Endocrine Abstracts (2010) 22 P224

Graves' disease, systemic lupus erythematosus, hypoparathyroidism: autoimmune polyglandular syndrome or coincidence?

Eugen Melcescu1, Elizabeth H Kemp2, Vikas Majithia1, Vani Vijayakumar1, Gabriel I Uwaifo1 & Christian A Koch1

1University of Mississippi, Jackson, MS, USA; 2University of Sheffield, Sheffield, S210 2JF, UK.

Data on coexisting Graves’ disease (GD), systemic lupus erythematosus (SLE), and hypoparathyroidism (hypop) are limited. Scanty case reports have described hypoparathyr or hypothyroidism (late complication) following external irradiation to the neck. The thyroid and parathyroid glands may be sensitive to the immunologic or irradiation damage.

A 34-year old AA woman presented with tetanic-like cramps, easy skin bruising, fatigue, weight gain, nocturia and back pain. No signs of Cushing syndrome or adrenal insufficiency were identified. She was diagnosed previously with GD in 2001 and underwent radioiodine therapy (RAI) in 9/01 using 6 mCi. PostRAI (Nov 2001) low serum calcium (5.2 mg/dl) and PTH (11 pg/ml) were recorded and she received calcium and vitD. Approx. 5-6 mo postRAI (2002), overt hypothyroidism was diagnosed with wt gain of 30 lbs, fatigue, depression, and TSH of 80 uU/ml. In 2007, SLE was diagnosed based on ACR criteria: malar rash, nephritis with proteinuria >0.5 g/d, positive Smith antibodies (1038 H U/ml), RNP antibodies (764H U/ml), Sjogren anti-SS-A (902 H U/ml) and positive ANA (1036H U/ml, speckled pattern). In Oct 2009, s-calcium and PTH were still low at 7.1 mg/dl and 9 pg/ml, respectively, although the patient denied symptoms on vitD and calcium supplementation. To identify possible autoimmune damage of the parathyroids we evaluated the presence of activating antibodies to the CaSR and also analyzed the DNA sequence of all 6 translated exons and flanking intronic sequences of her CaSR gene for a functionally significant CaSR mutation but neither was positive. The initial autoimmune damage to her thyroid and possibly parathyroid glands followed by irradiation of them seems to have contributed to her developing both hypoparathyroidism (11/01) and hypothyroidism (2002). The patient could potentially have had parathyroid autoantibodies in 2001 that disappeared by 2009 when the patient was tested for them. We consider that the multiple autoimmune conditions developed over the past decade of her life with the concurrent irradiation contributing to her brittle hypoparathyroidism. Select patients with GD and perhaps parathyroid autoantibodies with a slowly developing destructive impact on the parathyroid glands may then develop overt hyoparathyroidism with rather low dose RAI. Finally, we favor the hypothesis of mixed (radioimmunological) damage in this case.

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