- Email: [email protected]
Reborn after calcium infusion
European Geriatric Medicine 6 (2015) 58–60
Available online at
ScienceDirect www.sciencedirect.com
EGM clinical case
Reborn after calcium infusion F. van den Hanenberg *, K. Kalisvaart Kennemer Gasthuis Haarlem, Department of geriatric medicine, Boerhaavelaan 22, 2035 RC, Haarlem, The Netherlands
A R T I C L E I N F O
Article history: Received 2 June 2014 Accepted 6 June 2014 Available online 11 December 2014
1. Introduction The calcium ion plays a critical role in normal cellular function and signalling, regulating diverse physiologic processes such as neuromuscular signalling, cardiac contractility and hormone secretion. Parathyroid hormone (PTH) and calcitriol are involved in the calcium homeostasis and maintain the calcium concentrations within a narrow range [1].
25(OH)vitD3 24 nmol/L (normal 30–130 nmol/L). The parathyroid hormone level was 2.2 pmol/L (normal: 1–7.5 pmol/L). The electrocardiogram showed a prolonged QT interval of 495 milliseconds (Fig. 3). Cerebral-CT scan showed bilateral calcifications in the globus pallidus (Fig. 4). Intravenous calcium infusion and 1-a-OH-vitaminD3 was started. In the following week she felt much better, she had no muscles cramps anymore, the QTc time normalised and her mental functions improved (MMSE 29). She began to perform some daily activities herself again. She felt reborn. A few months later there were no signs of Parkinsonism anymore and she was painting and playing bridge as she did before.
[(Fig._1)TD$IG]
2. Case report A 77-year-old woman was referred to our outpatient clinic because of suspected M. Parkinson’s and dementia. A few months earlier she was admitted to the hospital because of pneumonia and congestive heart failure. Since the hospitalization she complained about falls caused by unsteady gait and muscle cramps. Furthermore, she suffered from hair loss, paresthesias and trembling hands. Hetero-anamnesis revealed impaired short-term memory, difficulties concentrating, apraxia and loss of interest in her hobbies (painting and playing bridge). Her daughter showed us two paintings her mother made, one a few weeks before presentation and the other 6 months earlier (Figs. 1 and 2). Beside signs of loss of self-care and oedematous legs, she seemed rather well on physical examination. Neurological examination revealed a mask like face, light tremor of the head, dysdiadochokinesia, decreased strength of the proximal leg muscles and an unsteady shuffling gait. The Chvosteck and Trousseau signs were present (Video 1) [2]. Her score on the Mini-Mental Examination Scale (MMSE) was 20. It showed impaired short-term memory, loss of attention, and visuospatial abilities. She had no disease awareness. Laboratory studies showed the following values: serum calcium 1.19 mmol/L (normal 2.10–2.60 mmol/L), albumin 42 g/L (normal 35–55 g/L), phosphate 1.89 mmol/L (normal 0.9–1.50 mmol/L), magnesium 0.60 mmol/L (normal 0.65–1.05 mmol/L), * Corresponding author. Tel.: +31647462727. E-mail address: [email protected] (F. van den Hanenberg).
Fig. 1. Painting made 6 months before presentation.
http://dx.doi.org/10.1016/j.eurger.2014.06.031 1878-7649/ß 2014 Elsevier Masson SAS and European Union Geriatric Medicine Society. All rights reserved.
