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Iron deficiency, as defined by one of the tests listed below (see 'Diagnosis' below), affects a large proportion of the world's population, especially women of childbearing age, children, and individuals living in low- and middle-income countries.
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reatment".) ●Adolescents – (See "Iron requirements and iron deficiency in adolescents".) ●Pregnancy – (See "Anemia in pregnancy" and "Nutrition in pregnancy", section on 'Iron'.) EPIDEMIOLOGY — <span>Iron deficiency, as defined by one of the tests listed below (see 'Diagnosis' below), affects a large proportion of the world's population, especially women of childbearing age, children, and individuals living in low- and middle-income countries. The absolute prevalence of iron deficiency depends on the population studied. In all of the studies that evaluate the scope of the problem, iron deficiency is more prevalent than iron d




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In all of the studies that evaluate the scope of the problem, iron deficiency is more prevalent than iron deficiency anemia (low hemoglobin or hematocrit caused by iron deficiency), and females are affected more than males.
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lation, especially women of childbearing age, children, and individuals living in low- and middle-income countries. The absolute prevalence of iron deficiency depends on the population studied. <span>In all of the studies that evaluate the scope of the problem, iron deficiency is more prevalent than iron deficiency anemia (low hemoglobin or hematocrit caused by iron deficiency), and females are affected more than males. As examples: ●A systematic analysis of the global burden of anemia from 1990 to 2010 found that the prevalence of iron deficiency anemia (and anemia overall) decreased but remained sign




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For females, iron deficiency anemia was present in nearly 20,000 per 100,000 population (approximately one in five). For both decades and for virtually every population (males, females, different regions of the world), iron deficiency accounted for the largest proportion of cases of anemia. These findings are illustrated in the figure (figure 1).
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xamples: ●A systematic analysis of the global burden of anemia from 1990 to 2010 found that the prevalence of iron deficiency anemia (and anemia overall) decreased but remained significant [1]. <span>For females, iron deficiency anemia was present in nearly 20,000 per 100,000 population (approximately one in five). For both decades and for virtually every population (males, females, different regions of the world), iron deficiency accounted for the largest proportion of cases of anemia. These findings are illustrated in the figure (figure 1). ●Data from the United States (US) general population have been collected periodically from various groups such as the National Health and Nutrition Examination Survey (NHANES) and the C




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Iron deficiency anemia in older adults is also greater than that seen in the general population. In a series of 190 adults in the community >65 years of age with anemia, 12 percent were due to iron deficiency [6].
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iron deficiency anemia in females of childbearing age is attributed to menstruation and childbirth, as discussed in detail separately. (See "Anemia in pregnancy", section on 'Iron deficiency'.) <span>Iron deficiency anemia in older adults is also greater than that seen in the general population. In a series of 190 adults in the community >65 years of age with anemia, 12 percent were due to iron deficiency [6]. Racial and ethnic disparities in iron deficiency are also present. Analysis of over 60,000 women in the Hemochromatosis and Iron Overload Screening (HEIRS) study in the United States fo




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Carrier status for a hereditary hemochromatosis variant in the HFE gene (C282Y or H63D) did not correlate with the prevalence of iron deficiency in any racial or age group in HEIRS participants.
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percent The prevalence of iron deficiency was 5.2 percent in Native Americans and 3.1 percent in Pacific Islanders, although fewer participants from these groups were included in the study [7]. <span>Carrier status for a hereditary hemochromatosis variant in the HFE gene (C282Y or H63D) did not correlate with the prevalence of iron deficiency in any racial or age group in HEIRS participants. Blood donors in the general population typically have slightly lower iron stores than non-donors, although this rarely translates to iron deficiency anemia [8]. Various blood donor seri




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Various blood donor series from a number of North American and European countries have estimated the rate of subclinical iron deficiency in the range of 5 to 15 percent [9,10]. This has led some experts to consider screening for iron deficiency and/or recommending iron supplementation for blood donors, as discussed separately.
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age group in HEIRS participants. Blood donors in the general population typically have slightly lower iron stores than non-donors, although this rarely translates to iron deficiency anemia [8]. <span>Various blood donor series from a number of North American and European countries have estimated the rate of subclinical iron deficiency in the range of 5 to 15 percent [9,10]. This has led some experts to consider screening for iron deficiency and/or recommending iron supplementation for blood donors, as discussed separately. (See "Blood donor screening: Procedures and processes to enhance safety for the blood recipient and the blood donor", section on 'Role of iron supplements'.) As discussed separately, ir




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The major causes of iron deficiency are decreased dietary intake, reduced absorption, and blood loss.
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series), suggesting that these women were likely iron deficient prior to becoming pregnant. (See "Anemia in pregnancy", section on 'Epidemiology'.) CAUSES AND RISK FACTORS FOR IRON DEFICIENCY — <span>The major causes of iron deficiency are decreased dietary intake, reduced absorption, and blood loss. In adults in resource-rich countries, dietary intake is almost always adequate, and it is usually reasonable to assume that the cause is blood loss until proven otherwise, with the impl




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Overt bleeding is obvious and not difficult for the clinician to recognize, often by history alone:

● Traumatic hemorrhage

● Hematemesis or melena

● Hemoptysis

● Heavy menstrual bleeding

● Pregnancy and delivery

● Hematuria

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tify the cause. (See 'Search for source of blood and iron loss' below.) Blood loss — The major cause of iron deficiency in resource-rich countries is blood loss, either overt or occult [11-16]. <span>Overt bleeding is obvious and not difficult for the clinician to recognize, often by history alone: ●Traumatic hemorrhage ●Hematemesis or melena ●Hemoptysis ●Heavy menstrual bleeding ●Pregnancy and delivery ●Hematuria Other causes of blood loss that may be overlooked include: ●Frequent blood donation ●Excessive diagnostic blood testing ●Underestimation of the degree of heavy menstrual bleeding ●Pregn




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Other causes of blood loss that may be overlooked include:

● Frequent blood donation

● Excessive diagnostic blood testing

● Underestimation of the degree of heavy menstrual bleeding

● Pregnancy and lactation, with a greater likelihood as the number of pregnancies increases

● Occult bleeding, typically gastrointestinal (eg, gastritis, malignancy, angiodysplasia) but may also include hemolysis with urinary losses

● Exercise-induced blood loss, often due to occult gastrointestinal bleeding (see "Exercise-related gastrointestinal disorders", section on 'Gastrointestinal bleeding')

● Gastrointestinal parasites (eg, hookworm, whipworm), especially in developing countries

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s and not difficult for the clinician to recognize, often by history alone: ●Traumatic hemorrhage ●Hematemesis or melena ●Hemoptysis ●Heavy menstrual bleeding ●Pregnancy and delivery ●Hematuria <span>Other causes of blood loss that may be overlooked include: ●Frequent blood donation ●Excessive diagnostic blood testing ●Underestimation of the degree of heavy menstrual bleeding ●Pregnancy and lactation, with a greater likelihood as the number of pregnancies increases ●Occult bleeding, typically gastrointestinal (eg, gastritis, malignancy, angiodysplasia) but may also include hemolysis with urinary losses ●Exercise-induced blood loss, often due to occult gastrointestinal bleeding (see "Exercise-related gastrointestinal disorders", section on 'Gastrointestinal bleeding') ●Gastrointestinal parasites (eg, hookworm, whipworm), especially in developing countries Typical iron loss during pregnancy has been estimated at approximately 1000 mg for pregnancy, delivery, and nursing. Menstrual blood losses account for approximately 1 mg of iron loss p




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Typical iron loss during pregnancy has been estimated at approximately 1000 mg for pregnancy, delivery, and nursing. Menstrual blood losses account for approximately 1 mg of iron loss per day.
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nal bleeding (see "Exercise-related gastrointestinal disorders", section on 'Gastrointestinal bleeding') ●Gastrointestinal parasites (eg, hookworm, whipworm), especially in developing countries <span>Typical iron loss during pregnancy has been estimated at approximately 1000 mg for pregnancy, delivery, and nursing. Menstrual blood losses account for approximately 1 mg of iron loss per day. (See "Anemia in pregnancy", section on 'Iron deficiency'.) Typical iron loss during hemodialysis may be as much as 2 g per year, which is highly likely to produce iron deficiency withou




