Suppressive Effects of Minocycline on the Pituitary-Thyroid Axis in Humans

Abstract

Minocycline has been thought to induce "black thyroid," a condition marked by discoloration due to brown deposits. However, its effect on thyroid function in humans is still obscure. We conducted a prospective study of thyroid hormone levels in 17 patients who were administered 200mg minocycline daily for 10 days. We found that minocycline significantly reduced the serum total thyroxine level (8.43 ± 0.61 to 7.09 ± 0.45μg/dl, mean ± SEM; <i>P</i><0.01), and free thyroxine level (1.12 ± 0.10 to 1.01 ± 0.08ng/dl, mean ± SEM; <i>P</i><0.01). There was also a slight, but insignificant, elevation of thyroid stimulating hormone (TSH) in patients treated with minocycline. Similar suppression of thyroxine and free thyroxine was not observed in control patients treated with β-lactam and/or aminoglycoside antibiotics. Risk factors for the reduction in these thyroxine levels included age and a high serum baseline level of free thyroxine. We found a significant correlation between the free baseline thyroxine level and a reduction in free thyroxine after minocycline administration (Y=0.420X-0.377, r=0.597; <i>P</i><0.01). Despite the observed alterations, the serum levels of all thyroid hormones after minocyctine therapy were still within the normal range. This antibiotic does not appear to induce clinical hypothyroidism, yet given the results of this study, we would like to recommend pituitary-thyroid axis monitoring during the use of this antibiotic.