NEUROIMAGES
Tertiary hyperparathyroidism presenting as posterior reversible encephalopathy syndrome Figure
Posterior reversible encephalopathy syndrome and ST elevation as manifestations of tertiary hyperparathyroidism
(A) CCT with frontal and occipital hypodense areas. MRI shows edema on coronal fluid-attenuated inversion recovery bilaterally in frontal (B, C) and occipital lobes (D). (E) ECG (excerpt) shows ST elevations in II, III, and aVF. (F) Sonography shows enlarged parathyroid gland (*) next to the common carotid artery and the internal jugular vein.
A man with hereditary hypophosphatemic rickets presented with seizures and coma. Brain MRI revealed edema typical of posterior reversible encephalopathy syndrome (PRES) and ECG showed ST elevations (figure). Coronary angiography was normal. Blood pressure was 165/90 mm Hg on admission; other known causes of PRES were absent. Severe hypercalcemia (3.83 mmol/L) was detected while parathyroid hormone was highly elevated (1,119 pg/mL). Sonography revealed an enlarged parathyroid gland. Subtotal parathyroidectomy led to prompt normalization of parathyroid hormone and calcium. The patient recovered fully. Tertiary hyperparathyroidism and hypercalcemic crises can be rare sequelae of long-term substitution treatment in hereditary hypophosphatemic rickets.1 Severe hypercalcemia has been recognized as a trigger for PRES (and ST elevations), yet the pathophysiologic mechanisms involved are unknown.2 Stoyan Popkirov, MD, Anja Figge, MD, Uwe Schlegel, MD, Sabine Skodda, MD From University Hospital Knappschaftskrankenhaus Bochum, Ruhr-University Bochum, Germany. Author contributions: Dr. Popkirov: study concept/design, analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Dr. Figge: analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Prof. Dr. Schlegel: analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Dr. Skodda: analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Study funding: No targeted funding reported. Disclosure: The authors report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures. Correspondence to Dr. Popkirov: [email protected] © 2016 American Academy of Neurology
695
ª 2016 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
1. 2.
696
Firth RG, Grant CS, Riggs BL. Development of hypercalcemic hyperparathyroidism after long-term phosphate supplementation in hypophosphatemic osteomalacia: report of two cases. Am J Med 1985;78:669–673. Nakajima N, Ueda M, Nagayama H, Yamazaki M, Katayama Y. Posterior reversible encephalopathy syndrome due to hypercalcemia associated with parathyroid hormone-related peptide: a case report and review of the literature. Intern Med 2013;52: 2465–2468.
Neurology 86
February 16, 2016
ª 2016 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
Tertiary hyperparathyroidism presenting as posterior reversible encephalopathy syndrome Stoyan Popkirov, Anja Figge, Uwe Schlegel, et al. Neurology 2016;86;695-696 DOI 10.1212/WNL.0000000000002378 This information is current as of February 15, 2016 Updated Information & Services
including high resolution figures, can be found at: http://www.neurology.org/content/86/7/695.full.html
References
This article cites 2 articles, 0 of which you can access for free at: http://www.neurology.org/content/86/7/695.full.html##ref-list-1
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This article, along with others on similar topics, appears in the following collection(s): Coma http://www.neurology.org//cgi/collection/coma Electrolyte http://www.neurology.org//cgi/collection/electrolyte Endocrine http://www.neurology.org//cgi/collection/endocrine Metabolic disease (inherited) http://www.neurology.org//cgi/collection/metabolic_disease_inherited
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Neurology ® is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright © 2016 American Academy of Neurology. All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.
Tertiary hyperparathyroidism presenting as posterior reversible encephalopathy syndrome Figure
Posterior reversible encephalopathy syndrome and ST elevation as manifestations of tertiary hyperparathyroidism
(A) CCT with frontal and occipital hypodense areas. MRI shows edema on coronal fluid-attenuated inversion recovery bilaterally in frontal (B, C) and occipital lobes (D). (E) ECG (excerpt) shows ST elevations in II, III, and aVF. (F) Sonography shows enlarged parathyroid gland (*) next to the common carotid artery and the internal jugular vein.
A man with hereditary hypophosphatemic rickets presented with seizures and coma. Brain MRI revealed edema typical of posterior reversible encephalopathy syndrome (PRES) and ECG showed ST elevations (figure). Coronary angiography was normal. Blood pressure was 165/90 mm Hg on admission; other known causes of PRES were absent. Severe hypercalcemia (3.83 mmol/L) was detected while parathyroid hormone was highly elevated (1,119 pg/mL). Sonography revealed an enlarged parathyroid gland. Subtotal parathyroidectomy led to prompt normalization of parathyroid hormone and calcium. The patient recovered fully. Tertiary hyperparathyroidism and hypercalcemic crises can be rare sequelae of long-term substitution treatment in hereditary hypophosphatemic rickets.1 Severe hypercalcemia has been recognized as a trigger for PRES (and ST elevations), yet the pathophysiologic mechanisms involved are unknown.2 Stoyan Popkirov, MD, Anja Figge, MD, Uwe Schlegel, MD, Sabine Skodda, MD From University Hospital Knappschaftskrankenhaus Bochum, Ruhr-University Bochum, Germany. Author contributions: Dr. Popkirov: study concept/design, analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Dr. Figge: analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Prof. Dr. Schlegel: analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Dr. Skodda: analysis/interpretation of data, drafting/revising the manuscript for content, including medical writing for content. Study funding: No targeted funding reported. Disclosure: The authors report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures. Correspondence to Dr. Popkirov: [email protected] © 2016 American Academy of Neurology
695
ª 2016 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
1. 2.
696
Firth RG, Grant CS, Riggs BL. Development of hypercalcemic hyperparathyroidism after long-term phosphate supplementation in hypophosphatemic osteomalacia: report of two cases. Am J Med 1985;78:669–673. Nakajima N, Ueda M, Nagayama H, Yamazaki M, Katayama Y. Posterior reversible encephalopathy syndrome due to hypercalcemia associated with parathyroid hormone-related peptide: a case report and review of the literature. Intern Med 2013;52: 2465–2468.
Neurology 86
February 16, 2016
ª 2016 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
Tertiary hyperparathyroidism presenting as posterior reversible encephalopathy syndrome Stoyan Popkirov, Anja Figge, Uwe Schlegel, et al. Neurology 2016;86;695-696 DOI 10.1212/WNL.0000000000002378 This information is current as of February 15, 2016 Updated Information & Services
including high resolution figures, can be found at: http://www.neurology.org/content/86/7/695.full.html
References
This article cites 2 articles, 0 of which you can access for free at: http://www.neurology.org/content/86/7/695.full.html##ref-list-1
Subspecialty Collections
This article, along with others on similar topics, appears in the following collection(s): Coma http://www.neurology.org//cgi/collection/coma Electrolyte http://www.neurology.org//cgi/collection/electrolyte Endocrine http://www.neurology.org//cgi/collection/endocrine Metabolic disease (inherited) http://www.neurology.org//cgi/collection/metabolic_disease_inherited
Permissions & Licensing
Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions
Reprints
Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus
Neurology ® is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright © 2016 American Academy of Neurology. All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.