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Typical iron loss during hemodialysis may be as much as 2 g per year, which is highly likely to produce iron deficiency without supplementation.
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pproximately 1000 mg for pregnancy, delivery, and nursing. Menstrual blood losses account for approximately 1 mg of iron loss per day. (See "Anemia in pregnancy", section on 'Iron deficiency'.) <span>Typical iron loss during hemodialysis may be as much as 2 g per year, which is highly likely to produce iron deficiency without supplementation. (See "Diagnosis of iron deficiency in chronic kidney disease" and "Treatment of iron deficiency in hemodialysis patients".) The likelihood that iron deficiency is due to an occult gastr




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In a 2012 series of 621 patients with definite or probable iron deficiency anemia, cancer and high-risk adenomas were identified in 51 of 310 (16 percent) of the individuals who underwent endoscopy [17].
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an occult gastrointestinal tumor has been illustrated in several case series; gastrointestinal disorders that reduce iron absorption are discussed below (see 'Reduced iron absorption' below): ●<span>In a 2012 series of 621 patients with definite or probable iron deficiency anemia, cancer and high-risk adenomas were identified in 51 of 310 (16 percent) of the individuals who underwent endoscopy [17]. ●In a 2005 series of 148 adults (median age, 66 years) with chronic iron deficiency who underwent endoscopy, 18 (12 percent) were found to have a malignant tumor [18]. ●In a 2002 report




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Iron is absorbed in the upper gastrointestinal tract; the duodenum is the site of maximal absorption [20].
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gs reinforce the importance of identifying the cause of blood loss, especially in men and postmenopausal women. (See 'Search for source of blood and iron loss' below.) Reduced iron absorption — <span>Iron is absorbed in the upper gastrointestinal tract; the duodenum is the site of maximal absorption [20]. Reduced absorption of iron is an uncommon cause of iron deficiency, especially in healthy individuals and in regions of the world where there is access to an iron-replete diet. However,




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The most clinically important are disorders that affect the mucosal cells responsible for iron absorption, such as celiac disease, atrophic gastritis, Helicobacter pylori infection, and bariatric surgery. Inherited disorders that interfere with iron absorption are very rare.
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e there is access to an iron-replete diet. However, several factors determine the efficiency of iron absorption, and certain medical conditions may interfere with normal uptake of dietary iron. <span>The most clinically important are disorders that affect the mucosal cells responsible for iron absorption, such as celiac disease, atrophic gastritis, Helicobacter pylori infection, and bariatric surgery. Inherited disorders that interfere with iron absorption are very rare. Sources of reduced iron absorption may be considered in individuals with gastrointestinal symptoms or those who do not have an adequate response to oral iron supplementation. Regardless




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Dietary heme iron (iron from meat rather than plant sources) is better absorbed than non-heme iron. A review of published studies that evaluated vegetarians and non-vegetarians found that those who consumed a vegetarian diet were more likely to be iron deficient [21]. However, non-heme iron is available from a wide array of vegetables and supplemented grains and cereals, as summarized in the table (table 1).
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of bleeding should be excluded. (See "Treatment of iron deficiency anemia in adults", section on 'Response to iron supplementation' and 'Search for source of blood and iron loss' below.) Diet — <span>Dietary heme iron (iron from meat rather than plant sources) is better absorbed than non-heme iron. A review of published studies that evaluated vegetarians and non-vegetarians found that those who consumed a vegetarian diet were more likely to be iron deficient [21]. However, non-heme iron is available from a wide array of vegetables and supplemented grains and cereals, as summarized in the table (table 1). A number of foods may impair iron absorption such as tannates, phosphates, phytates (mineral-binding compounds found in whole grains and seeds), and foods high in calcium (table 2). It




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A number of foods may impair iron absorption such as tannates, phosphates, phytates (mineral-binding compounds found in whole grains and seeds), and foods high in calcium (table 2).

It would be very difficult to develop iron deficiency solely due to these dietary factors, but they may contribute to iron deficiency in the setting of blood loss, or, less commonly, extremely low intake [16].

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n diet were more likely to be iron deficient [21]. However, non-heme iron is available from a wide array of vegetables and supplemented grains and cereals, as summarized in the table (table 1). <span>A number of foods may impair iron absorption such as tannates, phosphates, phytates (mineral-binding compounds found in whole grains and seeds), and foods high in calcium (table 2). It would be very difficult to develop iron deficiency solely due to these dietary factors, but they may contribute to iron deficiency in the setting of blood loss, or, less commonly, extremely low intake [16]. Celiac disease/atrophic gastritis/H. pylori — Celiac disease (also called gluten-sensitive enteropathy or nontropical sprue) is a disorder of small bowel inflammation triggered by expos




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Celiac disease (also called gluten-sensitive enteropathy or nontropical sprue) is a disorder of small bowel inflammation triggered by exposure to gluten in susceptible individuals. It predominantly affects White populations of northern European ancestry, with a prevalence of approximately 1 in 70 to 1 in 300 (0.3 to 1 percent) in these populations.
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ue to these dietary factors, but they may contribute to iron deficiency in the setting of blood loss, or, less commonly, extremely low intake [16]. Celiac disease/atrophic gastritis/H. pylori — <span>Celiac disease (also called gluten-sensitive enteropathy or nontropical sprue) is a disorder of small bowel inflammation triggered by exposure to gluten in susceptible individuals. It predominantly affects White populations of northern European ancestry, with a prevalence of approximately 1 in 70 to 1 in 300 (0.3 to 1 percent) in these populations. (See "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults".) ●Celiac disease – Celiac disease can contribute to anemia by several mechanisms, including i




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Celiac disease can contribute to anemia by several mechanisms, including iron deficiency, reduced absorption of supplemental iron, and malabsorption of other nutrients required for red blood cell (RBC) production including vitamin B12, folic acid, and copper [22]. There may also be a component of anemia of chronic disease/anemia of inflammation (ACD/AI) as well as blood loss, although the contribution (if any) of gastrointestinal blood loss from celiac disease to iron deficiency is unclear [22].
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ence of approximately 1 in 70 to 1 in 300 (0.3 to 1 percent) in these populations. (See "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults".) ●Celiac disease – <span>Celiac disease can contribute to anemia by several mechanisms, including iron deficiency, reduced absorption of supplemental iron, and malabsorption of other nutrients required for red blood cell (RBC) production including vitamin B12, folic acid, and copper [22]. There may also be a component of anemia of chronic disease/anemia of inflammation (ACD/AI) as well as blood loss, although the contribution (if any) of gastrointestinal blood loss from celiac disease to iron deficiency is unclear [22]. Various reports have commented on the unexpected presence of celiac disease in individuals with iron deficiency and vice versa. As an example, in a series of 102 patients diagnosed with




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Gastritis related to an autoimmune mechanism (eg, anti-parietal cell antibodies) or H. pylori has also been implicated in causing iron deficiency [25,26].
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ts with anemia who underwent testing for celiac disease, 10 (5 percent) were found to be positive by serologic testing confirmed by intestinal biopsy [24]. ●Autoimmune gastritis and H. pylori – <span>Gastritis related to an autoimmune mechanism (eg, anti-parietal cell antibodies) or H. pylori has also been implicated in causing iron deficiency [25,26]. The following studies demonstrate that these conditions may be more common than previously appreciated: •In a series of 373 individuals with iron deficiency that included 356 premenopau




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In another series of 71 patients with iron deficiency anemia who did not have an obvious source of blood loss and underwent upper and lower endoscopy, diagnoses related to reduced absorption included atrophic gastritis in 19 (27 percent) and H. pylori in 13 (18 percent), as well as celiac disease in four (6 percent) [14].
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ent was noted in 24 of 34 (71 percent) with anti-parietal cell antibodies and autoimmune gastritis, and in 15 of 22 (68 percent) with H. pylori (as well as all eight with celiac disease) [28]. •<span>In another series of 71 patients with iron deficiency anemia who did not have an obvious source of blood loss and underwent upper and lower endoscopy, diagnoses related to reduced absorption included atrophic gastritis in 19 (27 percent) and H. pylori in 13 (18 percent), as well as celiac disease in four (6 percent) [14]. The possibility of these conditions should be reviewed, and testing obtained, in individuals with unexplained iron deficiency, especially those at increased risk based on demographic fe




