Total Serum Phosphate Levels Less Than 3.0 Mg/Dl. • Mild Hypophosp

Total Page：16

File Type：pdf, Size：1020Kb

HYPOPHOSPHATEMIA DEFINITION: Total serum phosphate levels less than 3.0 mg/dL. Mild hypophosphatemia: 2.5-3.0 mg/dL. Moderate hypophosphatemia: 1.0-2.5 mg/dL. Severe hypophosphatemia: < 1.0 mg/dL. INCIDENCE IN CRITICAL ILLNESS: Common. ETIOLOGY: Transcellular shift: Refeeding syndrome (abrupt initiation of carbohydrate causes an insulin spike, which increases cellular phosphate uptake); exogenous administration of insulin; respiratory alkalosis. Renal loss: Diuretics; osmotic diuresis in diabetic ketoacidosis; hyperparathyroidism (primary and secondary; decreases urinary resorption of phosphate); proximal renal tubular dysfunction (Fanconi’s syndrome). Insufficient intestinal absorption: Malnutrition; phosphate-binding antacids; vitamin D deficiency; chronic diarrhea; nasogastric tube suction; malabsorption. Extreme catabolic states: Burns; trauma; sepsis. CLINICAL MANIFESTATIONS: Cardiovascular: Acute left ventricular dysfunction; reversible dilated cardiomyopathy. Hematologic: Acute hemolytic anemia; leukocyte dysfunction. Neuromuscular: Diffuse skeletal muscle weakness; rhabdomyolysis; bone demineralization; acute and chronic respiratory failure secondary to diaphragmatic weakness (impaired ventilator weaning); confusion and lethargy; gait disturbance; paresthesias. TREATMENT: It is impossible to accurately predict the exact quantity of phosphate repletion required because most phosphate is intracellular. Moderate hypophosphatemia: Oral supplementation is usually adequate (provided the gastrointestinal tract is functional). Severe hypophosphatemia: Intravenous repletion (sodium phosphate or potassium phosphate). However, IV repletion should be avoided in patients who have renal failure or hypercalcemia (risk of metastatic calcification). KEY REFERENCES: Knochel JP. The pathophysiology and clinical characteristics of severe hypophosphatemia. Arch Intern Med 1977;137:203-220. Marinella MA. The refeeding syndrome and hypophosphatemia. Nutr Rev 2003;61:320-323. Aubier M, Murciano D, Lecocguic Y, et al. Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure. N Engl J Med 1985;313:420-424. Maerz/Hypophosphatemia Page 1 .

Copy Link

Recommended publications

Randomized Trial of Intravenous Iron-Induced Hypophosphatemia
CLINICAL MEDICINE Randomized trial of intravenous iron-induced hypophosphatemia Myles Wolf,1,2 Glenn M. Chertow,3,4 Iain C. Macdougall,5 Robert Kaper,6 Julie Krop,6 and William Strauss6 1Division of Nephrology, Department of Medicine, and 2Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina, USA. 3Division of Nephrology, Department of Medicine and 4Department of Health Research and Policy, Stanford University, Stanford, California, USA. 5Renal Unit, King’s College Hospital, London, United Kingdom. 6AMAG Pharmaceuticals, Inc., Waltham, Massachusetts, USA. BACKGROUND. Hypophosphatemia can complicate intravenous iron therapy, but no head-to-head trials compared the effects of newer intravenous iron formulations on risks and mediators of hypophosphatemia. METHODS. In a randomized, double-blinded, controlled trial of adults with iron deficiency anemia from February 2016 to January 2017, we compared rates of hypophosphatemia in response to a single FDA-approved course of ferric carboxymaltose (n = 1,000) or ferumoxytol (n = 997). To investigate pathophysiological mediators of intravenous iron-induced hypophosphatemia, we nested within the parent trial a physiological substudy (ferric carboxymaltose, n = 98; ferumoxytol, n = 87) in which we measured fibroblast growth factor 23 (FGF23), calcitriol, and parathyroid hormone (PTH) at baseline and 1, 2, and 5 weeks later. RESULTS. The incidence of hypophosphatemia was significantly higher in the ferric carboxymaltose versus the ferumoxytol group (<2.0 mg/dl, 50.8% vs. 0.9%; <1.3 mg/dl, 10.0% vs. 0.0%; P < 0.001), and hypophosphatemia persisted through the end of the 5-week study period in 29.1% of ferric carboxymaltose–treated patients versus none of the ferumoxytol-treated patients (P < 0.001).
