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Muscle Dysfunction in Subclinical Hypothyroidism^d

CHU Brugmann and Department Erasme of Internal Medicine Brussels, Belgium

In a recent paper, Monzani et al. (1) showed that blood lactate levels increase more than normally during exercise in patients with subclinical hypothyroidism (sHT). They concluded that muscle energy metabolism is impaired in this condition. We have personal data supporting this hypothesis.

Thirteen patients (5 men, 8 women, ages 41–88 yr, mean 72.5 yr ± 14.6 SD), not admitted for thyroid disease and without any history of thyroid pathology, were recruted at admission in a general referal hospital on the basis of high blood levels of thyrotropin (TSH, ultrasensitive ICMA assay, Ciba Corning) and normal levels of free thyroid hormones (free thyroxine, FT4, and free triiodothyronine, FT3, RIA, Amerlex-Mab kit, Orange Medical). Serum creatine kinase (CK) activity (CK kit, Behring) was measured in these patients and history, physical examination, electrocardiogram, and CK isoenzyme analysis allowed us to exclude CK elevation due to heart or brain damage.

As shown in Fig. 1, CK levels were at the upper normal value or above in 6 out of the 13 patients. We observed a positive correlation between CK and TSH (r = 0.77, P < 0.01) and an inverse correlation between CK and FT4 (r = 0.55, P = 0.05), whereas the correlation between CK and FT3 (not shown) did not reach statistical significance (r = 0.28).

View larger version (18K): [in this window] [in a new window]   Figure 1. Correlation between serum creatine kinase (CK) concentrations and the circulating levels of thyrotropin (TSH) and free thyroxine (FT4). CK levels are represented on a logarithmic scale. The dotted lines indicate the range of normal values.

Monzani et al. thus demonstrated muscular abnormalities during exercise in sHT apparently related to the duration of this condition. In our cross-sectional analysis in patients at rest the statistical significance of the relationship between a biological parameter easy to measure, serum CK activity, and the degree of sHT sustains the hypothesis of muscular impairment. We agree with these authors in suggesting that sHT may require earlier treatment than previously thought.

Footnotes

Address correspondence to: Dr. I. W. Beyer, Department of Internal Medicine, CHU Brugmann, 4 place Van Gehuchten, Brussels, Belgium 1020.

Received January 14, 1998.

References

1. Monzani F, Caraccio N, Siciliano G, Manca L, Murri L, Ferrannini E. 1997 Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism. J Clin Endocrinol Metab. 82:3315–3318.[Abstract/Free Full Text]
2. Giampietro O, Clerico A, Buzzigoli G, Del Chicca MG, Boni C, Carpi A. 1984 Detection of hypothyroid myopathy by measurements of various serum muscle markers—myoglobin, creatine kinase, lactate deshydrogenase and their isoenzymes. Horm Res. 19:232–242.[Medline]
3. Burnett JR, Crooke MJ, Delahunt JW, Feek CM. 1994 Serum enzymes in hypothyroidism. N Z Med J. 107:355–356.[Medline]
4. Docherty I, Harrop JS, Hine KR, Hopton MR, Matthews HL, Taylor CJ. 1984 Myoglobin concentration, creatine kinase activity, and creatine kinase B subunit concentrations in serum during thyroid disease. Clin Chem. 30:42–45.[Abstract/Free Full Text]

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