Hashimoto's Thyroiditis in a Child with Familial Mediterranean Fever: a Case Report

Familial Mediterranean Fever (FMF) is an auto inflammatory disease[1] and also it can occur together with autoimmune disorders, such as Behçet's syndrome and systemic Lupus erythematosus[2,3]. Here, we present Familial Mediterranean fever and Hashimoto’s thyroiditis association in a 10-year-old girl. This girl was admitted to our hospital with a history of intermittent abdominal pain, fever, headache and chest pain. Her complaints have been recurring two or three times every month lasting 4-5 days for approximately two years. On admission, the physical findings were remarkable for fever and general abdominal tenderness. Laboratory studies revealed elevated levels of C-reactive protein and fibrinogen. Urinalysis and stool were normal. Abdominal ultrasonography and direct abdominal X-rays were unremarkable. So, she was diagnosed as FMF with periodic fever, abdominal and chest pain[4]. Her complaints resolved with colchicine treatment. DNA amplification analysis revealed a heterozygous E148Q mutation in the MEFV (Mediterranean fever) gene. On follow-up, after eight months of colchicine treatment she experienced some symptoms like progressively declining cognitive function, desire to sleep and fatigue. Her physical examination showed a smooth, painless thyroid enlargement. She had no other physical findings of hypothyroidism such as dry skin, hypothermia, decreased systolic blood pressure and increased diastolic blood pressure and edema of lower extremities. Complete blood count, glucose, calcium, electrolytes, renal and liver function test results were normal. Blood hormone levels were: TSH 2.03 mIU/mL (0.51-4.94), fT4 0.65 ng/dL (0.81.7), and fT3 4.2 pg/mL (2.3-4.2). The titers of thyroid antibodies were: anti-thyroid peroxidase (anti-TPO): >500 (0-60 IU/ml), antithyroglobulin (anti-TG): 370 (0-60 IU/ml). Other auto immune antibodies such as antigliadin antibody (AGA), antiendomysium antibody (EMA), antinuclear antibody (ANA), double-strand DNA antibody (Anti dsDNA) were negative. Ultrasonography of the thyroid gland revealed slight heterogeneity and slightly enlargement of the gland. These findings were compatible with HT[5]. Although her TSH level was normal, Levothyroxin treatment was started because of declining cognitive function, desire to sleep, fatigue and decreased fT4 level. After three months of treatment symptoms were resolved and the level of fT4 returned to normal. She has been followed for two years and has no additional problem. Hashimoto's Thyroiditis (HT) is the most common cause of autoimmune thyroid disease in children and adolescents. T cells play a critical role in disease pathogenesis by reacting with thyroid antigens and secreting inflammatory cytokines. Patients with HT thyroiditis have blocking antibodies to thyroid peroxidase, thyroglobulin, and the TSH receptor. These autoantibodies are secondary to thyroid follicular cell damage induced by T cells[6]. HT can be confirmed as the cause of hypothyroidism by measuring antithyroid antibodies, best done by measuring TPO Ab[5,7]. The patient with HT shows typical ultrasound changes such as scattered hypo and hyperechogenicity in thyroid gland[8]. Our patient had higher titers of antithyroid antibodies and revealed slight heterogeneity in thyroid ultrasonography so she was diagnosed as HT. The thyroid gland may be asymptomatically involved in most patients with systemic Letters to Editor Iran J Pediatr Aug 2013; Vol 23 (No 4), Pp: 489-492