scholarly journals MON-344 Uncommon Etiology of Hypophosphatemia and Secondary Hyperparathyroidism: Ferric Carboxymaltose Infusion

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sakine Sever
Keyword(s):  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Spinal Stenosis ◽  
Side Effect ◽  
Deficiency Anemia ◽  
Ferric Carboxymaltose ◽  
Left Femur ◽  
T Score ◽  
Fgf 23 ◽  
Work Up

Abstract Background: Hypophosphatemia has been recognized as one of the side effect of intravenous ferric carboxymaltose infusion. This effect is thought to be secondary to fibroblast growth factor 23 (FGF 23) mediated renal phosphate wasting and associated with calcitriol deficiency and secondary hyperparathyroidism. Clinical Case: A 76 years old male patient with medical problems including hypertension, type 2 diabetes mellitus, hyperlipidemia, paroxysmal atrial fibrillation, nephrolithiasis, spinal stenosis and chronic anemia was referred to endocrinology clinic for osteoporosis management. Bone density scan showed left femur neck T-score of -2.5 and L1-L4 lumbar spine T-score of 1.4. He reported pain on back and bilateral posterior thighs, difficulty with ambulation which were partly attributed to severe spinal stenosis that he was planned to have surgery for. Muscle strength was normal on examination. Laboratory studies were obtained for osteoporosis work up and showed: Calcium: 8.9 mg/dL (8.8-10.2 mg/dL), Creatinine: 0.77 mg/dL (0.74-1.35 mg/dL), GFR: 88 mL/min/BSA, Albumin 4.5 g/dL (3.5-5.0 g/dL), 25-Hydroxy vitamin D: 26 ng/mL, Magnesium 1.8 mg/dL (1.7-2.3 mg/mL), 1,25 Dihydroxy Vitamin D 24 pg/mL (18-64 pg/mL), Phosphorus: 1 mg/dL (2.5-4.5 mg/dL), PTH 163 pg/mL (15-65 pg/mL), Hemoglobin 12.9 mg/dL (13.2-16.6 mg/dL). Due to hypophosphatemia tumor induced osteomalacia diagnosis was entertained and further work up was considered in this regard however later noted that patient received ferric carboxymaltose 750 mg infusion two times within last 3 weeks for iron deficiency anemia. Hemoglobin level was 8.6 mg/dL before the infusions. After oral phosphate replacement the phosphate level improved to 2.4 mg/dL. Serum FGF 23 level was measured and it was normal at 108 RU/mL (<180 RU/mL). He was then started on bisphosphonate treatment for osteoporosis. Conclusion: Hypophosphatemia and secondary hyperparathyroidism can be seen after ferric carboxymaltose infusion due to FGF-23 mediated mechanism. In literature various presentations were reported from transient- asymptomatic hypophosphatemia to severe acute symptomatic hypophosphatemia along with persistent hypophosphatemia with osteomalacia and fragility fractures due to recurrent ferric carboxymaltose infusions. Thus, one should keep this possible side effect in mind during evaluation of hypophosphatemia and osteoporosis. References: 1. Wolf M, Chertow GM, Macdougall IC, Kaper R, Krop J, Strauss W. Randomized trial of intravenous iron-induced hypophosphatemia. JCI Insight. Dec 6 2018;3(23):e124486 2. Fang W, McMahon LP, Bloom S, Garg M. Symptomatic severe hypophosphatemia after intravenous ferric carboxymaltose. JGH Open. October 2019, volume 3, issue 5, P 438-440

scholarly journals The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1890 ◽  
Author(s):  
Chien-Lin Lu ◽  
Dong-Feng Yeih ◽  
Yi-Chou Hou ◽  
Guey-Mei Jow ◽  
Zong-Yu Li ◽  
...  
Keyword(s):  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Fibroblast Growth Factor 23 ◽  
Vitamin D Binding Protein ◽  
Hydroxylase Activity ◽  
Fgf 23 ◽  
Oxyphil Cell ◽  
Pth Level ◽  
Nutritional Vitamin

In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.

