Epidemiology and Diagnosis of Hypoparathyroidism

Total Page:16

File Type:pdf, Size:1020Kb

Epidemiology and Diagnosis of Hypoparathyroidism SPECIAL FEATURE Position Statement Epidemiology and Diagnosis of Hypoparathyroidism Bart L. Clarke, Edward M. Brown, Michael T. Collins, Harald Jüppner, Peter Lakatos, Michael A. Levine, Michael M. Mannstadt, John P. Bilezikian, Anatoly F. Romanischen, and Rajesh V. Thakker Mayo Clinic (B.L.C.), Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Rochester, Minnesota 55905; Harvard Medical School (E.M.B.), Division of Endocrinology, Diabetes and Hypertension, Boston, Massachusetts 02115; Skeletal Clinical Studies Unit (M.T.C.), Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892; Endocrine Unit and Pediatric Nephrology Unit (H.J.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114; First Department of Medicine (P.L.), Semmelweis University Medical School, Budapest 1085, Hungary; Division of Endocrinology and Diabetes (M.A.L.), Children’s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania 19104; Massachusetts General Hospital (M.M.M.), Boston, Massachusetts 02114; Columbia University College of Physicians & Surgeons (J.P.B.), New York, New York 10032; Department of Hospital Surgery and Oncology of St Petersburg State Pediatric Medical Academy (A.F.R.), St. Petersburg 194100, Russia; and Academic Endocrine Unit (R.V.T.), Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, OX3 7LJ, United Kingdom Context: Hypoparathyroidism is a disorder characterized by hypocalcemia due to insufficient secretion of PTH. Pseudohypoparathyroidism is a less common disorder due to target organ resistance to PTH. This report summarizes the results of the findings and recommendations of the Working Group on Epidemiology and Diagnosis of Hypoparathyroidism. Evidence Acquisition: Each contributing author reviewed the recent published literature regarding epidemi- ology and diagnosis of hypoparathyroidism using PubMed and other medical literature search engines. Evidence Synthesis: The prevalence of hypoparathyroidism is an estimated 37 per 100 000 person-years in the United States and 22 per 100 000 person-years in Denmark. The incidence in Denmark is approximately 0.8 per 100 000 person-years. Estimates of prevalence and incidence of hypoparathyroidism are currently lacking in most other countries. Hypoparathyroidism increases the risk of renal insufficiency, kidney stones, posterior subcapsular cataracts, and intracerebral calcifications, but it does not appear to increase overall mortality, cardiovascular disease, fractures, or malignancy. The diagnosis depends upon accurate mea- surement of PTH by second- and third-generation assays. The most common etiology is postsurgical hy- poparathyroidism, followed by autoimmune disorders and rarely genetic disorders. Even more rare are etiologies including parathyroid gland infiltration, external radiation treatment, and radioactive iodine therapy for thyroid disease. Differentiation between these different etiologies is aided by the clinical presentation, serum biochemistries, and in some cases, genetic testing. Conclusions: Hypoparathyroidism is often associated with complications and comorbidities. It is im- portant for endocrinologists and other physicians who care for these patients to be aware of recent advances in the epidemiology, diagnosis, and genetics of this disorder. (J Clin Endocrinol Metab 101: 2284–2299, 2016) ISSN Print 0021-972X ISSN Online 1945-7197 * Author affiliations are shown at the bottom of the next page. Printed in USA Abbreviations: ADH1, autosomal dominant hypocalcaemia type 1; AHO, Albright’s he- Copyright © 2016 by the Endocrine Society reditary osteodystrophy; CaSR, calcium-sensing receptor; CHARGE, coloboma-heart Received November 6, 2015. Accepted January 29, 2016. anomaly-choanal atresia-retardation-genital-ear; CHD7, chromodomain helicase DNA- First Published Online March 4, 2016 binding protein 7; CI, confidence interval; DGS, DiGeorge syndrome; DMR, differentially methylated region; GCM2, glial cells missing 2; HDR, hypoparathyroidism-deafness-renal For related articles see pages 2273, 2300, 2313 dysplasia; HR, hazard ratio; KSS, Kearns-Sayre syndrome; MELAS, mitochondrial enceph- alopathy, lactic acidosis, and stroke-like episodes; MTPDS, mitochondrial trifunctional pro- tein deficiency syndrome; NEBL, nebulette; 1,25(OH)2 vitamin D, 1,25-dihydroxyvitamin D; PDE4D, phosphodiesterase 4D; PHP, pseudohypoparathyroidism; PPHP, pseudopseudo- hypoparathyroidism; SEMA3E, sempahorin 3E; TBCE, tubulin-specific chaperone. 