Endocrine Abstracts

Introduction: Parkinson’s disease (PD) is one of the most common neurodegenerative disorders characterized by bradykinesia, tremor, rigidity and postural instability as well as neurocognitive impairment and depression. Studies found a significant association between thyroid dysfunction and an increased risk of PD. We report the case of a patient treated for PD who had also Hashimoto’s thyroiditis, and we discuss the association of thyroid dysfunction with risk of PD.

Case report : Female patient, aged 52 years. Followed for 2 and a half years for Parkinson’s disease, clinically retained for bradykinesia, rigidity, tremor, treated with L-Dopa Benserazide and trihexyphenidyl hydrochloride. She presented weight loss, palpitations and intermittent diarrhea. The clinical examination noted a goiter and normal heart rate to 70 bpm. Thyroid function tests showed hyperthyroidism TSH us < 0.01 uUl/ml, fT4: 51.9 pmol/I, fT3: 13.9 pmol/I. Anti-thyroid antibodies measurement indicated positive anti-tpo Ab to 663.5 IU/l and negative anti-TSH receptor Ab. Thyroid ultrasound examination revealed typical image of Hashimotós thyroiditis. The diagnosis of Hashitoxicosis was retained. In one month follow-up, fT4 level decreased to 34 pmol/l. Follow-up with biological monitoring is planned for the diagnosis and management of hypothyroidism stage.

Discussion: There is a correlation between thyroid function and PD, but the mechanism is not completely clear. Patients with thyroid dysfunction have an increased risk of developing PD. Oxidative stress is one of the chief contributing factors to dopaminergic neuron loss and PD progression. Both hyperthyroidism and hypothyroidism are related to oxidative stress and cellular damage. Patients with autoimmune diseases, such as Hashimoto’s thyroiditis, Graves disease, amyotrophic lateral sclerosis, multiple sclerosis, and rheumatoid myalgia, had an additional 33% risk of PD. Besides the direct effects of thyroid hormone on dopaminergic neuron and skeletal muscle function and shared genetic risk, the association may be driven by autoimmunity; autoimmune response and neuroinflammation may play a role in the pathogenesis of PD. In addition, studies have suggested that presence of thyroid auto antibodies (anti-thyroid peroxidase and antithyroglobulin) are associated with neurodegenerative disorders such as multiple system atrophy and cerebellar degeneration. However, it’s unknown whether and how thyroid autoantibodies affect the dopaminergic neurons and risk of PD.

Conclusion: Many studies have shown that there is a correlation between thyroid dysfunction and PD, but the mechanism is incompletely clear. Further investigations should be conducted to provide clear evidence and to identify the mechanism responsible for this association.