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Celiac and hypothyroidism: Celiac Disease and Autoimmune Thyroid Disease

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Celiac Disease and Autoimmune Thyroid Disease

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The Link Between Hypothyroidism and Celiac Disease

Sometimes these two autoimmune disorders can go hand in hand. Here’s what to do if you experience symptoms such as bloating, gas, and constipation.

By Beth W. OrensteinMedically Reviewed by Meeta Shah, MD

Reviewed:

Medically Reviewed

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Having hypothyroidism might increase your chances of having celiac disease, too.

“Celiac disease is an autoimmune disorder, and when you have one autoimmune disorder, there’s always an increased risk for developing others, including hypothyroidism,” says Norelle Rizkalla Reilly, MD, director of pediatric celiac disease at The Celiac Disease Center and an assistant professor of pediatrics at Columbia University Medical Center in New York.

“We can’t say that one autoimmune disorder causes the other, but they probably come from your genetic predisposition — so if you’re prone to one autoimmune disorder, you could be prone to another,” says Joseph Murray, MD, a gastroenterologist at the Mayo Clinic in Rochester, Minnesota.

In fact, a significant number of people with autoimmune thyroid disorders also have a number of other autoimmune disorders, including celiac disease, according to research published in the journal Autoimmunity Reviews in September 2016.

Symptoms of celiac disease include bloating or gas, constipation, depression, fatigue, irritability, and headaches, according to Beyond Celiac, an advocacy organization.  Adults with celiac disease may also experience anemia, acid reflux, a skin rash, and low bone density, says Sarah Nadeem, MD, an endocrinologist at Loyola University Health System in Maywood, Illinois.

Treating Celiac and Hypothyroidism

Some of the symptoms of celiac disease overlap with those of hypothyroidism, including constipation, depression, and fatigue.

“Symptoms of thyroid problems can be more vague and be incorrectly attributed to celiac disease if thyroid disease isn’t on your radar,” Dr. Reilly says.

If you have hypothyroidism, it makes sense to be screened for celiac disease, says Lawrence Schiller, MD, director of the division of gastroenterology at Baylor Scott & White Health in Dallas. Screening for celiac disease requires a simple blood test. And if you find you have both hypothyroidism and celiac disease, it’s important to treat both autoimmune disorders.

Treatment of celiac disease stays the same whether you have hypothyroidism or not, Dr. Nadeem says. It involves following a diet that’s 100 percent free of gluten — a protein found in wheat, rye, barley, and certain types of oats.

Your thyroid condition may improve on a gluten-free diet, Dr. Schiller says. “The reverse is not true,” he says. “Celiac disease will not improve with hypothyroidism treatment, but your doctor should know about the possibility of hypothyroidism, especially if your symptoms that are attributed to celiac disease do not improve with a gluten-free diet.”

The American Thyroid Association recommends that most people with hypothyroidism should be treated with the hormone replacement therapy levothyroxine. “Patients who have both celiac disease and hypothyroidism can choose a gluten-free form of levothyroxine,” Nadeem says.

Many people with hypothyroidism believe that following a “thyroid diet” can help, she says. “But no research has found a specific diet that will help with the thyroid. I recommend that my patients eat a healthy, well-balanced diet, with or without thyroid disease.”

Get Tested Regularly

If you have both hypothyroidism and celiac disease, you should have your thyroid checked every six months, especially in the first year after going gluten-free, Dr. Murray says. Once you treat your celiac disease, you may be able to better absorb your thyroid medication.

“Thyroid medication is very prone to not being absorbed properly,” he explains. “And celiac disease may actually cause you to not absorb your thyroid medication properly. If you treat your celiac disease and your body becomes better at absorbing your hormone replacement, your doctor may need to adjust your dose.”

Also, if you have hypothyroidism and you find you need to keep increasing your dose of thyroid replacement hormone, you should be screened for celiac disease, Murray says. “If your hormone levels are all over the place, it could be a sign of undiagnosed celiac disease.”

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Hypothyroidism is one of the most common forms of endocrine system dysfunction. In most cases, its diagnosis and therapy do not cause difficulties. Modern laboratory methods for assessing thyroid function can detect minimal deviations, and adequate replacement therapy with levothyroxine sodium can achieve target values ​​of thyroid-stimulating hormone in most cases of primary hypothyroidism, which in turn helps to normalize the condition and improve the quality of life of patients. Despite the fact that the therapy of overt and subclinical hypothyroidism does not cause difficulties, in some patients, due to certain factors, the achievement of clinical and biochemical euthyroidism can be difficult.
The article discusses the tactics of managing such groups of patients.

