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Hypocalcemia
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<h2 id="signs-and-symptoms">Signs and symptoms</h2> <p>The neuromuscular symptoms of hypocalcemia are caused by a positive <a href="/facts/Bathmotropic/vADrsB5G">bathmotropic</a> effect (i.e. increased responsiveness) due to the decreased interaction of calcium with <a href="/facts/Sodium_channel/pXb4n2Vz">sodium channels</a>. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization.<a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a> The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth. </p> <ul><li><a href="/facts/Petechiae/thXfeF1Q">Petechiae</a> which appear as on-off spots, then later become confluent, and appear as <a href="/facts/Purpura/bz0qayUG">purpura</a> (larger bruised areas, usually in dependent regions of the body).</li> <li>Oral, perioral, and acral <a href="/facts/Paresthesias/hRBAxluk">paresthesias</a>, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.</li> <li><a href="/facts/Carpopedal_spasm/dntSCQUJ">Carpopedal</a> and generalized <a href="/facts/Tetany_(medical_sign)/M2uVGcww">tetany</a> (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.</li> <li>Latent tetany <ul><li><a href="/facts/Trousseau_sign_of_latent_tetany/dntSCQUJ">Trousseau sign of latent tetany</a> (eliciting <a href="/facts/Trousseau_sign_of_latent_tetany/dntSCQUJ">carpal spasm</a> by inflating the <a href="/facts/Blood_pressure/VtqqSM2J">blood pressure</a> cuff and maintaining the cuff pressure above <a href="/facts/Systole_(medicine)/5KDbjw4B">systolic</a>)</li> <li><a href="/facts/Chvostek%2527s_sign/2MqjGbqe">Chvostek's sign</a> (tapping of the inferior portion of the <a href="/facts/Zygoma/MT8FTkKw">cheekbone</a> will produce facial spasms)<a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a></li></ul></li> <li>Tendon reflexes are hyperactive</li> <li>Life-threatening complications <ul><li><a href="/facts/Cardiac_arrhythmia/ooEpr46Q">Cardiac arrhythmias</a></li></ul></li> <li>Effects on cardiac output <ul><li>Negative <a href="/facts/Chronotropic/hRj7pBIC">chronotropic</a> effect, or a decrease in <a href="/facts/Heart_rate/YngB0bzg">heart rate</a>.</li> <li>Negative <a href="/facts/Inotropy/A58XE1pa">inotropic</a> effect, or a decrease in <a href="/facts/Contractility/e4A65oky">contractility</a></li> <li></li></ul></li> <li>ECG changes include the following: <ul><li>Intermittent <a href="/facts/QT_prolongation/kX1NAAUh">QT prolongation</a>, or intermittent prolongation of the QTc (corrected QT interval) on the ECG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predispose to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the person at high risk of <a href="/facts/Torsades_de_pointes/dsdr4HPF">torsades de pointes</a>, a specific type of <a href="/facts/Ventricular_tachycardia/UrRmY5Q6">ventricular tachycardia</a> which appears on an EKG (or ECG) as something that looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death unless the person can be medically or electrically cardioverted and returned to a normal cardiac rhythm.)</li></ul></li></ul> <h2 id="causes">Causes</h2> <p><a href="/facts/Hypoparathyroidism/Dd79cfqo">Hypoparathyroidism</a> is a common cause of hypocalcemia.<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a> Calcium is tightly regulated by the <a href="/facts/Parathyroid_hormone/Dh7Uld78">parathyroid hormone</a> (PTH). In response to low calcium levels, PTH levels rise, and conversely, if there are high calcium levels, then PTH secretion declines.<a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands.<a class="footnote-ref" id="fnref:21" href="#fn:21"><sup>21</sup></a> Hypoparathyroidism may also be due to an autoimmune problem.