Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 73 year old woman was hospitalized for recurrent occult gastrointestinal bleeding. She had been treated with iron replacement for a microcytic anemia at the age of 67 years remaining on iron and was well until 1989, when she again was hospitalized with symptomatic anemia (hemoglobin 5.4 9um/dl). Urea, electrolytes, liver function, serum vitamin B12 and red cell folate tests were normal. The gastrointestinal blood loss continued, and she became dependent on transfusions, receiving 60 unites of blood over the course of a year. Investigation confirmed iron deficiency with occult blood loss, and showed antibodies to gastric parietal cells, with a title of 1:160. At gastroscopy a series of longitudinally arrayed red streaks were seen radiating to the pylorus, the typical appearances of antral vascular ectasia or watermelon stomach. The diagnosis was confirmed histologically. Prednisolone therapy, initially at a dose of 30 mg, successfully stopped the bleeding and other drugs were withdrawn except from carbimazole and tolbutamide. Prednisolone also restored the gastric acid secretion to normal (basal acid output 2.7 mEq/hour, peak acid output 14 mEq/hour) with a corresponding fall in gastrin to 70 pg/ml. However, prednisolone caused hyperglycemia even at a reduced dose of 10 mg/day. It was replaced by a standard estrogen-progesterone pill (loestrin 30) containing 30 mcg of ethinyl estradiol and 1.5 mg of norethisterone taken daily for 3 weeks each month. After an endoscopic antral biopsy she received 4 units of blood, but otherwise maintained her hemoglobin concentration on iron alone over this period with a considerable reduction in gastrointestinal bleeding.
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PMID:Gastric antral vascular ectasia: maintenance treatment with oestrogen-progesterone. 161 93

A group of 50 patients (26 men and 24 women, mean age 50 +/- 19 years and range 21 to 67) on chronic hemodialysis (HD) and with basal levels of hemoglobin (Hb) less than or equal to 8 g/dl was treated with recombinant human erythropoietin (r-HuEpo) during 3 months. r-HuEpo was started at 50 U/kg I.V. 3 times a week, immediately after each session of HD, for 4 weeks, and this dose was increased in steps of 25 U/kg until a Hb level of 12 g/dl or a maximum dose of 100 U/kg were reached. Complete blood counts and biochemical profile were performed before the first dose of r-HuEpo and once weekly and monthly respectively during the period of treatment. In 8 patients the red-cell life span was studied with cromium 51 labelled erythrocytes just before and after treatment. One patient had a grand mal seizure and the r-HuEpo was discontinued. In 44 patients the mean hematocrit increased from 21.8% to 32.1% and in the other 5 there were no response because of iron deficiency. There were no changes in leucocytes and platelets counts and consistent decreases in iron and ferritin serum concentrations were observed despite oral supplementation of iron. In the 8 patients studied the shortened erythrocyte survival did not suffer any significant variation with r-HuEpo. Predialysis creatinine, urea and phosphorus blood levels increased significantly at 3th month of treatment but there was no increase in potassium. In 32.6% of previously normotensive and hypertensive patients an increase in blood pressure was founded. Thrombosis of arteriovenous fistulas and other severe clinical side effects were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of anemia in patients with chronic kidney insufficiency in hemodialysis with erythropoietin]. 222 Apr 24

