Discussion:
We report a case of acute polyarthritis revealing Hashimoto’s thyroiditis. Hashimoto’s thyroiditis is the most frequent auto-immune endocrine disorder [4] and the most common etiology of hypothyroidism [1]. It results from a diffuse lymphocytic infiltration of the thyroid.
The diagnosis of Hashimoto’s thyroiditis relies on clinical features which vary from subclinical hypothyroidism to typical myxedema, positivity of serum thyroid antibodies (mainly thyroperoxidase (90%) and thyroglobulin), and reduced echogenicity on thyroid ultrasonography [5].
Hashimoto’s thyroiditis can be responsible for various rhematic manifestations due to thyroid dysfunction. These manifestations often reveal this disease.
It is also closely associated with several autoimmune diseases, which can be themselves responsible for articular and muscular manifestations, such as Sjögren’s syndrome, rheumatoid arthritis, systemic lupus erythematosus, or scleroderma [6][7][8][9]. Therefore, it is necessary to rule out these diagnoses before attributing articular manifestations to Hashimoto’s thyroiditis.
In our case, apart from arthritis, there were no clinical nor immunological features for the diagnosis of systemic lupus erythematosus, Sjögren’s syndrome, or rheumatoid arthritis. Moreover, thyroid hormone replacement therapy led to a complete resolution of polyarthritis.
Musculoskeletal symptoms related to hypothyroidism [10] occur in 25 to 79% of cases. Muscular signs may include pain, cramps, and weakness.The muscle enzyme levels (CK, myoglobin, and lactate dehydrogenase) [10] can be increased. The CK levels correlated with TSH levels [11][12], and hypothyroid myopathy symptoms usually resolve after thyroxin supplementation [11][13].
Polyarthralgia is the most frequent rheumatic symptom occurring during hypothyroidism [3]. The classic clinical presentation of hypothyroid arthropathy is less frequent, it is characterized by synovial thickening and joint effusions typically affecting the knees, metacarpophalangeal, proximal interphalangeal, and metatarsophalangeal joints. Synovial fluid can be non-inflammatory with highly increased viscosity [14][15][16][17].
Other rheumatic manifestations were also reported in patients with hypothyroidism, such as frozen shoulder [18], chondrocalcinosis [19], and carpal tunnel syndrome [20]. The incidence of osteoarthritis seemed to be increased in patients with hypothyroidism [21].
Rheumatological manifestations in patients with hypothyroidism result from hormonal dysfunction [17] and deposition of mucopolysaccharides, notably hyaluronic acid in articular and peri-articular structures [22]. Indeed, the excess of hyaluronic acid in patients with primary hypothyroidism is due to the stimulation of hyaluronic acid synthesis by the increased TSH levels and the inhibition of hyaluronic acid degradation caused by thyroxine deficiency [23][24][25][26][17].
The role of TSH in the pathogenesis of arthropathy was also highlighted because normalization of TSH levels under thyroid hormone substitution therapy leads to improvement and complete resolution of articular symptoms [27][14][28][15][17][29].
However, other studies showed that rheumatic manifestations may occur in patients with chronic lymphocytic thyroiditis, even in those with TSH levels within normal ranges [3][30][31][25[[28]. Besides, LeRiche et al. [32] reported cases of inflammatory polyarthritis (joint stiffness, tenderness, and effusion) in patients with HT with no improvement of arthritis under thyroid replacement. These findings suggest that rheumatological manifestations can be related to either inflammatory or serological features of Hashimoto’s thyroiditis [32].