Erythrocyte carbonic anhydrase-I concentrations in patients with graves-disease and subacute thyroiditis reflect integrated thyroid-hormone levels over the previous few months
Abstract
We have recently reported that in patients with hyperthyroidism, red blood cell (RBC) zinc (Zn), most of which is present as the metal of carbonic anhydrase-I isozyme (CAI), reflects a patient's integrated thyroid hormone level over the previous few months. In the present report the RBC CAI concentration was measured by RIA in 26 healthy controls, 25 patients with hyperthyroid Graves' disease, 5 patients with primary hypothyroidism, and 10 subjects with subacute thyroiditis with elevated thyroid hormone levels. The mean (+/- SD) RBC CAI concentration in euthyroid controls was 380 +/- 70 nmol/g hemoglobin (Hb), and the normal range defined as the mean +/- 2 SD, was 240-520 nmol/g Hb. The mean RBC CAI in Graves' disease was decreased (180 +/- 53 nmol/g Hb), and 22 patients (88%) had subnormal values. The mean RBC CAI concentrations in hypothyroidism and subacute thyroiditis were not different from the control values. After treatment with antithyroid drugs, both mean the plasma T4 and T3 levels in 11 Graves' patients became normal within 4 weeks, but the normalization of RBC CAI lagged behind by about 2 months. Furthermore, the highest correlation was observed between the RBC CAI and plasma T4 and T3 levels measured 8 weeks earlier. During prednisolone therapy the RBC CAI in patients with subacute thyroiditis remained at a normal level. These results suggest that 1) not only RBC Zn but also the RBC CAI concentration in patients with Graves' disease reflect the patient's mean thyroid hormone level over the preceding several months; and 2) in patients with subacute thyroiditis, elevation of plasma thyroid hormone concentrations is transient and causes little change in the RBC CAI concentration.
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A concentration of 400 nmol/g Hb of erythrocytic CA would be about 40 μM CA in blood.
“A concentration of 400 nmol/g Hb [107] of erythrocytic CA would be about 40 μM CA in blood.”
From Mechanisms of nitrite bioactivation (2014) · cites this paper as [107]
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References 9 · Cited by 12
- Authors
- KISO, Y., YOSHIDA, K., KAISE, K., KAISE, N., FUKAZAWA, H., MORI, K., ABE, K., & YOSHINAGA, K.
- Affiliations
- Tohoku University (JP)
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 1991-02
- Volume
- 72
- Issue
- 2
- Pages
- 515-518
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2107234873
- Cited by
- 12
- References
- 9
- Citations by year
- 2021: 1 · 2013: 1
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Pathology and Forensic Medicine › Ophthalmology and Eye Disorders
- Keywords
- Graves' disease, subacute thyroiditis, hyperthyroidism, thyroid hormone levels, antithyroid drug therapy, prednisolone therapy
- MeSH terms
- Adolescent, Adult, Aged, Carbonic Anhydrases, Erythrocytes, Graves Disease, Humans, Middle Aged, Prednisolone, Thyroiditis, Subacute, Thyroxine, Triiodothyronine
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