The chemistry, pharmacology, pharmacokinetics, clinical uses and efficacy, adverse effects, drug interactions, dosage and administration, and formulary considerations of epoetin are described. Erythropoietin, a glycoprotein hormone primarily synthesized in the kidney, is the chief regulator of red blood cell production. Erythropoietin concentrations increase in response to a hypoxic state, resulting in increased red blood cell formation, accelerated hemoglobin production, and premature movement of reticulocytes into the circulation. The human gene responsible for the production of erythropoietin recently was cloned, and the recombinant product--epoetin--has been made available through mass production. The apparent volume of distribution of i.v. epoetin approximates the assumed plasma volume both in healthy volunteers and in patients with chronic renal failure. Little is known about the metabolism and route of elimination of epoetin and erythropoietin. Epoetin recently was approved by the FDA for treatment of anemia associated with chronic renal failure. Clinical trials in patients receiving hemodialysis or peritoneal dialysis and in predialysis patients with renal dysfunction demonstrate epoetin's efficacy. Other potential indications include augmentation of blood production in patients enrolled in autologous blood donation programs and treatment of anemias associated with rheumatoid arthritis, sickle cell disease, acquired immunodeficiency syndrome, cancer, and premature birth. The most frequent adverse effect associated with epoetin therapy is the worsening or development of hypertension. Other adverse effects include thrombocytosis, hyperkalemia, rise in serum urea concentration, iron deficiency, and flu-like symptoms. No drug interactions with epoetin have been reported in humans. The recommended starting epoetin dosage in patients with chronic renal failure is 50-100 IU/kg three times weekly. Epoetin is available only as an injection for i.v. or s.c. administration. Epoetin provides a new therapeutic approach to the treatment of anemia associated with chronic renal failure in hemodialysis, peritoneal dialysis, and predialysis patients. Benefits of epoetin therapy include reduced need for blood transfusions, the amelioration of anemic symptoms, and an improved quality of life.
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PMID:Epoetin: human recombinant erythropoietin. 268 Feb 41

The treatment efficacy of erythropoietin (EPO) in end-stage renal disease (ESRD) can be limited by deficiencies of iron, folate, or vitamin B12, by hyperparathyroidism, or by aluminum intoxication. Since EPO costs are significant, this study attempted to determine the cost-effectiveness of performing a panel of screening tests for anemia before starting EPO. Anemia screening was performed prospectively in 48 new-onset ESRD patients at the Ralph H. Johnson Veterans Affairs Medical Center before EPO treatment was started. Serum iron, transferrin, folate, vitamin B12, parathyroid hormone, and aluminum levels were determined, and transferrin saturation (Tfsat) was calculated at the first dialysis session. At presentation for dialysis, the mean hematocrit was 0.264 +/- 0.036 and the mean blood urea nitrogen was 32 +/- 2 mmol/L. Eighteen patients (37.5%) had a serum iron level lower than 7 micromol/L, suggesting iron deficiency. Twenty-five patients (52%) had Tfsat less than 0.20, consistent with overt iron deficiency. No patient was found to be vitamin B12 deficient, to be aluminum intoxicated, or to have significant hyperparathyroidism. One patient had folate deficiency. A cost-effectiveness analysis was performed assuming that (1) EPO would be given at an average starting dose of 6,000 U/wk at a cost of $14/2,000 U of EPO; (2) that without screening 1 month would elapse before a poor response was identified; and (3) that the failure to treat aluminum intoxication and hyperparathyroidism or to replete iron, vitamin B12, or folate deficiency would significantly impair the response to EPO. The Tfsat screen had a cost-effectiveness ratio of 0.2019, saving approximately $5.00 in EPO use for each dollar of test administration. All other screens had cost-effectiveness ratios greater than 1.0, indicating that their testing costs exceeded dollar savings in EPO use. In conclusion, iron deficiency is common in anemic patients starting dialysis, but other causes of anemia are not. It is imperative that current clinical practices be influenced by cost-effectiveness considerations. Given the cost of laboratory screens, and the relative ineffectiveness of the other screens examined here to identify factors known to impair the response to EPO, anemia screening before initiating EPO therapy should be limited to tests to identify iron deficiency.
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PMID:A cost-effectiveness analysis of anemia screening before erythropoietin in patients with end-stage renal disease. 915 97

