A Case of Subacute Thyroiditis Associated with Primary HIV Infection
Article Outline
To the Editor:
Subacute (De Quervain) thyroiditis (SAT) is a transient inflammatory process of the thyroid, sometimes caused by viral infections. To our knowledge, human immunodeficiency virus (HIV) infection has never been related to subacute thyroiditis in the literature. We describe the first case of subacute thyroiditis associated with primary HIV.
A 25-year-old man with no medical history or HIV risk factors was admitted to our Infectious Diseases department for fever (38.5°C), asthenia, deglutition disorders, and myalgia. Clinical examination revealed a painful palpation of the thyroid and cervical adenopathies of <1 cm diameter. Laboratory examinations showed hyperthyroidism (thyroid-stimulating hormone <.05 mUI/L, thyroxidine (T4) 46.8 pmol/L), moderate inflammatory syndrome (C-reactive protein 23 mg/L, fibrinogen 4.4 g/L, erythrocyte sedimentation rate 21 mm), hepatic disorders (aspartate aminotransferase 199 UI/L, alanine aminotransferase 352 UI/L, Gamma-glutamyl transferase 136 UI/L), and lymphopenia (590/mm3). Microbiological samples (blood cultures, urine cultures, and throat swab) were negative. Because of the high monocyte count (1900/mm3), suggesting mononucleosis syndrome, we screened for antibodies to cytomegalovirus, Epstein-Barr virus, hepatitis B virus, hepatitis C virus, and HIV (by enzyme-linked immunosorbent assay); all were negative. Thyroid peroxydase antibodies (252 U/mL) and thyroglobulin antibodies (184 UI/mL) were positive. Thyroid ultrasound examination showed bilateral hypoechoic areas.
Subacute thyroiditis was diagnosed and the patient received intravenous corticosteroids. He left the hospital after 5 days with oral corticosteroids for 10 days (decreasing dosage). All symptoms disappeared within 15 days; thyroid-stimulating hormone (0.01 mUI/L) and T4 (26 pmol/L) decreased.
The patient was referred to our department 5 months later for HIV infection, which had been diagnosed 1 month earlier in his wife after HIV testing during pregnancy. We thus suspected a primary HIV infection during subacute thyroiditis and retrospectively screened for HIV in stored plasma that had been collected at the time of the subacute thyroiditis. The result was positive, with an HIV viral load of 3.87 log copies/mL. At this time, we observed a complete resolution of the clinical and laboratory abnormalities (thyroid function and transaminases). The HIV viral load was 2.46 log copies/mL, and CD4 lymphocytes were at 616/mm3.
Thirty to fifty percent of primary HIV infections are symptomatic. The clinical signs are not specific and include: fever, adenopathies, odynophagia, rash, myalgia, asthenia, headaches, and neurological disorders.1, 2, 3 We believe that our patient concomitantly developed subacute thyroiditis and primary HIV infection. First, the absence of HIV-specific antibodies associated with the detection of the HIV genome in plasma is the typical pattern of primary HIV infection. Second, lymphopenia, mononucleosis syndrome, and cytolytic hepatitis observed at the time of the subacute thyroiditis were certainly related to acute HIV infection.
Several viruses, such as Coxsackie virus,4, 5 influenza virus,4 adenovirus,4 Epstein-Barr virus,6 and cytomegalovirus7 are thought to induce subacute thyroiditis. However, the mechanism by which viral infections can cause subacute thyroiditis is still unknown. In our case, subacute thyroiditis seemed to evolve independently of the HIV infection.
HIV infection should be added to the list of viral infections associated with subacute thyroiditis. Our data suggest that primary HIV infection should be screened for in patients with subacute thyroiditis, particularly in the presence of HIV risk factors.
References
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- . An infant with cytomegalovirus-induced subacute thyroiditis. J Pediatr Endocrinol Metab. 2008;21(2):191–193
Funding: There is no funding source.
Conflict of Interest: None of the authors of this work have any financial conflicts of interest to disclose.
Authorship: All authors had access to the data and a role in writing.
PII: S0002-9343(08)01180-7
doi:10.1016/j.amjmed.2008.11.010
© 2009 Elsevier Inc. All rights reserved.