2284 press.endocrine.org/journal/jcem J Clin Endocrinol Metab, June 2016, 101(6):2284–2299 doi: 10.1210/jc.2015-3908 The Endocrine Society. Downloaded from press.endocrine.org by [${individualUser.displayName}] on 05 July 2016. at 09:04 For personal use only. No other uses without permission. All rights reserved. doi: 10.1210/jc.2015-3908 press.endocrine.org/journal/jcem 2285 ypoparathyroidism is an uncommon disorder char- database over the interval studied. A surgical incidence H acterized by low serum calcium, increased serum estimate was based on calculation of the proportion of phosphorus, and deficient production of PTH (1, 2). The total neck operations resulting in transient (Ͻ6 months) or epidemiology of hypoparathyroidism has become better chronic (Ͼ6 months) hypoparathyroidism. A physician understood, with a number of recent studies quantitating primary market research study was conducted to assess aspects of the disease not previously appreciated. Pseudo- disease severity and to determine the percentage of new hypoparathyroidism (PHP), a disorder of PTH resistance, nonsurgical patients with hypoparathyroidism. Surgical is an even less common disease characterized by similarly incidence data were entered into an epidemiological model abnormal mineral biochemical abnormalities, but with in- to derive a second prevalence estimate. The surgical-based creased circulating levels of PTH (1). incidence approach gave an estimate of 117 342 relevant Operationally, hypoparathyroidism can be divided neck surgeries, resulting in 8901 cases of hypoparathy- into primary hypoparathyroidism due to intrinsic defects roidism over 12 months. Approximately 7.6% of surgeries within the parathyroid glands primarily due to genetic resulted in hypoparathyroidism, with 75% of these cases causes, and the much more common secondary or ac- being transient and 25% being chronic. The prevalence of quired forms due to etiologies that ablate, impair, or de- insured patients with chronic hypoparathyroidism in the stroy parathyroid gland function. Secondary causes of hy- surgical database was 58 625, similar to that obtained in poparathyroidism are by far the most common etiologies the diagnostic estimate. Assuming that 15.4% of the U.S. (2). Although the diagnosis of hypoparathyroidism is usu- population was uninsured at the time this study was done, ally straightforward once serum calcium, phosphorus, these findings were used to project an estimate of 77 000 and PTH levels are known, determining the cause of non- total insured and uninsured individuals in the United surgical hypoparathyroidism may be challenging. States that had hypoparathyroidism. Another estimate of the prevalence of hypoparathy- roidism comes from the longitudinal population-based Epidemiology of Hypoparathyroidism Rochester Epidemiology Project (Table 1) in which med- ical records linkage resources were used to identify all Anterior neck surgery is the most common cause of ac- persons residing in Olmsted County, Minnesota, in 2009 quired hypoparathyroidism and is responsible for about with any diagnosis of hypoparathyroidism assigned by a 75% of cases (1). The next most common acquired cause health care provider since 1945 (5). Detailed medical re- in adults is thought to be autoimmune disease, affecting cords were reviewed to confirm the diagnosis of hypo- either the parathyroid glands alone or multiple other en- parathyroidism and to assign an etiology. Subjects were docrine glands (2). Remaining cases of acquired hypo- assigned two age- and sex-matched controls per confirmed parathyroidism are secondary due to a variety of rare in- case. Fifty-four cases were confirmed, of mean age 58 Ϯ 20 filtrative disorders in which the parathyroid glands are years, with 71% female, giving a prevalence estimate of 37 affected by metastatic disease or iron or copper overload per 100 000 person-years. This prevalence estimate was or by ionizing radiation exposure. These latter causes of projected to approximately 115 000 patients in the United hypoparathyroidism are covered in more detail in the ac- States having hypoparathyroidism of any cause. Hypo- companying paper on presentation of hypoparathyroid- parathyroidism was caused by neck surgery in 78% of ism, including what little is known regarding the epide- cases, other secondary causes in 9%, familial disorders in miology of these disorders (3). Rare genetic disorders may 7%, and without an identified cause in 6%. also cause hypoparathyroidism. Only a few data exist on the epidemiology of hypo- parathyroidism in Europe. In a recent nationwide Danish Prevalence historic cohort study, the prevalence of hypoparathyroid- The best prevalence estimate of hypoparathyroidism in ism was estimated using data from the Danish National the United States is