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Bariatric surgery — Iron needs to be conjugated to vitamin C, amino acids, or sugars in the presence of gastric acid to protect it from the alkaline secretions in the proximal jejunum, which will otherwise convert the iron to ferric hydroxide (rust), which is unabsorbable. Bariatric surgery includes a number of procedures that promote weight loss by limiting gastric reservoir capacity and/or shortening the length of functional small intestine, which causes malabsorption. Procedures that bypass the duodenum such as roux-en-Y gastric bypass (RYGB) and biliopancreatic diversion with duodenal switch (BPD-DS) have the greatest risk of causing iron deficiency because they reduce the site of maximal absorption and in some cases reduce gastric acid availability.
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eased risk based on demographic features and those for whom oral iron therapy is ineffective. (See "Treatment of iron deficiency anemia in adults", section on 'Approaches to lack of response'.) <span>Bariatric surgery — Iron needs to be conjugated to vitamin C, amino acids, or sugars in the presence of gastric acid to protect it from the alkaline secretions in the proximal jejunum, which will otherwise convert the iron to ferric hydroxide (rust), which is unabsorbable. Bariatric surgery includes a number of procedures that promote weight loss by limiting gastric reservoir capacity and/or shortening the length of functional small intestine, which causes malabsorption. Procedures that bypass the duodenum such as roux-en-Y gastric bypass (RYGB) and biliopancreatic diversion with duodenal switch (BPD-DS) have the greatest risk of causing iron deficiency because they reduce the site of maximal absorption and in some cases reduce gastric acid availability. (See "Bariatric procedures for the management of severe obesity: Descriptions" and "Regulation of iron balance", section on 'Intestinal iron absorption'.) Routine iron supplementation a




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Medications — An acidic gastric environment facilitates absorption of iron, especially non-heme iron. However, reduced gastric acidity by itself is unlikely to cause clinically significant iron deficiency in an individual with an adequate dietary iron intake and a normally functioning gastrointestinal tract.
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n'.) Routine iron supplementation and monitoring of iron status with repletion as needed is used after most bariatric surgeries. (See "Bariatric surgery: Postoperative nutritional management".) <span>Medications — An acidic gastric environment facilitates absorption of iron, especially non-heme iron. However, reduced gastric acidity by itself is unlikely to cause clinically significant iron deficiency in an individual with an adequate dietary iron intake and a normally functioning gastrointestinal tract. Medications that reduce gastric acidity, especially proton pump inhibitors (PPIs), have been proposed to reduce iron absorption. This is mainly based on observational studies, which sug




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However, these studies indicate association rather than causation; individuals taking a PPI are more likely to have gastrointestinal conditions that lead to bleeding or reduced iron absorption, such as those listed above.
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duce iron absorption. This is mainly based on observational studies, which suggest a dose-response relationship between the dose of PPI (or duration of use) and risk of iron deficiency [29,30]. <span>However, these studies indicate association rather than causation; individuals taking a PPI are more likely to have gastrointestinal conditions that lead to bleeding or reduced iron absorption, such as those listed above. (See 'Celiac disease/atrophic gastritis/H. pylori' above.) If an individual with iron deficiency is taking a PPI, antacid, or histamine receptor blocker, we do not attribute iron defici




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If an individual with iron deficiency is taking a PPI, antacid, or histamine receptor blocker, we do not attribute iron deficiency to the medication without performing an evaluation for bleeding or reduced iron absorption as indicated for the individual. Further, we take the opportunity to re-evaluate whether the PPI is actually indicated, and we review the symptoms that led to PPI use and make sure they are properly evaluated.
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PPI are more likely to have gastrointestinal conditions that lead to bleeding or reduced iron absorption, such as those listed above. (See 'Celiac disease/atrophic gastritis/H. pylori' above.) <span>If an individual with iron deficiency is taking a PPI, antacid, or histamine receptor blocker, we do not attribute iron deficiency to the medication without performing an evaluation for bleeding or reduced iron absorption as indicated for the individual. Further, we take the opportunity to re-evaluate whether the PPI is actually indicated, and we review the symptoms that led to PPI use and make sure they are properly evaluated. (See "Proton pump inhibitors: Overview of use and adverse effects in the treatment of acid related disorders".) Medications that increase the risk of gastrointestinal bleeding may cause




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These individuals may lose an average of 2 g of iron per year, mainly from repeated blood testing and blood losses within the hemodialysis circuit [32]. Thus, iron deficiency will develop in almost all patients undergoing dialysis who are treated with EPO, as well as some individuals with chronic renal failure not receiving dialysis, unless supplemental iron is administered.
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iron requirements generated by this response in the short term can usually not be met by mobilization of the iron stores alone [31]. This is a particular problem with maintenance hemodialysis. <span>These individuals may lose an average of 2 g of iron per year, mainly from repeated blood testing and blood losses within the hemodialysis circuit [32]. Thus, iron deficiency will develop in almost all patients undergoing dialysis who are treated with EPO, as well as some individuals with chronic renal failure not receiving dialysis, unless supplemental iron is administered. This subject is discussed in detail in separate topic reviews. (See "Treatment of iron deficiency in nondialysis chronic kidney disease (CKD) patients" and "Treatment of iron deficiency




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Urinary – Chronic or intermittent intravascular hemolysis with hemosiderin accumulation in urinary epithelial cells may lead to iron loss through urinary shedding of these cells. Examples include individuals with intensive athletic training, prosthetic heart valve-associated hemolysis, or paroxysmal nocturnal hemoglobinuria (PNH).
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th cancer".) Urinary/pulmonary hemosiderosis — In some conditions, iron may be lost when there is shedding of iron-laden cells, especially over a prolonged period of time or multiple episodes. ●<span>Urinary – Chronic or intermittent intravascular hemolysis with hemosiderin accumulation in urinary epithelial cells may lead to iron loss through urinary shedding of these cells. Examples include individuals with intensive athletic training, prosthetic heart valve-associated hemolysis, or paroxysmal nocturnal hemoglobinuria (PNH). (See "Overview of the management of patients with prosthetic heart valves", section on 'Hemolytic anemia' and "Clinical manifestations and diagnosis of paroxysmal nocturnal hemoglobinur




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Pulmonary – Pulmonary hemosiderosis, such as in individuals with diffuse alveolar hemorrhage or idiopathic pulmonary hemosiderosis may lead to iron loss through iron-laden alveolar or bronchial epithelial cells. These conditions also may cause a component of functional iron deficiency, in which iron is trapped in pulmonary macrophages.
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management of patients with prosthetic heart valves", section on 'Hemolytic anemia' and "Clinical manifestations and diagnosis of paroxysmal nocturnal hemoglobinuria", section on 'Hemolysis'.) ●<span>Pulmonary – Pulmonary hemosiderosis, such as in individuals with diffuse alveolar hemorrhage or idiopathic pulmonary hemosiderosis may lead to iron loss through iron-laden alveolar or bronchial epithelial cells. These conditions also may cause a component of functional iron deficiency, in which iron is trapped in pulmonary macrophages. (See "Idiopathic pulmonary hemosiderosis" and "The diffuse alveolar hemorrhage syndromes".) Inherited disorders/IRIDA ●IRIDA due to TMPRSS6 mutation – Iron refractory iron deficiency an




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IRIDA due to TMPRSS6 mutation – Iron refractory iron deficiency anemia (IRIDA) is a rare inherited disorder in which absorption of oral iron is markedly impaired. IRIDA is caused by loss-of-function mutations of the TMPRSS6/matriptase 2 gene, which encodes a serine protease that cleaves membrane-bound hemojuvelin [33-42]. Membrane-bound hemojuvelin promotes hepcidin synthesis and impairs iron absorption in the gut; cleavage of membrane-bound hemojuvelin reduces hepcidin synthesis, increasing iron absorption. Loss of TMPRSS6 function thus causes iron deficiency due to inappropriately high hepcidin levels, with markedly reduced iron absorption and increased sequestration of iron in macrophages [39,43-48].
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tional iron deficiency, in which iron is trapped in pulmonary macrophages. (See "Idiopathic pulmonary hemosiderosis" and "The diffuse alveolar hemorrhage syndromes".) Inherited disorders/IRIDA ●<span>IRIDA due to TMPRSS6 mutation – Iron refractory iron deficiency anemia (IRIDA) is a rare inherited disorder in which absorption of oral iron is markedly impaired. IRIDA is caused by loss-of-function mutations of the TMPRSS6/matriptase 2 gene, which encodes a serine protease that cleaves membrane-bound hemojuvelin [33-42]. Membrane-bound hemojuvelin promotes hepcidin synthesis and impairs iron absorption in the gut; cleavage of membrane-bound hemojuvelin reduces hepcidin synthesis, increasing iron absorption. Loss of TMPRSS6 function thus causes iron deficiency due to inappropriately high hepcidin levels, with markedly reduced iron absorption and increased sequestration of iron in macrophages [39,43-48]. (See "Regulation of iron balance", section on 'Hemojuvelin'.) In published case reports as well as our own experience, patients with IRIDA are not anemic at birth, and the clinical phen




