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Oxidative stress is involved in the pathogenesis of Graves hyperthyroidism (GH) and Graves orbitopathy (GO) and an antioxidant approach has been proposed for both. In GH, a disbalance of the cell redox state is associated with thyroid hyperfunction and antithyroid medications may reduce oxidative stress. Tissue hypoxia participates in the pathogenesis of GO, and oxygen free radicals are involved in the typical changes of orbital tissues as reported by in vitro and clinical studies. Antioxidant agents, especially selenium, have been proposed as a therapeutic option for GH and GO. A clinical study regarding the use of selenium in mild GO has provided evidence for a beneficial effect in the short term, even though its beneficial effects in the long term are still to be investigated. In addition to selenium, a protective role of other antioxidant agents, i.e., quercetin, enalapril, vitamin C, N-acetyl-L-cysteine and melatonin has been suggested by in vitro studies, although clinical studies are lacking. Here, we review the role of oxidative stress and antioxidant agents in GH and GO.
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Background: Oculocutaneous albinism (OCA) is a heterogeneous autosomal recessive disorder characterized by reduced or absent melanin synthesis. Its prevalence is approximately one in 17,000 individuals worldwide. OCA causes a complete or partial absence of pigment in the skin, hair, and eyes. Reduction of melanin in the eyes results in reduced visual acuity, photophobia, and nystagmus. To our knowledge, the coexistence of albinism and thyroid autoimmune diseases has not been reported. Case Report: A 37-year-old male with OCA came to our observation for a familial history of autoimmune thyroiditis. He complained with mild asthenia. His brother was affected by OCA and autoimmune thyroiditis. Physical examination revealed the presence of fair skin, platinum white hair, and hypopigmentation of the iris. Laboratory data revealed the presence of subclinical hypothyroidism with positive serum anti-thyroid antibodies. Neck ultrasonography showed a markedly heterogeneously hypoechoic pattern of the thyroid, with a honeycomb-like appearance. Discussion: In the majority of cases, OCA in Caucasians is caused by mutations in the tyrosinase gene. The tyrosinase peptide is normally expressed on the surface of melanocytes, although recent studies have shown its presence in thyroid follicular epithelial cells of patients with Hashimoto’s thyroiditis. Therefore, although the mechanism is unclear, the present case report may suggest a pathogenetic link between OCA and Hashimoto’s thyroiditis.
Search for other papers by Elena Sabini in
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Background: Graves’ orbitopathy (GO) is believed to be the consequence of autoimmunity against antigens that are present both in the thyroid and orbital tissues. Massive release of thyroid antigens causes the appearance or deterioration of GO in patients with Graves’ hyperthyroidism (GH), as it occurs following radioiodine treatment. In theory, a similar release of autoantigens may occur at the eye level, for example due to an orbital trauma or surgical manipulation. To our knowledge, this is the first report of a case of de novo appearance of GO and then GH after an eye trauma, possibly reflecting spreading of autoantigens and activation of the immune system against shared orbital and thyroid antigens. Case Report: An otherwise healthy, 57-year-old man presented 6 months after the appearance of a monolateral right orbitopathy, which occurred 40 days after a trauma in the ipsilateral eye. His thyroid function was normal, with positive serum anti-TSH receptor autoantibodies. The thyroid was normal on ultrasound. A month later he developed hyperthyroidism and orbitopathy in the left eye. Discussion: The development of GO after an eye trauma may reflect tissue damage with release of autoantigens and consequent autoimmunity in a predisposed individual (our patient had a familial history of autoimmune thyroid disease). The subsequent development of hyperthyroidism is in keeping with the hypothesis that GH and GO are due to autoimmunity against antigens present both in the thyroid and in orbital tissues.
