The clinical utility of free thyroxine in oral levothyroxine absorption testing.

OBJECTIVE: Original absorption studies for levothyroxine (LT4) were validated using total thyroxine (TT4) measurements. Free thyroxine (FT4) has largely supplanted TT4 in clinical practice. The objective of our study was to assess the clinical utility of FT4 in oral LT4 absorption testing. METHODS: In this retrospective electronic health record analysis, we recorded data of patients who underwent LT4 oral absorption testing between November 2010 and January 2012 because of persistent hypothyroidism despite a greater than anticipated weight-based dose of LT4. Patients included had primary hypothyroidism and an absorption test with assessment of both TT4 and FT4 measured at times 0, 30, 60, 90, 120, 180, 240, 300, and 360 minutes. The test was conducted with 1 mg (five 200-µg tablets) of Synthroid® after an overnight fast by a standard nonisotopic method. RESULTS: A total of 10 patients (3 men/7 women) underwent absorption testing. Prior to testing, the median daily LT4 dose was 250 µg (range, 150 to 350 µg). Three patients were also on liothyronine (10, 20, or 50 µg daily). Based on the calculated amount absorbed, 1 patient demonstrated subnormal absorption, and 9 patients were normal. Median body mass index was 33 kg/m2 (range, 21 to 50 kg/m2). Median calculated absorption was 105% (range, 3.7 to 195.6%). The correlation comparing FT4 and TT4 was 0.88 (95% confidence interval, 0.56 to 0.97; P<.001), a significant correlation. CONCLUSION: FT4 and TT4 correlated highly, even in patients who were severely hypothyroid; FT4 may be used interchangeably with TT4 as a qualitative assessment of suspected malabsorption using an oral LT4 absorption test.

Is chronic nipple piercing associated with hyperprolactinemia?

Literature on hyperprolactinemia in the setting of a nipple piercing is limited to individuals with concomitant breast/chest wall infection. It is unclear if chronic nipple stimulation from a piercing alone can cause sustained elevations of serum prolactin. Nipple piercing is emerging as a more mainstream societal form of body art, and the answer to this clinical question would potentially alter patient management. Our aim was to assess serum prolactin levels in subjects with nipple piercing. Inclusion criteria were as follows: men and women ≥ 18 years old with nipple piercing(s) present > 6 months. Exclusion criteria included: women who are pregnant, lactating or < 6 months postpartum; subjects on medications known to increase prolactin levels; chest wall/breast infection at the time of phlebotomy or conditions known to be associated with hyperprolactinemia. Three men and eight women were enrolled. Median (range) ages for men and women were 33 (24-42) and 27 years (23-42), respectively. All except one subject had bilateral piercings. The median interval from nipple piercing to blood draw was 4.0 (2.0-12.0) years. None of the subjects had hyperprolactinemia. Median (range) prolactin levels for men and women were 5.6 ng/mL (3.8-7.4) and 8.0 ng/mL (2.8-10.9), respectively. Our results suggest that in the absence of any concomitant infection, chronic nipple piercing is not associated with hyperprolactinemia.

Epiphora after radioactive iodine ablation for thyroid cancer.

BACKGROUND: Epiphora is a condition in which an overflow of tears occurs because of excessive lacrimal secretion or insufficient drainage of tears due to obstruction of the nasolacrimal system. This ophthalmic complication can be an intermediate to late sequela of radioactive iodine ((131)I) therapy in thyroid cancer patients. PATIENT FINDINGS: We present a case of a 23-year-old woman with complaints of bilateral excessive tearing 6 months after (131)I therapy for well-differentiated thyroid cancer. She was diagnosed with epiphora secondary to nasolacrimal duct obstruction (NDO) and had bilateral endoscopic dacryocystorhinostomy, which resulted in complete resolution of her symptoms. SUMMARY: The sodium iodide symporter, present in cells of the lacrimal drainage system, is the potential mechanism by which (131)I therapy can cause inflammation, fibrosis, and ultimate obstruction of tear outflow. Risk factors such as (131)I dose, female sex, older age, and anatomical variations may also play a role in the obstruction. However, the precise pathophysiologic mechanisms remain incompletely understood. CONCLUSIONS: NDO is an under-recognized complication of (131)I therapy in thyroid cancer patients. Questions regarding eye symptoms should be an integral part of clinical follow-up in management of such patients so that effective intervention may be performed.