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SLC11A2 mutation – Iron deficiency anemia has also been described in individuals with mutations in the SLC11A2 gene, which encodes the divalent metal transporter DMT1 [49-53].
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chronic disease/inflammation [34]. The diagnosis of IRIDA is confirmed by demonstrating biallelic mutation in TMPRSS6; testing laboratories are listed on the Genetic Testing Registry website. ●<span>SLC11A2 mutation – Iron deficiency anemia has also been described in individuals with mutations in the SLC11A2 gene, which encodes the divalent metal transporter DMT1 [49-53]. (See "Regulation of iron balance", section on 'Divalent metal transporter 1'.) High-intensity athletics — Iron deficiency may be seen in some athletes due to gastrointestinal bleeding o




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High-intensity athletics — Iron deficiency may be seen in some athletes due to gastrointestinal bleeding or reduced iron intake [54,55]. Other causes of anemia may also contribute.
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ibed in individuals with mutations in the SLC11A2 gene, which encodes the divalent metal transporter DMT1 [49-53]. (See "Regulation of iron balance", section on 'Divalent metal transporter 1'.) <span>High-intensity athletics — Iron deficiency may be seen in some athletes due to gastrointestinal bleeding or reduced iron intake [54,55]. Other causes of anemia may also contribute. (See "Overtraining syndrome in athletes", section on 'Anemia and iron deficiency'.) STAGES OF IRON DEFICIENCY — The development of iron deficiency, and the rapidity with which it progre




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Normal body iron content — The normal body iron content in an adult is approximately 3 to 4 grams. The majority of iron is present in circulating red blood cells (RBCs), with additional iron in myoglobin and certain enzymes, as well as iron in storage and transport forms (figure 3)
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line iron stores, which are correlated with age, sex, and the steady state iron balance; as well as the degree, duration, and rapidity of iron or blood loss. (See "Regulation of iron balance".) <span>Normal body iron content — The normal body iron content in an adult is approximately 3 to 4 grams. The majority of iron is present in circulating red blood cells (RBCs), with additional iron in myoglobin and certain enzymes, as well as iron in storage and transport forms (figure 3). Typical amounts of iron in these sites is as follows (table 3): ●RBCs – Approximately 2 g, corresponding to approximately 2000 mL (25 to 30 mL/kg) of RBCs ●Iron-containing proteins (eg




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Typical amounts of iron in these sites is as follows ( table 3):

● RBCs – Approximately 2 g, corresponding to approximately 2000 mL (25 to 30 mL/kg) of RBCs

● Iron-containing proteins (eg, myoglobin, cytochromes, catalase) – Approximately 400 mg

● Plasma iron bound to transferrin – 3 to 7 mg

● Storage iron in the form of ferritin or hemosiderin – Approximately 0.8 to 1 g (men); approximately 0.4 to 0.5 g (women)

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4 grams. The majority of iron is present in circulating red blood cells (RBCs), with additional iron in myoglobin and certain enzymes, as well as iron in storage and transport forms (figure 3). <span>Typical amounts of iron in these sites is as follows (table 3): ●RBCs – Approximately 2 g, corresponding to approximately 2000 mL (25 to 30 mL/kg) of RBCs ●Iron-containing proteins (eg, myoglobin, cytochromes, catalase) – Approximately 400 mg ●Plasma iron bound to transferrin – 3 to 7 mg ●Storage iron in the form of ferritin or hemosiderin – Approximately 0.8 to 1 g (men); approximately 0.4 to 0.5 g (women) Storage iron in adult men has been estimated as being approximately 10 mg/kg, and is found mostly in the monocyte-macrophage system in the liver, spleen, and bone marrow. Adult women ha




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Storage iron in adult men has been estimated as being approximately 10 mg/kg, and is found mostly in the monocyte-macrophage system in the liver, spleen, and bone marrow. Adult women have less storage iron, depending upon the extent of menses, pregnancies, deliveries, lactation, and iron intake. In one study, 93 percent of women in the United States 20 to 45 years of age had iron stores of 5.5 ± 3.4 mg/kg, while the other 7 percent had an iron deficit of 3.9 ± 3.2 mg/kg [56].
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e) – Approximately 400 mg ●Plasma iron bound to transferrin – 3 to 7 mg ●Storage iron in the form of ferritin or hemosiderin – Approximately 0.8 to 1 g (men); approximately 0.4 to 0.5 g (women) <span>Storage iron in adult men has been estimated as being approximately 10 mg/kg, and is found mostly in the monocyte-macrophage system in the liver, spleen, and bone marrow. Adult women have less storage iron, depending upon the extent of menses, pregnancies, deliveries, lactation, and iron intake. In one study, 93 percent of women in the United States 20 to 45 years of age had iron stores of 5.5 ± 3.4 mg/kg, while the other 7 percent had an iron deficit of 3.9 ± 3.2 mg/kg [56]. Other estimates have suggested that up to 20 percent of menstruating women in the United States have absent iron stores [57]. The storage pool can be looked upon as a reserve of iron th




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Iron deficiency occurs in several stages, as illustrated by progressive changes in laboratory findings (table 4) [11,15]. These stages are defined by the extent of depletion, first of iron stores and then of iron available for hemoglobin synthesis. Eventually, if negative iron balance continues, production of iron-deficient RBCs and anemia occurs.
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ased need for hemoglobin synthesis, as in acute blood loss, growth in children and adolescents, pregnancy, lactation, and response to treatment with erythropoietin. Progressive iron depletion — <span>Iron deficiency occurs in several stages, as illustrated by progressive changes in laboratory findings (table 4) [11,15]. These stages are defined by the extent of depletion, first of iron stores and then of iron available for hemoglobin synthesis. Eventually, if negative iron balance continues, production of iron-deficient RBCs and anemia occurs. In the first stage, iron stores can be totally depleted without causing anemia. Once these stores are depleted, there is still enough iron present in the body within the "labile" iron p




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In the first stage, iron stores can be totally depleted without causing anemia. Once these stores are depleted, there is still enough iron present in the body within the "labile" iron pool from the daily turnover of red cells for normal hemoglobin synthesis, but the individual becomes vulnerable to development of anemia should there be further iron losses. Some individuals with extremely low levels of serum ferritin, but without anemia, may have symptoms of fatigue or show decreased exercise tolerance at this stage.
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tent of depletion, first of iron stores and then of iron available for hemoglobin synthesis. Eventually, if negative iron balance continues, production of iron-deficient RBCs and anemia occurs. <span>In the first stage, iron stores can be totally depleted without causing anemia. Once these stores are depleted, there is still enough iron present in the body within the "labile" iron pool from the daily turnover of red cells for normal hemoglobin synthesis, but the individual becomes vulnerable to development of anemia should there be further iron losses. Some individuals with extremely low levels of serum ferritin, but without anemia, may have symptoms of fatigue or show decreased exercise tolerance at this stage. Further loss of iron results in anemia, which is initially normocytic with a normal absolute reticulocyte count (table 4). This stage of iron deficiency is common in the United States.




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Further loss of iron results in anemia, which is initially normocytic with a normal absolute reticulocyte count (table 4). This stage of iron deficiency is common in the United States. As noted above, it has been estimated that the proportion of menstruating women in the United States who have minimal or absent iron reserves is at least 20 percent and may be as high as 65 percent [58,59]. Common laboratory findings at this stage include:

● Low levels of ferritin and serum iron (Fe).

● Increased levels of transferrin (Tf; total iron binding capacity [TIBC]). If only transferrin concentrations are available, they can be converted to the TIBC (in mcg/dL) by multiplying the transferrin concentration (in mg/dL) by 1.389.

● Low percent saturation of transferrin (ie, Fe/TIBC or Fe/Tf, stated as a percent).

