Levothyroxine Therapy in Gastric Malabsorptive Disorders

Abstract

Oral levothyroxine sodium is absorbed in the small intestine, mainly in the jejunum and the ileum being lower the absorption rate at duodenal level. The time interval between the ingestion of oral thyroxine and its appearance in the plasma renders unlike a gastric absorption of the hormone. However, several evidence confirm the key role of the stomach as a prerequisite for an efficient absorption of oral levothyroxine. In the stomach, in fact, occur key steps leading to the dissolution of thyroxine from the solid form, the process bringing the active ingredient from the pharmaceutical preparation to the aqueous solution. In particular, gastric juice pH, volume, viscosity, as well as gastric emptying time seem to be the most important limiting factors. These hypotheses are confirmed by the detection of an increased need for levothyroxine in patients with Helicobacter pylori infection, chronic atrophic gastritis, gastroparesis, or in simultaneous treatment with drugs interfering with gastric acidic output. The aim of the present article is to focus on the knowledge of pathophysiologic events that determine the absorptive fate of traditional (tablet) and alternative thyroxine preparations (softgel capsule and liquid solution) in patients bearing gastric disorders.

Keywords: Helicobacter pylori; gastritis; hypothyroidism; levothyroxine; liquid levothyroxine; malabsorption; proton pump inhibitors; softgel levothyroxine.

Figure 1

Delivery of active ingredient at gastric level: behavior of different thyroxine formulations.

Figure 2

The physiologic and pharmacologic biases of oral levothyroxine treatment that must be excluded before starting a diagnostic workup for malabsorptive disorders.