Recommended publications
  • Continuous Rhpth (1–34) Treatment in Chronic Hypoparathyroidism
    ID: 20-0009 -20-0009 C T Fuss and others Continuous rhPTH (1-34) in ID: 20-0009; May 2020 hypoparathyroidism DOI: 10.1530/EDM-20-0009 Continuous rhPTH (1–34) treatment in chronic hypoparathyroidism Carmina Teresa Fuss1, Stephanie Burger-Stritt1, Silke Horn1, Ann-Cathrin Koschker1, Kathrin Frey1, Almuth Meyer2 and Stefanie Hahner1 Correspondence should be addressed 1Division of Endocrinology and Diabetology, Department of Medicine I, University Hospital Würzburg, Würzburg, to S Hahner Germany and 2Division of Endocrinology and Diabetology, Department of Internal Medicine, Helios Klinikum Erfurt, Email Erfurt, Germany [email protected] Summary Standard treatment of hypoparathyroidism consists of supplementation of calcium and vitamin D analogues, which does not fully restore calcium homeostasis. In some patients, hypoparathyroidism is refractory to standard treatment with persistent low serum calcium levels and associated clinical complications. Here, we report on three patients (58-year-oldmale,52-year-oldfemale,and48-year-oldfemale)sufferingfromseveretreatment-refractorypostsurgical hypoparathyroidism. Two patients had persistent hypocalcemia despite oral treatment with up to 4 µg calcitriol and up to 4 g calcium per day necessitating additional i.v. administration of calcium gluconate 2–3 times per week, whereas the third patient presented with high frequencies of hypocalcemic and treatment-associated hypercalcemic episodes. S.c. administration of rhPTH (1–34) twice daily (40 µg/day) or rhPTH (1–84) (100 µg/day) only temporarily increased serum calcium levels but did not lead to long-term stabilization. In all three cases, treatment with rhPTH (1–34) as continuous s.c. infusion via insulin pump was initiated. Normalization of serum calcium and serum phosphate levels was observed within 1 week at daily 1–34 parathyroid hormone doses of 15 µg to 29.4 µg.
    [Show full text]
  • Calcium and Parathyroid Disease
    created EXCLUSIVELY FOR FINANCIAL PROFESSIONALS Rx FOR SUCCESS Calcium and Parathyroid Disease The parathyroid glands are four small glands located in the thyroid gland, which lies by the larynx at the front of the neck. The parathyroid glands regulate the calcium level in the blood and calcium deposition in the bone. Hyperparathyroidism is an increase in parathyroid hormone (PTH) secretion and results in a high blood calcium level. Hypoparathyroidism is a decrease in PTH and causes low blood calcium. Primary hyperparathyroidism (PHPT) is caused by excessive secretion of parathyroid hormone from one or more parathyroid glands. 85% of cases are due to a small benign parathyroid adenoma. The remaining cases are due to multiglandular disease (called parathyroid hyperplasia) or to malignancy. Most hyperparathyroidism is diagnosed in asymptomatic people by an incidental finding of elevated serum calcium. Most persons with PHPT have an elevated parathyroid hormone (PTH). Parathyroid related symptoms include osteoporosis (bone thinning), kidney stones, peptic ulcer, mental changes (fatigue, depression, confusion), loss of appetite, nausea, vomiting, constipation, EKG changes, and arrythmias. Surgery is the usual treatment but carries with it the risk of damage to the recurrent laryngeal nerve. Recurrence occurs in a small percentage of patients. Secondary hyperparathyroidism is characterized by an elevated PTH and a low or low-normal serum calcium. The most common cause is chronic renal failure. Other causes are vitamin D deficiency and renal hypercalciuria. Hypoparathyroidism is usually due to accidental removal of the parathyroid glands during thyroid surgery or removal of too much parathyroid tissue during surgery for hyperparathyroidism. It is characterized by low serum calcium levels and increased levels of blood phosphorus (hyperphosphatemia).