● Increased unsaturated iron binding capacity (UIBC = TIBC - Fe).

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there be further iron losses. Some individuals with extremely low levels of serum ferritin, but without anemia, may have symptoms of fatigue or show decreased exercise tolerance at this stage. <span>Further loss of iron results in anemia, which is initially normocytic with a normal absolute reticulocyte count (table 4). This stage of iron deficiency is common in the United States. As noted above, it has been estimated that the proportion of menstruating women in the United States who have minimal or absent iron reserves is at least 20 percent and may be as high as 65 percent [58,59]. Common laboratory findings at this stage include: ●Low levels of ferritin and serum iron (Fe). ●Increased levels of transferrin (Tf; total iron binding capacity [TIBC]). If only transferrin concentrations are available, they can be converted to the TIBC (in mcg/dL) by multiplying the transferrin concentration (in mg/dL) by 1.389. ●Low percent saturation of transferrin (ie, Fe/TIBC or Fe/Tf, stated as a percent). ●Increased unsaturated iron binding capacity (UIBC = TIBC - Fe). More profound deficiency results in the classical findings of anemia with RBCs that are hypochromic (low mean corpuscular hemoglobin [MCH]) and microcytic (low mean corpuscular volume [




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More profound deficiency results in the classical findings of anemia with RBCs that are hypochromic (low mean corpuscular hemoglobin [MCH]) and microcytic (low mean corpuscular volume [MCV]). Reticulocyte production cannot be increased in the setting of iron deficiency, and the reticulocyte count becomes inappropriately low (despite being in the "normal" range in many cases). It is worth noting, however, that other concomitant causes of anemia such as vitamin B12 deficiency may cause macrocytosis and obscure the microcytosis caused by iron deficiency.
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ansferrin concentration (in mg/dL) by 1.389. ●Low percent saturation of transferrin (ie, Fe/TIBC or Fe/Tf, stated as a percent). ●Increased unsaturated iron binding capacity (UIBC = TIBC - Fe). <span>More profound deficiency results in the classical findings of anemia with RBCs that are hypochromic (low mean corpuscular hemoglobin [MCH]) and microcytic (low mean corpuscular volume [MCV]). Reticulocyte production cannot be increased in the setting of iron deficiency, and the reticulocyte count becomes inappropriately low (despite being in the "normal" range in many cases). It is worth noting, however, that other concomitant causes of anemia such as vitamin B12 deficiency may cause macrocytosis and obscure the microcytosis caused by iron deficiency. (See 'Diagnostic evaluation' below.) The normal physiologic changes in response to iron deficiency produce a number of compensatory changes, including increased production of erythropoi




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Erythropoiesis-stimulating agents – Another mechanism of functional iron deficiency is treatment with erythropoiesis-stimulating agents (erythropoietin and darbepoetin) in individuals with renal insufficiency or cancer and chemotherapy-induced anemia. In these cases, iron stores may be available but their release into the circulation may not be rapid enough to support the increased erythropoietic rate; thus, these individuals have insufficient iron stores to respond to the ESA; this is also referred to as iron restricted erythropoiesis.
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(in certain individuals), or chronic medical conditions such as diabetes. Diagnosis and management are discussed in detail separately. (See "Anemia of chronic disease/anemia of inflammation".) •<span>Erythropoiesis-stimulating agents – Another mechanism of functional iron deficiency is treatment with erythropoiesis-stimulating agents (erythropoietin and darbepoetin) in individuals with renal insufficiency or cancer and chemotherapy-induced anemia. In these cases, iron stores may be available but their release into the circulation may not be rapid enough to support the increased erythropoietic rate; thus, these individuals have insufficient iron stores to respond to the ESA; this is also referred to as iron restricted erythropoiesis. (See 'Redistribution after erythropoietin/erythropoiesis-stimulating agents' above.) Thresholds for ferritin and transferrin saturation in absolute and functional iron deficiency are di




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Symptoms of anemia — The usual presenting symptoms in adults with iron deficiency are primarily due to anemia. The same symptoms may also be present in those with severely reduced iron stores and extremely low serum ferritin who are not anemic. Typical symptoms include [16]:

● Fatigue

● Pica (Pagophagia)

● Restless legs syndrome

● Headache

● Exercise intolerance

● Exertional dyspnea

● Weakness

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s-stimulating agents' above.) Thresholds for ferritin and transferrin saturation in absolute and functional iron deficiency are discussed below. (See 'Diagnosis' below.) CLINICAL MANIFESTATIONS <span>Symptoms of anemia — The usual presenting symptoms in adults with iron deficiency are primarily due to anemia. The same symptoms may also be present in those with severely reduced iron stores and extremely low serum ferritin who are not anemic. Typical symptoms include [16]: ●Fatigue ●Pica (Pagophagia) ●Restless legs syndrome ●Headache ●Exercise intolerance ●Exertional dyspnea ●Weakness These may be present in varying degrees and may not be appreciated at all until after iron deficiency is identified and treated. Many patients recognize in retrospect that they had fati




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The classic presentation pattern in a patient without comorbidities is a multigravid woman who presents with tiredness and fatigue and a complete blood count (CBC) that shows anemia with low MCV (eg, hemoglobin 8 g/dL, MCV 75 fL) and a peripheral blood smear that shows microcytic, hypochromic RBCs (picture 1). Iron studies are likely to show low iron in the range of 10 mcg/dL, low ferritin (below 30 ng/mL), and increased transferrin (around 400 mcg/dL) or high TIBC, with a low calculated transferrin saturation (TSAT; below 20 percent). Such a patient is likely to have a brisk response to iron therapy. It is also important to consider the possibility of gastrointestinal blood loss, even in a menstruating woman.
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ed and treated. Many patients recognize in retrospect that they had fatigue, weakness, exercise intolerance, and/or pica (see 'Pica and ice craving' below) only after successful iron repletion. <span>The classic presentation pattern in a patient without comorbidities is a multigravid woman who presents with tiredness and fatigue and a complete blood count (CBC) that shows anemia with low MCV (eg, hemoglobin 8 g/dL, MCV 75 fL) and a peripheral blood smear that shows microcytic, hypochromic RBCs (picture 1). Iron studies are likely to show low iron in the range of 10 mcg/dL, low ferritin (below 30 ng/mL), and increased transferrin (around 400 mcg/dL) or high TIBC, with a low calculated transferrin saturation (TSAT; below 20 percent). Such a patient is likely to have a brisk response to iron therapy. It is also important to consider the possibility of gastrointestinal blood loss, even in a menstruating woman. Pica and ice craving — Pica refers to a desire for or compulsion to eat substances not fit as food; the term is derived from the Latin word for magpie (Pica pica), a bird that gathers n




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Pica and ice craving — Pica refers to a desire for or compulsion to eat substances not fit as food; the term is derived from the Latin word for magpie (Pica pica), a bird that gathers non-food objects [62]. These substances may include earth substances such as clay or dirt (geophagia); paper products including wallpaper or toilet paper; starches including corn starch, laundry starch, fabric softener sheets, or raw rice or pasta (amylophagia); or ice (pagophagia).
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ow 20 percent). Such a patient is likely to have a brisk response to iron therapy. It is also important to consider the possibility of gastrointestinal blood loss, even in a menstruating woman. <span>Pica and ice craving — Pica refers to a desire for or compulsion to eat substances not fit as food; the term is derived from the Latin word for magpie (Pica pica), a bird that gathers non-food objects [62]. These substances may include earth substances such as clay or dirt (geophagia); paper products including wallpaper or toilet paper; starches including corn starch, laundry starch, fabric softener sheets, or raw rice or pasta (amylophagia); or ice (pagophagia). Other reported substances have included chalk, ashes, charcoal, coffee grounds, baby powder, and paint chips. The specific substances that are craved may depend on what is available and




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Overall, pica may be seen in many clinical settings and is not considered specific for iron deficiency. However, pagophagia (pica for ice) is considered quite specific for iron deficiency [63,65,66]. It may be present in patients who are not anemic and responds rapidly to treatment with iron (disappears during iron infusions), often before any increase is noted in the hemoglobin concentration. In one study of 55 unselected patients with iron deficiency anemia secondary to gastrointestinal blood loss, pica was present in 32 (58 percent), which manifested as pagophagia in 28 (51 percent of the total; 88 percent of those with pica) [65].
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considered culturally acceptable [63,64]. The craving for these non-food substances may be intense. In pregnant women, pica may also be misinterpreted as food cravings unrelated to iron status. <span>Overall, pica may be seen in many clinical settings and is not considered specific for iron deficiency. However, pagophagia (pica for ice) is considered quite specific for iron deficiency [63,65,66]. It may be present in patients who are not anemic and responds rapidly to treatment with iron (disappears during iron infusions), often before any increase is noted in the hemoglobin concentration. In one study of 55 unselected patients with iron deficiency anemia secondary to gastrointestinal blood loss, pica was present in 32 (58 percent), which manifested as pagophagia in 28 (51 percent of the total; 88 percent of those with pica) [65]. Pica may also contribute to iron deficiency by reducing iron absorption, depending on the substance ingested (see 'Reduced iron absorption' above). Its mechanism in individuals with iro




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Beeturia — Beeturia is a phenomenon in which the urine turns red following ingestion of beets. Beeturia is increased in individuals with iron deficiency but the finding is not specific for iron deficiency. It has been noted in approximately 10 to 14 percent of healthy individuals following ingestion of beets and in as much as 49 to 80 percent of individuals with iron deficiency [67-69].