Anemia in chronic renal failure is predominantly caused by diminished erythropoietin synthesis by diseased kidneys. While iron deficiency is often stated as a cause of anemia in chronic renal failure prior to end-stage renal disease, its relative contribution is debated. It is speculated that rather than frank 'iron deficiency', many patients with chronic renal failure may indeed have impaired utilization of iron. We analyzed 139 consecutive patients with chronic renal failure starting maintenance hemodialysis to determine the relationship between hematocrit, measures of renal function (blood urea nitrogen and serum creatinine concentration), and measures of iron availability (serum transferrin saturation, serum iron level and serum ferritin). The 139 study subjects (60 men, 79 women) comprised 116 blacks (83%), 15 hispanics (11%), and 8 whites (6%) of a mean age 56 +/- 15 years. Only 23 (17%) of 139 subjects had positive hemoccult stool test for blood. Their mean hematocrit was 24 +/- 4.5%, mean blood urea nitrogen concentration was 121 +/- 38, mean serum creatinine concentration was 12.6 +/- 5.2 mg/dl, mean serum transferrin saturation was 22 +/- 14%, mean serum ferritin level was 235 +/- 194 U/l, mean serum iron level was 55 +/- 40 U/l, and mean total iron binding capacity was 254 +/- 93%. Multiple regression analysis with hematocrit as the outcome variable, and blood urea nitrogen level, serum creatinine concentration, serum albumin concentration, serum transferrin saturation, and serum ferritin level as the independent variables, showed an inverse correlation between hematocrit and serum creatinine concentration (p = 0.002). We conclude that in patients with chronic renal failure starting uremia therapy, anemia does not correlate with any of the commonly measured indices of body iron stores. We infer that impaired utilization of iron may be a significant factor in the anemia of chronic renal failure.
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PMID:Relative contributions of body iron status and uremia severity to anemia in patients with advanced chronic renal failure. 937 26

Iron deficiency is an important factor for high erythropoietin (EPO) requirements. Some studies have shown a decrease in recombinant human erythropoietin (rHuEPO) dosage with correction of iron deficiency. This is a 2 year prospective study of 58 chronic hemodialysis (HD) patients in whom iron deficiency was corrected with intravenous iron therapy. Patients were stratified into two groups: Group 1 with 25 patients (EPO < 70 U/kg per HD), and Group 2 with 33 patients (EPO > 70 U/kg per HD). For Groups 1 and 2, respectively, differences in mean age (56.5 vs 64.1 years), rHuEPO dose (30.1 vs 148.7 U/kg per HD), and hematocrit concentration (36.5% vs 32.7%) were statistically significant (p < 0.05). Although iron saturation was 45% compared with 41.3% for Groups 1 and 2, respectively, serum parathyroid hormone, aluminum, and urea reduction ratio were similar for both. These data suggest that some patients continue to require a high rHuEPO dose in spite of adequate iron repletion. Further investigation into factors causing EPO resistance is important to decrease rHuEPO requirements and improve cost effectiveness.
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PMID:Erythropoietin (EPO) requirements remain high in EPO resistant patients after iron repletion. 980 3