[(Fig._2)TD$IG]
F. van den Hanenberg, K. Kalisvaart / European Geriatric Medicine 6 (2015) 58–60
59
Further exploration of the different causes of this case of hypoparathyroidism, showed no antibodies against the calcium receptor, no clues for the polyglandulair syndrome and no evidence for sarcoidosis, Wilson disease’s or a malignancy. There was no history of neck surgery and her family history was negative for hypocalcemia. Most likely our patient thus suffered from an acquired idiopathic hypoparathyroidism. 3. Discussion Acquired idiopathic hypoparathyroidism is a relatively rare condition. Acquired hypoparathyroidism not related to surgery is most often the result of an autoimmune disease [2,3]. Hypocalcemia may be associated with a spectrum of clinical manifestations, ranging from few if any symptoms if the hypocalcemia is mild, to life-threatening seizures, refractory heart failure, or laryngospasm if it is severe [2,3]. Extrapyramidal symptoms are seen in 4–12.5% of the patients with hypoparathyroidism [4,5]. The prevalence of hypothyroidism causing dementia is unknown. To our best knowledge only a few case reports have been published on this topic [6–9]. The prevalence of reversible dementia is very low. In elderly patients referred to a memory clinic, the prevalence of reversible dementia is estimated 1% [10,11]. In our case congestive heart failure was probably the first major sign of hypocalcemia. Congestive heart failure is most often the result of an irreversible cause. Hypocalcemia is one of the few reversible causes of heart failure [12–15]. 4. Conclusion Fig. 2. Painting made a few weeks before presentation.
[(Fig._3)TD$IG]
Patients with hypocalcemia may be asymptomatic if the decreases in serum calcium are relatively mild and chronic, or they may present with life-threatening complications. Dementia and congestive heart failure are reversible in some cases. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.
[(Fig._4)TD$IG]
Appendix A. Supplementary data
Fig. 3. A prolonged QTc interval.
Supplementary data associated with this article can be found, in the online version, at http://dx.doi.org/10.1016/j.eurger. 2014.06.031. References
Fig. 4. CT cerebrum: bilateral calcifications in the globus pallidus.
[1] Fauci A, Braunwald E, Kasper D, Hauser S, Longo D, Jameson J, et al. Harrison’s principles of internal medicine. In: Chapter 47 hypercalcemia and hypocalcemia 17th ed., Europe: McGraw-Hill Education; 2008. [2] Cooper MS, Gittoes NJL. Diagnoses and management of hypocalcaemia. BMJ 2008;336:1298–302. [3] Shoback D. Hypoparathyroidism. N Engl J Med 2008;359:391–403. [4] Abe S, Tojo K, Ichida K, Shigematsu T, Hasegawa T, Morita M, et al. A rare case of idiopathic hypoparathyroidism with varied neurological manifestations. Intern Med 1996;35:129–34. [5] Tambyah PA, Ong BK, Lee KO. Reversible Parkinsonism and asymptomatic hypocalcemia with basal ganglia calcification from hypoparathyroidism 26 years after thyroid surgery. Am J Med 1993;94:444. [6] Kowdley KV, Coull BM, Orwoll ES. Cognitive impairment and intracranial calcification in chronic hypoparathyroidism. Am J Med Sci 1999;317: 273–7. [7] Eraut D. Idiopathic hypoparathyroidism presenting dementia. Br Med J 1974;1(5905):429–30. [8] Slyter H. Idiopathic hypoparathyroidism presenting as dementia. Neurology 1979;29(3):393–4. [9] Kumar G, Kaur D, Aggarwal P, Khurana T. Hypoparathyroidism presenting as cognitive dysfunction. BMJ Case Rep 2013. http://dx.doi.org/10.1136/bcr2013-009220 [published online 23 May 2013].
60
F. van den Hanenberg, K. Kalisvaart / European Geriatric Medicine 6 (2015) 58–60
[10] Walstra GJ, Teunisse S, van Gool WA, van Crevel H. Reversible dementia in elderly patients referred to a memory clinic. J Neurol 1997;244:17–22. [11] Clarfield AM. The decreasing prevalence of reversible dementias: an updated meta-analysis. Arch Intern Med 2003;163:2219–29. [12] Kazmi AS, Wall BM. Reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism. Am J Med Sci 2007;333: 226–9.
[13] Catalano A, Basile G, Lasco A. Hypocalcemia: a sometimes overlooked cause of heart failure in the elderly. Aging Clin Exp Res 2012;24:400–3. [14] Connor TB, Rosen BL, Blaustein MP, Applefeld MM, Doyle LA. Hypocalcemia precipitating congestive heart failure. N Engl J Med 1982;30:307 [869–872]. [15] Bolk J, Ruiter JH, van Geelen JA. Hypocalcemia as a cause of reversible heart failure. Ned Tijdschr Geneeskd 2000;144:900–3.