[Show full text]
The Hematological Complications of Alcoholism
The Hematological Complications of Alcoholism HAROLD S. BALLARD, M.D. Alcohol has numerous adverse effects on the various types of blood cells and their functions. For example, heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells. Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections. Finally, alcohol adversely affects the platelets and other components of the blood-clotting system. Heavy alcohol consumption thus may increase the drinker’s risk of suffering a stroke. KEY WORDS: adverse drug effect; AODE (alcohol and other drug effects); blood function; cell growth and differentiation; erythrocytes; leukocytes; platelets; plasma proteins; bone marrow; anemia; blood coagulation; thrombocytopenia; fibrinolysis; macrophage; monocyte; stroke; bacterial disease; literature review eople who abuse alcohol1 are at both direct and indirect. The direct in the number and function of WBC’s risk for numerous alcohol-related consequences of excessive alcohol increases the drinker’s risk of serious Pmedical complications, includ- consumption include toxic effects on infection, and impaired platelet produc- ing those affecting the blood (i.e., the the bone marrow; the blood cell pre- tion and function interfere with blood cursors; and the mature red blood blood cells as well as proteins present clotting, leading to symptoms ranging in the blood plasma) and the bone cells (RBC’s), white blood cells from a simple nosebleed to bleeding in marrow, where the blood cells are (WBC’s), and platelets.
[Show full text]
A Rare Case of Multiple Phosphaturic Mesenchymal Tumors Along A
Arai et al. BMC Musculoskeletal Disorders (2017) 18:79 DOI 10.1186/s12891-017-1446-z CASEREPORT Open Access A rare case of multiple phosphaturic mesenchymal tumors along a tendon sheath inducing osteomalacia Ryuta Arai1* , Tomohiro Onodera1, Mohamad Alaa Terkawi1, Tomoko Mitsuhashi2, Eiji Kondo3 and Norimasa Iwasaki1 Abstract Background: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by renal phosphate wasting, hypophosphatemia, reduction of 1,25-dihydroxyl vitamin D, and bone calcification disorders. Tumors associated with TIO are typically phosphaturic mesenchymal tumors that are bone and soft tissue origin and often present as a solitary tumor. The high production of fibroblast growth factor 23 (FGF23) by the tumor is believed to be the causative factor responsible for the impaired renal tubular phosphate reabsorption, hypophosphatemia and osteomalacia. Complete removal of the tumors by surgery is the most effective procedure for treatment. Identification of the tumors by advanced imaging techniques is difficult because TIO is small and exist within bone and soft tissue. However, systemic venous sampling has been frequently reported to be useful for diagnosing TIO patients. Case presentation: We experienced a case of 39-year-old male with diffuse bone pain and multiple fragility fractures caused by multiple FGF23-secreting tumors found in the hallux. Laboratory testing showed hypophosphatemia due to renal phosphate wasting and high levels of serum FGF23. Contrast-enhanced MRI showed three soft tissue tumors and an intraosseous tumor located in the right hallux. Systemic venous sampling of FGF23 revealed an elevation in the right common iliac vein and external iliac vein, which suggested that the tumors in the right hallux were responsible for overproduction of FGF23.