Impaired erythropoiesis in continuous ambulatory peritoneal dialysis (CAPD) or continuous cyclic peritoneal dialysis (CCPD) patients receiving recombinant human erythropoietin (rHuEPO) is most often secondary to iron deficiency, either as a result of poor intestinal absorption or failure to take oral supplements as prescribed. The inconvenience of giving intravenous (i.v.) iron dextran (ID) to CAPD/CCPD patients precluded its use in this population. We therefore examined the efficacy of bolus intraperitoneal (i.p.) iron dextran (1000 mg) on erythropoiesis in a pilot study of 14 CAPD/CCPD patients. The patients ranged in age from 23-81 years, and all had iron deficiency (transferrin saturation 6%-23%; mean: 15.2% +/- 1.34%). Of the 14 patients studied, 13 were receiving rHuEPO. Pre-treatment hematocrit (Hct) ranged from 21%-38% (mean: 30.2% +/- 1.37%). After infusion of 2 L Dianeal (Baxter Healthcare Corp., Deerfield, Illinois, U.S.A.), 500 mg of undiluted ID was administered directly into the Tenckhoff catheter and subsequently flushed with 30 mm3 normal saline. The peritoneal dialysis (PD) exchange containing ID then dwelled for a period not < 6 hours before standard PD resumed. A second 500 mg dose ID was given to each patient by the same protocol 3-86 days later (mean: 14 days). No complications were seen. No patient complained of abdominal pain or other subjective symptoms during infusion or during the dwell. Repeat iron studies done 1-7 months post ID (mean: 2.8 months) showed a 1.1-fold to 4.9-fold increase (mean: 1.4-fold) in mean iron levels (40.4 +/- 3.9 mg/dL versus 57.5 +/- 5.5 mg/dL, p = 0.036); a 1.1-fold to 5.2-fold increase (mean: 1.6-fold) in mean transferrin saturation (15.2% +/- 1.3% versus 24.5% +/- 2.6%, p = 0.008); a 1.01-fold to 1.60-fold increase (mean: 1.12-fold) in mean Hct (30.2% +/- 1.37% versus 33.8% +/- 1.5%; p = 0.042). The mean dose of rHuEPO was statistically unchanged (170.0 +/- 47.4 U/kg body weight versus 178.8 +/- 49.6 U/kg body weight per week; p = 0.841). Peritoneal equilibration test (PET) score 1-4 months post ID (mean: 2 months) was 0.778 +/- 0.02 compared with a PET score at baseline of 0.767 +/- 0.03 (p = 0.734). No significant delta was observed in blood urea nitrogen (BUN) or creatinine values. We conclude that use of bolus i.p. ID is safe, effective, and convenient, and demonstrates no short-term negative effect on peritoneal membrane integrity. Long-term effects have yet to be determined.
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PMID:Use of bolus intraperitoneal iron dextran in continuous ambulatory peritoneal dialysis or continuous cyclic peritoneal dialysis patients receiving recombinant human erythropoietin. 1068 73

An analysis of the relationship between intermediate outcomes and duration of dialysis therapy in hemodialysis patients was performed by linking Health Care Financing Administration (HCFA) Core Indicators data with data obtained from HCFA form 2728 at the initiation of dialysis therapy. Patients who recently initiated hemodialysis therapy were less likely to meet Dialysis Outcomes Quality Initiative guidelines than patients with a longer duration of dialysis therapy. For both urea reduction ratio and Kt/V, odds ratios for adequate dialysis were approximately 0.20 for a duration of dialysis therapy less than 0.5 years and 0.42 to 0.63 for a duration of dialysis therapy of 0.5 to 1.0 years compared with a duration of dialysis therapy of 2.0 years or greater. For patients with a duration of dialysis therapy less than 0.5 years (compared with >/=2.0 years), the odds ratio for a hematocrit less than 28% was approximately 3.0, that for a hematocrit 33% or greater was approximately 0.6, and that for a serum albumin level of 3.5 g/dL or greater (bromcresol green method) or 3.2 g/dL or greater (bromcresol purple method) was approximately 0.4. There was a direct relationship between glomerular filtration rate at the initiation of dialysis therapy and both serum albumin and hematocrit values. Patients administered recombinant human erythropoietin (rHuEPO) predialysis were more likely to have greater hematocrits. There also was a direct relationship between hematocrit and serum albumin level. Therefore, several actionable items in regard to attentive overall medical care can result in an improvement in the percentage of patients newly started on hemodialysis therapy who meet intermediate outcomes, including the administration of rHuEPO predialysis, correction of iron deficiency, and timely placement of a permanent dialysis access.
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PMID:Duration of dialysis and its relationship to dialysis adequacy, anemia management, and serum albumin level. 1157 85