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Background: The pathogenesis of the extrathyroidal manifestations of Graves’ disease (GD) is not fully clarified. According to the most common hypothesis, they would reflect an autoimmune reaction against antigens constitutively expressed by the thyroid and by the extrathyroidal affected tissues. According to another hypothesis, the so-called Kriss’ hypothesis, soluble autoantigens released from the thyroid would reach the affected tissues, where they would become the target of the immune system. In this regard, a shift in gravity during sleep may favour antigen deposition. Case Report: A 59-year old man with GD came to our observation because of a dermopathy. He had been treated with radioactive iodine for Graves’ hyperthyroidism and with glucocorticoids and orbital decompression for a bilateral Graves’ orbitopathy (GO). The patient complained of a monolateral, untreated dermopathy, affecting the left leg and hand. At physical examination the skin of the left pretibial area and of the dorsal surface of the left hand appeared red and thickened, with an orange peel aspect. Interestingly, the patient reported that he usually slept laying on the left side of his body. Discussion: The observation of a patient with a monolateral dermopathy somehow reports to the Kriss’ hypothesis, especially in view of the patient’s habit of sleeping on the same side as dermopathy was present. Of course, this does not represent a proof that the Kriss’ hypothesis is correct, but it carries an element in favour of it. The fact that GO was bilateral is somehow against it, but does not exclude this possibility.
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Objectives: There is a general belief that Graves’ orbitopathy (GO) is a “chronic” disease, namely that patients’ eyes do not return to how they were before GO appeared. Here, we investigate this issue from both the patient’s and the physician’s point of view. Study Design: We studied the disappearance of GO, regardless of treatment, in all consecutive patients with a GO history of at least 10 years who came for a follow-up visit over a period of 5 years. Patients underwent an ophthalmological examination and were asked to answer a questionnaire on self-perception related to GO. Results: We studied 99 consecutive patients with a GO duration ≥10 years. Between the first and the last observation, patients received several types of treatment for their thyroid disease and/or for GO. At the end of follow-up, GO was considered disappeared based on objective criteria in 8 patients (∼8%) and based on subjective criteria in 24 patients (∼24%). When we considered both subjective and objective criteria, only 2 patients (∼2%) had all criteria fulfilled and could be considered as GO-free. Conclusions: GO is a chronic disease in the vast majority of patients. Even after a very long time since its onset, complete disappearance is rare, although a minority of patients believe they do not have GO anymore and an even lower proportion do not have relevant GO signs. Our findings have obvious implications in patient management and counseling.
Search for other papers by Giovanna Rotondo Dottore in
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Department of Surgical, Medical and Molecular Pathology, Division of Thoracic Surgery, University of Pisa and University Hospital of Pisa, Pisa, Italy
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Objectives: The thymus plays a central role in immune tolerance, which prevents autoimmunity. Myasthenia gravis (MG) is commonly associated with thymoma or thymus hyperplasia, and it can coexist with autoimmune thyroid diseases. However, the role of the thymus in thyroid autoimmunity remains to be clarified, which we investigated here. Study Design: The study design entailed the inclusion of consecutive MG patients and the measurement of anti-thyroid autoantibodies at baseline and, limited to autoantibody-positive patients, also at 24 and 48 weeks. One hundred and seven MG patients were studied. The main outcome measure was the behaviour of anti-thyroglobulin autoantibodies (TgAbs) and anti-thyroperoxidase autoantibodies (TPOAbs) over time in relation to thymectomy. Results: Serum TgAbs and/or TPOAbs were detected in ∼20% of patients in the absence of thyroid dysfunction. The prevalence of positive serum TgAbs and/or TPOAbs decreased significantly (p = 0.002) over the follow-up period in patients who underwent thymectomy, but not in patients who were not thymectomized. When the analysis was restricted to TgAbs or TPOAbs, findings were similar. On the same line, there was a general trend towards a reduction in the serum concentrations of anti-thyroid autoantibodies in patients who underwent thymectomy, which was significant for TPOAbs (p = 0.009). Conclusions: Our findings suggest a role of the thymus in the maintenance of humoral thyroid autoimmunity.