Beeturia is caused by increased intestinal absorption and subsequent excretion of the reddish pigment betalaine (betanin) present in beets. Betalaine, a redox indicator, is decolorized by ferric ions, which presumably explains the predisposition to beeturia when adequate amounts of iron are not available for decolorization of this pigment.

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iron deficiency by reducing iron absorption, depending on the substance ingested (see 'Reduced iron absorption' above). Its mechanism in individuals with iron deficiency is not well understood. <span>Beeturia — Beeturia is a phenomenon in which the urine turns red following ingestion of beets. Beeturia is increased in individuals with iron deficiency but the finding is not specific for iron deficiency. It has been noted in approximately 10 to 14 percent of healthy individuals following ingestion of beets and in as much as 49 to 80 percent of individuals with iron deficiency [67-69]. Beeturia is caused by increased intestinal absorption and subsequent excretion of the reddish pigment betalaine (betanin) present in beets. Betalaine, a redox indicator, is decolorized by ferric ions, which presumably explains the predisposition to beeturia when adequate amounts of iron are not available for decolorization of this pigment. (See "Urinalysis in the diagnosis of kidney disease", section on 'Red to brown urine'.) Restless legs syndrome — Restless legs syndrome (RLS), also called Willis-Ekbom disease, is a dis




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Restless legs syndrome — Restless legs syndrome (RLS), also called Willis-Ekbom disease, is a disorder in which there is an unpleasant or uncomfortable urge to move the legs during periods of inactivity. The discomfort is relieved by movement, often instantaneously. A number of changes in the central nervous system have been correlated with RLS. Of these, reduced iron in the central nervous system has been a consistent finding, regardless of total body iron stores.
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sposition to beeturia when adequate amounts of iron are not available for decolorization of this pigment. (See "Urinalysis in the diagnosis of kidney disease", section on 'Red to brown urine'.) <span>Restless legs syndrome — Restless legs syndrome (RLS), also called Willis-Ekbom disease, is a disorder in which there is an unpleasant or uncomfortable urge to move the legs during periods of inactivity. The discomfort is relieved by movement, often instantaneously. A number of changes in the central nervous system have been correlated with RLS. Of these, reduced iron in the central nervous system has been a consistent finding, regardless of total body iron stores. (See "Clinical features and diagnosis of restless legs syndrome and periodic limb movement disorder in adults", section on 'Pathophysiology'.) RLS is common in the general population, i




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RLS is common in the general population, in some series affecting 5 to 15 percent of adults, especially in White populations. Iron deficiency may be one of the more common causes of RLS, and RLS may be one of the more common clinical manifestations of iron deficiency. As an example, in a series of 251 patients with iron deficiency anemia referred to a community-based hematology practice, the prevalence of clinically significant RLS was 24 percent, approximately nine times higher than that seen in the control population [70].
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ent finding, regardless of total body iron stores. (See "Clinical features and diagnosis of restless legs syndrome and periodic limb movement disorder in adults", section on 'Pathophysiology'.) <span>RLS is common in the general population, in some series affecting 5 to 15 percent of adults, especially in White populations. Iron deficiency may be one of the more common causes of RLS, and RLS may be one of the more common clinical manifestations of iron deficiency. As an example, in a series of 251 patients with iron deficiency anemia referred to a community-based hematology practice, the prevalence of clinically significant RLS was 24 percent, approximately nine times higher than that seen in the control population [70]. While overall findings linking RLS to iron deficiency are not conclusive, they warrant the measurement of hemoglobin and iron parameters in individuals who present with this symptom, an




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While overall findings linking RLS to iron deficiency are not conclusive, they warrant the measurement of hemoglobin and iron parameters in individuals who present with this symptom, and administration of iron when stores are low.
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ia referred to a community-based hematology practice, the prevalence of clinically significant RLS was 24 percent, approximately nine times higher than that seen in the control population [70]. <span>While overall findings linking RLS to iron deficiency are not conclusive, they warrant the measurement of hemoglobin and iron parameters in individuals who present with this symptom, and administration of iron when stores are low. A 2018 guideline from the International Restless Legs Syndrome Study Group provides a consensus on intervention with oral or intravenous iron [71]. Some clinicians will give a trial of




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Findings on examination — The physical examination in individuals with iron deficiency (with or without anemia) may be normal or it may reveal one or more of the following findings [16,73]:

● Pallor

● Dry or rough skin

● Atrophic glossitis with loss of tongue papillae, which may be accompanied by tongue pain or dry mouth (picture 2 and picture 3) [74]

● Cheilosis (also called angular cheilitis) (picture 4 and picture 5)

● Koilonychia (spoon nails) (picture 6 and picture 7)

● Esophageal web, which may be accompanied by dysphagia (eg, Plummer-Vinson or Patterson-Kelly syndrome; rare)

● Alopecia (rare) in especially severe cases [75]

● Chlorosis (pale, faintly green complexion; extremely rare)

The more severe of these findings, including chlorosis and Plummer-Vinson syndrome, which were more common during the early 1900s, have virtually disappeared [76,77]. Patients with more severe anemia may have tachycardia, a cardiac murmur, or (rarely) hemodynamic instability [16].

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ned hearing loss of 2.4 (95% CI 1.9-3.0). The mechanism of the association is not known, and we do not perform a formal audiologic evaluation unless the patient reports difficulty with hearing. <span>Findings on examination — The physical examination in individuals with iron deficiency (with or without anemia) may be normal or it may reveal one or more of the following findings [16,73]: ●Pallor ●Dry or rough skin ●Atrophic glossitis with loss of tongue papillae, which may be accompanied by tongue pain or dry mouth (picture 2 and picture 3) [74] ●Cheilosis (also called angular cheilitis) (picture 4 and picture 5) ●Koilonychia (spoon nails) (picture 6 and picture 7) ●Esophageal web, which may be accompanied by dysphagia (eg, Plummer-Vinson or Patterson-Kelly syndrome; rare) ●Alopecia (rare) in especially severe cases [75] ●Chlorosis (pale, faintly green complexion; extremely rare) The more severe of these findings, including chlorosis and Plummer-Vinson syndrome, which were more common during the early 1900s, have virtually disappeared [76,77]. Patients with more severe anemia may have tachycardia, a cardiac murmur, or (rarely) hemodynamic instability [16]. For individuals with gastrointestinal blood loss, the stool may show overt or occult blood. However, absence of blood in the stool does not eliminate the possibilities of gastrointestin




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For individuals with gastrointestinal blood loss, the stool may show overt or occult blood. However, absence of blood in the stool does not eliminate the possibilities of gastrointestinal bleeding or iron deficiency (or the need to evaluate for a source of gastrointestinal bleeding when appropriate), because bleeding may be intermittent.