    [Show full text]
  • Parathyroid Carcinoma Presenting As Tertiary Hyperparathyroidism
    Postgrad Med J: first published as 10.1136/pgmj.61.713.243 on 1 March 1985. Downloaded from Postgraduate Medical Journal (1985) 61, 243-244 Parathyroid carcinoma presenting as tertiary hyperparathyroidism D.J. Sherlockl*, J. Newman2 and R.T.J. Holl-Allen' Departments of 'Surgery and 2Pathology, East Birmingham Hospital, Bordesley Green East, Birmingham B9 SST, UK. Summary: A case of malignant transformation in established secondary hyperparathyroidism presenting as tertiary hyperparathyroidism is reported. Althougb rare, this occurrence has important medical and surgical implications. Introduction A case of malignant transformation in established At operation a large hard 4.0cm x 2.0 cm gland was secondary hyperparathyroidism is reported; this removed from the left upper pole adherent firmly to presented as tertiary hyperparathyroidism and the the thyroid gland. The other three glands were re- histology is discussed. This case would appear to moved also, a portion of one being autotransplanted. support the concept of malignant transformation Histological examination indicated that the large occurring in benign parathyroid disease. Although gland was carcinoma. The tumour invaded the cap- rare, this predisposition has important implications, sule, thyroid gland and a few small veins (Figure 1). especially for borderline cases treated conservatively Focally it had a trabecular structure and showed copyright. at present. cytological pleomorphism together with a number of mitoses. The remaining three glands displayed nodular hyperplasia. Case report The serum calcium fell rapidly post-operatively, requiring administration of intravenous calcium A 42 year old dialysis patient with increasing hypercal- gluconate on several occasions. She remains well one caemia was referred for parathyroidectomy in early year post-surgery, and has been maintained on 1983.
    [Show full text]
  • Hypoparathyroidism, Sensorineural
    Joseph et al. BMC Endocrine Disorders (2019) 19:111 https://doi.org/10.1186/s12902-019-0438-4 CASE REPORT Open Access Hypoparathyroidism, Sensorineural deafness and renal disease (Barakat syndrome) caused by a reduced gene dosage in GATA3: a case report and review of literature Anne D. D. Joseph1* , Nirmala D. Sirisena2, Thirunavukarasu Kumanan1, Vathualan Sujanitha1, Veronika Strelow3, Raina Yamamoto3, Stefan Wieczorek3 and Vajira H. W. Dissanayake2 Abstract Background: Barakat syndrome is an autosomal dominant rare genetic disease caused by haploinsufficiency of the GATA binding protein 3 (GATA3) gene. It is also known as HDR syndrome, and is characterized by varying degrees of hypoparathyroidism, sensorineural deafness and renal disease. This is the first report of a heterozygous GATA3 whole gene deletion causing HDR syndrome in a Sri Lankan family. Case presentation: A 13-year-old boy with an acute febrile illness, hypocalcaemia and bilateral carpopedal spasm was referred for evaluation. A past medical history of treatment for persistent hypocalcaemic symptoms since the age of 7 months was obtained. Biochemical investigations showed persistent low serum corrected calcium levels with hyperphosphataemia, hypomagnesaemia, low parathyroid hormone levels, hypercalciuria, and low total 25-hydroxy vitamin D levels. His renal functions and renal sonography were normal. Audiometry showed bilateral moderate to severe sensorineural hearing loss. On screening, his mother was also found to have asymptomatic hypocalcaemia, hypomagnesaemia, hyperphosphataemia, hypercalciuria and low total 25-hydroxy vitamin D levels. She had impaired renal functions and chronic parenchymal changes in the renal scan. Audiometry showed bilateral profound sensorineural hearing loss. Genetic analysis using multiplex-ligation dependent probe amplification showed a reduced gene dosage for GATA3 that is consistent with a heterozygous whole gene deletion in both the child and mother.
