Adrenal, gonadal, and thyroid function were assessed in 40 asymptomatic subjects in whom infection with the human immunodeficiency virus (HIV) had recently been documented. None of the patients had historical or clinical evidence of endocrine dysfunction. Their mean serum hormone levels were also within the expected ranges, but several differences were noted compared to those of seronegative controls. Basal cortisol, basal aldosterone, and ACTH-stimulated cortisol were significantly lower in the HIV group. One subject (2.5%) had a subnormal cortisol response, and two (5%) had abnormal aldosterone responses to ACTH. PRA tended to be higher, and serum angiotensin-converting enzyme levels somewhat lower in the HIV group. Serum free testosterone was markedly elevated in the HIV patients and was associated with an exaggerated LH response to GnRH, but PRL, estradiol, and basal and peak GnRH-stimulated FSH did not differ between groups. Three subjects (8%) had subclinical hypothyroidism. Serum thyroid hormone levels were normal, but basal T3 was lower in the HIV group compared to control values. While of little immediate clinical importance, many subtle endocrine aberrations are evident very early in the course of HIV infection. These findings obtained in HIV-seropositive subjects without infections or tumors and who were not receiving medical therapy suggest an effect of HIV on each of the endocrine systems examined.

The hypothalamic-pituitary-testicular axis was evaluated in seven men with thyrotoxicosis due to Graves' disease. Loss of libido and decreased potency were present in 71% and 56%, respectively. All patients had normal testicular volume (25 ml in all) and gynecomastia was detected in two of seven patients. Total sperm counts were less than 40 million in four of the five men tested. There was an inverse correlation between basal serum 17 beta-estradiol (E2) levels and total sperm count (r = -0.87; P less than 0.05). Mean (+/- SE) total testosterone (T) and E2 levels (1008 +/- 104 ng/100 ml and 104 +/- 16 pg/ml) were significantly higher than in normal men (P less than 0.05). Free T (13.6 +/- 2.4 ng/100 ml) was indistinguishable from normal (15.3 +/- 1.5 ng/100 ml). The mean (+/- SE) response of serum T to hCG administration was blunted (80 +/- 40%) compared to controls (193 +/- 19%; P less than 0.02). Basal plasma LH levels (15.5 +/- 1.5 mIU/ml) were significantly higher (P less than 0.05) than in normal men (9.1 +/- 0.6 mIU/ml) and hyperresponded to 100 microgram LRH iv in five of seven patients. Basal plasma FSH levels and the FSH response to LRH were normal. These results suggest that men with hyperthyroidism have 1) partial Leydig cell failure, 2) impairment of spermatogenesis, and 3) blunting of the feedback effects of E2.

No abstract

CT is a peptide hormone produced predominantly by thyroid C cells and probably to a lesser extent by extrathyroidal tissues. Although its physiological function has not yet been established, it is a pharmacological inhibitor of osteoclastic bone resorption. There is currently no convincing evidence that naturally occurring or iatrogenic CT deficiency is involved in the pathogenesis of osteoporosis; however, a selective examination of patients with various rates of bone turnover would help to resolve this issue. As a pharmacological inhibitor of bone resorption, CT has potential usefulness in the therapy of osteoporosis. CT has been shown to stabilize or modestly increase indices of cortical and trabecular bone mass and total body calcium when administered to patients with established osteoporosis for periods of 1-2 yr. The increments in bone mass seen in some studies appear to be transient and are likely due to reductions in bone resorption with bone formation remaining unaffected until remodeling spaces are filled. The duration and magnitude of these increases are probably limited by the eventual decline in bone formation as remodeling equilibrium is reestablished. Therefore, reduction in the rate of bone loss with maintenance of the existing skeletal mass, rather than significant sustained increases in bone mass, should be considered the most realistic therapeutic goal with this agent. Whether or not a reduction in the rate of bone loss persists for longer periods needs further evaluation as does the important issue of subsequent fracture rates. The identification of patients with increased bone resorption rates (high turnover osteoporosis) should help provide a basis for more selective treatment of those patients who would be most likely to respond to this form of therapy. Whether there is additional benefit to using intermittent CT concurrently or sequentially with bone formation stimulating agents (coherence therapy) also needs to be explored. CT may also be of benefit in the prevention of osteoporosis, particularly in postmenopausal women who are unable or unwilling to take estrogen replacement. These potential benefits must be weighed carefully against the current cost of CT and the inconvenience of it having to be given by injection, problems which should be solved by future research.

To determine if differing degrees of levothyroxine (LT4) suppression therapy for benign and malignant thyroid disease are associated with proportionately increased rates of bone loss, this longitudinal assessment of bone densitometry changes (single-photon and dual-photon absorptiometry) was conducted in three groups of subjects: 24 thyroid cancer patients who were treated with near-total thyroidectomy, radioiodine ablation, and aggressive LT4-suppression; 44 patients who were treated with more conservative LT4-suppression for benign thyroid disorders; and 24 normal controls. Bone densitometry values were adjusted for age, weight, height, and menopausal status. The rates of bone loss in benign LT4-suppressed patients were greater than those in controls at the midradius, distal radius, lumbar spine, and femoral neck. The rates of loss in the thyroid cancer patients were also greater than those in the controls at all four sites and greater than in the benign LT4-suppressed patients at the midradius, distal radius, and femoral neck but not in the lumbar spine. Rates of bone loss were not significantly correlated with LT4 dose or with the serum level of T4 or TSH. LT4-suppression therapy for benign thyroid disease is associated with accelerated bone loss. More aggressive LT4-suppression for thyroid cancer is associated with even greater bone loss, particularly in cortical bone regions. These risks must be weighed against the benefits of LT4 therapy in individual patients.