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h were more common during the early 1900s, have virtually disappeared [76,77]. Patients with more severe anemia may have tachycardia, a cardiac murmur, or (rarely) hemodynamic instability [16]. <span>For individuals with gastrointestinal blood loss, the stool may show overt or occult blood. However, absence of blood in the stool does not eliminate the possibilities of gastrointestinal bleeding or iron deficiency (or the need to evaluate for a source of gastrointestinal bleeding when appropriate), because bleeding may be intermittent. DIAGNOSTIC EVALUATION Overview of evaluation — The possibility of iron deficiency should be addressed in the following adult populations: ●Virtually all adults with unexplained anemia,




INTRINSIC VALUE
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Tughlaq's Token coin
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Proton pump inhibitors (PPIs) effectively block gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump that resides on the luminal surface of the parietal cell membrane.
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Feb 2021. | This topic last updated: Jul 13, 2020. INTRODUCTION — <span>Proton pump inhibitors (PPIs) effectively block gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump that resides on the luminal surface of the parietal cell membrane. This topic review will provide an overview of the mechanism of action, pharmacokinetics, administration, and adverse effects of PPIs. The use and efficacy of PPIs in specific acid-relat




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Proton pump inhibitor (PPI) therapy is indicated in the following clinical situations:

Peptic ulcer disease – PPIs are first-line antisecretory therapy in the treatment of peptic ulcer disease. (See "Peptic ulcer disease: Treatment and secondary prevention", section on 'Initial antisecretory therapy'.)

Gastroesophageal reflux disease – PPIs are indicated in patients with gastroesophageal reflux disease, including for the treatment of erosive esophagitis and as maintenance therapy in patients with severe erosive esophagitis or Barrett’s esophagus. (See "Medical management of gastroesophageal reflux disease in adults", section on 'Severe or frequent symptoms or erosive esophagitis'.)

Zollinger-Ellison syndrome – PPIs, often in high doses, are required to control gastric acid hypersecretion in patients with gastrin-secreting tumors. (See "Management and prognosis of the Zollinger-Ellison syndrome (gastrinoma)", section on 'Proton pump inhibitors'.)

NSAID-associated ulcers – PPIs are indicated in the primary prevention of gastroduodenal ulcers associated with NSAID use. (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".)

Eradication of Helicobacter pylori – PPIs are a component of several first-line and salvage therapy regimens for H. pylori infection. (See "Treatment regimens for Helicobacter pylori in adults".)

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nd efficacy of PPIs in specific acid-related disorders is presented separately. (See "Antiulcer medications: Mechanism of action, pharmacology, and side effects".) INDICATIONS FOR PPI THERAPY — <span>Proton pump inhibitor (PPI) therapy is indicated in the following clinical situations: ●Peptic ulcer disease – PPIs are first-line antisecretory therapy in the treatment of peptic ulcer disease. (See "Peptic ulcer disease: Treatment and secondary prevention", section on 'Initial antisecretory therapy'.) ●Gastroesophageal reflux disease – PPIs are indicated in patients with gastroesophageal reflux disease, including for the treatment of erosive esophagitis and as maintenance therapy in patients with severe erosive esophagitis or Barrett’s esophagus. (See "Medical management of gastroesophageal reflux disease in adults", section on 'Severe or frequent symptoms or erosive esophagitis'.) ●Zollinger-Ellison syndrome – PPIs, often in high doses, are required to control gastric acid hypersecretion in patients with gastrin-secreting tumors. (See "Management and prognosis of the Zollinger-Ellison syndrome (gastrinoma)", section on 'Proton pump inhibitors'.) ●NSAID-associated ulcers – PPIs are indicated in the primary prevention of gastroduodenal ulcers associated with NSAID use. (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".) ●Eradication of Helicobacter pylori – PPIs are a component of several first-line and salvage therapy regimens for H. pylori infection. (See "Treatment regimens for Helicobacter pylori in adults".) PHARMACOLOGY ●Mechanism of action – Proton pump inhibitors (PPIs) inhibit H-K-ATPase, the final step of gastric acid secretion by parietal cells. PPIs are benzimidazole prodrugs which a




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PPIs are benzimidazole prodrugs which accumulate specifically and selectively in the secretory canaliculus of the parietal cell [1]. Within that space, they undergo an acid catalyzed conversion to a reactive species, the thiophilic sulfonamides, which are permanent cations. The rate of conversion varies among the compounds and is inversely proportional to the pKa of the benzimidazole (rabeprazole >omeprazole, esomeprazole, and lansoprazole >pantoprazole) (table 1) [2].
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t regimens for Helicobacter pylori in adults".) PHARMACOLOGY ●Mechanism of action – Proton pump inhibitors (PPIs) inhibit H-K-ATPase, the final step of gastric acid secretion by parietal cells. <span>PPIs are benzimidazole prodrugs which accumulate specifically and selectively in the secretory canaliculus of the parietal cell [1]. Within that space, they undergo an acid catalyzed conversion to a reactive species, the thiophilic sulfonamides, which are permanent cations. The rate of conversion varies among the compounds and is inversely proportional to the pKa of the benzimidazole (rabeprazole >omeprazole, esomeprazole, and lansoprazole >pantoprazole) (table 1) [2]. The reactive species interacts with the external surface of the H-K-ATPase that faces the lumen of the secretory space of the parietal cell, resulting in disulfide bond formation with c




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Proton pump inhibitors (PPIs) inhibit H-K-ATPase, the final step of gastric acid secretion by parietal cells.
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PIs are a component of several first-line and salvage therapy regimens for H. pylori infection. (See "Treatment regimens for Helicobacter pylori in adults".) PHARMACOLOGY ●Mechanism of action – <span>Proton pump inhibitors (PPIs) inhibit H-K-ATPase, the final step of gastric acid secretion by parietal cells. PPIs are benzimidazole prodrugs which accumulate specifically and selectively in the secretory canaliculus of the parietal cell [1]. Within that space, they undergo an acid catalyzed co




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PPIs are similar in structure and mechanism of action, but PPIs differ in their pKa, bioavailability, peak plasma levels, and route of excretion (table 1). The magnitude of these differences are small and their clinical relevance has not been established.
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transport. This covalent inhibition of the enzyme results in a specific and long-lasting impairment of gastric acid secretion. (See "Physiology of gastric acid secretion".) ●Pharmacokinetics – <span>PPIs are similar in structure and mechanism of action, but PPIs differ in their pKa, bioavailability, peak plasma levels, and route of excretion (table 1). The magnitude of these differences are small and their clinical relevance has not been established. PPIs are most effective when the parietal cell is stimulated to secrete acid postprandially, a relationship that has important clinical implications for timing of administration. Becaus




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PPIs are most effective when the parietal cell is stimulated to secrete acid postprandially, a relationship that has important clinical implications for timing of administration. Because the amount of H-K-ATPase present in the parietal cell is greatest after a prolonged fast, PPIs should be administered before the first meal of the day. In most individuals, once-daily dosing is sufficient to produce the desired level of acid inhibition, and a second dose, which is occasionally necessary, should be administered before the evening meal [1]
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s differ in their pKa, bioavailability, peak plasma levels, and route of excretion (table 1). The magnitude of these differences are small and their clinical relevance has not been established. <span>PPIs are most effective when the parietal cell is stimulated to secrete acid postprandially, a relationship that has important clinical implications for timing of administration. Because the amount of H-K-ATPase present in the parietal cell is greatest after a prolonged fast, PPIs should be administered before the first meal of the day. In most individuals, once-daily dosing is sufficient to produce the desired level of acid inhibition, and a second dose, which is occasionally necessary, should be administered before the evening meal [1]. (See 'Dose and timing of administration' below.) Once-daily PPI dosing for five days inhibits maximal gastric acid output by approximately 66 percent. Since PPIs inhibit only activated




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Once-daily PPI dosing for five days inhibits maximal gastric acid output by approximately 66 percent. Since PPIs inhibit only activated enzyme present in the canalicular membrane, the reduction of gastric acid secretion after an initial dose will probably be suboptimal. As inactive enzyme is recruited into the secretory canaliculus, acid secretion will resume, albeit at a reduced level. After the second dose is given on the next day, more H-K-ATPase will have been recruited and subsequently inhibited, and after the third dose, additional recruitment and further acid inhibition will probably occur. Thus, the occasional use of a PPI taken on an "as needed" basis does not reliably provide adequate acid inhibition and does not produce a consistent or satisfactory clinical response (in contrast to the H2 antagonists, which have a more rapid onset of action) [1].
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ce the desired level of acid inhibition, and a second dose, which is occasionally necessary, should be administered before the evening meal [1]. (See 'Dose and timing of administration' below.) <span>Once-daily PPI dosing for five days inhibits maximal gastric acid output by approximately 66 percent. Since PPIs inhibit only activated enzyme present in the canalicular membrane, the reduction of gastric acid secretion after an initial dose will probably be suboptimal. As inactive enzyme is recruited into the secretory canaliculus, acid secretion will resume, albeit at a reduced level. After the second dose is given on the next day, more H-K-ATPase will have been recruited and subsequently inhibited, and after the third dose, additional recruitment and further acid inhibition will probably occur. Thus, the occasional use of a PPI taken on an "as needed" basis does not reliably provide adequate acid inhibition and does not produce a consistent or satisfactory clinical response (in contrast to the H2 antagonists, which have a more rapid onset of action) [1]. Restoration of acid secretion after discontinuing PPIs depends upon enzyme turnover and the biological reversibility of the disulfide bond. Maximal acid secretory capacity may not be re