Drugs affecting the dose of levothyroxine

Hypothyroidism is one of the most common forms of thyroid dysfunction and, at first glance, the simplest thyroid disease for diagnosis, differential diagnosis and therapy.

The etiology and pathogenesis of hypothyroidism are well understood. The most common cause of its development, especially in regions without pronounced iodine deficiency, is autoimmune thyroiditis (AIT), a chronic autoimmune pathology of the thyroid gland, characterized by lymphocytic infiltration and atrophy of thyroid follicular cells, followed by a decrease in the number of functionally active thyrocytes and the development of hypothyroidism [1]. Autoimmune thyroiditis can occur in the form of classic Hashimoto’s thyroiditis with goiter or in an atrophic form with a small thyroid volume. The latter option is increasingly observed in clinical practice. The second place among the causes of hypothyroidism is occupied by the consequences of radical methods of treating thyroid pathology – post-radiation and postoperative hypothyroidism.

The prevalence of overt hypothyroidism in the general European population is 0.2–5.3%, depending on age and gender. At the same time, women suffer from hypothyroidism five to ten times more often than men [2].

Replacement therapy with levothyroxine sodium, a synthetic levorotatory isomer of thyroxine synthesized by the thyroid gland, remains the gold standard for the treatment of hypothyroidism of various etiologies. The dose of levothyroxine depends on a number of factors – primarily on weight, age and the presence of concomitant cardiovascular pathology. It is also important to take into account the target level of thyroid-stimulating hormone (TSH), planned or ongoing pregnancy, and the etiology of hypothyroidism. Thus, the dose of levothyroxine is relatively higher in patients after thyroidectomy than in patients with hypothyroidism due to autoimmune thyroiditis.

The algorithm for starting replacement therapy provides for either the appointment of an initial estimated dose of levothyroxine sodium 1.6–1.8 µg/kg, or small doses of 12.5–25.0 µg with gradual titration. The latter option is mandatory for patients with cardiovascular diseases (primarily coronary heart disease and arrhythmia) and the elderly due to the possibility of latent, previously undiagnosed cardiovascular pathology. However, for young, potentially healthy patients, the strategy of prescribing low starting doses of levothyroxine with subsequent titration can be chosen, especially in the case of subclinical hypothyroidism or a relatively small increase in TSH levels.

The goal of replacement therapy is to achieve normal values ​​of laboratory markers of thyroid function – TSH for primary hypothyroidism and free thyroxine (free T4) for central hypothyroidism.

To date, only tablet forms of levothyroxine sodium are available on the domestic pharmaceutical market, and gelatin capsules and solutions are also available on the world market. Preparations of different forms of release and brands may differ in bioavailability, which depends on their composition. In particular, different ingredients affect the absorption of levothyroxine in the small intestine in different ways. In this regard, it is recommended to use the same drug during therapy, and in case of changing it to a drug from another manufacturer, extraordinary TSH monitoring to assess the effectiveness of therapy and exclude overdose or underdose.

In most cases, the tactics of treating overt and subclinical hypothyroidism does not cause doubts and difficulties. However, about a third of patients have difficulty compensating for hypothyroidism due to various factors, which requires more frequent dose titration and monitoring of thyroid function. The most common cause of insufficient control of the disease is low compliance with the regimen of taking levothyroxine sodium – in the morning, strictly on an empty stomach, drinking water, 30-40 minutes before a meal. Often this leads to pseudo-malabsorption and unjustified dose titration.

Special groups of patients with primary hypothyroidism and their management are discussed below.

Patients with malabsorption syndrome

When taken orally on an empty stomach, levothyroxine sodium is characterized by high bioavailability – up to 80%. The drug is absorbed mainly in the duodenum and small intestine within three hours after ingestion [3].

It has been established that the bioavailability of levothyroxine sodium is reduced by various gastrointestinal diseases, joint intake with other drugs and food.

In the absence of clinical and biochemical compensation of hypothyroidism against the background of high doses of levothyroxine (> 2 μg/kg of body weight), it is necessary to exclude the presence of gastrointestinal pathology [4, 5].