scholarly journals AB0922 BUROSUMAB (ANTI-FGF23 MONOCLONAL ANTIBODY) IN THE TREATMENT OF A PATIENT WITH RECURRENT TUMOR INDUCED OSTEOMALACIA.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1762.3-1762
Author(s):  
C. Crotti ◽  
F. Zucchi ◽  
P. Messa ◽  
R. Caporali ◽  
M. Varenna
Keyword(s):  
Monoclonal Antibody ◽  
Vitamin D ◽  
Great Trochanter ◽  
Fibroblast Growth Factor 23 ◽  
Well Being ◽  
Hypophosphatemic Rickets ◽  
Imaging Evaluation ◽  
Left Femur ◽  
Pet Ct ◽  
Fgf 23

Background:Tumor-induced Osteomalacia (TIO) is a rare paraneoplastic syndrome caused by tumoral overproduction of fibroblast growth factor 23 (FGF23), resulting in hyperphospaturia, hypophosphatemia and osteomalacia. Surgery is the only curative treatment, but tumor can locally recur, even after years from primary surgery. Furthermore, some tumors cannot be removed by surgery due to their location.Objectives:To describe a case of a 53-year-old woman affected by recurrent TIO after three surgical attempts of removal treated with Burosumab.Methods:We describe the case of a 53 years old woman with TIO treated with Burosumab, an anti-FGF-23 monoclonal antibody at present approved for X-linked hypophosphatemic rickets only.Results:A 46-year-old Caucasian female was referred to our Bone Unit after experiencing several fractures in different sites. She reported being in good health until three years prior consultation. At the time of symptoms onset, she experienced a progressive muscle pain, enabling her to stand for a long period. During imaging evaluation for atraumatic fracture of right great trochanter, the MRI abdomen and18FDG- PET-CT showed a metabolic pre-sacral lesion. She unsuccessfully underwent to an exploratory laparotomy of that lesion. Then, she suffered from atraumatic intertrochanteric fracture of right femur, surgically treated, and after 3 months, she had an insufficiency dyaphiseal fracture of the left femur, surgically treated. Furthermore, she experienced several ribs fractures. At the time of first evaluation, lab works showed: serum-Phosophate (PS) 1.2 mg/dL (reference range (RR) 2.5-4.5 mg/dL), urinary-phosphate of 24h (PU) 842 mg/24h, alkaline phosphatase (ALP) 565 UI (RR<300), 1,25(OH)2vitamin D327 ng/L (RR 25-86.5), PTH 24 (RR<75 pg/mL), intact-FGF-23 117 (RR 25-45 pg/mL), normal serum and 24h-urinary Calcium. Patient underwent to68Ga-DOTATATE-PET-CT that showed a pre-sacral lesion, who was studied with MRI and CT before surgery. In 2013 patient underwent surgical excision of the pre-sacral region. After 18 months of well-being, patient complained worsening of articular pain and muscle weakness, and further ribs fractures. Another68Ga-DOTATATE-PET-CT reported a relapse of the previous pre-sacral lesion (32x12x47 mm) with an increase of FGF-23levels (54.6 pg/mL). Even the subsequent surgery was not able to remove the tumor. Since 2015, patient was maintained in phosphorus supplements and 1,25(OH)2vitamin D3, but PS levels never normalized. We asked for compassionate use of Burosumab and, after ethical committee approval, in September 2019 she was started on Burosumab, at a dose of 30 mg per month (0.3 mg/kg). At baseline, she had PS 1.2 mg/dL, PU 1874 mg/24h, TRP 25.96%. After two months, she improved in pain symptom (VAS reduction from 65 to 12 mm), which allow her to walk and stand without crutches. She did not normalize her PS levels (1.3 mg/dL), while PU reduced to 1000 mg/24h. We titred Burosumab dose at 40 mg per month (0.6 mg/kg) and patient is still under therapy, waiting for next blood works.Conclusion:This is the first European patient affected by TIO treated with Burosumab. Burosumab could be a promising therapy in the medical treatment of TIO refractory or not eligible for definitive surgery. Further data are needed to standardize the proper dose regimen.Disclosure of Interests:Chiara Crotti: None declared, Francesca Zucchi: None declared, Piergiorgio Messa: None declared, Roberto Caporali Consultant of: AbbVie; Gilead Sciences, Inc.; Lilly; Merck Sharp & Dohme; Celgene; Bristol-Myers Squibb; Pfizer; UCB, Speakers bureau: Abbvie; Bristol-Myers Squibb; Celgene; Lilly; Gilead Sciences, Inc; MSD; Pfizer; Roche; UCB, Massimo Varenna: None declared