[Show full text]
Wilson Disease Presenting As a Case of Resistant Rickets
Wilson disease presenting as a case of resistant rickets Manjari Basu 1 Sri Lanka Journal of Child Health 2014; 43 (2): 106-107 (Key words: Wilson disease; resistant rickets) Case report Urine examination showed phosphaturia and glycosuria. Thus we diagnosed the case as Wilson A 9 year old Muslim boy, born of a consanguineous disease causing resistant rickets with osseo-muscular marriage, presented with knock knees which were type genu valgum. We started treatment with D- progressively increasing over the past year. He was penicillamine, pyridoxine and zinc. active and playful. There was no history of convulsions, jaundice, drug intake or malabsorption. Parents continued the treatment for 1 month but after that discontinued it due to the high cost and came to On examination, his build and nutrition were average. follow-up long after 1year. By that time he had There was genu valgum and widening of wrists. several neurological manifestations including chorea, There was no alopecia or dental abnormality. There tremor, and abnormal gait. was no family history of similar abnormality. Discussion X-ray of wrist was suggestive of rickets. Serum calcium was 9.5 mg/dl (normal range: 8.8-10.8 Wilson disease is a rare autosomal recessive disorder mg/dl), serum phosphate 2.5 mg/dl (normal range: characterized by a toxic accumulation of copper in 3.7-5.6 mg/dl) and serum alkaline phosphatase (ALP) liver, brain, cornea, skeletal system and other 2311 U/L (normal range: 145-420 U/L). Parathyroid tissues 1. The abnormal gene of Wilson disease is hormone (PTH) level was normal.
[Show full text]
Less Phosphorus, More Problems: Hypophosphatemia Induced Polymorphic Ventricular Tachycardia in a Young Male Robin Jacob1*, Ritesh S
ISSN: 2378-2951 Jacob et al. Int J Clin Cardiol 2018, 5:112 DOI: 10.23937/2378-2951/1410112 Volume 5 | Issue 2 International Journal of Open Access Clinical Cardiology CASE REPORT Less Phosphorus, More Problems: Hypophosphatemia Induced Polymorphic Ventricular Tachycardia in a Young Male Robin Jacob1*, Ritesh S. Patel1 and Francisco Fuentes2 Check for 1Resident, Department of Medicine, UT Health Science Center, Houston, Texas, USA updates 2Professor, Cardiovascular Medicine, UT Health Science Center, Houston, Texas, USA *Corresponding author: Robin Jacob, Resident, Department of Medicine, UT Health Science Center, Houston, Texas, USA, Tel: 678-200-6759, E-mail: [email protected] mal left ventricular size and systolic function (ejection Keywords fraction 60-65%) with normal left ventricular diastolic Hypophosphatemia, Phosphorus, Polymorphic ventricular filling and no abnormal findings. Electrocardiogram ev- tachycardia, Arrhythmia idenced normal sinus rhythm. Introduction During his stay, patient’s overnight telemetry re- vealed intermittent, non-sustained ventricular tachycar- It is well known that electrolyte derangements such dia (Figure 1). He was asymptomatic at the time, deny- as hypokalemia, hypomagnesaemia, and hypocalcae- ing any chest pain, shortness of breath, palpitations, or mia can potentially cause dangerous arrhythmias in dizziness. Patient denied any personal or family history hospitalized patients. This can be a common concern of heart failure or arrhythmias. Of note, he had not eat- for acute care physicians, as the occurrence of arrhyth- en the day prior to the event, and had remained noth- mias predisposes patients to higher morbidity, mortali- ing per oral (NPO) on admission. Labs were checked and ty, and longer length of stay.