Heart failure in hypophosphatemic rickets: complications from high-dose phosphate therapy.

OBJECTIVE: To report a rare case of hypophosphatemic rickets (HR) leading to extensive cardiac complications. METHODS: We present the clinical course and autopsy findings of a patient with HR, treated with chronic phosphate-only therapy as a child, who subsequently developed tertiary hyperparathyroidism leading to extensive cardiac calcifications and complications. We also review the literature on the pathophysiology of calcifications from HR. RESULTS: A 34-year-old man was diagnosed with HR at 4 years of age after presenting with growth delay and leg bowing. Family history was negative for the disease. He was initiated on high-dose phosphate therapy (2-6 g of elemental phosphorus/day) with sporadic calcitriol use between 4-18 years of age. For 6 years he received phosphate-only therapy. Subsequently, he developed nephrocalcinosis, heart valve calcifications, severe calcific coronary artery disease, heart block, and congestive heart failure. At a young age, he required an aortic valve replacement and a biventricular pacemaker that was subsequently upgraded to an implantable cardioverter defibrillator. Autopsy showed extensive endocardial, myocardial, and coronary artery calcifications. CONCLUSION: Cardiac calcification is a known sequela of tertiary hyperparathyroidism when it occurs in patients with renal failure, but it is rarely seen in HR due to high phosphate therapy. Phosphate alone should never be used to treat HR; high doses, even with calcitriol, should be avoided. It is important to be cognizant of high-dose phosphate effects and to consider parathyroidectomy for autonomous function, if needed. This case emphasizes the importance of appropriate therapy, monitoring, and management of patients with HR.

Hypothyroidism as a cause of hyponatremia: fact or fiction?

OBJECTIVE: To illustrate that severe primary hypothyroidism alone may not be enough to cause hyponatremia in the otherwise healthy ambulatory patient. METHODS: A retrospective chart review was conducted using an academic health center enterprise-wide electronic health record to identify 10 patients with primary hypothyroidism and same-day serum thyroid-stimulating hormone (TSH), sodium, creatinine, and calculated glomerular filtration rate (GFR). Same-day free triiodothyronine or free thyroxine was also recorded if tested. Patients were included in our case series if they met the following inclusion criteria: TSH level >100 µU/mL and same-day sodium and creatinine levels. All laboratory tests were collected on an outpatient basis. RESULTS: The 10 subjects (2 men and 8 women) were ages 19 to 97 years (median, 51.5 years). Median TSH was 193 µU/mL (range, 104.2 to 515.6 µU/mL; normal, 0.40 to 5.50 µU/mL) with median sodium of 138 mmol/L (range, 136 to 142 mmol/L; normal, 135 to 146 mmol/L). The lowest sodium was 136 mmol/L with concurrent TSH of 469.7 µU/mL, free triiodothyronine of 1.0 pg/mL (normal, 1.8 to 4.6 pg/mL), and free thyroxine of 0.2 ng/dL (normal, 0.7 to 1.8 ng/dL). Median GFR was 67.5 mL/min/1.73 m2 (range, 44 to 114 mL/min/1.73 m2; normal, 90 to 120 mL/min/1.73 m2). CONCLUSION: In our small series of patients with extreme TSH elevations, none had a serum sodium level below normal (<135 mmol/L), even in the presence of a reduced GFR. Hyponatremia can be a common occurrence in hospitalized and/or chronically ill patients; however, in an otherwise relatively healthy ambulatory patient, hypothyroidism, even when severely undertreated, may be a less clinically relevant cause of hyponatremia.