All co-authors take full responsibility for the integrity of the study and the final manuscript. Funding Not applicable. Availability of data and materials All data generated or analyzed during this study are included in this published article. Declarations Ethics approval and consent to participateEthics approval was waived. onset of Guillain-Barr syndrome, helper T cells became predominantly type 1, effector B cells increased in number, and thyroid-stimulating antibodies were produced, leading to the conclusion that Hashimoto’s disease progressed to Graves’ disease. Therefore, it is necessary to pay attention to the transition of thyroid function during Guillain-Barr syndrome. Female, Male, Guillain-Barr syndrome Miller Fisher syndrome The transition mechanism from Hashimoto’s to Graves’ disease is through the dominance of Th1 cells, increased effector Cinchocaine B cells, and TSAb production [2, 3]. In addition, helper T Cinchocaine cells are predominantly Th17, and this increase correlates with goiter enlargement and TSAb [2, 3]. On the other hand, Th1 and Th17 become dominant during the onset of Guillain-Barr syndrome [9]. In this case, the onset of Guillain-Barr syndrome increased Th1 and Th17, possibly leading to Hashimoto’s disease transitioning into Graves’ disease due to the production of TSAb. However, the issue of whether Graves disease is biased toward the Th1 or Th2 functional subset remains controversial [2]. As an alternative hypothesis, Graves’ disease can be triggered by viral infection [10]. It is possible that an unidentified pathogen could have caused both Guillain-Barr syndrome and Graves’ disease simultaneously. However, it is highly unlikely that a Cinchocaine viral infection triggered both Guillain-Barr syndrome and Graves’ disease concurrently. Patients with autoimmune thyroid disorders (i.e., Hashimoto’s disease and Graves’ disease) often have multiple autoimmune diseases [11]. This results from a complex interaction between genetic predisposition and environmental/endogenous factors [11]. In particular, it has been reported that multiple autoimmune diseases are more predominant in adult patients than in pediatric/adolescent patients [12]. In the current case, it is assumed that the patient had an original predisposition to Hashimoto’s disease and had endogenous factors predisposing her to Guillain-Barr syndrome, a type of autoimmune disease. In conclusion, this report presents Cinchocaine a case wherein Hashimoto’s disease changed into Graves’ disease as a result of Guillain-Barr syndrome. Although rare, Guillain-Barr syndrome can develop in patients with thyroid disease. If a patient with Hashimoto’s disease Cinchocaine develops Guillain-Barr syndrome, it may progress to Graves’ disease; thus, it is necessary to pay attention to the transition of thyroid function during the course of Guillain-Barr syndrome. Acknowledgements In diagnosing Fzd10 the pathophysiology of this case, Dr. Susumu Kusunoki, Department of Neurology, Kinki University Hospital, tested for anti-glycolipid antibodies. Abbreviations AbAntibodyTRAbAutoantibodies to the thyrotropin receptorTSAbThyroid stimulating antibodyMMTManual muscle testCSFCerebrospinal fluid Authors contributions MA managed the case and prepared and revised the manuscript. TK assisted with the preparation and revision of the manuscript. All co-authors approved the final manuscript as submitted and agreed to be accountable for all aspects of the work. All co-authors take full responsibility for the integrity of the study and the final manuscript. Funding Not applicable. Availability of data and materials All data generated or analyzed during this study are included in this published article. Declarations Ethics approval and consent to participateEthics approval was waived. As this is a case report no consent for participation is required. Consent for publicationWritten informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editor of this journal. Competing interestsThe authors declare that they have no competing interests. Footnotes Publishers note Springer nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations..