Exaggerated Levothyroxine Malabsorption Due to Calcium Carbonate Supplementation in Gastrointestinal Disorders

Csákó, György; McGriff, Nayahmka J; Rotman-Pikielny, Pnina; Sarlis, Nicholas J.; Pucino, Frank

doi:10.1345/aph.1a031

Cited by 34 publications

(18 citation statements)

References 25 publications

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“…A number of studies have shown that both iron and calcium supplements can potentially decrease the absorption of thyroxine through the formation of a nonabsorbable complex in the gut 9,10. Given the increased incidence of hypothyroidism in the elderly population and the association of both osteoporosis and anemia with this condition, it is important to consider the interaction of these supplements with thyroxine as a potential cause for treatment failure.…”

Section: Discussionmentioning

confidence: 99%

Pituitary hyperplasia: a complication of the pseudomalabsorption of thyroxine

Doyle¹,

Lochnan²

2013

IJGM

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Objective“The pseudomalabsorption of thyroxine” has been used to describe patients with hypothyroidism who fail to comply with their treatment. We describe a unique case of a 32-year-old with hypothyroidism who developed pituitary hyperplasia and hyperprolactinemia secondary to the pseudomalabsorption of thyroxine.Investigations and treatmentAfter baseline thyroid-function tests were performed, the patient was administered levothyroxine 0.5 mg under the supervision of a registered nurse. Thyroid function testing was repeated at 30, 60, 120, and 180 minutes. Arrangements were made for further daily supervised loading of levothyroxine 0.1 mg.ResultsWith the administration of 0.5 mg levothyroxine, free thyroxine levels increased by 120 minutes, and with daily supervised dosing of 0.1 mg there was normalization of the thyroid hormone levels and a reduction of thyroid-stimulating hormone levels. Maintenance of thyroid-stimulating hormone < 15 mU/L for 2 weeks led to a reduction in prolactin levels and regression in the size of the pituitary on magnetic resonance imaging.ConclusionIf left untreated, these patients face significant morbidity and are at risk of developing pituitary hyperplasia, complications from an increase in pituitary size, hyperprolactinemia, and potentially myxedema coma. Recognizing pituitary hyperplasia and hyperprolactinemia as a complication from the pseudomalabsorption of levothyroxine may prevent the potential of a misdiagnosis of a prolactinoma leading to unnecessary investigations and inappropriate treatment. Patient awareness of this serious complication and the rapid, demonstrable resolution with adequate thyroid hormone replacement may provide motivation to comply with supervised dosing of levothyroxine. It has also been suggested that supervised treatment enables the individual to maintain their patient status, which may be in part the motivation behind this disorder.

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Section: Discussionmentioning

confidence: 99%

Pituitary hyperplasia: a complication of the pseudomalabsorption of thyroxine

Doyle¹,

Lochnan²

2013

IJGM

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“…4 -6 Other medications include sucralfate, aluminum hydroxide, sodium polystyrene sulfonate. [7][8][9] Enhanced metabolism of L-thyroxine by medications such as phenytoin, rifampin, carbamazepine, and phenobarbital can also reduce its bioavailability. 10 -13 Other medications interfering with thyroid hormone homeostasis include estrogen and lithium.…”

Section: Discussionmentioning

confidence: 99%

“…The patient had been diagnosed with primary hypothyroidism approximately 1 year prior to the referral, at which time the patient presented to her family physician with fatigue and cold intolerance. She had clinical and biochemical evidence of primary hypothyroidism; the thyroid-stimulating hormone (TSH) was Ͼ100 U/mL (0.5-5.0), total thyroxine was 1.4 g/dL (5)(6)(7)(8)(9)(10)(11)(12), and antithyroid peroxidase and antithyroglobulin antibodies were positive. The patient was started on 125 g of L-thyroxine, with which her symptoms improved.…”

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A Case of Celiac Disease Presenting With Malabsorption of l-Thyroxine

