+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Subclinical Hypothyroidism in HIV-Infected Patients Is Not an Autoimmune Disease

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Aims and Methods: A study of 350 HIV+ patients in our region showed that 16% suffered from hypothyroidism. Twenty-two HIV+ hypothyroid patients (10 with subclinical hypothyroidism, 12 with low FT4 levels (LT4) (confirmed by a dialysis equilibrium assay) and 22 HIV+ euthyroid controls receiving highly active anti-retroviral therapy were included in an additional study. Results: No goiter or anti-thyroid antibodies were detected. Use of stavudine was more frequent in the LT4 subgroup (p < 0.01) and subclinical hypothyroidism group (p = 0.04). Use of didanosine (OR, 12.5, p < 0.01) and ritonavir (OR, 33.0, p < 0.01) was more frequent in the LT4 subgroup, with a greater didanosine cumulative dose (616.7 mg [180.0, 1,260.0] vs. 263.7 [63.0, 948.0], p = 0.01). Reverse T3, binding protein levels, the TSH response to thyrotropin-releasing hormone, urinary iodine, plasma selenium and thiocyanate levels did not differ. IFNγ levels were lower in the subclinical hypothyroidism group (pg/ml) (9.1 [0.0, 22.7] vs. 19.5 [0.0, 40.9], p = 0.03). Conclusion: None of the investigated mechanisms are able to explain the occurrence of hypothyroidism in HIV patients receiving highly active anti-retroviral therapy except the anti-retroviral treatment. In light of the absence of autoimmunity, the normal adenohypophysis and thyroid responses to thyrotropin-releasing hormone, central hypothyroidism is suspected and could explain LT4 and high TSH levels. Underlying mechanisms need further exploration.

          Related collections

          Most cited references 21

          • Record: found
          • Abstract: found
          • Article: not found

          The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.

          Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
            • Record: found
            • Abstract: not found
            • Article: not found

            HIV and autoimmunity

              • Record: found
              • Abstract: found
              • Article: not found

              Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease.

              Experimental evidence from animal models has provided a framework for our current understanding of autoimmune disease pathogenesis and supports the importance of genetic predisposition, molecular mimicry, and immune dysregulation. However, only recently has evidence emerged to support the role of immune dysregulation in human organ-specific autoimmune disease. In the current study of the "late" manifestation of autoimmune thyroid disease (AITD) in a cohort of human immunodeficiency virus (HIV)-positive patients following highly active antiretroviral therapy (HAART), we discuss how immune dysregulation and factors associated with the immunopathology of HIV infection fit the current understanding of autoimmunity and provide a plausible basis for our clinical observations. De novo diagnoses of thyroid disease were identified between 1996 and 2002 in 7 HIV treatment centers (5/7 centers completed the study). Patients were diagnosed as clinical case entities and not discovered through thyroid function test screening. Paired plasma specimens were used to demonstrate sequential rise in thyroid antibodies. Seventeen patients were diagnosed with AITD (median age, 38 yr; 65% were of black African or black Caribbean ethnicity; and 82% were female). The median duration of immune reconstitution was 17 months. Graves disease (GD) was diagnosed in 15 of 17 patients. One patient developed hashithyrotoxicosis with atypically raised C-reactive protein, and another developed hypothyroidism. One GD patient had associated secondary hypoadrenalism. The estimated combined prevalence of GD for 4 treatment centers for female patients was 7/234 and for males was 2/1289. The denominator numbers were matched controls, from 4 centers able to provide data, who commenced HAART during the same time (January 1996 to July 2002) and who did not develop clinical AITD. The mean baseline pre-HAART CD4 count was 67 cells/mL, and the mean increase from nadir to AITD presentation was 355 cells/mL. AITD patients were more likely than controls (95% confidence interval, chi-square test) to be severely compromised at baseline (as defined by a CD4 count < 200 cells/mL or the presence of an acquired immunodeficiency syndrome [AIDS]-defining diagnosis), and to experience greater CD4 increments following HAART. AITD may be a late manifestation of immune reconstitution in HIV-positive patients taking HAART, and immune dysregulation may be an important factor.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                June 2006
                23 June 2006
                : 66
                : 1
                : 21-26
                Departments of aEndocrinology, bInfectious Diseases and cBiophysics and Nuclear Medicine Units, University of Picardie-Jules Verne, Amiens, France
                93228 Horm Res 2006;66:21–26
                © 2006 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 3, References: 34, Pages: 6
                Original Paper


                Comment on this article