[Show full text]
Practical Management of Iron Overload Disorder (IOD) in Black Rhinoceros (BR; Diceros Bicornis)
animals Review Practical Management of Iron Overload Disorder (IOD) in Black Rhinoceros (BR; Diceros bicornis) Kathleen E. Sullivan, Natalie D. Mylniczenko , Steven E. Nelson Jr. , Brandy Coffin and Shana R. Lavin * Disney’s Animal Kingdom®, Animals, Science and Environment, Bay Lake, FL 32830, USA; [email protected] (K.E.S.); [email protected] (N.D.M.); [email protected] (S.E.N.J.); Brandy.Coffi[email protected] (B.C.) * Correspondence: [email protected]; Tel.: +1-407-938-1572 Received: 29 September 2020; Accepted: 26 October 2020; Published: 29 October 2020 Simple Summary: Black rhinoceros under human care are predisposed to Iron Overload Disorder that is unlike the hereditary condition seen in humans. We aim to address the black rhino caretaker community at multiple perspectives (keeper, curator, veterinarian, nutritionist, veterinary technician, and researcher) to describe approaches to Iron Overload Disorder in black rhinos and share learnings. This report includes sections on (1) background on how iron functions in comparative species and how Iron Overload Disorder appears to work in black rhinos, (2) practical recommendations for known diagnostics, (3) a brief review of current investigations on inflammatory and other potential biomarkers, (4) nutrition knowledge and advice as prevention, and (5) an overview of treatment options including information on chelation and details on performing large volume voluntary phlebotomy. The aim is to use evidence to support the successful management of this disorder to ensure optimal animal health, welfare, and longevity for a sustainable black rhinoceros population. Abstract: Critically endangered black rhinoceros (BR) under human care are predisposed to non-hemochromatosis Iron Overload Disorder (IOD).
[Show full text]
Iron Deficiency Anemia (IRIDA) • Rare
Iron Deficiency: Review Melinda Wu, MD, MCR Oregon Health & Science University OHSU10/17/2019 Disclosure Information: a) Moderators/panelists/presenters: Melinda Wu has nothing to disclose. OHSUb) Funding sources: NIH/NHLBI- K08 HL133493 Objectives 1) To review iron body homeostasis 2) To review the etiologies of iron deficiency OHSU3) To review various treatment options of iron deficiency Part I: Review of Iron Body OHSUHomeostasis Iron Balance in the Body Iron is required for growth of all cells, not just hemoglobin! Heme proteins: cytochromes, catalase, peroxidase, cytochrome oxidase Flavoproteins: cytochrome C reductase, succinic dehydrogenase, NADH oxidase, xanthine oxidase Too little Too much Not enough for essential Accumulates in organs proteins: Promotes the formation of: • Hemoglobin • Oxygen radicals •OHSURibonucleotide reductase • Lipid peroxidation (DNA synthesis) • DNA damage • Cytochromes • Tissue fibrosis • Oxidases Iron Economy • The average adult has 4-5 g of body iron. • ~10% of dietary iron absorbed, exclusively in duodenum • Varies with: • Iron content of diet • Bioavailability of dietary iron • Iron stores in body • Erythropoietic demand • Hypoxia • Inflammation • More than half is incorporated into erythroid precursors/mature erythrocytes OHSU• Only ~1-2 mg of iron enters and leaves the body in a day on average. • About 1 mg of iron is lost daily in menstruating women. Lesjak, M.; K. S. Srai, S. Role of Dietary Flavonoids in Iron Homeostasis. Pharmaceuticals 2019 Systemic Iron Regulation: Absorption Iron status is regulated entirely at the level of absorption! • Heme iron (30-70%) > non-heme iron (<5%) • 2 stable oxidation states: Ferrous (Fe 2+) > Ferric (Fe 3+) • Elemental iron must be reduced to Fe2+ iron to be absorbed 1.