Khandwala

Chibbar

Worobetz

2005

The Endocrinologist

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A 26-year-old-female with a history of primary hypothyroidism was referred to the endocrinology clinic for evaluation of persistent hypothyroidism despite a dose of 2.7 g/kg/d of Lthyroxine. After excluding issues with compliance and drug interactions, the possibility of malabsorption was considered; tissue transglutaminase antibody was elevated at 83 kU/L (positive Ͼ25), and the duodenal biopsy demonstrated complete villous atrophy. The diagnosis of celiac disease was established, and the patient was subsequently placed on a gluten-free diet. Malabsorption of Lthyroxine can be the only clue to the underlying diagnosis of celiac disease. As the prevalence of celiac disease is increased in patients with autoimmune thyroid disorders, the diagnosis of celiac disease should be considered in patients requiring high doses of L-thyroxine to achieve euthyroidism. (The Endocrinologist 2005;15: 14 -17) C eliac disease and primary hypothyroidism are relatively common disorders; both are considered to be autoimmune in nature. An increased prevalence of celiac disease in patients with other autoimmune diseases, particularly type 1 diabetes and Hashimoto thyroiditis, has been reported. 1 We present a case of a 26-year-old female with Hashimoto thyroiditis in whom the only clue to the underlying presence of celiac disease was malabsorption of L-thyroxine. CASE REPORTA 26-year-old Caucasion female was referred to the endocrinology clinic for evaluation of persistent hypothyroidism. The patient had been diagnosed with primary hypothyroidism approximately 1 year prior to the referral, at which time the patient presented to her family physician with fatigue and cold intolerance. She had clinical and biochemical evidence of primary hypothyroidism; the thyroid-stimulating hormone (TSH) was Ͼ100 U/mL (0.5-5.0), total thyroxine was 1.4 g/dL (5-12), and antithyroid peroxidase and antithyroglobulin antibodies were positive. The patient was started on 125 g of L-thyroxine, with which her symptoms improved. Six months after the diagnosis, the patient noticed insomnia and, although she was subclinically hypothyroid at the time (TSH 7.6 U/mL and free thyroxine 1.05 ng/dL ͓0.7-2.0͔), decided to discontinue treatment. Two months later, she became symptomatically hypothyroid and was found to have a TSH of 61 U/mL and a free thyroxine of 0.56 ng/dL. Treatment was restarted, this time with 75 g of L-thyroxine, and the patient was referred to the endocrinology clinic. After restarting L-thyroxine, the patient felt better and was euthyroid by symptoms.Her past medical history was unremarkable and was specifically negative for anemia or gastrointestinal symptoms. There was no family history of thyroid or other autoimmune diseases. Her medications at the time included 75 g of L-thyroxine, an oral contraceptive, and 500 mg of calcium carbonate a day. Her examination was remarkable for a weight of 46.1 kg and a body mass index (BMI) of 17.7 kg/m 2 . The thyroid was normal to palpation; there was no lymphadenopathy or splenomegaly. She did not have e...

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“…Thus, gastrointestinal diseases and/or anatomic abnormalities, as well as some drugs taken together with L-T 4 , causing reduced absorption and bioavailability of L-T 4 , may lead to uncorrected neuropsychological development [2,3,4,5,6]. …”

Section: Introductionmentioning

confidence: 99%

Increased Risk of Coeliac Disease in Patients with Congenital Hypothyroidism

Stagi

Manoni²,

Cecchi³

et al. 2011

Horm Res Paediatr

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Background: In patients with congenital hypothyroidism (CH), the presence of coeliac disease (CD) has been sporadically described. Methods: Seventy-nine consecutive children (58 females and 21 males; age range 3.1–12.1 years) with permanent CH were studied. For all patients, a family history of autoimmune diseases as far as second-degree relatives was collected, and total serum IgA, antigliadin, anti-endomysium and anti-transglutaminase antibodies were evaluated. In the subjects positive for CD antibodies, the CD diagnosis was confirmed by jejunal biopsy. One hundred and eighty-two Italian children from the same geographical area, matched for age and sex, acted as controls. Results: In CH patients, a statistically significant difference was found in the familial occurrence of autoimmune diseases compared to controls (22 vs. 7.9%; p < 0.001). A total of 6 patients (4 girls, 2 boys; 7.6 vs. 1%; p < 0.005) were positive for CD antibodies. In 5 of these patients (6.3%), the diagnosis of CD was confirmed histologically. Conclusion: Our data show a higher prevalence of CD in children with permanent CH and suggest that these patients should be monitored carefully for CD. Other studies are needed to confirm our results and to explain the causes of this possible relationship.

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Exaggerated Levothyroxine Malabsorption Due to Calcium Carbonate Supplementation in Gastrointestinal Disorders

Abstract: Decreased absorption of levothyroxine when given with calcium carbonate may be particularly pronounced in patients with preexisting malabsorption disorders. Once recognized, a change in drug administration schedule usually minimizes or eliminates this interaction.

Cited by 34 publications

References 25 publications

Pituitary hyperplasia: a complication of the pseudomalabsorption of thyroxine

Pituitary hyperplasia: a complication of the pseudomalabsorption of thyroxine

A Case of Celiac Disease Presenting With Malabsorption of l-Thyroxine

Increased Risk of Coeliac Disease in Patients with Congenital Hypothyroidism

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