Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12188/25768
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dc.contributor.authorTodorova, Biljanaen_US
dc.contributor.authorBitoska, Iskraen_US
dc.contributor.authorJovanovska Mishevska, Sashaen_US
dc.contributor.authorStevcevska, Aleksandraen_US
dc.contributor.authorJanev Georgieva, Oliveraen_US
dc.contributor.authorMilenkovikj, Tatjanaen_US
dc.date.accessioned2023-02-20T10:22:34Z-
dc.date.available2023-02-20T10:22:34Z-
dc.date.issued2023-01-18-
dc.identifier.urihttp://hdl.handle.net/20.500.12188/25768-
dc.description.abstractHashimoto's thyroiditis and Graves’ disease are the most common autoimmune thyroid conditions and are more common in women than in men. Thyrotropin receptor (TSHR) antibodies that stimulate the thyroid (TSAb) cause Graves’ hyperthyroidism and TSHR antibodies which block thyrotropin action (TBAb) are occasionally responsible for hypothyroidism. Unusual patients switch from TSAb to TBAb (or vice versa) with concomitant thyroid function changes.The most common scenario is the evolution from Graves’ disease (GD) to Hashimoto's thyroiditis (HT), whereas the switch from HT into GD seems to be less common. 53-year-old woman presented with a several month's history of tiredness, cold intolerance and hoarseness in October 2020. She was diagnosed with autoimmune hypothyroidism and achieved euthyroid status following treatment with Tbl. Levothyroxine a 50 mcg S. 1×1. This almost stable status was interestingly interrupted after 9 months (January 2021) when the patient on a regular checkup got laboratory results that showed suppressed TSH levels and a high fT4. The substitution therapy was discontinued immediately. The ultrasound of the thyroid gland showed nonspecific changes: hypoechoic, inhomogeneous gland without any markable pathological formations. The patient was feeling tired, she had palpitations, sweating that is not connected to a physical activity, shaking of the hands and uncontrolled movements of the extremities and neck. Her hair started to fall rapidly in the past few months. She was given Tbl. Metoprolol a 100 mg S.1×1 and Tbl ASA a 100 mg S. 1X1.In October 2021, the new laboratory results showed TSH <0.005 mU/l; fT4 =33.36, aTP-O= 22.77 iU/ml thyroglobulin =46,62, Calcitonin=2.99, Vit. D3=27.3, TSH receptor antibodies= 15.40. Antithyroid therapy was required, and she was given Tbl Thiamazole, Tbl. Propronalol because of the developed clinically and laboratory confirmed hyperthyroidism. There were oscillations in the thyroid status in the first months after the switch to hyperthyroidism, and in December 2021 there was a discontinuation of the Thiamazole treatment for one month because of the unstable TSH level, but afterwards from January 2022 the therapy is administered again and the patient is so far clinically stable under regular control. The patient is feeling good. Conclusion:This rare switch from a state of hypothyroidism to a state of hyperthyroidism is not very common in the clinical endocrinology practice, but should not be missed or misdiagnosed. Suspicion should be raised in the very first moment of tapering the levothyroxine doses in any patient with diagnosed HT during a regular follow up. Our recommendation is doing the TRABs (if available) at the moment of lowering the levothyroxine doses along with the regular laboratory tests of fT4, TSH, ATP-O. If there are any TRABs elevated, the leading way is to think and manage the possible and probable onset of hyperthyroidismen_US
dc.language.isoenen_US
dc.publisherThe Endocrine Societyen_US
dc.relation.ispartofJCEM Case Reportsen_US
dc.subjecthyperthyroidismen_US
dc.titleCase report on a switch from hypothyroidism to hyperthyroidismen_US
dc.typeProceeding articleen_US
dc.relation.conferenceEndoBridge, Antalya, Turkeyen_US
dc.identifier.doi10.1210/jcemcr/luac014.059-
dc.identifier.urlhttps://academic.oup.com/jcemcr/article-pdf/1/Supplement_1/luac014.059/48943090/luac014.059.pdf-
dc.identifier.urlhttps://academic.oup.com/jcemcr/article-pdf/1/Supplement_1/luac014.059/48943090/luac014.059.pdf-
dc.identifier.volume1-
dc.identifier.issueSupplement_1-
item.grantfulltextnone-
item.fulltextNo Fulltext-
crisitem.author.deptFaculty of Medicine-
crisitem.author.deptFaculty of Medicine-
crisitem.author.deptFaculty of Medicine-
Appears in Collections:Faculty of Medicine: Conference papers
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