    [Show full text]
  • Hypercalcemia Secondary to Parathyroid Hormone Secretion from Metastatic Lesions in Liver
    Medical Case Studies Vol. 3(1), pp. 1-3, January 2012 Available online at http://www.academicjournals.org/MCS DOI: 10.5897/MCS11.026 ISSN 2141-6532 ©2012 Academic Journals Case Report Hypercalcemia secondary to parathyroid hormone secretion from metastatic lesions in liver Jennifer R. Dubay1, Veena Patil1, Neha Rickson1, Anthony Morrison2 and David L. Vesely1* 1James A. Haley Veterans Medical Center-151, 13000 Bruce B. Downs Blvd. Tampa, Florida 33612, USA. 2University of South Florida Health Sciences Center, Tampa, Florida 33647 USA. Accepted 30 November, 2011 Parathyroid cancer is a rare malignancy with a prevalence of 0.005% of all registered cancer cases in the United States. Metastases are rare but when they occur the metastatic lesions are usually in the lungs and lymph nodes. There has been only one reported metastasis to the liver in the 233 combined year experience of several major medical centers. A 35-year-old man had 9 metastatic lesions in his liver which produced approximately 1500 mg/dl PTH and sustained hypercalcemia (12.3 mg/dl) even after surgical resection of the parathyroid cancer and a transient hypocalcemia. Key words: Hypercalcemia, parathyroid hormone, liver secretion, metastases, parathyroid cancer. INTRODUCTION Parathyroid cancer is a rare endocrine malignancy with a This is the first case of a parathyroid cancer metastasis to prevalence of 0.005% of all registered cancer cases in liver that produced functional parathyroid hormone (PTH) the United States (Hundahl et al., 1999). It is also an and hypercalcemia. It is, thus, important to remember uncommon cause of hypercalcemia in persons with that hypercalcemia secondary parathyroid disease may parathyroid disease with only 0.4 to 3% of patients with not involve lesions in the neck but lesions elsewhere.
    [Show full text]
  • Primary Hyperparathyroidism
    A FOCUS MEETING REPORT FROM: 2nd Expert Workshop on Parathyroid Disorders 27-28 June 2019, Santpoort, The Netherlands PARAT Steering Group: Jens Bollerslev (Norway) Claudio Marcocci (Italy) Lars Rejnmark (Denmark) Camilla Schalin-Jäntti (Finland) Wim Van Hul (Belgium) PARAT Expert Meeting Faculty: Bart L. Clarke (USA) Neil Gittoes (UK) Ghada El-Hajj Fuleihan (Lebanon) Hans Morreau (The Netherlands) Stefan Pilz (Austria) Lars Rolighed (Denmark) Heide Siggelkow (Germany) Antonio Sitges-Serra (Spain) Rajesh Thakker (UK) FREE access to presentation summaries and slide decks at: www.ese-hormones.org/ parat Calcium and Bone Contents Contents What is PARAT? | Steering Group 3 Faculty 2019 4 Participants 2019 5 Special Inherited Forms of Parathyroid Dysfunction 6 Inherited Forms of Primary Hyperparathyroidism (MEN1,2,4, HPT-JT and FIHP): Diagnosis and Management Camilla Schalin-Jantti, Finland CaSR-mutations (FHH – ADH): Genetic and Clinical Perspective, Ghada El-Hajj Fuleihan, Lebanon 7 PTH-receptor Mutation (PseudoHypoPT, Acrodysostosis), Lars Rejnmark, Denmark 8 Breakout Summary 9 Special Aspects of Hypoparathyroidism and Hyperparathyroidism 11 Management of Hypoparathyroidism during Pregnancy, Bart L. Clarke, USA Bone Metabolism and Fractures in Chronic Hypoparathyroidism in Adults, Jens Bollerslev, Norway 12 How to Avoid Surgical Damage to the Parathyroid Glands: 13 Part I: Current Best Practice. Antonio Sitges-Serra, Spain Part II: Prospective Techniques. Lars Rolighed, Denmark Breakout Summary 14 Primary and Secondary HPT and Atypical Adenomas 16 Atypical Parathyroid Adenoma Management Part I: Definitions and Characteristics. Claudio Marcocci, Italy Part II: A Diagnostic View. Hans Morreau, The Netherlands Secondary Hyperparathyroidism: Causes, Consequences and Non-Surgical Management. 18 Stefan Pilz, Austria Primary Hyperparathyroidism – NICE Guidelines.
