Hypothyroidism during second-line treatment of multidrug-resistant tuberculosis: a prospective study.
Hypothyroidism is an adverse effect of certain anti-tuberculosis drugs.



This is a prospective study of the frequency and possible pathomechanisms associated with hypothyroidism due to second-line treatment of multidrug-resistant tuberculosis. Fifty human immunodeficiency virus negative patients and 20 controls were included. All participants underwent ultrasonography of the thyroid and measurement of thyroid stimulating hormone (TSH). TSH levels were checked every 3 months. If hypothyroidism was present, T3, T4 and thyroid peroxidase autoantibodies were measured, and imaging extended to scintigraphy and repeated ultrasonography.



Before treatment, 7 patients (14%) and 1 control (5%) were hypothyreotic. During the first 6 months of treatment, TSH levels increased in 41 patients (82%), 39 (78%) had values above the normal range and 19 (38%) had overt hypothyroidism. As none of the patients had signs of autoimmune thyroiditis, interaction with anti-tuberculosis drugs was assumed to be the cause of hypothyroidism. Nine patients died during treatment, all of whom had developed hypothyroidism. In seven, the metabolic situation at their death was known, and they had become euthyreotic following levothyroxine substitution.



TSH levels should be checked before initiating anti-tuberculosis treatment and after 3 and 6 months to start timely replacement of levothyroxine. Further studies are needed to elucidate the exact pathomechanism involved in hypothyroidism and whether hypothyroidism can be used as predictor of treatment failure.
Department of Nuclear Medicine and Clinical Molecular Imaging, University Hospital Tuebingen, Germany.
R
R
Bares
Rawalpindi Leprosy Hospital, Rawalpindi, Pakistan.
N
N
Khalid
Rawalpindi Leprosy Hospital, Rawalpindi, Pakistan.
H
H
Daniel
Department of Nuclear Medicine and Clinical Molecular Imaging, University Hospital Tuebingen, Germany.
H
H
Dittmann
Department of Nuclear Medicine and Clinical Molecular Imaging, University Hospital Tuebingen, Germany.
M
M
Reimold
Department of Internal Medicine, Division of Endocrinology, University Hospital Tuebingen, Germany.
B
B
Gallwitz
Rawalpindi Leprosy Hospital, Rawalpindi, Pakistan.
C
C
Schmotzer
D000293:Adolescent; D000328:Adult; D000995:Antitubercular Agents / Q000009:adverse effects*; D001323:Autoantibodies / Q000097:blood; D001324:Autoantigens / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000097:blood / Q000139:chemically induced* / Q000000981:diagnostic imaging; D007453:Iodide Peroxidase / Q000276:immunology; D033862:Iron-Binding Proteins / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009169:Mycobacterium tuberculosis / Q000187:drug effects*; D011446:Prospective Studies; D012307:Risk Factors; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D016896:Treatment Outcome; D014284:Triiodothyronine / Q000097:blood; D018088:Tuberculosis, Multidrug-Resistant / Q000175:diagnosis / Q000188:drug therapy* / Q000382:microbiology; D014463:Ultrasonography; D055815:Young Adult
D000995:Antitubercular Agents; D001323:Autoantibodies; D001324:Autoantigens; D015415:Biomarkers; D033862:Iron-Binding Proteins; D014284:Triiodothyronine; D013972:Thyrotropin; C056658:TPO protein, human; D007453:Iodide Peroxidase; D013974:Thyroxine