We reported a case of thyroiditis-induced thyrotoxicosis that suddenly led to normocytic anemia within 4 weeks after the patient’s last visit to our hospital. The patient’s TSH receptor antibody was negative, his FT3/FT4 ratio was low, and the destructive findings on thyroid ultrasonography indicated painless thyroiditis. This is the first report of secondary anemia associated with painless thyroiditis. Although the levels remained within the normal range, mild leukopenia and thrombocytopenia presented at disease onset, suggesting pancytopenia due to thyrotoxicosis3. Pancytopenia completely disappeared by 12 weeks after onset, with spontaneous remission of thyrotoxicosis.
Painless thyroiditis (silent thyroiditis) is a self-limiting inflammatory disorder of the thyroid gland characterized by an early thyrotoxicosis phase caused by the release of thyroid hormones and a late hypothyroidism phase, with complete resolution in most cases [4, 6]. The pathophysiologic mechanism of painless thyroiditis is unknown, but the possibility of immune disorder involvement has been suggested [6, 7]. Painless thyroiditis generally manifests as a lymphocyte infiltration of the thyroid follicles, causing thyroid follicular cell damage. In our case, we observed a typical course of painless thyroiditis. The secondary anemia caused by thyrotoxicosis has improved, but we would like to carefully follow up on the continuation of thyroid hormone replacement therapy.
The mechanism by which anemia develops in thyrotoxicosis is not clear. Shortened erythrocyte survival or ineffective erythropoiesis have been suggested as potential causes of anemia in thyrotoxicosis [2, 3]. Moreover, mild leukopenia and thrombocytopenia were observed in our case, which could have been due to a variety of mechanisms. The involvement of autoantibodies in leukocytes and platelets has been reported . The involvement of immune processes in the onset of painless thyroiditis could help explain the pathophysiology of pancytopenia . The patient had an history of acute pancreatitis. It is interesting to assume the immune mechanisms as the pathogenesis of acute and chronic pancreatitis .
In addition to the clinical course of thyrotoxicosis and associated anemia, the present case provided interesting laboratory data. First, sIL-2R was high at onset but normalized by 16 weeks after onset of anemia. Elevated levels of sIL-2R have been reported in hyperthyroidism of Graves' disease  and thyrotoxicosis due to painless thyroiditis , and it is known that thyroid hormones directly enhance sIL-2R production in lymphocytes . Second, LDL-C and HDL-C levels decreased due to thyrotoxicosis but then normalized. Excessive thyroid hormone levels lower serum LDL-C levels via LDL receptor  and PCSK9  and lower HDL-C levels via increased CETP activity . In addition, we previously reported that increased sIL-2R cause significant decreases levels in HDL-C and LDL-C in patients with hematologic malignancies . Increased cytokines were recently reported to be associated with hypolipidemia in COVID-19 patients . Presumably, increases in levels of both thyroid hormones and sIL-2R induce the decreases in HDL-C and LDL-C. In addition, slight decreases in HDL-C and LDL-C levels were observed 4 weeks before onset, which may have preceded the anemia. Third, slight increases in liver enzyme levels and a decrease in serum albumin were observed, but these changes disappeared with normalization of thyroid function. However, the time to disappearance was several weeks behind the normalization of Hgb, LDL-C, and HDL-C. The reason for this is unknown. The duration of propranolol administration and the deterioration of liver function did not match. These data suggest that autoimmune processes in the liver could be associated with the different time courses in the normalization of cholesterol and hepatic enzyme levels .
In conclusion, we reported the case of a diabetes patient with secondary anemia resulting from thyrotoxicosis. Thyrotoxicosis was caused by painless thyroiditis, but there have been no reports of secondary anemia induced by painless thyroiditis. Changes in sIL-2R, HDL-C, LDL-C and liver function were also observed during the clinical course of thyrotoxicosis and anemia.