    [Show full text]
  • Jcem3307.Pdf
    SPECIAL FEATURE Editorial Hypoparathyroidism: Is It Time for Replacement Therapy? Mara J. Horwitz and Andrew F. Stewart Division of Endocrinology and Metabolism, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213 ndocrine diseases caused by hormone deficiencies are com- iopathic, and autosomal dominant hypoparathyroidism are Downloaded from https://academic.oup.com/jcem/article/93/9/3307/2596495 by guest on 01 October 2021 E monly treated by replacement of the deficient hormones. the most common varieties. For example, Addison’s disease is treated with oral glucocorti- Why does PTH deficiency cause hypocalcemia? Although coids, autoimmune hypothyroidism with oral thyroxine, and bone turnover is dramatically reduced in hypoparathyroidism, it premature ovarian failure with oral estrogen and progesterone. does not play a major role in causing hypocalcemia in hypopar- The availability of orally deliverable drugs makes this straight- athyroidism. Instead, the hypocalcemia in hypoparathyroidism forward. However, when the deficient hormone in question is a results principally from two other mechanisms (5–9). First, the protein, oral treatment presents problems because proteins are loss of PTH results in a failure of renal 1,25 dihydroxyvitamin D generally degraded by proteolytic digestive enzymes when de- [1,25(OH)2D] production, with a resultant reduction in the abil- livered orally. This obstacle commonly is circumvented by sc ity to absorb dietary calcium. Second, PTH is a potent antical- injection of the peptide hormone in question (i.e. GH, insulin, ciuric agent in the distal convoluted tubule. Therefore, its loss 1-desamino-␤-D-arginine vasopressin). So what is different results in striking increases in renal calcium excretion.
    [Show full text]
  • Symptomatic Hypoparathyroidism Based on a 22Q11 Deletion First Diagnosed in a 43-Year-Old Woman
    CAsE rEPorT symptomatic hypoparathyroidism based on a 22q11 deletion first diagnosed in a 43-year-old woman K. van den Berge1, K. Diderich2, P. Poddighe2, A. Berghout1* 1Department of Medicine, Medical Centre Rijnmond Zuid, Rotterdam, the Netherlands, 2Department of Clinical Genetics, Erasmus Medical Centre – Erasmus University Rotterdam, the Netherlands, *corresponding author: e-mail: [email protected] A b s T r act Congenital hypoparathyroidism usually manifests in early for cataract and a significant learning disability. Her childhood with hypocalcaemia with or without clinical medication consisted of levetiracetam and salbutamol. characteristics. This report describes a Caucasian woman At physical examination we saw a woman of short stature who, at the age of 43 years, was diagnosed with dysgenesis who was noted to have subtle facial dysmorphisms (figure of the parathyroid glands due to a de novo microdeletion in 1), i.e. a high forehead, a long philtrum, mild ptosis and chromosome 22q11 or diGeorge syndrome. This syndrome is characterised by a considerable variability in clinical symptoms, including heart defects, thymic hypoplasia and mental retardation. our patient presented with generalised figure 1. Close up photograph of the patient with convulsions due to extreme, symptomatic hypocalcaemia. hypoparathyroidism, showing the high forehead, a long The convulsions had been apparent for 18 months at the philtrum, mild ptosis and upslanting palpebral fissures time of the diagnosis. remarkably, whereas parathyroid hormone levels were undetectable, the 1,25-dihydroxy vitamin d level was normal. Chromosome 22q11 deletion was confirmed by fluorescence in situ hybridisation analysis. Keywords 22q11, DiGeorge, hypocalcaemia, hypoparathyroidism CAsE rEPorT A 43-year-old Caucasian woman was evaluated for thrombocytopenia.