Helicobacter pylori infection . The effect of H. pylori infection on the bioavailability of levothyroxine sodium has been proven in many studies [6, 7]. The proposed mechanism is considered to be a decrease in the secretion of hydrochloric acid in the stomach and hypochlorhydria, which leads to a decrease in the absorption of levothyroxine. It was shown that the level of TSH in blood serum and the need for levothyroxine are significantly higher in patients with H. pylori [6]. Eradication of H. pylori leads to a decrease in the level of TSH and the dose of levothyroxine. In a study by M.S. Bugdaci et al. 21% of patients after eradication of H. pylori developed artificial thyrotoxicosis, which confirms the role of infection in the increased need for levothyroxine sodium [7].

Autoimmune atrophic gastritis . Autoimmune gastritis is characterized by the appearance of autoantibodies to the parietal cells of the stomach and the internal factor of Castle and, as a result, lymphocytic infiltration and atrophy of the own glands of the stomach, as well as focal intestinal metaplasia. The achlorhydria that develops at the same time can disrupt the absorption of levothyroxine, leading to decompensation of hypothyroidism and an increase in the need for a dose of levothyroxine.

The association of atrophic gastritis with autoimmune thyroid pathology has been proven. About 13-42% of patients with AIT are carriers of parietal antibodies, up to 40% of patients with atrophic gastritis have AIT [8, 9].

S. Checchi et al. found that the need for levothyroxine sodium was significantly higher in carriers of parietal antibodies. Autoimmune gastritis has become an additional factor influencing the need for levothyroxine [10].

Celiac disease is a chronic autoimmune enteropathy characterized by persistent intolerance to cereals and gluten with the development of malabsorption syndrome. Celiac disease is also associated with autoimmune thyroid diseases.

According to a meta-analysis, celiac disease occurs in 1.4% of patients with AIT, which was confirmed by the data of a histological study of biopsies of the gastric mucosa [11]. At the same time, a gluten-free diet made it possible to control not only the symptoms of celiac disease, but also the need for levothyroxine.

Another reason for reduced absorption of levothyroxine in the small intestine may be lactose intolerance . Lactose intolerance is a pathological condition associated with a violation of the breakdown of lactose due to a deficiency of the lactase enzyme and is clinically manifested by malabsorption when taking lactose-containing products. In patients with hypothyroidism, lactase deficiency can be the cause of uncompensated hypothyroidism. Limiting the consumption of dairy products and taking lactose-free forms of levothyroxine sodium will increase the bioavailability of the drug and achieve target TSH levels.

Currently, due to the prevalence of obesity, the number of bariatric surgical interventions is increasing. An expected side effect of this therapy option is also malabsorption syndrome. At the same time, the need for levothyroxine in the early and late postoperative periods can be very variable. On the one hand, against the background of malabsorption, the absorption of levothyroxine is disturbed and the need for it increases, on the other hand, a significant decrease in body weight is accompanied by a decrease in the need for a dose of levothyroxine [12].

Parasitic infestations can also cause subcompensation of hypothyroidism.

Patients taking concomitant medications

A number of drugs affect the metabolism of levothyroxine sodium; therefore, concomitant drug therapy should be evaluated for effects on thyroid function and serum levels of levothyroxine sodium (table). First of all, we are talking about drugs that affect the absorption and bioavailability of levothyroxine: antacids, iron, calcium, sucralfate, cholestyramine, orlistat, sevelamer, proton pump inhibitors. Patients with end-stage chronic kidney disease and concomitant hypothyroidism may have difficulty achieving the target TSH level due to the use of several groups of drugs that reduce the absorption of levothyroxine at once. These include phosphate binders, sevelamer, and calcium preparations, widely prescribed for hyperphosphatemia in patients with chronic kidney disease receiving renal replacement therapy [13]. These patients often take iron supplements and antacids for anemia and/or proton pump inhibitors for gastritis and reflux esophagitis.

Thus, in patients with hypothyroidism during therapy with drugs that affect the absorption of levothyroxine, the need for it and, as a result, for dose titration increases. To reduce these risks, it is advisable to take levothyroxine and these drugs separately with an interval of two to four hours, control TSH and adjust the dose of levothyroxine at the beginning and end of therapy with these drugs. Taking liquid forms and gelatin capsules of levothyroxine can also improve its bioavailability.

An increase in the dose of levothyroxine may be required when taking drugs that increase the metabolism and clearance of levothyroxine, such as phenytoin, carbamazepine, rifampicin, phenobarbital.

