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Biochemical Markers in Bone Metabolism in Patients with Graves' Disease
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences. (Experimentell endokrinkirurgi)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
(English)Manuscript (preprint) (Other academic)
Keyword [en]
Graves' Disease, Bone metabolism, Calcium sensing receptor, Hypocalcaemia, Total thyroidectomy
National Category
Clinical Medicine
Research subject
Medical Science
Identifiers
URN: urn:nbn:se:uu:diva-282595OAI: oai:DiVA.org:uu-282595DiVA: diva2:918146
Available from: 2016-04-10 Created: 2016-04-05 Last updated: 2016-06-01
In thesis
1. Calcium Homeostasis in Patients with Graves' Disease
Open this publication in new window or tab >>Calcium Homeostasis in Patients with Graves' Disease
2016 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Patients with Graves´ Disease (GD) have a higher risk of developing more severe and prolonged hypocalcaemia after total thyroidectomy (TT) than patients who undergo surgery for benign atoxic goitre. Since TT is the most effective treatment for GD, it is crucial to identify mechanisms for postoperative hypocalcaemia. The aim of this thesis was to study the mechanisms of calcium metabolism in patients with GD.

It is safe to operate on GD patients with TT. Results in Paper I showed fewer recurrences and equal complication rates compared to patients who underwent subtotal thyroidectomy (ST). The transient lowering of PTH seen in the hypocalcaemic patients was fully restored one month after surgery (Papers II and V).

The calcium-sensing receptor (CaSR) is crucial for maintaining plasma calcium, and single nucleotide polymorphisms (SNPs) in the gene may alter the sensing function. Thus, we analysed SNPs in CaSR in GD patients (Paper II) and showed that they had a more left-shifted calcium-PTH set-point compared to controls, implicating higher sensitivity. This is also supported by the results in the group of postoperatively hypocalcaemic patients. They already had lower plasma calcium preoperatively (Papers II, IV and V) and lacked the T/G G/A G/C, a haplotype shown in Paper III to have a close relationship to higher p-calcium levels. Moreover, a lack of the T allele in rs1801725 was seen in the group of patients needing permanent treatment with calcium and vitamin D, i.e. > 12 months, (paper V).

Patients who became hypocalcaemic (p-calcium < 2.00 mmol/L) on day one postoperatively, had lower preoperative levels of thyroid stimulating hormone (TSH) and higher levels of  T3, this was also applied to the patient groups requiring temporary or permanent postoperative treatment (Papers II and V). In addition, hypocalcaemic patients treated for less than six months with anti-thyroid drugs had higher levels of bone metabolism markers CTX and P1NP than normocalcaemic patients (Paper V).

In conclusion, the postoperative period of hypocalcaemia seen in patients with GD is a complex medical condition, caused by a combination of surgical trauma, different SNPs in CaSR, and high bone metabolism related to preoperative thyroid metabolism.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2016. 51 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1212
Keyword
Graves' Disease, Calcium homeostasis, Total thyroidectomy, Bone metabolism, Calcium sensing receptor
National Category
Clinical Medicine
Research subject
Surgery
Identifiers
urn:nbn:se:uu:diva-283075 (URN)978-91-554-9552-7 (ISBN)
Public defence
2016-06-02, Föreläsningssalen Falu Lasarett, Söderbaums väg 8, entré I, Falun, 10:00 (Swedish)
Opponent
Supervisors
Available from: 2016-05-12 Created: 2016-04-10 Last updated: 2016-06-01

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Annerbo, Maria

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