scholarly journals Iron Therapy Induced Leukopenia

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 39-40
Author(s):  
Hussam A Almasri ◽  
Ashraf Tawfiq Soliman ◽  
Vincenzo Desanctis ◽  
Arwa E Alsaud ◽  
Ruoa Alhashimy ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Iron Deficiency ◽  
Tract Infection ◽  
Iron Deficiency Anemia ◽  
Side Effect ◽  
Iron Therapy ◽  
Deficiency Anemia ◽  
Ferric Carboxymaltose ◽  
Iv Iron ◽  
Iron Replacement

Introduction Iron deficiency anemia (IDA) is the most common cause of anemia in both developed and developing countries, particularly affecting females in the child bearing age and children. The treatment of IDA is a major health goal, it consists of treating the underlying cause and iron supplements. Iron replacement comes in form of oral or intravenous, there are certain side effects of this therapy including constipation and allergy. Leukopenia as a side effect of iron therapy is under reported in the literature as only sporadic cases were prescribed. We conducted a study to clarify this issue and to check for its clinical significance. Objective: To assess the relationship between iron therapy (intravenous) and leukopenia, neutropenia or lymphocytopenia, and its impact on patient's clinical settings. Materials and Methods We retrospectively reviewed the electronic medical records of patients attended Haematology clinic for iron deficiency anemia and treated with intravenous iron (ferric carboxymaltose or iron saccharide) over 2 years in Hamad Medical Corporation, Doha/Qatar. Adult female patients with IDA cases who received IV iron were included. anemia due to other nutrients deficienciesa nd conditions (including other medications) that may alter WBCs count were excluded.Age, Ethnicity, BMI, Complete blood count and iron studies data were collected before and after treatment with IV iron therapy. Infection occurrence at the time of IDA and leukopenia, the use of antibiotics and infection related complications were also collected. Leukopenia was defined as WBCs count to be less than 4000/microlitre, Neutropenia as ANC less than 1500/microlitre and lymphocytopenia as lymphocytes less than 1000/mocrolitre. Statistical analysis was done using mean , SD and t test. Results After iron therapy, out of 1567 case of iron deficiency anemia, 30 cases (1.914%) have leukopenia,15 cases (0.957%) have neutropenia and 12 cases (0.765%) have lymphocytopenia. All had normal readings before treatment. 2 patients (6.66%) had infection, 1 had upper respiratory tract infection and 1 urinary tract infection, the latter was treated with antibiotics, none reported infection related complications Discussion Leukocytopenia is defined as low WBCs circulating in the blood and this can be caused by low neutrophils count, low lymphocytes count, other WBCs components or combined. Some previous reported cases generated the idea of a possible connection between iron supplement therapy and leukopenia, Brito-Babapulle et al reported a case of fatal bone marrow suppression linked to ferric carboxymaltose therapy in a patient with IDA. The pathophysiology is not well understood but thought to be a toxic effect of iron on bone marrow and it can affect all cell lineages. Our findings suggest possible iron replacement side effect as there was significant drop of the WBCs count after treating IDA patients with IV iron, however this association was not common. There was no life threatening or serious infections in the affected patients, which can suggest that most of these cases are mild and transient. More studies are needed to address this issue, particularly on larger scales. Patient education also may be appreciated before treatment with IV iron. Conclusions: Leukopenia in form of neutropenia or lymphocytopenia maybe a side effect of IV iron therapy. Clinical significance is limited in view of current literature further studies needed to elaborate more in this important adverse event. Disclosures No relevant conflicts of interest to declare.

