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Remember the hormones
Dementia can form a vicious cycle with several endocrine conditions.
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A 74-year-old wom-an comes in for an initial consultation, and is accompanied by her daughter. She has received a referral from her geriatrician because of worsening dementia.
The patient has a history of thyroidectomy and radioactive iodine ablation in her 20s for thyroid cancer; there has been no recurrence since, and she has not seen an endocrinologist in years. In addition to postsurgical hypothyroidism, she also has a history of vitamin D deficiency, impaired memory and arthritis. Surgical history is notable for total knee arthroplasty, appendectomy, hysterectomy and cataract removal.
On review of symptoms, she reports fatigue, cold intolerance and feeling “slow,” and denies palpitations, heat intolerance, weight change, nervousness, jitteriness, labile mood, hair loss, gastrointestinal symptoms or hoarseness. The daughter is concerned about her mother’s impaired memory.
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She does not come with a medication list but reports adherence to the prescribed medical regimen of levothyroxine 50 mcg daily, conjugated estrogens 0.625 mg daily, and vitamin D and calcium; she denies drug allergies. Family history is positive for acquired hypothyroidism. The patient, a widow who lives alone but within driving distance from her daughter, does not smoke and has one drink per day. She is a retired typist.
The patient is barely participatory in the conversation and appears absent and withdrawn. Most history is submitted by the daughter, who then coaxes her mother to either agree or disagree.
On exam, her blood pressure is 140/90 mm Hg, pulse 96, weight 123 lb, BMI 21. The patient has a scar after thyroidectomy and no palpable thyroid tissue. She has normal judgment and insight, appears oriented to time and person but is not completely oriented to place. Physical exam is otherwise unremarkable.
Labs from three months ago show a mildly elevated calcium of 10.5 mg/dL (upper limit of normal at that lab = 10.3 mg/dL) but no albumin. Creatinine was elevated at 1.5 mg/dL.
Patient and daughter leave the practice, and labs come back later that night: calcium 12.8 mg/dL; albumin 4.5 g/dL; creatinine 2.2 mg/dL; parathyroid hormone ≤ 3 pg/mL.
What is the next best step?
A. Call the patient’s daughter and convene a family meeting with an oncologist and an estate lawyer because the most likely cause of hypercalcemia in this patient is advanced malignancy.
B. Send the patient a letter and advise her to drink more water.
C. Call the lab to add on a vitamin D 25(OH) level, then call the patient at home and ask her to read every label of every medication she is taking.
D. Start paroxetine for depression.
E. Emergently refer the patient for hemodialysis.
Case Discussion:
This is a mildly disoriented elderly woman with a history of postsurgical hypothyroidism and an old lab report with mild hypercalcemia. We frequently find incidental parathyroid adenomas because older patients have a mildly elevated calcium level on routine chemistry. Hypercalcemia would be one explanation of the patient’s affect and poor memory, not clinical depression (D).
I was surprised by the extent of her hypercalcemia, renal impairment and unmeasurable PTH. Although the creatinine was not helping matters, I felt that increased fluid intake, especially if delayed by a week or so after sending out a letter (B), would not address the actual cause of the symptoms. However, this was a condition that had been building up for at least three months, and there was no need for an emergent lowering of calcium levels by dialysis (E).
Because primary hyperparathyroidism was ruled out by the low PTH, one has to assume that common things are common, and in elderly patients this means hypercalcemia of malignancy. I am all for establishing advanced directives and initiating timely care, but before we divide the patient’s estate and start a tumor search, more banal reasons of hypercalcemia should be considered.
One is vitamin D intoxication. When I called the patient that night, she read me all of her medications. In addition to calcium carbonate 667 mg twice daily, she was taking vitamin D2, 50,000 units daily. I immediately instructed her to stop taking vitamin D and calcium, then called the patient’s daughter and asked her to remove the pill bottles from the household so that the mother would not accidentally take them.
Her vitamin D 25(OH) level came back elevated at 119 ng/mL a few days later. As a fat-soluble compound, vitamin D is stored and was therefore still high at 98 ng/mL one month later, when the patient returned. Her calcium was still high-normal, at 10.6 mg/dL, but she was much more engaged in the conversation, no longer appeared depressed and had a much better memory.
Ronald Tamler, MD, PhD, MBA, is Assistant Professor in the Division of Endocrinology at Mount Sinai School of Medicine, N.Y.