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In reply: Postsurgical hypoparathyroidism is not primary hypoparathyroidism

In Reply: We thank Dr. Parmar and appreciate his important comments.

Regarding the difference between primary and secondary hypoparathyroidism, the definition varies among investigators. Some define primary hypoparathyroidism as a condition characterized by primary absence or deficiency of parathyroid hormone (PTH), which results in hypocalcemia and which can be congenital or acquired, including postsurgical hypoparathyroidism.1–4 In principle, this is similar to the classification of disorders affecting other endocrine glands as primary and secondary. For example, primary hypothyroidism refers to a state of low thyroid hormones resulting from impairment or loss of function of the thyroid gland itself, such as in Hashimoto thyroiditis, radioactive iodine therapy, or thyroidectomy, among others.5 We adopted this definition in our article. In contrast, secondary hypoparathyroidism is characterized by low PTH secretion in response to certain conditions that cause hypercalcemia. Non-PTH-mediated hypercalcemia is a more common term used to describe this state of secondary hypoparathyroidism.

Other investigators restrict the term “primary hypoparathyroidism” to nonacquired (congenital or hereditary) etiologies, while applying the term “secondary hypoparathyroidism” to acquired etiologies.6

Concerning the association between diabetes mellitus and hypomagnesemia, we agree that diabetes does not need to be uncontrolled to cause hypomagnesemia. However, the patient described in our article presented with severe hypomagnesemia (serum level 0.6 mg/dL), which is not commonly associated with diabetes. Most cases of hypomagnesemia in patients with type 2 diabetes mellitus are mild and asymptomatic, whereas severe manifestations including seizures, cardiac arrhythmias, and acute tetany are rarely encountered in clinical practice.7 Furthermore, numerous studies have shown a negative correlation between serum magnesium level and glycemic control.7–11 A recent study reported that plasma triglyceride and glucose levels are the main determinants of the plasma magnesium concentration in patients with type 2 diabetes.12

Our patient’s diabetes was uncontrolled, as evidenced by her hemoglobin A1c level of 9.7% and her random serum glucose level of 224 mg/dL. Therefore, it is more likely that “uncontrolled diabetes mellitus” (in addition to diuretic use) was the cause of her symptomatic severe hypomagnesemia rather than controlled diabetes mellitus.

References
  1. Mendes EM, Meireles-Brandão L, Meira C, Morais N, Ribeiro C, Guerra D. Primary hypoparathyroidism presenting as basal ganglia calcification secondary to extreme hypocalcemia. Clin Pract 2018; 8(1):1007. doi:10.4081/cp.2018.1007
  2. Vadiveloo T, Donnan PT, Leese GP. A population-based study of the epidemiology of chronic hypoparathyroidism. J Bone Miner Res 2018; 33(3):478-485. doi:10.1002/jbmr.3329
  3. Hendy GN, Cole DEC, Bastepe M. Hypoparathyroidism and pseudohypoparathyroidism. In: De Groot LJ, Chrousos G, Dungan K, et al, eds. Endotext [Internet], South Dartmouth (MA): MDText.com, Inc.; 2017. www.ncbi.nlm.nih.gov/books/NBK279165. Accessed August 20, 2018.
  4. Rosa RG, Barros AJ, de Lima AR, et al. Mood disorder as a manifestation of primary hypoparathyroidism: a case report. J Med Case Rep 2014; 8:326. doi:10.1186/1752-1947-8-326
  5. Almandoz JP, Gharib H. Hypothyroidism: etiology, diagnosis, and management. Med Clin North Am 2012; 96(2):203–221. doi:10.1016/j.mcna.2012.01.005
  6. Fouda UM, Fouda RM, Ammar HM, Salem M, Darouti ME. Impetigo herpetiformis during the puerperium triggered by secondary hypoparathyroidism: a case report. Cases J 2009; 2:9338. doi:10.1186/1757-1626-2-9338
  7. Tosiello L. Hypomagnesemia and diabetes mellitus. A review of clinical implications. Arch Intern Med 1996; 156(11):1143–1148. pmid: 8639008
  8. Pham PC, Pham PM, Pham PA, et al. Lower serum magnesium levels are associated with more rapid decline of renal function in patients with diabetes mellitus type 2. Clin Nephrol 2005; 63(6):429–436. pmid:15960144
  9. Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med 2005; 20(1):3–17. doi:10.1177/0885066604271539
  10. Resnick LM, Altura BT, Gupta RK, Laragh JH, Alderman MH, Altura BM. Intracellular and extracellular magnesium depletion in type 2 (non-insulin-independent) diabetes mellitus. Diabetologia 1993; 36(8):767–770. pmid:8405745
  11. Pun KK, Ho PW. Subclinical hyponatremia, hyperkalemia and hypomagnesemia in patients with poorly controlled diabetes mellitus. Diabetes Res Clin Pract 1989; 7(3)163–167. pmid: 2605984
  12. Kurstjens S, de Baaij JH, Bouras H, Bindels RJ, Tack CJ, Hoenderop JG. Determinants of hypomagnesemia in patients with type 2 diabetes mellitus. Eur J Endocrinol 2017; 176(1):11–19. doi:10.1530/EJE-16-0517
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Sohab S. Radwan, MD
The University of Jordan, Amman, Jordan

