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Reversible Alteration of Red Cell Lithium-Sodium Countertransport in Patients with Thyroid Disease^*

GREGORY A. BRENT, MITZY CANESSA and ROBERT G. DLUHY

Endocrine-Hypertension Unit, Brigham and Women’s Hospital Boston, Massachusetts 02115

Address all correspondences and requests for reprints to: Dr. Gregory A. Brent, Thyroid Unit, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.

Thyroid hormones may alter red blood cell (RBC) sodium content and transport. The functional importance of lithium-sodium (Li-Na) countertransport in regulating sodium (Na) transport in vascular smooth muscle and kidney by Na-H countertransport and the potential effect of thyroid hormone on these processes led us to study Li-Na countertransport and other sodium transporters in RBCs of patients with thyroid dysfunction.

Patients with untreated hypothyroidism (10) and hyperthyroidism (10) were studied, along with normal subjects (10). The mean value for Li-Na countertransport was significantly higher in the hypothyroid group [0.46 ± 0.08 (±SE) mmol/L cell-h; P < 0.05] and lower in the hyperthyroid group (0.15 ± 0.04 mmol/ L cell · h; P < 0.05) compared to that in the normal subjects (0.25 ± 0.03 mmol/L cell·h). When all groups were combined, significant negative correlations were found between Li-Na countertransport and serum T₄ (r = –0.48; P < 0.01), free T₄ index (r = –0.42; P < 0.05), and serum T₃ (r = –0.38; P < 0.05). Li-Na countertransport was positively correlated with serum triglyceride (r = 0.57; P < 0.01), but not with serum cholesterol levels (r = 0.28; P = NS). The values became normal in subsets of the hypothyroid (n = 5) and hyperthyroid groups (n = 5) during treatment.

We found a bidirectional effect of thyroid status on RBC Li-Na countertransport, which was reversible when serum thyroid hormone levels became normal. Changes in Li-Na countertransport, a pathway of Na-H exchange, may influence renal sodium handling and vascular tone in patients with thyroid disease and contribute to abnormalities such as hypertension that occur in patients with hypothyroidism.

^* This work was performed at the Clinical Research Center at Brigham and Women’s Hospital (Boston, MA), and data were organized and analyzed using the Clinfo data management and analysis system at Brigham and Women’s Hospital, Boston, MA. Clinfo and the Clinical Research Center are supported by GCRC Grant MOI-RR-02635-05. Additional support was provided by NIH Grant SCOR 5P50-36568.

Supported by NIH Institutional Physician-Scientist Program Award 5K12-AM 01401.

Received June 29, 1988.

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