The unmasking of primary hypothyroidism by steroid replacement in profound Addison's Disease

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 1-16-Adrenal Insufficiency
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-2
Sudeep Dhillon*1 and Xiangbing Wang2
1UMDNJ-RWJMS, New Brunswick, NJ, 2UMDNJ- RWJMS, New Brunswick, NJ
Objective:  To discuss a patient with Addison’s Disease and the diagnostic implications of steroid replacement on thyroid function.

Case Report:  38 y/o F with history of hypothyroidism diagnosed at 12 years old, presents with 6 month history of fatigue, 10 lb weight loss, and skin darkening.   Due to symptoms of worsening fatigue, patient reports stopping thyroid replacement at the onset of these symptoms.   No menstrual irregularities, polyuria, or polydipsia were present.  Physical exam was significant for patient’s thin stature – BMI 17.92 kg/m2–buccal and generalized hyperpigmentation, mild thyromegaly, dry skin, and mild, diffuse proximal muscle weakness.  Laboratory evaluation the previous month showed the following:  cortisol 0.5 mcg/dL; ACTH 1306 pg/mL; TSH 2.28 uIU/L; T4 8.3 ug/dL; T3 158 ng/dL. 

Patient was given decadron 1 mg for 3 days prior to returning for ACTH stimulation test and further studies: TSH 160.80 uIU/L. FT4 0.51 ng/dL; IGF-1 107 ng/mL; LH 4.7mIU/mL; FSH 6.0 mIU/mL; 21-OH Antibody - 19 U/mL; prolactin 65 ng/mL; Electrolytes and PTH within normal range.  250 mcg ACTH stim test: pre-dose cortisol <1 mcg/dL; 1 hour post-dose cortisol <1 mcg/dL;    TPO ab 578 IU/mL; Hemoglobin A1C 5.5%.  Celiac antibody negative;  MRI brain unremarkable.  CT Abdomen showed atrophied adrenal glands.  Patient started on daily  hydrocortisone 30 mg and levothyroxine 50 mcg.  4 weeks later, repeat labs were as follows: TSH 21.180 uIU/mL; T4 7.8 ug/dL; T3 104 ng/dL; FT4 1.12 ng/dL.

Discussion:  This patient has features of polyglandular autoimmune syndrome type 2, namely autoimmune adrenalitis and autoimmune thyroid disease.  This endocrinopathy occurs in approximately 14-20 people per million and has a 3:1 female to male propensity with peak incidence at 30-40 years of age. 

In this acutely ill Addisonian patient with a history of known hypothyroidism, her TSH without LT4 replacement for 6 months was within normal range.  The administration of high physiologic doses of steroids for just 3 days was followed by a reversion to an unequivocally hypothyroid pattern, which was further confirmed by an elevated TSH a few weeks after thyroid replacement therapy was started.  The explanation for the dramatic changes in thyroid function is not entirely  understood, but contributory mechanisms for the initial ‘normal’ thyroid function may include “sick euthyroid” as well as severe cortisol deficiency leading to abnormal thyroid hormone metabolism  

Conclusion:  This presentation highlights a truly unique pattern of thyroid function in a patient initially diagnosed with Addison’s Disease.  The diagnosis of hypothyroidism would have been missed if thyroid function were not reassessed after steroids were started.  In conclusion, in the setting of Addison’s Disease, clinicians should not assume euthyroidism based on pretreatment lab data and should preferentially evaluate thyroid function after initiating steroid replacement.

Nothing to Disclose: SD, XW

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