Khair M. Hamo, MD
The University of Jordan, Amman, Jordan

Ayman A. Zayed, MD, MSc, FACE, FACP
The University of Jordan, Amman, Jordan

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Cleveland Clinic Journal of Medicine - 85(10)
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735-737
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hypoparathyroidism, postsurgical hypoparathyroidism, secondary hypoparathyroidism, parathyroid hormone, PTH, low PTH, hypomagnesemia, magnesium, Mg, diabetes mellitus, glycemic control, Sohab Radwan, Khair Hamo, Ayman Zayed
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Sohab S. Radwan, MD
The University of Jordan, Amman, Jordan

Khair M. Hamo, MD
The University of Jordan, Amman, Jordan

Ayman A. Zayed, MD, MSc, FACE, FACP
The University of Jordan, Amman, Jordan

Author and Disclosure Information

Sohab S. Radwan, MD
The University of Jordan, Amman, Jordan

Khair M. Hamo, MD
The University of Jordan, Amman, Jordan

Ayman A. Zayed, MD, MSc, FACE, FACP
The University of Jordan, Amman, Jordan

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In Reply: We thank Dr. Parmar and appreciate his important comments.

Regarding the difference between primary and secondary hypoparathyroidism, the definition varies among investigators. Some define primary hypoparathyroidism as a condition characterized by primary absence or deficiency of parathyroid hormone (PTH), which results in hypocalcemia and which can be congenital or acquired, including postsurgical hypoparathyroidism.1–4 In principle, this is similar to the classification of disorders affecting other endocrine glands as primary and secondary. For example, primary hypothyroidism refers to a state of low thyroid hormones resulting from impairment or loss of function of the thyroid gland itself, such as in Hashimoto thyroiditis, radioactive iodine therapy, or thyroidectomy, among others.5 We adopted this definition in our article. In contrast, secondary hypoparathyroidism is characterized by low PTH secretion in response to certain conditions that cause hypercalcemia. Non-PTH-mediated hypercalcemia is a more common term used to describe this state of secondary hypoparathyroidism.

Other investigators restrict the term “primary hypoparathyroidism” to nonacquired (congenital or hereditary) etiologies, while applying the term “secondary hypoparathyroidism” to acquired etiologies.6

Concerning the association between diabetes mellitus and hypomagnesemia, we agree that diabetes does not need to be uncontrolled to cause hypomagnesemia. However, the patient described in our article presented with severe hypomagnesemia (serum level 0.6 mg/dL), which is not commonly associated with diabetes. Most cases of hypomagnesemia in patients with type 2 diabetes mellitus are mild and asymptomatic, whereas severe manifestations including seizures, cardiac arrhythmias, and acute tetany are rarely encountered in clinical practice.7 Furthermore, numerous studies have shown a negative correlation between serum magnesium level and glycemic control.7–11 A recent study reported that plasma triglyceride and glucose levels are the main determinants of the plasma magnesium concentration in patients with type 2 diabetes.12

Our patient’s diabetes was uncontrolled, as evidenced by her hemoglobin A1c level of 9.7% and her random serum glucose level of 224 mg/dL. Therefore, it is more likely that “uncontrolled diabetes mellitus” (in addition to diuretic use) was the cause of her symptomatic severe hypomagnesemia rather than controlled diabetes mellitus.

In Reply: We thank Dr. Parmar and appreciate his important comments.

