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

Autor: Rachel Desailloud, S. Beltran, François-Xavier Lescure, I. El Esper, J.L. Schmit
Rok vydání: 2006
Předmět:
Adult
endocrine system
medicine.medical_specialty
Triiodothyronine
Reverse
endocrine system diseases
Endocrinology
Diabetes and Metabolism
Thyroid Gland
Human immunodeficiency virus (HIV)
Thyrotropin
Thyrotropin-releasing hormone
HIV Infections
medicine.disease_cause
Gastroenterology
Autoimmune Diseases
Interferon-gamma
Endocrinology
Hypothyroidism
Antiretroviral Therapy
Highly Active
Internal medicine
medicine
Humans
Hiv infected patients
Prospective Studies
Prospective cohort study
Thyrotropin-Releasing Hormone
Autoantibodies
Ultrasonography
Subclinical infection
Autoimmune disease
business.industry
Hypogonadism
Thyroid
Autoantibody
virus diseases
Middle Aged
medicine.disease
Thyroxine
medicine.anatomical_structure
Pediatrics
Perinatology and Child Health
Immunology
Triiodothyronine
business
hormones
hormone substitutes
and hormone antagonists
Iodine
Zdroj: Hormone Research in Paediatrics. 66:21-26
ISSN: 1663-2826
1663-2818
DOI: 10.1159/000093228
Popis: 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.
Databáze: OpenAIRE
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