Letter to the Editor from Valdes-Socin et al: “Genetic Study in a Large Cohort Supported Different Pathogenesis of Graves’ Disease and Hashimoto’s Hypothyroidism”

Abstract

Objective: The conversion of Hashimoto's thyroiditis (HT) to hyperthyroidism due to thyrotropin receptor antibodies is intriguing and considered rare. The contribution of TSH receptor blocking antibodies (TRAb), which may be stimulators (TSAb) or blockers (TBAb), is suspected. We describe clinical and biological variables in a series of patients switching from Hashimoto's thyroiditis to Grave's disease. Subjects and methods: Retrospective case study of 24 patients with Hashimoto's thyroiditis followed during 48 ± 36 months that developed later Graves' disease (GD). These variables were analysed in the hypo and hyperthyroid phase: age, sex, initial TSH, free triiodothyronine (fT3), free thyroxine (fT4), anti-TPO, TBII antibodies, parietal cell autoantibodies, time between hypo and hyperthyroidism, thyroid volume and levothyroxine doses (LT). Results: In HT, mean TSH was 9.4 ± 26.1 UI/L and levothyroxine treatment was 66.2 ± 30.8 µg/day. The switch to GD was observed 38 ± 45 months after HT diagnosis. As expected, we found significant differences on TSH, FT3, FT4 and TBAb levels. Three out of 14 patients had parietal cell autoantibodies. In two of these three cases there was an Helicobacter pylori infection. There were no significant differences between HT and GD groups with respect to thyroid volume. Conclusions: To our knowledge, large series documenting the conversion of HT to GD are scarce. Although rare, this phenomenon should not be misdiagnosed. Suspicion should be raised whenever thyroxine posology must be tapered down during the followup of HT patients. Further immunological and genetic studies are needed to explain this unusual autoimmune change.

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“…The mechanism of H. pylori -induced Vit. B12 deficiency could be related to the failure of gastric parietal cells to produce intrinsic factor in patients with H. pylori-associated corpus-predominant chronic gastritis [26] .…”

“…Primary immune thrombocytopenia (ITP) is an autoimmune disorder, linked to H. pylori infection [26] . The putative pathogenic mechanism of this association is a molecular mimicry between platelet surface glycoproteins and amino acid sequences of H. pylori virulence factors, such as H. pylori lipopolysaccharide (LPS), Vac A , CagA , and urease B [25 , 27] .…”

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“…Although he additionally postulated that the kidneys are its pharmacological target, it was not until the 1970s that inhibition of renal tubular glucose reabsorption was specified as the mechanism of action of phlorizin [16], while Rosetti et al demonstrated an amelioration of insulin resistance and hyperglycemia after phlorizin administration in 1987 [17]. The development of the first orally absorbable, phlorizin-derived SGLT-1 and -2-inhibitor was followed by a rapid discovery of more orally active agents and in 2013, canagliflozin was the first SGLT2-inhibitors that received Food and Drug Administration (FDA) approval for the treatment of type 2 diabetes, followed by Dapagliflozin and Empagliflozin in 2014 [18]. SGLT co-transporters are subdivided into two categories: SGLT-1 and SGLT-2 co-transporters.…”