Health & Medicine

In this case abdominal pain did not ring a bell. Still, I told Roger I’d double-check. The chapter on hyperthyroidism in Harrison’s Principles of Internal Medicine lists a table of symptoms. I scanned it twice: No abdominal pain.

We returned to Kim’s bedside.

“And your periods have been regular?” I asked.

“Yes, doctor,” she replied.

“Do you ever get nervous, shaky?”

“Well, I worry about this pain.”

“Can you hold out your hands for me?”

She held them out like a diver on a board: No tremor. I gently propped up her right knee and tapped on the patellar tendon with my middle finger. The lower leg jerked, but it wasn’t a bounce-off-the-ceiling hyperthyroid reflex.

I felt her belly one more time: soft. I told Roger there was no need for a CT scan.

I told Kim, “You’re going to be OK.” She gave me a relieved smile and spared me the embarrassing question: Then why does my stomach hurt on and off?

Two hours later, I saw Roger preparing to discharge her. A sheepish grin played on his face.

“You were right,” he said. “The CT scan I took was negative.”

“Did you do the thyroid tests?”

“A thyroid problem seems like a stretch,” he said.

“But the tachycardia . . .”

“I sent ’em, I sent ’em,” he said, laughing. “They just take two days.”

Worldwide, the bulk of thyroid disease arises from iodine deficiency. The thyroid gland needs iodine to make its hormone, and if the diet is iodine-poor, the thyroid gland must work harder to produce an ever-dwindling amount of hormone. In the process, the gland often balloons into an unsightly neck mass called a goiter. Nowadays, with iodine in common table salt, the vast majority of cases in the United States arise from a mysterious cause: autoimmunity in the form of antibodies that attack home turf. One type of autoantibody mimics the pituitary hormone that stimulates the thyroid, hoodwinking it—despite the pituitary’s shutting off its own secretion of thyroid-stimulating hormone—into massive overproduction. The result is Graves’ disease, the most common form of hyperthyroidism, best known for the eye-bulging look it confers as a result of the antibodies stimulating connective-tissue cells behind the eyes. Another type of autoantibody can attack the thyroid itself, destroying the gland. So women—who are much more prone than men to autoimmune disorders—are 5 to 10 times more likely to suffer from various thyroid diseases.

Confusing as the clinical picture is, laboratory diagnosis has become a snap, thanks to sensitive new tests of the pituitary’s thyroid-stimulating hormone, or TSH: A low TSH means the pituitary is trying to rein in a runaway thyroid; high TSH equals hypothyroidism. Some experts even advocate routine screening of such high-risk groups as postmenopausal women. The mainstay of treatment for hyperthyroidism is radioactive iodine, which homes in on the gland and prunes it back; for hypothyroidism, a once-a-day supplement of thyroid hormone usually does the trick.

Two days later, I cornered Roger.

“Well?” I asked.

“TSH practically zero. The T4 was 26,” Roger said, meaning that Kim’s thyroid hormone was twice the normal level. He shook his head and muttered, “Remarkable.”

In 1931 the physician J. R. Verbrycke reported on 34 cases of “gastrointestinal hyperthyroidism” that he had diagnosed over three years. He admitted becoming clued in only after someone in his family had it, and he cringed at the misdiagnoses he might have committed up to that point.

I surveyed half a dozen medical textbooks. Some do mention abdominal pain as a possible symptom of hyperthyroidism. Those that don’t, keeping excellent company with two emergency doctors of my acquaintance, prove again the old adage “The only thing new is the history you don’t know yet.”

Three months later, I called Kim to ask how the treatment for Graves’ disease was going. Fine, she told me.

And the belly pain? “All gone, doctor.”