Abstract

Background Patients with thyroid disease have a high prevalence of iron-deficiency, but this is often times overlooked in the medical community. Treating a patient’s iron levels may be all that is needed to reverse his or her thyroid condition. Iodine is one of the main components of thyroid hormones; however, iodine requires iron in order for it to be fully utilized. Iron is an element that is essential for the human body to synthesize and metabolize the thyroid hormones. The body is dependent upon iron to convert thyroxine (T4) into the active hormone triiodothyronine (T3) via thyroid peroxidase (TPO). As such, low iron levels can impede thyroid function and patients can present with hypothyroid-like symptoms. Clinical Case A 50-year old female with no significant past medical history presented to our facility with chief complaints of fatigue and dizziness. She was referred by her PCP to our ED for anemia after her labs drawn the day prior were remarkable for a hemoglobin of 4.5 g/dL (n=12-16 g/dL). In the ED, her workup was remarkable for a hemoglobin of 4.9 g/dL and a TSH of 870.44 mIU/L and 719.84 mIU/L on re-check (n=0.36-3.74 mIU/L). Therefore, she was admitted for iron-deficiency anemia (IDA) and hypothyroidism. Her free T4 was undetectable at <0.40 ng/dL (n=0.76-1.46 ng/dL), her free T3 was low at 1.0 pg/mL (n=2.3-4.2 pg/mL), her total T4 was undetectable at <3.0 ug/dL (n=4.8-11.7 ug/dL), and total T3 was low at 0.27 pg/mL (n=0.60-1.81 pg/mL). Patient was given 2 units pRBC and her hemoglobin improved to 8.7 g/dL. She had an iron panel drawn which showed decreased iron at 13 ug/dL (n=39-150 ug/dL), elevated TIBC at 680 ug/dL (n=241-421 ug/dL), elevated transferrin at 450 mg/dL (n=200-360 mg/dL), decreased transferrin saturation at 2% (n=15-50%), and decreased ferritin at 2 ng/mL (n=8-252 ng/mL). Patient was given a one-time dose of IV iron sucrose 200 mg as well as two injections of levothyroxine (100 mcg and 50 mcg, respectively) in the hospital. Pt was also given IV hydrocortisone 100 mg every 8 hours for 2 days. Patient was discharged from the hospital in a stable fashion on PO levothyroxine 125 mcg daily and PO hydrocortisone 20 mg in AM and 10 mg in PM. She was also started on ferrous sulfate 142 mg daily extended-release tablets. Patient followed-up with an endocrinologist as an outpatient, and she was encouraged to continue taking PO levothyroxine 125 mcg daily. Her last TSH was 0.28 mIU/L (n=0.36-3.74 mIU/L) and she now reports feeling well. Conclusion The etiology for patient’s hypothyroidism was due to iron-deficiency anemia. Upon further questioning, patient stated she was diagnosed with IDA at age 17 secondary to heavy menstrual periods; however, she did not take iron supplements. Patient reported her last menstrual period to be in May 2018. In conclusion, it is always imperative to consider iron-deficiency as an etiology for hypothyroidism.

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