7 Thyroid dysfunction in HIV infection

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During infection with HIV, overt clinical or biochemical thyroid dysfunctions are rare. When present, thyroid failure generally results from the destruction of the thyroid gland by opportunistic infections such as Pneumocystis carinii, or tumoural processes such as KS. Less frequently, hypothalamic-pituitary failure due to central nervous system infections is involved. Some cases of thyroiditis with thyrotoxicosis or hypothyroidism due to Pneumocystis carinii have also been reported. Subtle alterations of thyroid function tests are more common in HIV infection and are sometimes already detectable in the early phase of the disease. Contrary to what is observed in severe non-thyroidal illnesses, the low T3 syndrome and the sick euthyroid syndrome are less marked; these changes are mainly present in the final stage of the disease, when anorexia and weight loss occur, and indicate a poor outcome. Unique abnormalities of thyroid function indices have also been recently documented. A progressive elevation in serum TBG--but not in other binding proteins such as CBG and SHBG--accompanying the decline of the CD4 lymphocyte count, and associated with a concomitant increase in the serum T4 value, has been reported. An unusual prolonged maintenance of normal T3 levels with a paradoxical decrease in serum rT3 values has also been recognized. Finally, a hypothyroid-like regulation of the pituitary-thyroid axis, possibly directed to limit hypermetabolism in HIV infection, has been observed. The recognition of these particular thyroid profiles is of clinical importance as serum TBG appears to be a specific marker of the progression of HIV infection and serum T3 a reliable prognostic indicator for AIDS.