Human immunodeficiency virus (HIV) infection has progressed to a chronic disease and HIV positive individuals are living longer lives. This has lead to an increase in morbidity and mortality due to secondary issues, one being HIV bone disease. HIV infected pediatric and adult populations have a greater incidence in reduction of BMD as compared to the controls. Osteoporosis has been reported to be present in up to 15 % of HIV positive patients. We are starting to understand the mechanism behind the changes in HIV bone disease. Viral proteins interfere with osteoblastic activity either by direct interaction or by the inflammatory process that they induce. Anti-viral management, including highly active antiretroviral therapy (HAART), protease inhibitors, and nucleoside/nucleotide reverse transcriptase inhibitors (NRTI) also are involved in disrupting proper bone metabolism. Vitamin D levels have strong correlation with bone disease in HIV patients, and are dependent not only to chronic disease state, but interaction of pharmacologic management and inflammatory process as well. Work up of the secondary causes of osteopenia and osteoporosis should be undertaken in all patients. DEXA scan is recommended in all post-menopausal women with HIV, all HIV infected men 50 years of age or older and in those with a history of fragility fractures regardless of age or gender. Preventive measures include adequate nutrition, calcium and Vitamin D intake daily, muscle strengthening and balance exercises to increase BMD and reduce fractures. Bisphosphonates are considered to be the first line for the treatment of HIV associated bone disease. This review will describe how the balanced mechanism of bone metabolism is interrupted by the HIV infection itself, the complications that arise from HIV/AIDS, and its treatment options.

Context We hypothesize that impaired glucocorticoid sensitivity (GC Sensitivity) plays a role in the development of Premature Adrenarche (PA) and polycystic ovarian syndrome (PCOS) by increasing androgen synthesis. Objective To study glucocorticoid sensitivity in vitro in subjects with Premature Adrenarche and PCOS. Patients and Methods 14 subjects (10 girls, 4 boys, 6.9 ± 0.6 yrs.) with Premature Adrenarche; 27 subjects with PCOS (17 ± 2.5 yrs.) and 31 healthy controls were enrolled in the study. All subjects and controls underwent GC sensitivity analysis in vitro using a F-DEX assay. A GC sensitivity index (GCSI) was calculated as area under the curve of the F-DEX assay results. Subjects were classified as GC resistant, if the GCSI ≤ 264 and GC sensitive if the GCSI ≥ 386. Results In the Premature Adrenarche group, 8 out of 14 subjects were resistant with GCSI of 179.7 ± 39.9, 4 were within the normal range with GCSI of 299.6 ± 27.9 and 2 had increased GC sensitivity with GCSI of 423.5 ± 47.9. In the PCOS group, 18 out of 27 subjects were GC-resistant with GCSI of 180.9 ± 58.2; 8 were within the normal range with GCSI of 310.7 ± 26.4 and 1 had increased GCSI of 395.4. In the PCOS GC-resistant subgroup, cortisol was higher compared to PCOS with normal GCSI (p<0.05). In the combined PCOS plus female control group GCSI correlated negatively with cortisol and testosterone (p<0.05). Conclusion GC resistance was found in more than 50% of patients with PCOS and Premature Adrenarche. The findings strongly suggest that GC resistance is associated with states of Premature Adrenarche and PCOS.

Excessive thyroid hormone production, as seen in Graves' disease, stimulates osteoblast-mediated bone turnover in favor of bone resorption. Acute reversal of bone resorption can lead to hungry bone syndrome (HBS), a state of rapid calcium deposition into newly synthesized osteoid resulting in hypocalcemia. Hypocalcemia due to subsequent functional or relative hypoparathyroidism is a recognized complication of therapy for Graves' disease. HBS is most recognized as an outcome of rapid correction of vitamin D deficiency or of acute hypoparathyroidism in cases of parathyroid gland function disruption after surgical removal of the thyroid. We report the case of an adolescent boy with Graves' disease who presented with hypocalcemia after radioactive iodine (131I) therapy due to HBS. Our report highlights the risk of HBS and severe hypocalcemia following treatment for Graves' disease in pediatric patients and also underscores the importance of pretreatment assessment and intervention for coexistent vitamin D deficiency.

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