A 46-year-old female presented with recurrent and aggravated weakness, palpitation, and distending pain in the eyes for 10 days in April 2009. The patient experienced fatigue and palpitation 1 month previously. She experienced weak legs and shaking hands, and was examined twice in a local clinic. The plasma potassium level was 2.57–3.0 mM, which is less than normal physiological levels (3.5–5.5 mM). The patient was administered with a potassium supplement, and the above symptoms disappeared. Ten days before admission (April, 2009), the patient again showed weakness, palpitation, shaking hands, distending pain in the eyes, and no appetite. Diagnosis at the Endocrine Department of the clinic showed abnormal thyroid and liver functions as well as a high level of fasting blood glucose (FBG). The patient was then hospitalized for systemic examination. Inspection of her disease course revealed that after the occurrence of the above symptoms, she had polydipsia, no fever, no hyperhidrosis, no dysphoria, and no increasing food intake or rapid hungering. The patient lost 5 kg in the 15 days before admission. The patient had no history of viral hepatitis (HBV markers was negative 3 years ago), tuberculosis, high blood pressure, diabetes mellitus, or thyroid disease. In addition, there was no history of surgery, trauma, blood transfusion, or HBV carriers among her family members. Physical examination showed conscious admission, a pulse rate of 98 beats per min, and bright eyes. The exophthalmometric values of her left and right eyes were both 18 mm. There was no Stellwag’s sign, no von Graefe’s sign, no Joffroy’s sign, and no Mobiud sign. The thyroid gland was pliable and had mild swelling. There was no thyroid nodule or tenderness. Vascular bruit was negative, and there were no liver palms or spider angioma. In addition, there were no abnormalities of the heart, lung, or abdomen, and there was no swelling of the legs. Laboratory examination showed the following: HbsAg+; HBeAg+; HBcAg IgM+; HBV DNA >5.0 × 107 copies/mL; an alanine transaminase (ALT) level of 351 U/L; negative for HAV-Ab, HCV-Ab, HEV-Ab,EBV-Ab,CMV-Ab and CMV DNA; increased levels of free triiodothyronine (FT3, 18.13 pM) and free thyroxine (FT4, 39.98 pM); decreased levels of thyroid-stimulating hormone (TSH) (0.0364 mIU/L), TRAb+, and TPO Ab-; and an abnormal oral glucose tolerance test. The color Doppler flow imaging (CDFI) of the thyroid showed a swollen thyroid gland and lymph nodes of the bilateral neck, while the CDFI of the liver was normal. The patient was diagnosed acute HBV infection and Graves’ hyperthyroidism. As a middle-aged female who was TRAb positive, the patient belongs to the population with a high incidence of autoimmune diseases. In addition, because she had no history of hyperthyroidism or HBV, and both appeared at once, the incipient hyperthyroidism was considered as an extrahepatic manifestation of acute HBV infection. Therefore, the patient was not given antithyroid medicine or radioactive 131I therapy but only propranolol (10 mg, tid, po), as a symptomatic treatment, and entecavir (0.5 mg per day, os) to treat the HBV infection. The thyroid and liver functions as well as HBsAg levels were monitored. After 12 weeks of treatment, the FT3 level decreased to 3.80 pM, the FT4 level decreased to 12.23 pM, the TSH level increased to 1.4899 mIU/L, the HBV DNA level decreased to 8100 copies/mL, the ALT level was 112 U/L, the FBG level was 5.35 mM, and the postprandial blood glucose (PBG) level was 7.19 mM. At 24 weeks post-treatment, the HBV DNA level became undetectable, the HBsAg and HBeAg test results were negative, while the detection of HBeAb became positive, and that of HBsAb remained negative. In addition, the ALT level was 16 U/L, and the FBG, PBG, and thyroid functional parameters ranged within normal levels. Therefore, antiviral entacavir was stopped and the patient continued to be monitored. At 48 weeks post-treatment, HBV DNA remained undetectable, the ALT level stabilized at 17 U/L, HBsAg and HBeAg remained negative, and HBsAb became positive. In addition, the patient had normal thyroid functions. At the last follow up at 3 years post-treatment, the TSH, FBG, and ALT levels were normal and the HBsAg test was negative.