Intravenous ferric carboxymaltose-associated hypophosphatemia in patients with iron deficiency anemia. A common side effect

2015 ◽  
Vol 145 (3) ◽  
pp. 108-111
Author(s):  
Rebeca Sánchez González ◽  
Hugo Guillermo Ternavasio-de la Vega ◽  
Leticia Moralejo Alonso ◽  
Sandra Inés Revuelta ◽  
Aurelio Fuertes Martín
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Side Effect ◽  
Deficiency Anemia ◽  
Common Side Effect ◽  
Ferric Carboxymaltose

scholarly journals Normal Parathyroid Function with Decreased Bone Mineral Density in Treated Celiac Disease

2001 ◽  
Vol 15 (5) ◽  
pp. 302-307 ◽  
Author(s):  
Bernard Lemieux ◽  
Michel Boivin ◽  
Jean-Hugues Brossard ◽  
Raymond Lepage ◽  
Daniel Picard ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Vitamin D ◽  
Celiac Disease ◽  
Lumbar Spine ◽  
Secondary Hyperparathyroidism ◽  
Bone Mineral ◽  
Reference Population ◽  
Mineral Density ◽  
T Score ◽  
Parathyroid Function

Decreased bone mineral density (BMD) has been reported in patients with celiac disease in association with secondary hyperparathyroidism. The present study investigated whether basal parathyroid hormone (PTH) remained elevated and whether abnormalities of parathyroid function were still present in celiac disease patients treated with a gluten-free diet. Basal seric measurements of calcium and phosphate homeostasis and BMD were obtained in 17 biopsy-proven patients under treatment for a mean period of 5.7±3.7 years (range 1.1 to 15.9). In addition, parathyroid function was studied with calcium chloride and sodium citrate infusions in seven patients. Basal measurements of patients were compared with those of 26 normal individuals, while parathyroid function results were compared with those of seven sex- and age-matched controls. Basal results were similar in patients and controls except for intact PTH (I-PTH) (3.77±0.88 pmol/L versus 2.28±0.63 pmol/L, P<0.001), which was higher in the former group but still within normal limits. Mean 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D values were normal in patients. Parathyroid function results were also found to be similar in both groups. Compared with a reference population of the same age (Z score), patients had significantly lower BMDs of the hip (-0.60±0.96 SDs, P<0.05) and lumbar spine (-0.76±1.15 SDs, P<0.05). T scores were also decreased for the hip (-1.3±0.9 SDs, P<0.0001) and lumbar spine (-1.4±1.35 SDs, P<0.0001), with two to three patients being osteoporotic (T score less than -2.5 SDs) and seven to eight osteopenic (T score less than -1 SDs but greater than or equal to -2.5 SDs) in at least one site. Height and weight were the only important determinants of BMD values by multivariate or logistical regression analysis in these patients. The results show higher basal I-PTH values with normal parathyroid function in treated celiac disease. Height and weight values are, but I-PTH values are not, an important determinant of the actual bone mass of patients. Normal parathyroid function in treated patients suggests a lack of previous severe secondary hyperparathyroidism and/or complete adaptation to prior changes in parathyroid function.

scholarly journals Symptomatic hypophosphataemia after intravenous iron therapy: an underrated adverse reaction

2019 ◽  
Vol 2019 ◽  
Author(s):  
Eseoghene Ifie ◽  
Samson O Oyibo ◽  
Hareesh Joshi ◽  
Olugbenro O Akintade
Keyword(s):  
Vitamin D ◽  
Iron Deficiency ◽  
Side Effect ◽  
Case Reports ◽  
Intravenous Iron ◽  
Iron Therapy ◽  
Common Side Effect ◽  
Ferric Carboxymaltose ◽  
Infusion Therapy ◽  
List Type

Summary Iron (ferric carboxymaltose) infusion therapy is used to treat severe iron deficiency which is not responding to the first-line oral iron therapy. However, it can also cause severe renal wasting of phosphate resulting in severe hypophosphataemia in some patients. Despite the growing number of case reports, this side effect is not well known to healthcare professionals. The product labelling information sheet does mention that hypophosphataemia can be a side effect, but also says that this side effect is usually transient and asymptomatic. We report a challenging case of a patient who developed severe, symptomatic and prolonged hypophosphataemia after an intravenous iron infusion for severe iron deficiency. Learning points: Clinicians prescribing ferric carboxymaltose (Ferinject®) should be aware of the common side effect of hypophosphataemia, which could be mild, moderate or severe. Patients receiving iron infusion should be educated concerning this potential side effect. Pre-existing vitamin D deficiency, low calcium levels, low phosphate levels or raised parathyroid hormone levels may be risk factors, and these should be evaluated and corrected before administering intravenous iron. Patients may require phosphate and vitamin D replacement along with monitoring for a long period after iron infusion-induced hypophosphataemia. Every incident should be reported to the designated body so that the true prevalence and management thereof can be ascertained.

scholarly journals Intravenous Iron Administration and Hypophosphatemia in Clinical Practice

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
S. Hardy ◽  
X. Vandemergel
Keyword(s):  
Vitamin D ◽  
Iron Deficiency ◽  
Intravenous Iron ◽  
Deficiency Anemia ◽  
Ferric Carboxymaltose ◽  
Clinical Consequence ◽  
Iron Administration ◽  
Vitamin D Levels ◽  
Persistent Fatigue ◽  
Parenteral Iron

Introduction. Parenteral iron formulations are frequently used to correct iron deficiency anemia (IDA) and iron deficiency (ID). Intravenous formulation efficacy on ferritin and hemoglobin level improvement is greater than that of oral formulations while they are associated with lower gastrointestinal side effects. Ferric carboxymaltose- (FCM-) related hypophosphatemia is frequent and appears without clinical significance. The aim of this study was to assess the prevalence, duration, and potential consequences of hypophosphatemia after iron injection.Patients and Methods. The medical records of all patients who underwent parenteral iron injection between 2012 and 2014 were retrospectively reviewed. Pre- and postinjection hemoglobin, ferritin, plasma phosphate, creatinine, and vitamin D levels were assessed. Patients who developed moderate (range: 0.32–0.80 mmol/L) or severe (<0.32 mmol/L) hypophosphatemia were questioned for symptoms.Results. During the study period, 234 patients received iron preparations but 104 were excluded because of missing data. Among the 130 patients included, 52 received iron sucrose (FS) and 78 FCM formulations. Among FS-treated patients, 22% developed hypophosphatemia versus 51% of FCM-treated patients, including 13% who developed profound hypophosphatemia. Hypophosphatemia severity correlated with the dose of FCM (p=0.04) but not with the initial ferritin, hemoglobin, or vitamin D level. Mean hypophosphatemia duration was 6 months. No immediate clinical consequence was found except for persistent fatigue despite anemia correction in some patients.Conclusions. Hypophosphatemia is frequent after parenteral FCM injection and may have clinical consequences, including persistent fatigue. Further studies of chronic hypophosphatemia long-term consequences, especially bone assessments, are needed.

scholarly journals MON-338 Severe Hypophosphatemia Induced by Intravenous Ferric Carboxymaltose Therapy for Iron Deficiency Anemia

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Matthew Tam ◽  
Ruchi Bhabhra
Keyword(s):  
Vitamin D ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Muscle Weakness ◽  
Bypass Surgery ◽  
Intravenous Iron ◽  
Hypophosphatemic Rickets ◽  
Deficiency Anemia ◽  
Ferric Carboxymaltose ◽  
Vitamin D Levels

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.

scholarly journals Intravenous Iron Induced Cytopenias(Leukopenia,Neutropenia,Lymphocytopenia) Among Arab Population with Iron Deficiency Anemia

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 18-19
Author(s):  
Hussam A Almasri ◽  
Ashraf Tawfiq Soliman ◽  
Vincenzo Desanctis ◽  
Rita Wafik Ahmad ◽  
Mustafa A Al-Tikrity ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Side Effect ◽  
Intravenous Iron ◽  
Iron Therapy ◽  
Deficiency Anemia ◽  
Ferric Carboxymaltose ◽  
Iv Iron ◽  
Iron Replacement