Regarding the difference between primary and secondary hypoparathyroidism, the definition varies among investigators. Some define primary hypoparathyroidism as a condition characterized by primary absence or deficiency of parathyroid hormone (PTH), which results in hypocalcemia and which can be congenital or acquired, including postsurgical hypoparathyroidism.1–4 In principle, this is similar to the classification of disorders affecting other endocrine glands as primary and secondary. For example, primary hypothyroidism refers to a state of low thyroid hormones resulting from impairment or loss of function of the thyroid gland itself, such as in Hashimoto thyroiditis, radioactive iodine therapy, or thyroidectomy, among others.5 We adopted this definition in our article. In contrast, secondary hypoparathyroidism is characterized by low PTH secretion in response to certain conditions that cause hypercalcemia. Non-PTH-mediated hypercalcemia is a more common term used to describe this state of secondary hypoparathyroidism.

Other investigators restrict the term “primary hypoparathyroidism” to nonacquired (congenital or hereditary) etiologies, while applying the term “secondary hypoparathyroidism” to acquired etiologies.6

Concerning the association between diabetes mellitus and hypomagnesemia, we agree that diabetes does not need to be uncontrolled to cause hypomagnesemia. However, the patient described in our article presented with severe hypomagnesemia (serum level 0.6 mg/dL), which is not commonly associated with diabetes. Most cases of hypomagnesemia in patients with type 2 diabetes mellitus are mild and asymptomatic, whereas severe manifestations including seizures, cardiac arrhythmias, and acute tetany are rarely encountered in clinical practice.7 Furthermore, numerous studies have shown a negative correlation between serum magnesium level and glycemic control.7–11 A recent study reported that plasma triglyceride and glucose levels are the main determinants of the plasma magnesium concentration in patients with type 2 diabetes.12

Our patient’s diabetes was uncontrolled, as evidenced by her hemoglobin A1c level of 9.7% and her random serum glucose level of 224 mg/dL. Therefore, it is more likely that “uncontrolled diabetes mellitus” (in addition to diuretic use) was the cause of her symptomatic severe hypomagnesemia rather than controlled diabetes mellitus.