Available online at
ScienceDirect www.sciencedirect.com
EGM clinical case
Reborn after calcium infusion F. van den Hanenberg *, K. Kalisvaart Kennemer Gasthuis Haarlem, Department of geriatric medicine, Boerhaavelaan 22, 2035 RC, Haarlem, The Netherlands
A R T I C L E I N F O
Article history: Received 2 June 2014 Accepted 6 June 2014 Available online 11 December 2014
1. Introduction The calcium ion plays a critical role in normal cellular function and signalling, regulating diverse physiologic processes such as neuromuscular signalling, cardiac contractility and hormone secretion. Parathyroid hormone (PTH) and calcitriol are involved in the calcium homeostasis and maintain the calcium concentrations within a narrow range [1].
25(OH)vitD3 24 nmol/L (normal 30–130 nmol/L). The parathyroid hormone level was 2.2 pmol/L (normal: 1–7.5 pmol/L). The electrocardiogram showed a prolonged QT interval of 495 milliseconds (Fig. 3). Cerebral-CT scan showed bilateral calcifications in the globus pallidus (Fig. 4). Intravenous calcium infusion and 1-a-OH-vitaminD3 was started. In the following week she felt much better, she had no muscles cramps anymore, the QTc time normalised and her mental functions improved (MMSE 29). She began to perform some daily activities herself again. She felt reborn. A few months later there were no signs of Parkinsonism anymore and she was painting and playing bridge as she did before.
[(Fig._1)TD$IG]
2. Case report A 77-year-old woman was referred to our outpatient clinic because of suspected M. Parkinson’s and dementia. A few months earlier she was admitted to the hospital because of pneumonia and congestive heart failure. Since the hospitalization she complained about falls caused by unsteady gait and muscle cramps. Furthermore, she suffered from hair loss, paresthesias and trembling hands. Hetero-anamnesis revealed impaired short-term memory, difficulties concentrating, apraxia and loss of interest in her hobbies (painting and playing bridge). Her daughter showed us two paintings her mother made, one a few weeks before presentation and the other 6 months earlier (Figs. 1 and 2). Beside signs of loss of self-care and oedematous legs, she seemed rather well on physical examination. Neurological examination revealed a mask like face, light tremor of the head, dysdiadochokinesia, decreased strength of the proximal leg muscles and an unsteady shuffling gait. The Chvosteck and Trousseau signs were present (Video 1) [2]. Her score on the Mini-Mental Examination Scale (MMSE) was 20. It showed impaired short-term memory, loss of attention, and visuospatial abilities. She had no disease awareness. Laboratory studies showed the following values: serum calcium 1.19 mmol/L (normal 2.10–2.60 mmol/L), albumin 42 g/L (normal 35–55 g/L), phosphate 1.89 mmol/L (normal 0.9–1.50 mmol/L), magnesium 0.60 mmol/L (normal 0.65–1.05 mmol/L), * Corresponding author. Tel.: +31647462727. E-mail address: [email protected] (F. van den Hanenberg).
Fig. 1. Painting made 6 months before presentation.
http://dx.doi.org/10.1016/j.eurger.2014.06.031 1878-7649/ß 2014 Elsevier Masson SAS and European Union Geriatric Medicine Society. All rights reserved.
[(Fig._2)TD$IG]
F. van den Hanenberg, K. Kalisvaart / European Geriatric Medicine 6 (2015) 58–60
59
Further exploration of the different causes of this case of hypoparathyroidism, showed no antibodies against the calcium receptor, no clues for the polyglandulair syndrome and no evidence for sarcoidosis, Wilson disease’s or a malignancy. There was no history of neck surgery and her family history was negative for hypocalcemia. Most likely our patient thus suffered from an acquired idiopathic hypoparathyroidism. 3. Discussion Acquired idiopathic hypoparathyroidism is a relatively rare condition. Acquired hypoparathyroidism not related to surgery is most often the result of an autoimmune disease [2,3]. Hypocalcemia may be associated with a spectrum of clinical manifestations, ranging from few if any symptoms if the hypocalcemia is mild, to life-threatening seizures, refractory heart failure, or laryngospasm if it is severe [2,3]. Extrapyramidal symptoms are seen in 4–12.5% of the patients with hypoparathyroidism [4,5]. The prevalence of hypothyroidism causing dementia is unknown. To our best knowledge only a few case reports have been published on this topic [6–9]. The prevalence of reversible dementia is very low. In elderly patients referred to a memory clinic, the prevalence of reversible dementia is estimated 1% [10,11]. In our case congestive heart failure was probably the first major sign of hypocalcemia. Congestive heart failure is most often the result of an irreversible cause. Hypocalcemia is one of the few reversible causes of heart failure [12–15]. 4. Conclusion Fig. 2. Painting made a few weeks before presentation.
