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DOI: 10.1055/s-2000-7369
Verlauf einer hypothyreoten Schilddrüsenfunktionslage mit positiven Thyreoglobulin-Autoantikörpern unter Kortikoidsubstitution bei einem 54-jährigen Mann mit isoliertem ACTH-Mangel
Hypothyreoidism with thyroglobulin antibodies during corticoid replacement in a 54-year-old man with isolated ACTH deficiencyPublication History
Publication Date:
31 December 2000 (online)

Anamnese und klinischer Befund: Ein 54-jähriger Patient litt seit 3 Jahren an Abgeschlagenheit, Diarrhoe und Gewichtsverlust. Bei der körperlichen Untersuchung fielen eine trockene, aber normal pigmentierte Haut sowie deutlich abgeschwächte Achillesehnenreflexe beidseits auf.
Untersuchungen: Die Blutsenkungsgeschwindigkeit nach Westergreen war mit 32 mm/h leicht erhöht. Die Hämoglobinkonzentration lag bei 12,4 mg/dl, bei normalen Indices der korpuskulären Bestandteile. Die Serumelektrolytwerte und der Serumbikarbonatwert lagen im Referenzbereich. Deutlich erhöht war der Spiegel des basalen Thyreoidea-stimulierenden Hormons (TSH) mit 8,5 µU/ml bei einem Normalwert des freien peripheren Trijodthyronins (fT3) von 3,2 pg/ml (2,3-4,2) und leicht erniedrigtem freiem Thyroxin (fT4) von 0,7 ng/d (0,8-1,8l). Die Sonographie der Schilddrüse ergab einen Normalbefund; leicht positiv waren die antinukleären Antikörper (ANA), doppelsträngige DNA-Antikörper (ds-DNA) konnten allerdings nicht nachgewiesen werden. Antithyreoglobulin-Antikörper (TGA) waren mit 1012 IU/ml (<350) mäßig erhöht. Das basale adrenokortikotrope Hormon (ACTH) wurde bei wiederholter Messung unterhalb der Nachweisgrenze gemessen, bei nicht messbarem Plasmakortisol und fehlender Kortisolausscheidung im 24-h-Sammelurin. Eine Kernspintomographie war unauffällig. Da die Kortisolsynthese weder durch den kurzen ACTH-Test, noch durch CRH stimuliert werden konnte, bestand bei intakter sonstiger anteriorer hypophysärer Funktion ein isolierter ACTH-Mangel auf Ebene der Hypophyse.
Therapie und Verlauf: Unter Substitution mit Hydrokortison 30 mg/d und Thyroxin 100 µg/d besserte sich der Zustand des Patienten rasch. Die Thyreoglobulin-Autoantikörper sowie die Antinukleären Antikörper (ANA) ließen sich 6 Monate nach Beginn der Substitutionstherapie nicht mehr nachweisen. Nach 15 Monaten setzten wir die Therapie mit Thyroxin aus. Die zeitlich enge Kontrolle der Schilddrüsenfunktionsparameter ergab in den folgenden 2 Jahren jeweils Euthyreose.
Folgerung: Eine subnormale Konzentration der peripheren Schilddrüsenwerte in Kombination mit einem erhöhten TSH kann durch eine reversible Störung der Schilddrüsenfunktion im Falle eines Hypokortisolismus auftreten.
Hypothyroidism with thyroglobulin antibodies during corticoid replacement in a 54-year-old man with isolated ACTH deficiency
History and admission findings: A 54-year-old previously healthy man was admitted because of fatigue, tiredness, diarrhoea and weight loss for the last 3 years. Physical examination revealed dry but normally pigmented skin and markedly reduced Achilles reflex bilaterally.
Investigations: Erythrocyte sedimentation rate was slightly elevated at 32 mm/h, C-reactive protein was normal. Both haemoglobin (12.4 mg/dl) and the corpuscular indices were normal, as were serum electrolytes, and sodium bicarbonate. But basal levels of thyroid stimulating hormone (TSH, 8.5 mU/ml) was markedly elevated, while free peripheral triiodothyronine (3.2pg/ml) was normal and free thyroxine (fT4) at 0.7 ng/d was slightly reduced. Thyroid ultrasound was normal. Test for antinuclear antibodies was slightly positive, but double-strand DNA was not demonstrated. Antithyroglobulin antibodies were slightly raised to 1012 IU/ml (normal <350). The basic level of ACTH was repeatedly below detection, as were plasma cortisol and cortisol excretion in 24-hour urine. Nuclear magnetic imaging was normal. Failure to stimulate corticol synthesis in the short ACTH test and by CRH indicated an isolated ACTH deficiency at the level of the anterior pituitary, while other hypophyseal functions were unaffected.
Treatment and course: The patient"s condition rapidly improved on replacement with hydrocortisone, 30 mg/d, and thyroxine, 100 mg/d. No thyroglobulin antibodies or antinuclear antibodies were demonstrable after 6 months. Thyroxine was discontinued after 15 months. Frequent monitoring of thyroid function over the next 2 years always indicated a euthyroid state.
Conclusion: Subnormal concentration of peripheral thyroid hormone combined with elevated TSH levels can, in the presence of hypercorticolism, be due to reversible abnormal thyroid function.
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