Requirement for multiple lymphocyte subsets in protection by a live attenuated vaccine against retroviral infection

STUDY DESIGN: A case report and literature review of thoracic hyperkyphosis deformity secondary to glucocorticoid-induced osteoporosis in Cushing's disease. OBJECTIVES: To identify the pathophysiology of glucocorticoid-induced osteoporosis and to outline the diagnosis and treatment options for a patient with severe spinal deformity secondary to unrecognized excess glucocorticoid activity. SUMMARY OF BACKGROUND DATA: Glucocorticoid-induced osteoporosis is seen in patients exposed to supraphysiologic levels of endogenous or exogenously administered glucocorticoids. In these patients, glucocorticoids act to suppress bone formation and increase bone resorption by indirect and direct effects. These patients have a high prevalence of trabecular bone loss, resulting in much higher rates of vertebral body collapse and pathologic fracture and thus causing an increased propensity toward kyphotic spinal malalignment. METHODS: The literature was reviewed and case reports studied. This case report highlights the pathophysiology of the disease process that caused the spinal deformity and the surgical intervention used to correct the kyphotic deformity after the metabolic problem was resolved. RESULTS: This patient has responded well to treatment and surgical intervention to correct a thoracic hyperkyphotic deformity without complication. CONCLUSIONS: Unrecognized endogenous production of glucocorticoids in Cushing's disease should be considered in young adult patients with progressive osteoporotic spinal deformities.