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Nuklearmedizin 1990; 29(01): 40-43
DOI: 10.1055/s-0038-1629511
Fallbericht – Case Report
Schattauer GmbH

Transient Prealbumin- Associated Hyperthyroxinemia in TSH-Producing Pituitary Adenoma

Transiente Präalbumin-assoziierte Hyperthyroxinämie in TSH-produzierenden Hypophysenadenomen
P. Lind
1   From the Department of Internal Medicine, Barmherzige Brüder Hospital, Eggenberg, University of Graz, Austria
,
W. Langsteger
1   From the Department of Internal Medicine, Barmherzige Brüder Hospital, Eggenberg, University of Graz, Austria
,
P. Költringer
1   From the Department of Internal Medicine, Barmherzige Brüder Hospital, Eggenberg, University of Graz, Austria
,
P. Wakonig
1   From the Department of Internal Medicine, Barmherzige Brüder Hospital, Eggenberg, University of Graz, Austria
,
B. Eber
2   The department of Internal Medicine, University of Graz, Austria
,
M. Mokry
3   The institute of Neurosurgery, University of Graz, Austria
,
A. Beham
4   And the institute of Pathology, Medical School, University of Graz, Austria
,
O. Eber
1   From the Department of Internal Medicine, Barmherzige Brüder Hospital, Eggenberg, University of Graz, Austria
› Author Affiliations
Further Information

Publication History

Received: 12 November 1989

Publication Date:
04 February 2018 (online)

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This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/ATSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.

Zusammenfassung

Es wird über einen 38jährigen Patienten berichtet, der wegen klinisch milder Zeichen einer Hyperthyreose, erhöhter Schilddrüsenhormonwerte und erhöhtem basalen TSH zur weiteren Abklärung stationär aufgenommen wurde. Die erhöhten Gesamthormonspiegel, die erhöhten freien Schilddrüsenhormone und das im TRH-Test praktisch nicht stimulierbare, bereits basal erhöhte TSH ließen ein Hypophysenadenom mit inappro- priater TSH-Inkretion vermuten. Die Sella-CT bestätigte die Verdachtsdiagnose mit einer 16 mm großen intrasellären Expansion. Die neoplastische TSH-Produktion wurde durch eine erhöhte a-Subunit und eine erhöhte molare a-Sub/TSH Ratio untermauert. In der T4-Proteinverteilung an Präalbumin (PA, TTR), Albumin (A) und thyroxinbindendem Globulin (TBG) ergab sich jedoch zusätzlich eine deutlich erhöhte Bindung an PA. Die Absolutwerte für PA, A und TBG lagen im Normbereich. Nach operativer Entfernung des TSH-produzierenden Adenoms kam es zur Normalisierung des TSH, der freien Schilddrüsenhormone und der T4-Bindung an PA. Die präalbuminassoziierte Hyperthyroxinämie war daher als passager im Rahmen der sekundären Hyperthyreose (T4-Shift von TBG zu Präalbumin) und nicht als genetisch determinierte Proteinbindungsanomalie zu interpretieren.

 

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