%. Ten patients received iron substitution before rEPO. During rEPO therapy five further patients had to be supplemented with iron; all patients needed an increase in the oral iron doses and three required i.v. iron. During the correction phase mean serum
ferritin
dropped from 203 micrograms/l to a minimum of 71 micrograms/l and was 102 micrograms/l after six months. Serum iron and TIBC changed only moderately. It thus appears that iron demand rises markedly during rEPO therapy, requiring iron substitution in most patients. Serum
ferritin
is the most sensitive parameter for development of iron deficiency.
...
PMID:Iron metabolism under rEPO therapy in patients on maintenance hemodialysis. 234 53
There is little data available on the use of
erythropoietin
in CAPD patients. The available pharmacokinetic and clinical data suggest that a low dose of subcutaneous
erythropoietin
might be effective. Seven CAPD patients, without active malignancy or infection, self-administered
erythropoietin
, 2,000 units (a mean of 32 units/kg) subcutaneously, three times a week. The Hct rose from 23% to 31% in a mean treatment time of 7 weeks, or a rate of rise of 1.2% per week. Three of the patients had previously been transfusion dependent. One of these patients and two additional had iron overload (
ferritin
level greater than 2,000 ng/ml). The drug was paid for by Medicaid (two patients) or private insurance, with the patient paying the uncovered portion, generally 20%. Side effects were minimal. Low dose subcutaneous
erythropoietin
is effective in CAPD patients.
...
PMID:The use of subcutaneous erythropoietin in CAPD patients. 235 Sep 7
A 41-year-old hemodialyzed woman developed ascites and was found to have secondary iron overload. The dose of administered iron was approximately 11-12 g, and her serum
ferritin
level was 15,000 ng/ml (15,000 micrograms/l). There were no signs of congestive heart failure, fluid overload, or liver cirrhosis. A program of weekly phlebotomy combined with recombinant human
erythropoietin
(rhEPO) therapy was tried to eliminate the iron congestion. After 9 months of this therapy, about 5 g of iron had been removed. The ascites completely disappeared, and her serum
ferritin
level fell to 5,800 ng/ml (5,800 micrograms/l). This suggests that such combined therapy would be useful when iron overload must be corrected rapidly. Before therapy, the sterile ascitic fluid showed exudative characteristics with 3.7 g/dl (37 g/l) of total protein. The serum-ascites albumin difference was 0.6 g/dl (6 g/l), and the fluid contained 1,400 inflammatory cells/mm3 (1.4 X 10(9)/l). Notably, the serum-ascites albumin difference increased in parallel with iron elimination. These findings suggested that iron deposition may have played a role in changing the permeability of the peritoneum, or in impairing lymphatic drainage, both of which are presumed to be pathogenetic factors of nephrogenic ascites.
...
PMID:Treatment of a patient with end-stage renal disease, severe iron overload and ascites by weekly phlebotomy combined with recombinant human erythropoietin. 236 36
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