Introduction Iron deficiency anemia (IDA) is the most common cause of anemia in both developed and developing countries, particularly affecting females in the child bearing age and children. The treatment of IDA is a major health goal, it consists of treating the underlying cause and iron supplements. Iron replacement comes in form of oral or intravenous, there are certain side effects of this therapy including constipation and allergy. Leukopenia as a side effect of iron therapy is under reported in the literature as only sporadic cases were prescribed. We conducted a study to clarify this issue and to check for its clinical significance. Objective: To assess the relationship between iron therapy (intravenous) and leukopenia, neutropenia or lymphocytopenia, and its impact on patient's clinical settings. Materials and Methods We retrospectively reviewed the electronic medical records of patients attended Haematology clinic for iron deficiency anemia and treated with intravenous iron (ferric carboxymaltose or iron saccharide) over 2 years in Hamad Medical Corporation, Doha/Qatar. Adult female patients with IDA cases who received IV iron were included. anemia due to other nutrients deficienciesa nd conditions (including other medications) that may alter WBCs count were excluded.Age, Ethnicity, BMI, Complete blood count and iron studies data were collected before and after treatment with IV iron therapy. Infection occurrence at the time of IDA and leukopenia, the use of antibiotics and infection related complications were also collected. Leukopenia was defined as WBCs count to be less than 4000/microlitre, Neutropenia as ANC less than 1500/microlitre and lymphocytopenia as lymphocytes less than 1000/mocrolitre. Statistical analysis was done using mean , SD and t test. Results After iron therapy, out of 1567 case of iron deficiency anemia, 30 cases (1.914%) have leukopenia,15 cases (0.957%) have neutropenia and 12 cases (0.765%) have lymphocytopenia. All had normal readings before treatment. 2 patients (6.66%) had infection, 1 had upper respiratory tract infection and 1 urinary tract infection, the latter was treated with antibiotics, none reported infection related complications Discussion Leukocytopenia is defined as low WBCs circulating in the blood and this can be caused by low neutrophils count, low lymphocytes count, other WBCs components or combined. Some previous reported cases generated the idea of a possible connection between iron supplement therapy and leukopenia, Brito-Babapulle et al reported a case of fatal bone marrow suppression linked to ferric carboxymaltose therapy in a patient with IDA. The pathophysiology is not well understood but thought to be a toxic effect of iron on bone marrow and it can affect all cell lineages. Our findings suggest possible iron replacement side effect as there was significant drop of the WBCs count after treating IDA patients with IV iron, however this association was not common. There was no life threatening or serious infections in the affected patients, which can suggest that most of these cases are mild and transient. More studies are needed to address this issue, particularly on larger scales. Patient education also may be appreciated before treatment with IV iron. Conclusions: Leukopenia in form of neutropenia or lymphocytopenia maybe a side effect of IV iron therapy. Clinical significance is limited in view of current literature further studies needed to elaborate more in this important adverse event. Figure Disclosures No relevant conflicts of interest to declare.

Vitamin D Deficiency and Intoxication - A concern either way

JMS SKIMS ◽  
2011 ◽  
Vol 14 (2) ◽  
pp. 40-42
Author(s):  
Muzafar Maqsood Wani ◽  
Imtiaz Ahmed Wani
Keyword(s):  
Vitamin D ◽  
Cell Growth ◽  
Bone Turnover ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Bone Mineralization ◽  
Normal Blood ◽  
Blood Levels ◽  
Calcium And Phosphorus ◽  
Biologic Function

Major biologic function of activated vitamin D is to maintain normal blood levels of calcium and phosphorus, thus regulating bone mineralization. Research suggests that vitamin D may help in immunomodulation, regulating cell growth and 1,4 differentiation as well as some diverse unspecified functions. Overt vitamin D deficiency leads to hypocalcaemia, secondary hyperparathyroidism and increased bone turnover, which in prolonged and severe cases may cause rickets in children and osteomalacia in elderly.... JMS 2011;14(2):40-42

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