Nondiabetic Ketoacidosis Caused by Severe Hyperthyroidism

Emily T. Wood; William B. Kinlaw

Disclosures

Thyroid. 2004;14(8) 

In This Article

Case Presentation

A 41-year-old woman presented with a 6-week history of diarrhea, vomiting, palpitation and an approximately 40-pound weight loss. She denied eye problems, rash, neck pain, alcohol abuse, and family history of thyroid or other metabolic diseases. Her diarrhea had been treated with antibiotics for several weeks without improvement. At another hospital she was found to be hyperthyroid and was given propranolol. There, her symptoms accelerated after administration of iodinated contrast for a computed tomography(CT) scan. Two days after discharge, the patient presented to our hospital with continued vomiting, heat intolerance and palpitation.

On physical examination, her heart rate was 112 beats per minute, she was afebrile, and her blood pressure was 146/75mm Hg. Body mass index was 27.3. She had tremor and proximal muscle weakness. The thyroid was approximately five times normal size with a bruit. Exophthalmos and pretibial myxedema were absent. Laboratory data are summarized in Table 1 .

The patient was given propranolol 240 mg/day andpropylthiouracil 1200 mg/d that produced symptomatic improvement within 72 hours. Saturated solution of potassium iodide, 300 mg/d, was then added, and the thyroid hormone indices continued to fall (Fig. 1). She was also treated with thiamine to avoid Wernicke-Korsakoff syndrome.

Time course of treatments, thyroid hormone levels, and acidosis. FT3I indicates the free T3 index calculated by dividing the total T3 by the Tup. Black and gray lines indicate the upper limits of normal for the FT3I and anion gap, respectively. PTU, propylthiouracil; SSKI, saturated solution of potassium iodine; T3, triiodothyronine; T4, thyroxine.

Ketonuria and an elevation of the serum anion gap were noted on admission. This worsened on day 3, prompting measurement of β-hydroxybutyrate (β-OHB), which was 5.21 mmol/L (normal, 0.03–0.30). Arterial blood gas revealed pH 7.36, pCO226 mm Hg, and bicarbonate 14.5 mmol/L, reflecting a severe metabolic acidosis with respiratory compensation.

Fasting insulin and glucose levels were normal. The homeostasis model assessment of insulin resistance (HOMA-IR) was 0.659, indicating normal insulin sensitivity.[3] Serum urea nitrogen and creatinine were normal. Importantly, L-lactate concentrations were also normal, implicating ketoacids as the cause of her acidosis. The acidosis normalized as her thyroid hormone indices fell, and the patient was discharged on propylthiouracil, propranolol,and potassium iodide. A thyroidectomy was performed for cosmetic reasons several months later at another institution, and the pathology was consistent with Graves' disease.

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