[Show full text]
25. C:\Documents and Settings\Kwang-Il\My
The human disease network Goh K-I, Cusick ME, Valle D, Childs B, Vidal M, Barabasi′ A-L (2007) Proc Natl Acad Sci USA 104:8685-8690 Disorder Class Bone Coats Cancer Urolithiasise Osteopetrosis disease NDP Caffey van_Buchem Exudative Cardiovascular disease disease vitreoretinopathy Norrie SLC34A1 disease 439 LRP5 Connective tissue disorder Nevo Hyperostosis, syndrome COL1A1 endosteal Dermatological PLOD1 217 PAX9 Oligodontia Osteogenesis Osteoporosis 1164 Developmental Ehlers-Danlos imperfecta syndrome Arthropathy COL3A1 Hypodontia Ear, Nose, Throat Aneurysm, COL1A2 familial_arterial Myasthenic Witkop 733 syndrome Heart syndrome Pseudoachondroplasia Endocrine 3-methylglutaconicaciduria OPA3 WISP3 Optic Marfan block MSX1 atrophy OPA1 Aortic syndrome Paramyotonia Sick_sinus Gastrointestinal aneurysm congenita syndrome 3558 Intervertebral_disc Brugada SCN4A disease syndrome Syndactyly Spondyloepiphyseal COMP COL9A2 Hematological Glaucoma Weill-Marchesani Shprintzen-Goldberg Cramps, SCN5A Zlotogora-Ogur Cleft dysplasia syndrome syndrome potassium-aggravated Myotonia 2785 syndrome palate Parkes_Weber Basal_cell FBN1 congenita Oculodentodigital COL9A3 1432 Immunological 1414 CYP1B1 syndrome nevus_syndrome MASS Hypokalemic Acquired dysplasia Peters long_QT_syndrome Epiphyseal FLNB RASA1 PTCH Keratitis syndrome periodic MATN3 Metabolic SHH anomaly Eye Ectopia Thyrotoxic paralysis dysplasia Atelosteogenesis anomalies Marshall Larson Capillary Basal_cell Holoprosencephaly Coloboma, periodic KCNH2 PVRL1 malformations GJA1 Incontinentia syndrome SLC26A2
[Show full text]
Kyowa Kirin Announces Approval of CRYSVITA® (Burosumab) in Switzerland for the Treatment of Adults and Children with X-Linked Hypophosphatemia (XLH)
Kyowa Kirin Announces Approval of CRYSVITA® (burosumab) in Switzerland for the Treatment of Adults and Children with X-Linked Hypophosphatemia (XLH) CRYSVITA is the first and only treatment for XLH that targets the underlying cause of the disease TOKYO, Japan, February 25, 2020 – Kyowa Kirin Co., Ltd., (Kyowa Kirin) today announced the approval of CRYSVITA (burosumab) by Swissmedic (dispensing category B) for the treatment of adults, adolescents and children (1 year of age and older) with X-linked hypophosphatemia (XLH), a rare genetic disease that causes abnormalities in the bones, muscles and joints.1,2,3 The product is expected to be available for prescription in Switzerland in accordance with the provisions of Article 71 of the KVV (Verordnung über die Krankenversicherung). “X-linked hypophosphatemia is the most common form of hereditary rickets,” said Abdul Mullick, President of Kyowa Kirin International. “Many patients experience debilitating symptoms on a daily basis, including joint and bone pain, stiffness and fatigue, and may have trouble walking. Bringing this important treatment to adults and children with XLH in Switzerland is a very important milestone for our company and for the treatment of this rare, progressive disease.” “CRYSVITA (burosumab) is the first and only treatment available in Switzerland for patients with XLH that targets the underlying cause of the disease,” said Tomohiro Sudo, Head of Global Product Management Office of Kyowa Kirin. "We are proud that CRYSVITA is now available to patients in Switzerland and
[Show full text]
EUROCAT Syndrome Guide
JRC - Central Registry european surveillance of congenital anomalies EUROCAT Syndrome Guide Definition and Coding of Syndromes Version July 2017 Revised in 2016 by Ingeborg Barisic, approved by the Coding & Classification Committee in 2017: Ester Garne, Diana Wellesley, David Tucker, Jorieke Bergman and Ingeborg Barisic Revised 2008 by Ingeborg Barisic, Helen Dolk and Ester Garne and discussed and approved by the Coding & Classification Committee 2008: Elisa Calzolari, Diana Wellesley, David Tucker, Ingeborg Barisic, Ester Garne The list of syndromes contained in the previous EUROCAT “Guide to the Coding of Eponyms and Syndromes” (Josephine Weatherall, 1979) was revised by Ingeborg Barisic, Helen Dolk, Ester Garne, Claude Stoll and Diana Wellesley at a meeting in London in November 2003. Approved by the members EUROCAT Coding & Classification Committee 2004: Ingeborg