ABSTRACT
I. Introduction ............................................................................. 84
II. Clinical Protocols ..................................................................... 88 A. Therapeutic Regimes ....................................................... 88 B. Doses ................................................................................ 88
III. Clinical Outcomes .................................................................... 89 A. Fractures Due to Osteoporosis........................................ 89 B. Bone Mass ........................................................................ 89 C. Histology.......................................................................... 92 D. Calcium Balance Studies ................................................. 92
IV. Serum Biochemical Changes During PTH Therapy ............... 93
V. Biochemical Markers of Bone Metabolism ............................. 95
VI. Analysis of Concurrent Therapies Used with PTH Protocols .......................................................................... 96
VII. Pharmacokinetics of PTH Administration.............................. 99 A. Summary of Pharmacokinetics and
Pharmacodynamics ....................................................... 101
VIII. Other Analogs and Delivery Systems ................................... 101
IX. Immunological Responses to Exogenous PTH..................... 102
X. Side Effects During PTH Therapy......................................... 102
XI. Conclusion.............................................................................. 103
References ......................................................................................... 104
Current concepts of therapy to reduce the fracture risk consequences of osteoporosis can be divided into antiresorptive and anabolic approaches. These are schematically shown in Figure 4.1. As bone mass falls with age, antiresorptive drugs (e.g., estrogen, calcitonin, and the bisphosphonates) have been shown to arrest bone loss and even increase bone mass. As will be discussed later, small gains in bone mass in patients with osteoporosis and established fractures translate into clinically important reductions in future fracture risk. By contrast, anabolic agents such as sodium fluoride and parathyroid hormone (PTH) have the potential to cause accelerated gains in bone mass over short periods (2 to 4 years), which might offer particular protection to patients with very low bone mass. Recent studies of PTH and several peptide analogs of PTH have provided evidence for a potent anabolic action on bone in both laboratory and clinical osteoporosis. This chapter focuses on the clinical information currently available and, when possible, contrasts this with the established efficacy of antiresorptive therapy.
