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Common subclinical hypothyroidism during Whipple’s disease

BACKGROUND: Classic Whipple’s disease is caused by T. whipplei and likely involves genetic predispositions, such as the HLA alleles DRB1*13 and DQB1*06, that are more frequently observed in patients. T. whipplei carriage occurs in 2-4% of the general population in France. Subclinical hypothyroidism,...

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Autores principales: Lagier, Jean-Christophe, Fenollar, Florence, Chiaroni, Jacques, Picard, Christophe, Oddoze, Christiane, Abi-Rached, Laurent, Raoult, Didier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4099391/
https://www.ncbi.nlm.nih.gov/pubmed/24996424
http://dx.doi.org/10.1186/1471-2334-14-370
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author Lagier, Jean-Christophe
Fenollar, Florence
Chiaroni, Jacques
Picard, Christophe
Oddoze, Christiane
Abi-Rached, Laurent
Raoult, Didier
author_facet Lagier, Jean-Christophe
Fenollar, Florence
Chiaroni, Jacques
Picard, Christophe
Oddoze, Christiane
Abi-Rached, Laurent
Raoult, Didier
author_sort Lagier, Jean-Christophe
collection PubMed
description BACKGROUND: Classic Whipple’s disease is caused by T. whipplei and likely involves genetic predispositions, such as the HLA alleles DRB1*13 and DQB1*06, that are more frequently observed in patients. T. whipplei carriage occurs in 2-4% of the general population in France. Subclinical hypothyroidism, characterized by high levels of TSH and normal free tetra-iodothyronine (fT4) dosage, has been rarely associated with specific HLA factors. METHODS: We retrospectively tested TSHus in 80 patients and 42 carriers. In cases of dysthyroidism, we tested the levels of free-T4 and anti-thyroid antibodies, and the HLA genotypes were also determined for seven to eight patients. RESULTS: In this study, 72-74% of patients and carriers were male, and among the 80 patients, 14 (17%) individuals had a high level of TSH, whereas none of the carriers did (p < 0 · 01). In the 14 patients with no clinical manifestations, the T4 levels were normal, and no specific antibodies were present. Four patients treated with antibiotics, without thyroxine supplementation, showed normal levels of TSHus after one or two years. One patient displayed a second episode of subclinical hypothyroidism during a Whipple’s disease relapse five years later, but the subclinical hypothyroidism regressed after antibiotic treatment. HLA typing revealed nine alleles that appeared more frequently in patients than in the control cohort, but none of these differences reached significance due to the small size of the patient group. CONCLUSION: Regardless of the substratum, classic Whipple’s disease could lead to subclinical hypothyroidism. We recommend systematically testing the TSH levels in patients with Whipple’s disease.
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spelling pubmed-40993912014-07-17 Common subclinical hypothyroidism during Whipple’s disease Lagier, Jean-Christophe Fenollar, Florence Chiaroni, Jacques Picard, Christophe Oddoze, Christiane Abi-Rached, Laurent Raoult, Didier BMC Infect Dis Research Article BACKGROUND: Classic Whipple’s disease is caused by T. whipplei and likely involves genetic predispositions, such as the HLA alleles DRB1*13 and DQB1*06, that are more frequently observed in patients. T. whipplei carriage occurs in 2-4% of the general population in France. Subclinical hypothyroidism, characterized by high levels of TSH and normal free tetra-iodothyronine (fT4) dosage, has been rarely associated with specific HLA factors. METHODS: We retrospectively tested TSHus in 80 patients and 42 carriers. In cases of dysthyroidism, we tested the levels of free-T4 and anti-thyroid antibodies, and the HLA genotypes were also determined for seven to eight patients. RESULTS: In this study, 72-74% of patients and carriers were male, and among the 80 patients, 14 (17%) individuals had a high level of TSH, whereas none of the carriers did (p < 0 · 01). In the 14 patients with no clinical manifestations, the T4 levels were normal, and no specific antibodies were present. Four patients treated with antibiotics, without thyroxine supplementation, showed normal levels of TSHus after one or two years. One patient displayed a second episode of subclinical hypothyroidism during a Whipple’s disease relapse five years later, but the subclinical hypothyroidism regressed after antibiotic treatment. HLA typing revealed nine alleles that appeared more frequently in patients than in the control cohort, but none of these differences reached significance due to the small size of the patient group. CONCLUSION: Regardless of the substratum, classic Whipple’s disease could lead to subclinical hypothyroidism. We recommend systematically testing the TSH levels in patients with Whipple’s disease. BioMed Central 2014-07-04 /pmc/articles/PMC4099391/ /pubmed/24996424 http://dx.doi.org/10.1186/1471-2334-14-370 Text en Copyright © 2014 Lagier et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Lagier, Jean-Christophe
Fenollar, Florence
Chiaroni, Jacques
Picard, Christophe
Oddoze, Christiane
Abi-Rached, Laurent
Raoult, Didier
Common subclinical hypothyroidism during Whipple’s disease
title Common subclinical hypothyroidism during Whipple’s disease
title_full Common subclinical hypothyroidism during Whipple’s disease
title_fullStr Common subclinical hypothyroidism during Whipple’s disease
title_full_unstemmed Common subclinical hypothyroidism during Whipple’s disease
title_short Common subclinical hypothyroidism during Whipple’s disease
title_sort common subclinical hypothyroidism during whipple’s disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4099391/
https://www.ncbi.nlm.nih.gov/pubmed/24996424
http://dx.doi.org/10.1186/1471-2334-14-370
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