A TALE TO TELL: HOW LUPUS LED TO

GRAVES’ DISEASE
Madalina Musat 1,2, Camelia Giurca2, Daniela Aflorei2, Anca Lupu2, Mirela Ivan2, Anda Dumitrascu2, Mihaela
Milicescu1,3 Cristina Popescu1,4, Rucsandra Danciulescu1,5, Catalina Poiana1,2
1. Carol Davila University of Medicine and Pharmacy, Bucharest, Romania 2. C.I Parhon National Institute of Endocrinology,
Bucharest, Romania; 3. Department of Internal Medicine, Dr. I. Cantacuzino Hospital, Bucharest, Romania, 4. Institute of
Infectious Disease, M. Bals, Bucharest, Romania, 5. Institute of Diabetes, Nutrition and Metabolic Disease Prof. Dr. N.C.
INTRODUCERE
Paulescu, Bucharest, Romania

Introduction: 19.06.2009 Thyroid scan

Despite the presence of antinuclear antibodies and anti DNA
antibodies in Graves’ disease the association with Systemic
Lupus Erythematosus (SLE) is rare. Responsible for this
association seem to be mutations in the PTPN22 gene located
on chromosome 1p13.

Case Report:
We report a case of a 27-year old woman, who presented in
January 2009 in our department, at 6 months postpartum, after
being extensively investigated for autoimmunity, having 19.06.2009 She was re-screened for SLE and found positive.
negative results for polymyositis and SLE, but positive for
Normal values
TSHR antibodies (4,171 U/L). ANA Positive Negative
At presentation the patient had no signs or symptoms of Ac antiADN ds Positive Negative
Graves’ disease, only a mild rush of the zygomatic region, CORTIZOL 9,21 4,30-22,40 µg/dl
neck and anterior thorax, and hyperemic oedema of the ACTH 5,11 1-66 pg/mL

inferior eyelid regions. FSH 5,67 3,85-8,78 mUI/ml

Laboratory : E2 60,85 24-114 pg/ml

TSH 2 0,5-4,5 µUI/ml
28.01.2009
TT3 193 80-200 ng/dl
Normal values TT4 10,3 4,5-13 µg/dl
TSH 0,0197 0,35 - 5,50 µUI/ml

FT3 2,84 2,30-4,20 pg/nL Final diagnostic:

FT4 1,60 0,89-1,76 ng/dL SUBCLINICAL GRAVES’ DISEASE

TSHR-antibody 4,71 <1 UI/l SYSTEMIC LUPUS ERYTHEMATOSUS
ATPO 344 <70 UI/ml Management:
Antitiroglobulin 74,2 <270 UI/ml • Methymazole 5 mg once a day
antibodies
ANA <2 <3 UI/ml
• Methylprednisolone 32 mg once a day
• Hydroxichlorochine 200 mg once a day
Ac antiADN ds <7 <25 UI/ml
• Azathioprine 50 mg once a day

Radioiodine uptake: 2h: 6% and at 24 hours: 21% • Follow-up: SLE remission, controlled Graves Disease.

Ophtalmologic evaluation: proptosis: RE=15mm, LE=15mm, DISCUSSIONS

normal motility, bilateral eyelid edema, eyelid congestion.
Orbit CT scan: There were no CT signs of Graves orbitopathy,
only infiltrative aspect of the bilateral inferior eyelid regions
At this point the patient was diagnosed with
SUBCLINICAL GRAVES’ DISEASE
Management methymazole 20 mg once per day,
oral corticosteroid (methylprednisolone 32 mg/day)
followed by improvement of facial erythema.
Corticosteroid therapy was tapered in 3 months and the patient
returned after a pause of 2 months, in the summer with an
exacerbation of facial and thoracic rush.
The reported prevalence of autoimmune thyroid disease (3.9–24%) and
antithyroid antibodies (11–51%) in SLE varies considerably.
In our case at onset SLE didn’t meet sufficient diagnostic criteria, but
screening for autoimmune conditions was revelatory of subclinical Graves
SLE improvement after corticosteroid therapy (aimed to alleviate a presumed
Graves ophthalmopathy) was followed by clinical and immune rebound of
SLE at steroid withdrawal.
We were not able to screen for genetic mutations of PTPN22 gene, which is
supposed to encode a lymphoid-specific phosphatase, a negative regulator of
T cell activation. A coding SNP at nucleotide 1858 of PTPN22 that causes an
arginine to tryptophan substitution at position 620 (R620W) was found to be
strongly associated with several autoimmune diseases.
CONCLUSIONS
1.Screening for Graves’ disease in young women suspected of
SLE should be more largely used.
2. Facial rash in young women with Graves’ disease could be a
clue to diagnosis of SLE.