    [Show full text]
  • Prediction of Transient and Permanent Hypoparathyroidism After Total
    J Endocr Surg. 2017 Sep;17(3):104-113 https://doi.org/10.16956/jes.2017.17.3.104 pISSN 2508-8149·eISSN 2508-8459 Original Article Prediction of Transient and Permanent Hypoparathyroidism after Total Thyroidectomy Using the Postoperative Serum Parathyroid Hormone Test: When Is the Best Time to Check? Hyunju Kim 1, Hyeong Won Yu 1, In Eui Bae 1, Jin Wook Yi 2, 5 2,4 3,4 1,4 Received: Jul 6, 2017 Joon-Hyop Lee , Su-jin Kim , Young Jun Chai , June Young Choi , Revised: Aug 2, 2017 Kyu Eun Lee 2,4 Accepted: Aug 21, 2017 1Department of Surgery, Seoul National University Bundang Hospital, Seongnam, Korea Correspondence to 2Department of Surgery, Seoul National University Hospital, Seoul National University College of Medicine, June Young Choi Seoul, Korea Department of Surgery, Seoul National 3Department of Surgery, Seoul Metropolitan Government-Seoul National University Boramae Medical University Bundang Hospital, 82 Gumi-ro Center, Seoul, Korea 4 173-beon-gil, Bundang-gu, Seongnam 13620, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea 5 Korea. Department of Surgery, Gachon University Gil Medical Center, Incheon, Korea Tel: +82-31-787-7107 Fax: +82-31-787-4078 E-mail: [email protected] ABSTRACT Copyright © 2017. Korean Association of Purpose: Thyroid and Endocrine Surgeons; KATES The usefulness of serum intact parathyroid hormone (iPTH) levels for predicting This is an Open Access article distributed hypocalcemia after total thyroidectomy is well established. This retrospective cohort under the terms of the Creative Commons study aimed to identify the best time iPTH levels should be checked, and determine the Attribution Non-Commercial License (https:// postoperative day 1 iPTH level that most safely predict the development of permanent creativecommons.org/licenses/by-nc/4.0/).
    [Show full text]
  • Hypoparathyroidism and Digeorge Syndrome
    Endocrinology and Diabetes Clinic Disorders of Calcium 4480 Oak Street, Vancouver, BC V6H 3V4 604-875-2117 1-888-300-3088 x2117 and Phosphorus http://endodiab.bcchildrens.ca Hypoparathyroidism the parathyroid cells. The body has developed cells that destroy some of its Hypoparathyroidism occurs when the body own tissue. This may include other does not produce enough parathyroid organs and endocrine glands, causing hormone (PTH). This hormone is made in 4 type 1 diabetes, Addison disease or or 5 parathyroid glands, located behind the other autoimmune diseases. thyroid tissue in the neck area. They are 2. Surgery or radiation to the thyroid gland very small—the size of peas. Their only job which damages the parathyroid glands. is to produce PTH, which keeps the calcium levels in the blood in the right range. 3. Iron deposits in the parathyroid glands, a side-effect of repeated transfusions to The name “hypo-parathyroid-ism”, means a treat thalassemia or other blood condition of low parathyroid hormone. diseases What does PTH do? How is hypoparathyroidism diagnosed? PTH balances the calcium level in the blood, keeping it in the right range. When the Something will have happened to make your calcium level is low, PTH is produced and it doctor request special blood tests. Perhaps raises the calcium level by: a heart problem is discovered during a routine pregnancy ultrasound or at birth, or 1. Moving calcium from the bones into the perhaps your baby or child became very sick blood. with symptoms of low blood calcium (see 2. Decreasing how much calcium is handout Disorders of Calcium and eliminated from the blood into the urine Phosphorus).