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Restoration of acid secretion after discontinuing PPIs depends upon enzyme turnover and the biological reversibility of the disulfide bond. Maximal acid secretory capacity may not be restored for 24 to 48 hours [1].
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t reliably provide adequate acid inhibition and does not produce a consistent or satisfactory clinical response (in contrast to the H2 antagonists, which have a more rapid onset of action) [1]. <span>Restoration of acid secretion after discontinuing PPIs depends upon enzyme turnover and the biological reversibility of the disulfide bond. Maximal acid secretory capacity may not be restored for 24 to 48 hours [1]. (See 'Discontinuing PPIs' below.) ●Metabolism – PPIs are metabolized via hepatic cytochrome P450 enzymes, with CYP2C19 having the dominant role. However, the dominance of CYP2C19 over o




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Plasma levels of PPI correlate with their metabolism, and differences may contribute to varying dose requirements and clinical efficacy. As an example, one study examined the effect of variable metabolism of omeprazole when using this agent to treat H. pylori in 62 Japanese patients [3]. While eradication was achieved in all individuals homozygous for a CYP2C19 mutation (ie, slow metabolizers), successful treatment was achieved in only 60 and 29 percent of heterozygotes and wild type homozygotes, respectively.
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e metabolism of PPIs by this route may be delayed in these individuals [4]. Homozygotes for the wild type gene rapidly metabolize these drugs, while heterozygotes are intermediate metabolizers. <span>Plasma levels of PPI correlate with their metabolism, and differences may contribute to varying dose requirements and clinical efficacy. As an example, one study examined the effect of variable metabolism of omeprazole when using this agent to treat H. pylori in 62 Japanese patients [3]. While eradication was achieved in all individuals homozygous for a CYP2C19 mutation (ie, slow metabolizers), successful treatment was achieved in only 60 and 29 percent of heterozygotes and wild type homozygotes, respectively. In another study that evaluated the efficacy of lansoprazole in the treatment of 65 patients with gastroesophageal reflux disease (GERD), slow metabolizers were much more likely to be a




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HIV protease inhibitors - PPIs may decrease the absorption of certain HIV protease inhibitors. PPIs are contraindicated in patients being treated with rilpivirine. Atazanavir should not be used in patients who require a PPI dose equivalent to >20 mg omeprazole daily.
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evance of these data remains highly controversial. The interaction of clopidogrel and PPIs are discussed in detail separately. (See "Clopidogrel resistance and clopidogrel treatment failure".) ●<span>HIV protease inhibitors - PPIs may decrease the absorption of certain HIV protease inhibitors. PPIs are contraindicated in patients being treated with rilpivirine. Atazanavir should not be used in patients who require a PPI dose equivalent to >20 mg omeprazole daily. (See "Overview of antiretroviral agents used to treat HIV", section on 'Protease inhibitors (PIs)'.) ●Methotrexate - Coadministration of PPIs with high dose methotrexate appears to be c




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Methotrexate - Coadministration of PPIs with high dose methotrexate appears to be correlated with delayed methotrexate elimination and potentially may lead to methotrexate toxicity if not monitored appropriately.
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ld not be used in patients who require a PPI dose equivalent to >20 mg omeprazole daily. (See "Overview of antiretroviral agents used to treat HIV", section on 'Protease inhibitors (PIs)'.) ●<span>Methotrexate - Coadministration of PPIs with high dose methotrexate appears to be correlated with delayed methotrexate elimination and potentially may lead to methotrexate toxicity if not monitored appropriately. For additional information on drug interactions, use the Lexicomp drug interactions program provided by UpToDate. (See "Overview of the non-acute management of unstable angina and non-S




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Clopidogrel - Some data suggest decreased activation of clopidogrel when used in conjunction with omeprazole due to shared hepatic cytochrome P450-mediated metabolism. In 2009, the United States Food and Drug Administration concluded that patients taking clopidogrel should consult with their clinician if they are taking or considering taking a PPI, including over-the-counter PPI preparations [13,14]. However, the relevance of these data remains highly controversial. The interaction of clopidogrel and PPIs are discussed in detail separately.
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0 enzymes involved in PPI metabolism and the potential for interactions among PPIs varies considerably (table 2) [6-12]. Some other important drug interactions with PPIs include the following: ●<span>Clopidogrel - Some data suggest decreased activation of clopidogrel when used in conjunction with omeprazole due to shared hepatic cytochrome P450-mediated metabolism. In 2009, the United States Food and Drug Administration concluded that patients taking clopidogrel should consult with their clinician if they are taking or considering taking a PPI, including over-the-counter PPI preparations [13,14]. However, the relevance of these data remains highly controversial. The interaction of clopidogrel and PPIs are discussed in detail separately. (See "Clopidogrel resistance and clopidogrel treatment failure".) ●HIV protease inhibitors - PPIs may decrease the absorption of certain HIV protease inhibitors. PPIs are contraindicate




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Magnesium – We obtain serum magnesium levels prior to starting a PPI in patients who are expected to be on long-term (≥1 year) treatment or in patients who take PPIs in conjunction with other medications associated with hypomagnesemia (eg, diuretics). In addition, we obtain magnesium levels periodically in such patients while they are taking a PPI. The frequency of testing is based on the clinical history and the presence of symptoms of hypomagnesemia. As an example, in patients with a history of arrhythmias or QT interval prolongation, we monitor magnesium levels every six months. The management of hypomagnesemia is discussed in detail separately.
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le angina and non-ST elevation myocardial infarction", section on 'Gastrointestinal prophylaxis'.) Laboratory testing — We limit routine laboratory testing to selected patients on PPI therapy. ●<span>Magnesium – We obtain serum magnesium levels prior to starting a PPI in patients who are expected to be on long-term (≥1 year) treatment or in patients who take PPIs in conjunction with other medications associated with hypomagnesemia (eg, diuretics). In addition, we obtain magnesium levels periodically in such patients while they are taking a PPI. The frequency of testing is based on the clinical history and the presence of symptoms of hypomagnesemia. As an example, in patients with a history of arrhythmias or QT interval prolongation, we monitor magnesium levels every six months. The management of hypomagnesemia is discussed in detail separately. (See "Hypomagnesemia: Evaluation and treatment".) ●Vitamin B12 – We also obtain vitamin B12 levels yearly in patients on long-term PPIs [15]. However, routinely monitoring vitamin B12 l




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Vitamin B12 – We also obtain vitamin B12 levels yearly in patients on long-term PPIs [15]. However, routinely monitoring vitamin B12 levels is controversial.
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or QT interval prolongation, we monitor magnesium levels every six months. The management of hypomagnesemia is discussed in detail separately. (See "Hypomagnesemia: Evaluation and treatment".) ●<span>Vitamin B12 – We also obtain vitamin B12 levels yearly in patients on long-term PPIs [15]. However, routinely monitoring vitamin B12 levels is controversial. (See 'Magnesium malabsorption' below and 'Vitamin B12 malabsorption' below.) There are insufficient evidence to support routine bone density monitoring or calcium supplementation due to




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There are insufficient evidence to support routine bone density monitoring or calcium supplementation due to proton pump inhibitor use alone [16].
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levels yearly in patients on long-term PPIs [15]. However, routinely monitoring vitamin B12 levels is controversial. (See 'Magnesium malabsorption' below and 'Vitamin B12 malabsorption' below.) <span>There are insufficient evidence to support routine bone density monitoring or calcium supplementation due to proton pump inhibitor use alone [16]. ADMINISTRATION Intravenous regimen — IV PPIs are indicated prior to endoscopic evaluation in patients with clinically significant upper gastrointestinal bleeding from a suspected peptic