<a class="footnote-ref" id="fnref:22" href="#fn:22"><sup>22</sup></a><a class="footnote-ref" id="fnref:23" href="#fn:23"><sup>23</sup></a> Some causes of hypocalcaemia are as follows: </p> <ul><li><a href="/facts/Hyperphosphatemia/mbCIQHbx">Hyperphosphatemia</a><a class="footnote-ref" id="fnref:24" href="#fn:24"><sup>24</sup></a></li> <li><a href="/facts/Vitamin_D_deficiency/lWMkWjEm">Vitamin D deficiency</a></li> <li><a href="/facts/Cirrhosis/bkLuLvCD">Chronic liver disease</a></li> <li><a href="/facts/Edetate_disodium/XvHgKQyD">Edetate disodium</a><a class="footnote-ref" id="fnref:25" href="#fn:25"><sup>25</sup></a></li> <li><a href="/facts/Magnesium_deficiency/GBVGeFw9">Magnesium deficiency</a><a class="footnote-ref" id="fnref:26" href="#fn:26"><sup>26</sup></a></li> <li>Prolonged use of medications/laxatives (magnesium)<a class="footnote-ref" id="fnref:27" href="#fn:27"><sup>27</sup></a></li> <li><a href="/facts/Osteomalacia/dQbx3aRe">Osteomalacia</a><a class="footnote-ref" id="fnref:28" href="#fn:28"><sup>28</sup></a></li> <li><a href="/facts/Chronic_kidney_failure/4YKH9wpo">Chronic kidney failure</a><a class="footnote-ref" id="fnref:29" href="#fn:29"><sup>29</sup></a></li> <li>Ineffective active vitamin D<a class="footnote-ref" id="fnref:30" href="#fn:30"><sup>30</sup></a></li> <li><a href="/facts/Hypoparathyroidism/Dd79cfqo">Hypoparathyroidism</a>/genetic<a class="footnote-ref" id="fnref:31" href="#fn:31"><sup>31</sup></a></li> <li>After surgery <a href="/facts/Hypoparathyroidism/Dd79cfqo">hypoparathyroidism</a><a class="footnote-ref" id="fnref:32" href="#fn:32"><sup>32</sup></a></li> <li><a href="/facts/Hungry_bone_syndrome/yBaUxzsU">Hungry bone syndrome</a></li> <li><a href="/facts/Tumour_lysis_syndrome/rSHyRzrN">Tumour lysis syndrome</a><a class="footnote-ref" id="fnref:33" href="#fn:33"><sup>33</sup></a></li> <li><a href="/facts/Acute_kidney_injury/dYg8l5P8">Acute kidney injury</a><a class="footnote-ref" id="fnref:34" href="#fn:34"><sup>34</sup></a></li> <li><a href="/facts/Rhabdomyolysis/Cs08YHfR">Rhabdomyolysis</a> (initial stage)<a class="footnote-ref" id="fnref:35" href="#fn:35"><sup>35</sup></a></li> <li>As a complication of <a href="/facts/Pancreatitis/gmbNTcCG">pancreatitis</a><a class="footnote-ref" id="fnref:36" href="#fn:36"><sup>36</sup></a></li> <li><a href="/facts/Alkalosis/SoUSH8No">Alkalosis</a><a class="footnote-ref" id="fnref:37" href="#fn:37"><sup>37</sup></a></li> <li>Massive <a href="/facts/Red_blood_cell/Kggpq8Jh">red blood cell</a> transfusion due to excess <a href="/facts/Citrate/EgKGQBdl">citrate</a> in the blood</li> <li>As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation.</li> <li><a href="/facts/Neonatal_hypocalcemia/lBINyzWP">Neonatal hypocalcemia</a><a class="footnote-ref" id="fnref:38" href="#fn:38"><sup>38</sup></a></li> <li>Gain of function mutations of the <a href="/facts/Calcium-sensing_receptor/z8aIKyEh">calcium-sensing receptor</a></li> <li><a href="/facts/Foscarnet/yayguTSI">Foscarnet</a> use</li> <li><a href="/facts/Loop_diuretic/eEgJ4qpf">Loop diuretic</a> use</li> <li><a href="/facts/Crohn_disease/zm55cBtd">Crohn disease</a></li> <li>High level of <a href="/facts/Lactic_acid/BsVRFx7s">lactic acid</a> in the blood</li> <li><a href="/facts/Pseudohypoparathyroidism/cDrGtwPH">Pseudohypoparathyroidism</a></li> <li><a href="/facts/Major_trauma/vAIyyy22">Trauma</a><a class="footnote-ref" id="fnref:39" href="#fn:39"><sup>39</sup></a></li></ul> <h2 id="pathophysiology">Pathophysiology</h2> <p>Physiologically, blood calcium is tightly regulated within a narrow range for proper cellular processes. Calcium in the blood exists in three primary states: bound to proteins (mainly <a href="/facts/Albumin/gDmSgAH2">albumin</a>), bound to anions such as <a href="/facts/Phosphate/FDGVCxUG">phosphate</a> and <a href="/facts/Citric_acid/EgKGQBdl">citrate</a>, and as free (unbound) <a href="/facts/Ionized_calcium/wgUxKej5">ionized calcium</a>. Only the unbound ionized calcium is physiologically active. Normal blood calcium level is between 8.5 and 10.5 mg/dL (2.12 to 2.62 mmol/L) and that of unbound calcium is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L).<a class="footnote-ref" id="fnref:40" href="#fn:40"><sup>40</sup></a> </p> <h3>Mechanism</h3> <p>Extracellular Ca2+ levels modulate the opening propensity of <a href="/facts/Voltage-gated_sodium_channel/pXb4n2Vz">voltage-gated sodium channels</a>, presumably by binding onto the external aspect of the channel, thus altering the local electrical charge at the channel. With decreasing extracellulars Ca2+ levels, Na+ channels will be able open at progressively more negative <a href="/facts/Membrane_potential/DpNG14c7">membrane potentials</a>, causing nervous overexcitability. When extracellular Ca2+ concentrations reach half of normal, overexcitability of the Na+ channels becomes sufficient to cause some peripheral nerves to begin discharging spontaneously.