An increasing number of reports documenting resistance to human recombinant erythropoietin (rHuEPO) therapy are challenging the concept that erythropoietin deficiency is the main cause of the anaemia of chronic kidney disease (CKD). In an attempt to establish whether other factors play a more predominant role in the anaemia of CKD, 988 patients receiving dialysis were assessed for a wide range of variables. Data were collected on haematocrit (Hct) levels, rHuEPO dose, dry weight, serum ferritin, transferrin saturation, serum albumin, serum aluminium, serum parathyroid hormone intact, eKt/V for urea, gender, dose of i.v. iron administered, time in hospital, and use of i.v. vancomycin. Hyporesponsiveness to rHuEPO was defined as patients requiring >500 IU/kg/week or failing to achieve Hct levels of >30%. Ninety-two (9.2%) of the 988 patients met the above criteria for hyporesponsiveness to rHuEPO. In 21 of these patients, Hct concentrations remained <30% at 6-month follow-up. There were known haematological causes of refractoriness to rHuEPO in nine of these patients. During extended follow-up, probable causes of hyporesponsiveness were discovered in all but two of the remaining 13 patients. Of 62 dialysis patients who received rHuEPO at doses >500 IU/kg/week, 45 (73%) had Hct concentrations of 33-42%. These patients were responding to the higher doses of rHuEPO with no obvious adverse effects. Lower values of serum ferritin, transferrin saturation, and eKt/V, or higher levels of parathyroid hormone or serum aluminium were not associated with higher rHuEPO dose requirements. These results suggest that erythropoietin deficiency is still the main cause of the anaemia of CKD. Erythropoietin replacement therapy can correct the anaemia in almost all iron replete patients providing enough hormone is given, functional iron deficiency is avoided, aluminium levels and parathyroid toxicities are controlled and that no de novo haematological condition that affects erythropoiesis or red blood cell survival develops. Consideration should be given to modifying the definition of rHuEPO hyporesponsiveness. The US Hct target of 33-36% for haemodialysis patients is narrow and the European target of Hct >33% may be significantly more practical and physiologically relevant.
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PMID:Is it time for a paradigm shift? Is erythropoietin deficiency still the main cause of renal anaemia? 1209 99

Anaemia is one of the most common disorders in pregnancy. The most common cause is iron deficiency. Iron deficiency anaemia is relatively easy to diagnose using a serum ferritin of <15 ng/ml. However, because ferritin is an acute phase reactant, the diagnosis of iron deficiency anaemia in hospitalised or ill patients may be difficult, since serum ferritin may be normal or raised, even in the face of iron deficiency. Soluble transferrin receptor assay (STfR) may be useful in these situations because it reflects the degree of iron requirement in relation to supply, and it is not an acute phase reactant. This study was undertaken to detect subclinical anaemia in pregnant women and to correlate STfR assay with the current diagnostic tests for iron deficiency anaemia. One hundred and fifty-three consenting pregnant women seen at the antenatal clinic at King Edward VIII Hospital (KEH) were recruited. Women on haemantinics, who had renal failure, haemoglinopathy and blood transfusion in the past 3 months, were excluded. An ELISA technique was used for the assay of STfR while standard methodology was used for the other biochemical and haematological assays (FBC, urea, creatinine, c reactive protein and iron studies). One hundred and fifty subjects were included in the final analysis. Seventy-two (48%) had varying degrees of iron deficiency anaemia. In 70% (105) of the samples analysed, serum ferritin and STfR agreed on the presence/absence of iron deficiency anaemia. STfR and S:F were 75% and 86% sensitive; 63% and 82% specific, respectively. The calculated positive and negative predictive values are: STfR 64% and 75%; S:F 84% and 87%; Hb 58% and 57%; mean corpuscular volume 91% and 55%, respectively. Ferritin remains the gold standard for the diagnosis of iron deficiency anaemia. However, because ferritin is an acute phase reactant, soluble transferrin receptor assay may be a better test in ill and hospitalised patients where ferritin may be normal or elevated, despite iron deficiency.
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PMID:Soluble transferrin receptors in anaemia of pregnancy. 1252 53


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