In addition, estrogen intake and conditions accompanied by hyperestrogenism, due to an increase in the level of thyroxin-binding globulin and, as a result, a decrease in the level of free thyroid hormones, may require an increase in the dose of levothyroxine.

It should be noted that in patients with hypothyroidism due to AIT, especially subclinical hypothyroidism, decompensation of hypothyroidism while taking drugs that affect the biosynthesis of thyroid hormones, primarily amiodarone and lithium preparations, is not excluded.

Patients with a special working regime and work schedule

A number of studies have established a relationship between the level of TSH and thyroid pathology with the night work schedule. A meta-analysis, the purpose of which was to assess the effect of night work on the development of thyroid pathology (n = 4074), showed a significantly higher level of TSH in those who worked at night than in those who worked during the day. A higher level of TSH was explained by a violation of the circadian rhythm and the sleep-wake cycle, as well as eating behavior [14].

For a number of professions, maintaining a stable euthyroidism is a mandatory criterion for admission to work. Thus, hypothyroidism of any etiology and severity is considered as a temporary contraindication for flight work (pilots, flight attendants who control aircraft traffic, etc.) [15]. Employees are allowed to work to achieve and maintain stable euthyroidism against the background of replacement therapy, followed by regular monitoring of thyroid function during a medical examination.

Patients with hypothyroidism after thyroidectomy are not considered fit for military service.

Compensated hypothyroidism due to AIT or other etiology is not a contraindication for military service. Depending on the state, such persons may be recognized as fit for military service, fit for military service with minor restrictions, limited fit for military service [16].

The work schedule and work schedule can affect patient compliance and the degree of compensation for hypothyroidism. In particular, low adherence of patients to therapy may be due to difficulties in taking levothyroxine on an empty stomach in the morning.

In a study by N. Bolk et al. it has been shown that the transfer of levothyroxine intake to the evening (after dinner) can improve the absorption of levothyroxine, as evidenced by a decrease in the level of TSH in the blood serum [17]. In a study by T.G. Bach-Huynh et al. the transfer of the time of taking levothyroxine from morning to evening, on the contrary, was accompanied by an increase in the concentration of TSH and a decrease in the level of free blood. T4 [18]. In general, most studies have demonstrated comparable efficacy of levothyroxine when used in the morning and evening hours [19, 20]. The main condition remains the observance of the intervals between taking the drug and food – at least 30-40 minutes before breakfast and at least two to four hours after dinner.

Thus, patients who cannot take levothyroxine sodium in the morning on an empty stomach and maintain the required interval before meals can take it in the evening after dinner.

Conclusion

The difficulty in achieving the target TSH, the need for high doses of levothyroxine, the instability of the dose of levothyroxine, and concomitant micro- or macrocytic anemia require the exclusion of concomitant gastrointestinal pathology and malabsorption as the causes of uncompensated hypothyroidism in patients with satisfactory compliance. Adequate therapy of atrophic gastritis, infections H. pylori , celiac disease, lactase deficiency and other gastrointestinal pathology accompanied by malabsorption syndrome improves the control of hypothyroidism [4]. St. level T4 on the background of taking levothyroxine makes it possible to differentiate the syndrome of malabsorption and pseudomalabsorption with low compliance of patients [21].

When planning the treatment of hypothyroidism, it is important to take into account the comorbidities and medications taken, vital activity, the mode and nature of the work of patients.

The main conditions for successful treatment of hypothyroidism are high adherence to treatment and regular monitoring of thyroid function.

Related Diseases – Gluten Free Living

Celiac disease is an autoimmune disease, so people with celiac disease are at greater risk of developing other autoimmune diseases such as diabetes or thyroid disease. Some people with celiac disease may also be lactose intolerant.

Diabetes

Diabetes mellitus (Latin name “ diabetes mellitus “) is a disease that mainly occurs when the body has low insulin levels and metabolic disorders. Diabetes mellitus develops with some endocrine disorders. As with other types of diabetes, there is an increase in urination (polyuria) and an increase in fluid intake (polydipsia). Diabetes is characterized by high levels of glucose (sugar) in the blood (hyperglycemia). Diabetes mellitus is characterized by a chronic course and a gradual disruption of all types of metabolism in the body.

The causes of diabetes depend on the type of diabetes.

Type 1 diabetes may be caused by pre-existing pancreatic disease or autoimmune disease.

Type 2 diabetes is caused by obesity, high blood pressure, smoking, low HDL cholesterol and/or elevated blood triglycerides.

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