References
  1. Mendes EM, Meireles-Brandão L, Meira C, Morais N, Ribeiro C, Guerra D. Primary hypoparathyroidism presenting as basal ganglia calcification secondary to extreme hypocalcemia. Clin Pract 2018; 8(1):1007. doi:10.4081/cp.2018.1007
  2. Vadiveloo T, Donnan PT, Leese GP. A population-based study of the epidemiology of chronic hypoparathyroidism. J Bone Miner Res 2018; 33(3):478-485. doi:10.1002/jbmr.3329
  3. Hendy GN, Cole DEC, Bastepe M. Hypoparathyroidism and pseudohypoparathyroidism. In: De Groot LJ, Chrousos G, Dungan K, et al, eds. Endotext [Internet], South Dartmouth (MA): MDText.com, Inc.; 2017. www.ncbi.nlm.nih.gov/books/NBK279165. Accessed August 20, 2018.
  4. Rosa RG, Barros AJ, de Lima AR, et al. Mood disorder as a manifestation of primary hypoparathyroidism: a case report. J Med Case Rep 2014; 8:326. doi:10.1186/1752-1947-8-326
  5. Almandoz JP, Gharib H. Hypothyroidism: etiology, diagnosis, and management. Med Clin North Am 2012; 96(2):203–221. doi:10.1016/j.mcna.2012.01.005
  6. Fouda UM, Fouda RM, Ammar HM, Salem M, Darouti ME. Impetigo herpetiformis during the puerperium triggered by secondary hypoparathyroidism: a case report. Cases J 2009; 2:9338. doi:10.1186/1757-1626-2-9338
  7. Tosiello L. Hypomagnesemia and diabetes mellitus. A review of clinical implications. Arch Intern Med 1996; 156(11):1143–1148. pmid: 8639008
  8. Pham PC, Pham PM, Pham PA, et al. Lower serum magnesium levels are associated with more rapid decline of renal function in patients with diabetes mellitus type 2. Clin Nephrol 2005; 63(6):429–436. pmid:15960144
  9. Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med 2005; 20(1):3–17. doi:10.1177/0885066604271539
  10. Resnick LM, Altura BT, Gupta RK, Laragh JH, Alderman MH, Altura BM. Intracellular and extracellular magnesium depletion in type 2 (non-insulin-independent) diabetes mellitus. Diabetologia 1993; 36(8):767–770. pmid:8405745
  11. Pun KK, Ho PW. Subclinical hyponatremia, hyperkalemia and hypomagnesemia in patients with poorly controlled diabetes mellitus. Diabetes Res Clin Pract 1989; 7(3)163–167. pmid: 2605984
  12. Kurstjens S, de Baaij JH, Bouras H, Bindels RJ, Tack CJ, Hoenderop JG. Determinants of hypomagnesemia in patients with type 2 diabetes mellitus. Eur J Endocrinol 2017; 176(1):11–19. doi:10.1530/EJE-16-0517
References
  1. Mendes EM, Meireles-Brandão L, Meira C, Morais N, Ribeiro C, Guerra D. Primary hypoparathyroidism presenting as basal ganglia calcification secondary to extreme hypocalcemia. Clin Pract 2018; 8(1):1007. doi:10.4081/cp.2018.1007
  2. Vadiveloo T, Donnan PT, Leese GP. A population-based study of the epidemiology of chronic hypoparathyroidism. J Bone Miner Res 2018; 33(3):478-485. doi:10.1002/jbmr.3329
  3. Hendy GN, Cole DEC, Bastepe M. Hypoparathyroidism and pseudohypoparathyroidism. In: De Groot LJ, Chrousos G, Dungan K, et al, eds. Endotext [Internet], South Dartmouth (MA): MDText.com, Inc.; 2017. www.ncbi.nlm.nih.gov/books/NBK279165. Accessed August 20, 2018.
  4. Rosa RG, Barros AJ, de Lima AR, et al. Mood disorder as a manifestation of primary hypoparathyroidism: a case report. J Med Case Rep 2014; 8:326. doi:10.1186/1752-1947-8-326
  5. Almandoz JP, Gharib H. Hypothyroidism: etiology, diagnosis, and management. Med Clin North Am 2012; 96(2):203–221. doi:10.1016/j.mcna.2012.01.005
  6. Fouda UM, Fouda RM, Ammar HM, Salem M, Darouti ME. Impetigo herpetiformis during the puerperium triggered by secondary hypoparathyroidism: a case report. Cases J 2009; 2:9338. doi:10.1186/1757-1626-2-9338
  7. Tosiello L. Hypomagnesemia and diabetes mellitus. A review of clinical implications. Arch Intern Med 1996; 156(11):1143–1148. pmid: 8639008
  8. Pham PC, Pham PM, Pham PA, et al. Lower serum magnesium levels are associated with more rapid decline of renal function in patients with diabetes mellitus type 2. Clin Nephrol 2005; 63(6):429–436. pmid:15960144
  9. Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med 2005; 20(1):3–17. doi:10.1177/0885066604271539
  10. Resnick LM, Altura BT, Gupta RK, Laragh JH, Alderman MH, Altura BM. Intracellular and extracellular magnesium depletion in type 2 (non-insulin-independent) diabetes mellitus. Diabetologia 1993; 36(8):767–770. pmid:8405745
  11. Pun KK, Ho PW. Subclinical hyponatremia, hyperkalemia and hypomagnesemia in patients with poorly controlled diabetes mellitus. Diabetes Res Clin Pract 1989; 7(3)163–167. pmid: 2605984
  12. Kurstjens S, de Baaij JH, Bouras H, Bindels RJ, Tack CJ, Hoenderop JG. Determinants of hypomagnesemia in patients with type 2 diabetes mellitus. Eur J Endocrinol 2017; 176(1):11–19. doi:10.1530/EJE-16-0517
Issue
Cleveland Clinic Journal of Medicine - 85(10)
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Cleveland Clinic Journal of Medicine - 85(10)
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735-737
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In reply: Postsurgical hypoparathyroidism is not primary hypoparathyroidism
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In reply: Postsurgical hypoparathyroidism is not primary hypoparathyroidism
Legacy Keywords
hypoparathyroidism, postsurgical hypoparathyroidism, secondary hypoparathyroidism, parathyroid hormone, PTH, low PTH, hypomagnesemia, magnesium, Mg, diabetes mellitus, glycemic control, Sohab Radwan, Khair Hamo, Ayman Zayed
Legacy Keywords
hypoparathyroidism, postsurgical hypoparathyroidism, secondary hypoparathyroidism, parathyroid hormone, PTH, low PTH, hypomagnesemia, magnesium, Mg, diabetes mellitus, glycemic control, Sohab Radwan, Khair Hamo, Ayman Zayed
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