Proton-pump inhibitors (PPIs) impair tablet levothyroxine (LT4) intestinal absorption by increasing the gastric pH and decreasing LT4 dissolution in the stomach. The purpose of this study was to verify whether a liquid formulation of LT4 would correct LT4 malabsorption induced by PPIs. This was a prospective observational cohort study. The study was conducted from 2012 to 2013, and the mean duration of the follow-up was 23.7 ± 11.9 weeks. The study was conducted in a tertiary university hospital outpatients clinic. Upon informed consent, we recruited 24 consecutive adult patients (18 women and 6 men), who took LT4 for replacement (n = 14) or suppressive purposes (n = 10) and who had absorption of tablet LT4 impaired by PPIs. The 24 patients were switched from the tablet to the oral solution LT4 at the same daily dose. Significantly lower mean TSH levels were seen with the oral solution than with the tablet as were significantly greater rates of serum TSH less than or equal to the specified cutoff values (replacement [REP] group) or ≤ 0.10 mU/L (suppressive [SUP] group) with the oral solution than with the tablet. Serum TSH was lower with the oral solution than with the tablet formulation (REP group, 1.7 ± 1.0 mU/L vs 5.4 ± 4.3, P < .0001; SUP group, 0.1 ± 0.3 mU/L vs 2.1 ± 2.7, P < .0001). In the REP group, the rate of TSH values of ≤ 4.12 or ≤ 2.5 mU/L was 29 of 30 (96.7%) or 24 of 30 (80.0%) postswitch but only 17 of 36 (47.2%) or 9 of 36 (25.0%) preswitch (P < .0001). In the SUP group, the rate of serum TSH values of ≤ 0.10 mU/L was 26 of 35 (74.3%) postswitch but 0 of 22 (0%) preswitch (P < .0001). These data demonstrate the continued absorption of liquid LT4 despite the increased gastric pH due to PPI therapy.

Levothyroxine (l-T4) is the mainstay of treating hypothyroidism. The tablet is the traditional formulation of l-T4. Tablet l-T4 malabsorption results from either hindered gastric dissolution of the tablet or binding of l-T4 by sequestrants in the intestinal lumen. This review provides an overview of the pharmacokinetics of l-T4 formulations available in the market: the tablet, the soft gel capsule and the oral solution. We review literature on the new formulations and anticipate the areas of future research. Failure of l-T4 treatment to reach target serum thyroid-stimulating hormone levels generally prompts the physicians to increase l-T4 daily dose. In vitro studies have shown that the soft gel capsule releases the active ingredient more consistently at varying pH than the tablet. In addition, in vivo studies have confirmed the in vitro data and have demonstrated that both the soft gel capsule and the liquid formulation are capable to solve tablet l-T4 malabsorption caused by certain drugs, bariatric surgery or coffee. These new formulations may be attractive also for patients who cannot/do not want to change their (improper) habits of l-T4 ingestion. Finally, the oral solution l-T4 could be suitable for patients who cannot swallow the solid formulations.

Thyroid hormones act on testis in multiple ways and exert their effect on different cell types, including Leydig and Sertoli cells, and germ cells. An excess or deficit of thyroid hormones results in alterations of testis function, including semen abnormalities. More frequently, hyperthyroidism has been associated with reduced semen volume and reduced sperm density, motility, and morphology, whereas hypothyroidism is associated with reduced sperm morphology. Therefore, thyroid function tests should be part of the diagnostic workup of the infertile man. This article is aimed at (1) elucidating how hyperthyroidism and hypothyroidism lead to a reduction in semen quality, briefly reviewing the current literature on murine models and humans, and (2) pinpointing the limitations of the studies carried out so far and identifying new perspectives for future research.

The number of thyroid cancers is increasing. Standard treatment usually includes primary surgery, thyroid-stimulating hormone suppressive therapy, and ablation of the thyroid remnant with radioactive iodine (RAI). Despite the generally good prognosis of thyroid carcinoma, about 5% of patients will develop metastatic disease, which fails to respond to RAI, exhibiting a more aggressive behavior. The lack of specific, effective and well-tolerated drugs, the scarcity of data about the association of multi-targeting drugs, and the limited role of radioiodine for dedifferentiated thyroid cancer, call for further efforts in the field of new drugs development. Rearranged during transfection (RET)/papillary thyroid carcinoma gene rearrangements, BRAF (B-RAF proto-oncogene, serine/threonine kinase) gene mutations, RAS (rat sarcoma) mutations, and vascular endothelial growth factor receptor 2 angiogenesis pathways are some of the known pathways playing a crucial role in the development of thyroid cancer. Targeted novel compounds have been demonstrated to induce clinical responses and stabilization of disease. Sorafenib has been approved for differentiated thyroid cancer refractory to RAI.