Barisic, Elisa Calzolari, Ester Garne, Annukka Ritvanen, Claude Stoll, Diana Wellesley 1 TABLE OF CONTENTS Introduction and Definitions 6 Coding Notes and Explanation of Guide 10 List of conditions to be coded in the syndrome field 13 List of conditions which should not be coded as syndromes 14 Syndromes – monogenic or unknown etiology Aarskog syndrome 18 Acrocephalopolysyndactyly (all types) 19 Alagille syndrome 20 Alport syndrome 21 Angelman syndrome 22 Aniridia-Wilms tumor syndrome, WAGR 23 Apert syndrome 24 Bardet-Biedl syndrome 25 Beckwith-Wiedemann syndrome (EMG syndrome) 26 Blepharophimosis-ptosis syndrome 28 Branchiootorenal syndrome (Melnick-Fraser syndrome) 29 CHARGE
[Show full text]
Severe Hypophosphataemia After Intravenous Iron Administration
sPeCIAL ARTI CLE severe hypophosphataemia after intravenous iron administration A. Blazevic, J. Hunze, J.M.M. Boots* Department of Internal Medicine and Nephrology, Maasstad Hospital, the Netherlands, *corresponding author: tel.: +31 (0)10-2911833, e-mail: [email protected] a B s t r a C t Currently, in many centres, intravenous administration of iron is becoming increasingly popular because of What was known on this topic? higher efficacy and decreased side effects, mainly gastro- Intravenous iron supplements are highly effective in intestinal, compared with oral iron therapy. Studies of treating iron deficiency anaemia. Besides a transient, intravenous ferric carboxymaltose administration in the asymptomatic hypophosphataemia, there are few postpartum setting and in patients with non-dialysis- adverse effects of these intravenous preparations dependent chronic kidney disease revealed a decrease in compared with oral iron supplements. serum phosphate levels that was generally asymptomatic and transient. What does this add? Here, we report four cases of severe and symptomatic This article emphasises the importance of hypophosphataemia after intravenous iron administration. determining pre-existent disorders in phosphate All patients received this as therapy for iron deficiency homeostasis and continuous monitoring of anaemia due to heavy menstrual bleeding. In most cases, a serum phosphate levels after intravenous ferric pre-existent disorder in the phosphate homeostasis existed, carboxymaltose administration as the provoked
[Show full text]
6C48bb2ef8da97b11f9a7c35f49
Open Access Case Report DOI: 10.7759/cureus.10874 X-Linked Hypophosphatemic Rickets Manifesting as Sclerotic Bone Disease and Enthesopathy Hiya Boro 1 , Shailendra Singh Naik 2 , Charandeep Singh 3 , Saurav Khatiwada 3 , Rajesh Khadgawat 1 1. Endocrinology, All India Institute of Medical Sciences, New Delhi, IND 2. Radiology, All India Institute of Medical Sciences, New Delhi, IND 3. Endocrinology, Diabetes and Metabolism, All India Institute of Medical Sciences, New Delhi, IND Corresponding author: Hiya Boro, [email protected] Abstract X-linked hypophosphatemic (XLH) rickets is a genetic disease caused due to the inactivation of the PHEX gene (phosphate regulating gene with homology to endopeptidase on the X chromosome). The usual presentation is with rickets and osteomalacia, and dental abscesses leading to premature loss of teeth. However, enthesopathy and sclerotic bone disease in XLH have also been reported in a few case reports. In this report, we describe the case of a 23-year-old female patient who presented to us with severe bone deformities, proximal myopathy, truncal weakness, and recent onset of pain and stiffness around the joints. She was diagnosed with XLH and was found to have severe enthesopathy along with heterotopic ossification. Categories: Endocrinology/Diabetes/Metabolism Keywords: rickets, enthesopathy, osteosclerosis, dental abscess, hypophosphatemia Introduction X-linked hypophosphatemic (XLH) rickets is a disease characterized by rachitic manifestations and osteomalacia in the form of bone pain, bone deformities, proximal myopathy, and poor dental health. It is caused by the inactivating mutation of the PHEX gene (phosphate regulating gene with homology to endopeptidase on the X chromosome). The PHEX gene encodes for an endopeptidase that causes cleavage of fibroblast growth factor 23 (FGF23), a phosphatonin that causes phosphate wastage from the body.
[Show full text]