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].