[(Fig._3)TD$IG]
Patients with hypocalcemia may be asymptomatic if the decreases in serum calcium are relatively mild and chronic, or they may present with life-threatening complications. Dementia and congestive heart failure are reversible in some cases. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.
[(Fig._4)TD$IG]
Appendix A. Supplementary data
Fig. 3. A prolonged QTc interval.
Supplementary data associated with this article can be found, in the online version, at http://dx.doi.org/10.1016/j.eurger. 2014.06.031. References
Fig. 4. CT cerebrum: bilateral calcifications in the globus pallidus.
[1] Fauci A, Braunwald E, Kasper D, Hauser S, Longo D, Jameson J, et al. Harrison’s principles of internal medicine. In: Chapter 47 hypercalcemia and hypocalcemia 17th ed., Europe: McGraw-Hill Education; 2008. [2] Cooper MS, Gittoes NJL. Diagnoses and management of hypocalcaemia. BMJ 2008;336:1298–302. [3] Shoback D. Hypoparathyroidism. N Engl J Med 2008;359:391–403. [4] Abe S, Tojo K, Ichida K, Shigematsu T, Hasegawa T, Morita M, et al. A rare case of idiopathic hypoparathyroidism with varied neurological manifestations. Intern Med 1996;35:129–34. [5] Tambyah PA, Ong BK, Lee KO. Reversible Parkinsonism and asymptomatic hypocalcemia with basal ganglia calcification from hypoparathyroidism 26 years after thyroid surgery. Am J Med 1993;94:444. [6] Kowdley KV, Coull BM, Orwoll ES. Cognitive impairment and intracranial calcification in chronic hypoparathyroidism. Am J Med Sci 1999;317: 273–7. [7] Eraut D. Idiopathic hypoparathyroidism presenting dementia. Br Med J 1974;1(5905):429–30. [8] Slyter H. Idiopathic hypoparathyroidism presenting as dementia. Neurology 1979;29(3):393–4. [9] Kumar G, Kaur D, Aggarwal P, Khurana T. Hypoparathyroidism presenting as cognitive dysfunction. BMJ Case Rep 2013. http://dx.doi.org/10.1136/bcr2013-009220 [published online 23 May 2013].
60
F. van den Hanenberg, K. Kalisvaart / European Geriatric Medicine 6 (2015) 58–60
[10] Walstra GJ, Teunisse S, van Gool WA, van Crevel H. Reversible dementia in elderly patients referred to a memory clinic. J Neurol 1997;244:17–22. [11] Clarfield AM. The decreasing prevalence of reversible dementias: an updated meta-analysis. Arch Intern Med 2003;163:2219–29. [12] Kazmi AS, Wall BM. Reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism. Am J Med Sci 2007;333: 226–9.
[13] Catalano A, Basile G, Lasco A. Hypocalcemia: a sometimes overlooked cause of heart failure in the elderly. Aging Clin Exp Res 2012;24:400–3. [14] Connor TB, Rosen BL, Blaustein MP, Applefeld MM, Doyle LA. Hypocalcemia precipitating congestive heart failure. N Engl J Med 1982;30:307 [869–872]. [15] Bolk J, Ruiter JH, van Geelen JA. Hypocalcemia as a cause of reversible heart failure. Ned Tijdschr Geneeskd 2000;144:900–3.