    [Show full text]
  • Hypoparathyroidism • Always Carry Spare Medication with You
    Taking Tablets Living with hypoparathyroidism • Always carry spare medication with you. Many people with Hypopara can expect to lead Hypoparathyroidism • Try to maintain a month’s supply in reserve. normal lives with a normal life span. • Carry an extra supply of medication on holiday. • With permanent but mild Hypopara, temporary • Carry your medication in your hand luggage symptoms may occur from time to time. when travelling by plane, with prescription • Severe Hypopara is rare but you may experience labels visible. constantly unstable calcium levels (or brittle Hypopara) and a range of symptoms which can Does anything affect my calcium level? be very challenging. You should be referred to a • Diet: It is better to get your calcium from your specialist in calcium metabolism. food than from supplements. However, some • You may experience episodes of unusual fatigue foods, e.g. too much wholemeal bread, spinach Further information and support are available or muscle weakness. At times you will need to from Hypopara UK, a national voluntary patient or tomatoes, alcohol and fizzy drinks can deplete allow your body to catch up, with extra rest. calcium. Dehydration also affects calcium levels: organisation, working to support people with all • Women with Hypopara can have a healthy drink eight glasses of water daily. forms of hypoparathyroidism and to promote pregnancy and a normal childbirth. Calcium, better medical understanding of this rare • Calcium levels can be affected by: vitamin D and thyroid hormone doses may need parathyroid condition. illness, infection, fever, sweating, vomiting, adjusting throughout pregnancy. diarrhoea,dehydration, surgery (including Free Membership|Support Groups|Information • You may need extra medication during strenuous dental), stress, smoking, menstrual periods, physical exercise.
    [Show full text]
  • Hypoparathyroidism, Nephrocalcinosis
    P160 A Case report: Hypoparathyroidism, nephrocalcinosis and replacement therapy Boysan S Nur1, Ozgen Zeren2, Sahin Tuna3 1 Department of Endocrinology 2 Department of Nephrology 3 Department of Radiology Kahramanmaras Necip Fazıl City Hospital ,Kahramanmaras, Turkey Introduction Results of the 6th month • The objectives of treatment in hypoparathyroidism are Calcium 8.8 mg/dl controlling symptoms and maintaining serum calcium in the Phosphorus 4.1 mg/dl low-normal range and serum phosphorus within a normal Creatinine 1.3 mg/dl range without developing hypercalciuria and • Renal ultrasonography showed slightly increased hyper nephrocalcinosis. echogenity of medullary more distinctive in the left renal • We present a case who has hypocalcemia and images. hyperphosphatemia and also nephrocalcinosis. Case Report Medical history • A fifty-years old man was admitted to hospital for routine visit . • At the age of 24, in Neurology department basal ganglion Right renal image Left renal image calcification was diagnosed caused by hypoparathyroidism. Conclusion • Medical treatment was included oral daily 1,25(OH)2D • In autosomal dominant hypoparathyroidism, heterozygous 0.25 mcg, 1333 IU Vit D, and 2500 mg calcium carbonate activating mutations of the CaR gene reset parathyroid and and also 880 IU Vit D3. kidney causing hypocalcemia and hypercalciuria. Laboratory • Vitamin D treatment results in further hypercalciuria and Calcium 7.6 mg/dl nephrocalcinosis.. Phosphorus 5 mg/dl • Some literature suggests the use of injectable Parathormon 4 pg/dl parathormon(1-34) when nephrocalcinosis developed in Creatinine 1.3 mg/dl the treatment of hypoparathyroidism but some results Radiology showed no difference when compared with conventional therapy. • Renal ultrasonograpy showed bilateral extensive • In addition, parathormon is not approved by FDA for use in medullary hyperdense images diagnosed as hypoparathyroidism in USA because of the unknown risk of nephrocalcinosis.
    [Show full text]