<a class="footnote-ref" id="fnref:41" href="#fn:41"><sup>41</sup></a> </p> <h2 id="diagnosis">Diagnosis</h2> <p>Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: <a href="/facts/Corrected_calcium/wgUxKej5">Corrected calcium</a> (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]).<a class="footnote-ref" id="fnref:42" href="#fn:42"><sup>42</sup></a> </p><p>Since calcium is also bound to small anions, it may be more useful to correct total calcium for both albumin and the <a href="/facts/Anion_gap/Cn1UXy35">anion gap</a>.<a class="footnote-ref" id="fnref:43" href="#fn:43"><sup>43</sup></a><a class="footnote-ref" id="fnref:44" href="#fn:44"><sup>44</sup></a> </p> <h2 id="management">Management</h2> <p>Management of this condition includes: </p> <ul><li><a href="/facts/Intravenous/AwwuD3Nu">Intravenous</a> <a href="/facts/Calcium_gluconate/ErtaRtbU">calcium gluconate</a> 10% can be administered, or if the hypocalcaemia is severe, <a href="/facts/Calcium_chloride/e1EwNPGF">calcium chloride</a> is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium but rather exacerbated. Such rapid administration of calcium would result in effective over-correction – symptoms of hypercalcemia would follow.</li> <li>However, in either circumstance, maintenance doses of both calcium and vitamin D (often as 1,25-(OH)2-D3, i.e., <a href="/facts/Calcitriol/3SXesdFb">calcitriol</a>) are often necessary to prevent further decline.</li></ul> <h2 id="see-also">See also</h2> <ul><li><a href="/facts/Milk_fever/BXXWKnAh">Milk fever</a> (hypocalcemia in animals)</li> <li><a href="/facts/Calcium_deficiency_(plant_disorder)/rg1Saj3y">Calcium deficiency (plant disorder)</a></li> <li><a href="/facts/Hypomagnesemia_with_secondary_hypocalcemia/WyBISf0C">Hypomagnesemia with secondary hypocalcemia</a></li></ul> <h2 id="external-links">External links</h2> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>LeMone, Priscilla; Burke, Karen; Dwyer, Trudy; Levett-Jones, Tracy; Moxham, Lorna; Reid-Searl, Kerry (2015). Medical-Surgical Nursing. Pearson Higher Education AU. p. 237. ISBN 9781486014408. Archived from the original on 2016-10-02. <a href="9781486014408" target="_blank">9781486014408</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Pathy, M.S. John (2006). "Appendix 1: Conversion of SI Units to Standard Units". Principles and practice of geriatric medicine. Vol. 2 (4. ed.). Chichester [u.a.]: Wiley. p. Appendix. doi:10.1002/047009057X.app01. ISBN 9780470090558. <a href="9780470090558" target="_blank">9780470090558</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>Minisola, S; Pepe, J; Piemonte, S; Cipriani, C (2 June 2015). "The diagnosis and management of hypercalcaemia". BMJ (Clinical Research Ed.). 350: h2723. doi:10.1136/bmj.h2723. PMID 26037642. S2CID 28462200. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care". Canadian Family Physician. 58 (2): 158–62. PMC 3279267. PMID 22439169. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>Cooper, MS; Gittoes, NJ (7 June 2008). "Diagnosis and management of hypocalcaemia". BMJ (Clinical Research Ed.). 336 (7656): 1298–302. doi:10.1136/bmj.39582.589433.be. PMC 2413335. PMID 18535072. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413335" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413335</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></p></li> <li id="fn:8"><p>Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care". Canadian Family Physician. 58 (2): 158–62. PMC 3279267. PMID 22439169. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267</a> <a href="#fnref:8" class="footnote-back-ref">↩</a></p></li> <li id="fn:9"><p>Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care". Canadian Family Physician. 58 (2): 158–62. PMC 3279267. PMID 22439169. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267</a> <a href="#fnref:9" class="footnote-back-ref">↩</a></p></li> <li id="fn:10"><p>Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:10" class="footnote-back-ref">↩</a></p></li> <li id="fn:11"><p>Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care". Canadian Family Physician. 58 (2): 158–62. PMC 3279267. PMID 22439169. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267</a> <a href="#fnref:11" class="footnote-back-ref">↩</a></p></li> <li id="fn:12"><p>Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:12" class="footnote-back-ref">↩</a></p></li> <li id="fn:13"><p>Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:13" class="footnote-back-ref">↩</a></p></li> <li id="fn:14"><p>Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care". Canadian Family Physician. 58 (2): 158–62. PMC 3279267. PMID 22439169. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267</a> <a href="#fnref:14" class="footnote-back-ref">↩</a></p></li> <li id="fn:15"><p>Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care". Canadian Family Physician. 58 (2): 158–62. PMC 3279267. PMID 22439169. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267</a> <a href="#fnref:15" class="footnote-back-ref">↩</a></p></li> <li id="fn:16"><p>Cooper, MS; Gittoes, NJ (7 June 2008). "Diagnosis and management of hypocalcaemia". BMJ (Clinical Research Ed.). 336 (7656): 1298–302. doi:10.1136/bmj.39582.589433.be. PMC 2413335. PMID 18535072. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413335" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413335</a> <a href="#fnref:16" class="footnote-back-ref">↩</a></p></li> <li id="fn:17"><p>Armstrong, C. M.; Cota, Gabriel (1999). "Calcium block of Na+ channels and its effect on closing rate". Proceedings of the National Academy of Sciences of the United States of America. 96 (7): 4154–4157. Bibcode:1999PNAS...96.4154A. doi:10.1073/pnas.96.7.4154. PMC 22436. PMID 10097179. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC22436" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC22436</a> <a href="#fnref:17" class="footnote-back-ref">↩</a></p></li> <li id="fn:18"><p>Durlach, J; Bac, P; Durlach, V; Bara, M; Guiet-Bara, A (June 1997). "Neurotic, neuromuscular and autonomic nervous form of magnesium imbalance". Magnesium Research. 10 (2): 169–95. PMID 9368238. <a href="/wiki/PMID_(identifier)" target="_blank">/wiki/PMID_(identifier)</a> <a href="#fnref:18" class="footnote-back-ref">↩</a></p></li> <li id="fn:19"><p>Nussey, S. S.; Whitehead, S. A. (2013-04-08). Endocrinology: An Integrated Approach. CRC Press. p. 194. ISBN 9780203450437. <a href="9780203450437" target="_blank">9780203450437</a> <a href="#fnref:19" class="footnote-back-ref">↩</a></p></li> <li id="fn:20"><p>Bijlani, R. L.; Manjunatha, S. (2010-11-26). Understanding Medical Physiology: A Textbook for Medical Students. Jaypee Brothers Publishers. p. 465. ISBN 9789380704814.[permanent dead link] <a href="9789380704814" target="_blank">9789380704814</a> <a href="#fnref:20" class="footnote-back-ref">↩</a></p></li> <li id="fn:21"><p>Nussey, S. S.; Whitehead, S. A. (2013-04-08). Endocrinology: An Integrated Approach. CRC Press. p. 194. ISBN 9780203450437. <a href="9780203450437" target="_blank">9780203450437</a> <a href="#fnref:21" class="footnote-back-ref">↩</a></p></li> <li id="fn:22"><p>"Hypoparathyroidism. Parathyroid symptoms and disease | Patient". Patient. Retrieved 2015-09-05. <a href="https://patient.info/doctor/hypoparathyroidism-pro" target="_blank">https://patient.info/doctor/hypoparathyroidism-pro</a> <a href="#fnref:22" class="footnote-back-ref">↩</a></p></li> <li id="fn:23"><p>"Hypoparathyroidism". NORD (National Organization for Rare Disorders). Retrieved 2019-01-09. These cases may be called autoimmune hypoparathyroidism and develop when the body's immune system mistakenly attacks parathyroid tissue and leads to the loss of the secretion of parathyroid hormone. <a href="https://rarediseases.org/rare-diseases/hypoparathyroidism/" target="_blank">https://rarediseases.org/rare-diseases/hypoparathyroidism/</a> <a href="#fnref:23" class="footnote-back-ref">↩</a></p></li> <li id="fn:24"><p>Metheny, Norma (2012). Fluid and electrolyte balance : nursing considerations (5th ed.). Sudbury, MA: Jones & Bartlett Learning. p. 93. ISBN 978-0-7637-8164-4. Retrieved 4 September 2015. <a href="978-0-7637-8164-4" target="_blank">978-0-7637-8164-4</a> <a href="#fnref:24" class="footnote-back-ref">↩</a></p></li> <li id="fn:25"><p>Metheny, Norma (2012). Fluid and electrolyte balance : nursing considerations (5th ed.). Sudbury, MA: Jones & Bartlett Learning. p. 93. ISBN 978-0-7637-8164-4. 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