Iron Deficiency Anemia Diagnosed in the Private Practice Setting,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3186-3186
Author(s):  
Thomas A Bensinger ◽  
Ayana M Elliott ◽  
Laura Hostovich ◽  
Martin D. Weltz

Abstract Abstract 3186 Introduction: Iron deficiency anemia (IDA) continues to be a problem in the United States in the 21st Century. Differentiating IDA from anemia of chronic disease (ACD) is important in the clinical practice setting because iron supplementation has been shown to be beneficial for IDA and may deleteriously affect ACD patients. We examined consecutive patients referred for a diagnosis of anemia in a single community-based hematology-oncology practice in the suburbs of a major city over an 8 month period. IDA was found amongst these patients. The common possible causes, symptoms and usual treatment for this subset of patients are reported. Methods: Records of all adult patients referred to the practice with a diagnosis of anemia and were then confirmed to be iron deficiency anemia from March 2010 until November 2010 were reviewed. Chart review analysis was performed to identify differences in gender, causes, symptoms, treatment plans, treatment efficacy, pertinent history and physical findings including laboratory studies - CBC, ferritin, iron/TIBC, reticulocyte count, review of the peripheral blood film, and often but not always, an erythropoietin level. Results: A significant number of patients (n = 130) demonstrated iron deficiency anemia. The vast majority of these patients were female (94%). Most patients were also premenopausal. Four patients were pregnant. The most common cause of iron deficiency anemia was heavy menstrual blood loss associated with the presence of uterine fibroids (67%) followed by, gastric bypass surgery (24%). Interestingly, a subset of patients (12%) had a history of both gastric bypass and heavy menstrual blood loss. Other associated causes found to be linked to IDA were gastrointestinal lesions, such as AV malformations, gastritis, including medication induced gastritis (nonsteroidal anti-inflammatory drugs), hiatal hernia and at least one colon cancer. Subjective symptoms of IDA included tiredness, weakness, exhaustion, brittle nails and hair loss. The finding of pica was quite extensive and often not reported by the patient unless questioned in detail. Pica symptoms included the desire for ice (pagophagia), clay or starch, and also revealed some unusual urges, including eating toilet paper or paper towels, dirt from a patient's rose garden, or the urge to chew gum with the amount exceeding several packages of greater than 10 sticks each per day. One patient reported eating leaves which were stripped from a garden plant. Laboratory studies on these patient subset revealed only 3 had a ferritin level greater than 20 ng/mL (3%). The MCV was less than 80 fl in 111 of the 130 patients. Thrombocytosis (a platelet count of greater than 400,000.103 ml) was an associated finding of IDA and occurred 40 of 130 patients (30%). The platelet count returned to normal in all but one patient post treatment. Conclusion: Iron deficiency is a pervasive problem that is not adequately assessed and treated. Many of our clinic patients developed iron deficiency anemia as a result of surgical intervention, such as gastric bypass surgery. We recommend identifying IDA early to treat patients efficaciously for optimal outcomes. Close attention should be given to key clinical indicators including low MCV and variant forms of pica syndrome which is a valid symptom of iron deficiency. Our experience with administering intravenous iron preparations suggests that patients have improvements in overall well being often within a few days of the first infusion. The pica syndrome resolved in approximately two weeks post the first dose of iron in most patients, even prior to demonstrating any significant improvement in the hemoglobin and hematocrit or the MCV levels. This may imply that iron deficiency affects fundamental enzymes for metabolic processes found in the oral mucosa leading to the PICA. Intravenous iron administration was often used in our practice to bring the hemoglobin and hematocrit to more favorable levels in order to reduce symptoms of iron deficiency or to undergo surgical procedures and childbirth as needed. There was an occasional reaction to intravenous iron that included pruritis, back pain and an unusual swelling in the joints (e.g., knees). We have treated these patients with 100 mg of hydrocortisone intravenously and 25 mg of diphenhydramine intravenously. All reactions usually abated within 30 minutes. We had no fatal reactions to the use of intravenous iron preparations. Disclosures: No relevant conflicts of interest to declare.

2013 ◽  
Vol 9 (1) ◽  
pp. 129-132 ◽  
Author(s):  
Zachariah DeFilipp ◽  
John Lister ◽  
Daniel Gagné ◽  
Richard K. Shadduck ◽  
Lori Prendergast ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Matthew Tam ◽  
Ruchi Bhabhra

Abstract Background: Ferric carboxymaltose (Injectafer), a newer intravenous iron agent permits larger iron concentrations to be delivered in fewer doses compared to traditional preparations of intravenous iron. However, ferric carboxymaltose has been shown to up-regulate fibroblast growth factor 23 (FGF23) which can result in severe hypophosphatemia. We present a case illustrating this phenomenon. Clinical Case: A 48 year-old Caucasian female was admitted to the emergency department with complaints of gradual onset muscle weakness and severe exhaustion. Over the course of several months she noticed significant muscle weakness in all extremities. Her co-morbidities included morbid obesity (status-post Roux-en-y bypass surgery), asthma, and hereditary angioedema. Due to her history of gastric bypass surgery, the patient required monthly iron sucrose infusions over the previous two years. Her regimen was changed to ferric carboxymaltose (Injectafer) about five months prior to the admission, receiving 750mg treatments twice monthly. On admission, she was found to have severe hypophosphatemia of 1.5 mg/dL (2.1 – 4.7 mg/dL) with 25-OH vitamin D 21 ng/mL and PTH of 155 pg/mL. A random urinary phosphate was 72 mg/dL with a urine creatinine of 45 mg/dL, with calculated fractional excretion of phosphorus of 74%. Further diagnostic tests including EMG / nerve conduction studies, inflammatory markers, autoimmune workup, and creatine kinase were negative. She was found to have a ferritin of 2159 ng/mL (11 – 306 ng/mL) from previous baseline of 12.8 ng/mL with normal ESR and CRP. This was elucidated to be due to iron overload from IV iron infusions out of proportion to her needs. Therefore, ferrric carboxymaltose was discontinued. Her symptoms gradually improved with phosphorus and vitamin D supplementation. Two months later, when seen by Endocrinology, her ferritin was 1220 ng/mL, PTH 44 pg/mL, and phosphorus normalized to 2.6 mg/dL. Conclusion: Ferric carboxymaltose can cause profound phosphaturia and hypophosphatemia by inhibiting the cleavage of intact FGF23 to the inactive form, a mechanism similar to autosomal dominant hypophosphatemic rickets. Previous clinical trials show the incidence of hypophosphatemia to be as high as 41-70%. We conclude that baseline phosphorus and vitamin D levels should be obtained prior to therapy and monitored closely during treatment. Reference: Adkinson NF et al. Comparative safety of intravenous ferumoxytol versus ferric carboxymaltose in iron deficiency anemia: A randomized trial. Am J Hematol. 2018;93(5):683.


Author(s):  
Abdul-Kareem Al-Momen ◽  
Abdulaziz Al-Meshari ◽  
Lulu Al-Nuaim ◽  
Abdulaziz Saddique ◽  
Zainab Abotalib ◽  
...  

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