A 30-year-old woman comes to the office due to tingling and numbness in both of her distal lower extremities for the last 3 months. Her symptoms are gradually worsening. She also has had intense fatigue. She has not had any weight change, constipation, skin dryness, headaches, or visual changes. The patient was diagnosed with primary hypothyroidism secondary to Hashimoto thyroiditis when she was 10 years old. She is currently on 100 mcg per day of levothyroxine orally. Her mother also has hypothyroidism. The patient does not use tobacco, alcohol, or recreational drugs. Her menstrual cycles have been irregular for the last 6 months. Her last menstrual period was 2 months ago. She is sexually active with one partner. Blood pressure is 114/78 mm Hg and pulse is 72/min. She weighs 69 kg (152 lbs) and is 163 cm (5'4") tall. Her thyroid is nonpalpable. Her mucous membranes are moist and pale. Her tongue appears to be bald. She does not have any scleral icterus. Vibration and proprioception are decreased in both of her lower extremities distally. Pain and temperature sensations appear normal. Her ankle jerks are absent, but other reflexes are brisk. Babinski is present, and Romberg signs is positive. The rest of the physical examination is unremarkable. Stool obtained from the rectal examination is negative for occult blood. Laboratory results reveal a hemoglobin of 8 g/dL and hematocrit of 24%. Her total leukocyte count is 3,200/mm³. Her platelet count is 300,000/mm³. Basic serum chemistries are within normal limits. Her total T4 level is 8.2 mcg/dL (normal 4-12 mcg/dL) and TSH level is 2.4 micro IU/mL.
What is the next best step in the management of this patient?

Question

Quizplus · Accepted Answer

Explanation: The patient's primary hypothyroidism predisposed her to other autoimmune disorders such as pernicious anemia. Involvement of the posterior column (loss of proprioception), lateral column (brisk reflexes), and peripheral nerves (loss of ankle jerks) indicate neurologic involvement due to vitamin B12 deficiency, which resulted from atrophic gastritis (pernicious anemia). Dietary vitamin B12 binds to intrinsic factor secreted by the parietal cells in the gastric mucosa. The intrinsic factor-vitamin B12 complex is then carried to the terminal ileum for receptor-mediated absorption. Pernicious anemia results from the autoimmune destruction of parietal cells, leading to achlorhydria and decreased production of the intrinsic factor. The lack of intrinsic factor leads to vitamin B12 deficiency. The red blood cells are macrocytic due to ineffective erythropoiesis due to defective nucleic acid synthesis. Neurologic involvement is characterized by involvement of posterior and lateral columns in the spinal cord ("subacute combined degeneration") and leads to ataxia, loss of proprioceptive, and vibratory sensations. Severe spasticity, weakness, and peripheral nerve involvement can occur. Symptoms and signs are more prominent in the lower than the upper extremities. (Choice A) Increasing the levothyroxine dose is not the appropriate choice for this patient because her thyroid function tests are within normal limits. The fatigue in this patient is most likely due to anemia. (Choice B) Although neurologic involvement can indicate cord compression, the history and other features of this patient suggest otherwise; therefore, MRI is unnecessary. (Choice C) Endocrinopathy with polyneuropathy can be seen with POEMS(polyneuropathy, organomegaly, endocrinopathy, M-proteins and skin changes) syndrome. SPEP is done to look for an M-spike. This patient does not have organomegaly or skin changes. (Choice E) Folate levels may be obtained to determine the cause of macrocytic anemia; however, the patient's history of autoimmune hypothyroidism and characteristic neurological picture is more suggestive of vitamin B12 deficiency. Educational objective: Patients with primary hypothyroidism are predisposed to get other autoimmune diseases such as pernicious anemia. Vitamin B12 deficiency in pernicious anemia is due to a deficiency of intrinsic factor secreted by the stomach. Neurologic involvement in Vitamin B12 deficiency is characterized by subacute combined degeneration of the spinal cord and peripheral neuropathy.

A 30-Year-Old Woman Comes to the Office Due to Tingling