Iron deficiency

[Dr.Vad]

Уважаемые коллеги!

Последний номер журнала "Best practice and research in clinical haematology" посвящен "железным" проблемам: Volume 18, Issue 2, Pages 157-380 (June 2005); Iron Diseases; Edited by Chaim Hershko.

Будучи основным "промотором" на этом форуме по проблемам преимущественно железодефицита при различной соматической патологии, предлагаю Вашему вниманию некоторые из обзоров, посвященные наиболее клинически-ориентированным проблемам в терапии:

Diagnosis and management of iron-deficiency anaemia

James D. Cook MD, MSc (Med), Philips Professor of Medicine

Department of Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA

Anaemia is typically the first clue to iron deficiency, but an isolated haemoglobin measurement has both low specificity and low sensitivity. The latter can be improved by including measures of iron-deficient erythropoiesis such as the transferrin iron saturation, mean corpuscular haemoglobin concentration, erythrocyte zinc protoporphyrin, percentage of hypochromic erythrocytes or reticulocyte haemoglobin concentration. However, the changes in these measurements with iron deficiency are indistinguishable from those seen in patients with the anaemia of chronic disease. The optimal diagnostic approach is to measure the serum ferritin as an index of iron stores and the serum transferrin receptor as a index of tissue iron deficiency. The treatment of iron deficiency should always be initiated with oral iron. When this fails because of large blood losses, iron malabsorption, or intolerance to oral iron, parenteral iron can be given using iron dextran, iron gluconate or iron sucrose.

Definitions of impaired iron status
Laboratory diagnosis of iron deficiency
Screening measurements
Storage iron
Tissue iron
Clinical diagnosis of iron deficiency
Isolated iron deficiency
Iron deficiency with chronic disease
Defining the cause of iron deficiency
Physiological iron deficiency
Pathological iron deficiency
Treatment of iron deficiency
Oral iron therapy
Parenteral iron therapy
Iron dextran
Iron gluconate
Iron sucrose
Summary

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Iron requirements in erythropoietin therapy

Joseph Wetherill Eschbach MD, , Senior Research Advisor, Clinical Professor of Medicine, Emeritus

Northwest Kidney Centers, University of Washington, Seattle, WA, USA

When erythropoietin (epoetins or darbepoetin) is used to treat the anemias of chronic renal failure, cancer chemotherapy, inflammatory bowel diseases, HIV infection and rheumatoid arthritis, functional iron deficiency rapidly ensues unless individuals are iron-overloaded from prior transfusions. Therefore, iron therapy is essential when using erythropoietin to maximize erythropoiesis by avoiding absolute and functional iron deficiency. Body iron stores (800–1200 mg) are best maintained by providing this much iron intravenously in a year, or more if blood loss is significant (in hemodialysis patients this can be 1–3 g). There is no ideal method for monitoring iron therapy, but serum ferritin and transferrin iron saturation are the most common tests. Iron deficiency is also detected by measuring the percentage of hypochromic red blood cells, content of hemoglobin in reticulocytes, soluble transferrin receptor levels, and free erythrocyte protoporphyrin values, but iron overload is not monitored by these tests. Iron gluconate and iron sucrose are the safest intravenous medications.

Normal iron metabolism
Epoetin-responsive conditions
Iron metabolism in the anemia of chronic renal disease
Iron metabolism in other anemias
Functional iron deficiency
Effect of epoetin on iron metabolism in healthy subjects
Iron requirements associated with epoetin therapy
Chronic renal disease/failure
Cancer-related chemotherapy
Inflammatory bowel disease
Rheumatoid arthritis
Severe chronic heart failure
Monitoring iron therapy
Potential adverse effects of iron therapy
Summary

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Gastropathic sideropenia

Chaim Hershko MD,, Professor, Chief, Amnon Lahad MD and Dan Kereth MD

Department of Haematology, Shaare Zedek Medical Center, Hebrew University Hadassah Medical School, Jerusalem 91031, Israel
Department of Family Medicine, Clalit Health Services, Jerusalem, and Hebrew University Hadassah Medical School, Jerusalem, Israel
Department of Gastroenterology, Clalit Health Services, Jerusalem, and Hebrew University Hadassah Medical School, Jerusalem, Israel

There has been an increasing awareness recently of subtle, non-bleeding gastrointestinal conditions that may result in abnormal iron absorption leading to iron-deficiency anaemia (IDA) in the absence of gastrointestinal symptoms. Thus, the importance of coeliac disease as a possible cause of IDA refractory to oral iron treatment, without other manifestations of malabsorption syndrome, is increasingly being recognized. In addition, Helicobacter pylori has been implicated in several recent studies as a cause of IDA refractory to oral iron treatment, and the anaemia responds favourably to H. pylori eradication. Likewise, achlorhydric gastric atrophy or atrophic body gastritis (ABG), a condition associated with chronic idiopathic iron deficiency, has been shown to be responsible for refractory IDA in over 20% of patients with no evidence of gastrointestinal blood loss. It has also been suggested that H. pylori gastritis may represent an early phase of ABG in which infection may trigger an autoimmune process directed against gastric parietal cells by means of antigenic mimicry. In this review we examine in a critical manner the role of H. pylori gastritis in the causation of IDA, the role of ABG in the pathogenesis of iron malabsorption, the evidence supporting a possible cause-and-effect relationship between H. pylori gastritis and ABG, and the implications of these findings for the diagnostic work-up and management of IDA.

Helicobacter pylori and IDA
Population studies
Effect of H. pylori eradication on anaemia
Mechanism of iron deficiency in H. pylori gastritis
Occult gastrointestinal bleeding
Competition for dietary iron
Effect on gastric secretion
Atrophic gastritis and IDA
Possible role of H. pylori in the pathogenesis of ABG
Evidence based on population studies
Histological evaluation
Effect of H. pylori eradication
Prevalence of H. pylori and ABG in the diagnostic work-up of IDA
Implications for diagnostic work-up and management of IDA
References