Case Report: Myxedema Coma Caused by Immunoglobulin A Vasculitis in a Patient With Severe Hypothyroidism

Abstract

Myxedema coma is a critical disorder with high mortality rates. Disruption of the compensatory mechanism for severe and long-term hypothyroidism by various causes leads to critical conditions, including hypothermia, respiratory failure, circulatory failure, and central nervous system dysfunction. Infectious diseases, stroke, myocardial infarction, sedative drugs, and cold exposure are considered the main triggers for myxedema coma. A 59-year-old Japanese woman presented with bilateral painful purpura on her lower legs. She was diagnosed with coexisting immunoglobulin A (IgA) vasculitis and severe IgA vasculitis with nephritis and was consequently treated with intravenous methylprednisolone (125 mg/day). However, she rapidly developed multiple organ failure due to the exacerbation of severe hypothyroidism, i.e., myxedema. Her condition improved significantly following oral administration of prednisolone along with thyroxine. There was a delayed increase in the serum free triiodothyronine level, while the serum free thyroxine level was quickly restored to normal. Rapid deterioration of the patient's condition after admission led us to diagnose her as having myxedema coma triggered by IgA vasculitis. Hence, clinicians should be aware of the risks of dynamic exacerbations in patients with hypothyroidism. Furthermore, our study suggested that combination therapy with thyroxine and liothyronine might prove effective for patients with myxedema coma, especially for those who require high-dose glucocorticoid administration.

Keywords: Hashimoto’s thyroiditis; IgA vasculitis; glucocorticoid; levothyroxine; liothyronine; myxedema coma.

Figure 1

Images of the lower legs, chest X-ray, chest computed tomography, electrocardiogram, and echocardiogram. (A) Purpura and edema on both lower legs. (B) Chest X-ray on admission showed mild pulmonary congestion. (C) No abnormalities were found on the electrocardiogram at the time of admission. (D) Chest computed tomography showed atelectasis and mild pulmonary congestion. (E) Thyroid echo showed diffuse atrophy of the thyroid gland, irregular surface, and rough and low echo levels inside the thyroid gland. The thickness of the isthmus is 2.6 mm in diameter, which is indicated as broken line 1.

Figure 2

Clinical course after admission. Physical findings: body temperature (closed circles with solid lines), systolic blood pressure (closed triangles with solid lines), and heart rate (square with broken lines) [lower]; laboratory findings: serum albumin (closed triangles with solid lines), proteinuria (square with broken lines), and TSH levels (closed circles with solid lines) [middle]; and the contents of medication therapies [upper] are presented.

Figure 3

Progress of FT3 and FT4 during hospitalization. Time course of serum FT4 and FT3 levels are shown. Serum FT4 and FT3 levels are denoted by closed triangles and circles, respectively. FT4 levels increased and reached above the normal range following levothyroxine administration after 20th day. However, FT3 levels did not increase sufficiently. The shadows represent the normal ranges of serum free T4 and free T3 levels.