Parenteral nutrition-associated metabolic bone disease

JPEN: Journal of Parenteral and Enteral Nutrition,  Sep/Oct 2002  by Seidner, Douglas L

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ABSTRACT. The incidence of parenteral nutrition-- associated metabolic bone disease is unknown. Initial reports from the early 1980s suggested that both osteoporosis and osteomalacia were quite common in patients who receive long-term parenteral nutrition. The findings described in these early surveys provide a snapshot into the many factors that contribute to the development of metabolic bone disease. More recent evidence suggests that bone loss may not be as great with the initiation of parenteral nutrition as once was thought, and that most of the metabolic bone disease that is noted may be related to the patient's underlying illness. Although this recent

information is reassuring, it is of the utmost importance to provide parenteral nutrition that minimizes further bone loss and promotes the formation of new bone. This review will describe the general features of metabolic bone disease and the abnormalities noted with parenteral nutrition-associated metabolic bone disease, highlight the importance of preexisting illness and parenteral nutrition associated factors that contribute to the development of metabolic bone disease, and finally discuss an approach to avoid this debilitating complication of longterm parenteral nutrition. (Journal of Parenteral and Enteral Nutrition 26:S37-542, 2002)

BONE FUNCTION, METABOLISM, AND METABOLIC BONE DISEASES

Bone is the major structural component of the skeleton and provides a rigid frame for locomotion and protection of the vital organs of the body. Bone is also a site for hematopoiesis and provides a reservoir of calcium, phosphorus, and magnesium. There are two major types of bone, cortical and trabecular bone. Cortical bone is composed of densely packed layers of mineralized collagen and is the major component of the shafts of the long bones. Trabecular bone makes up the inner lace-like bone which surrounds the bone marrow and gives bone its compressive strength. Trabecular bone, which is also referred to as cancellous bone, makes up the major portion of the vertebrae, pelvis, and ends of long bones.

Bone responds to mechanical stress by undergoing continuous breakdown and renewal in a process referred to as bone remodeling.' New bone is initially laid down through the formation of osteoid, a protein matrix that is predominantly made up of collagen. Osteoid is then mineralized with calcium and phosphorus, a process that is carefully regulated by parathyroid hormone (PTH) and requires adequate blood levels of vitamin D, calcium, magnesium, and phosphorus. Old bone is removed by reabsorption of the mineral and organic components of the bone. At a cellular level, bone remodeling is directed by osteoclasts that resorb bone, osteoblasts that direct new bone formation, and osteocytes that regulate mineral metabolism. Bone mass increases through childhood and adolescence and peaks at the end of the second to third decade of life. Although bone mass remains fairly stable throughout adult life, there is a gradual decline with senescence that is most often of no clinical consequence. Although there are several types of metabolic bone disease (MBD), the two predominant forms are osteoporosis and osteomalacia.

Osteoporosis

Osteoporosis is the most common form of MBD and is responsible for over one million fractures in the United States each year. In osteoporosis, there is a decrease in the total amount of bone with a normal ratio of bone matrix to bone mineral. Although bone may appear to be histologically normal, microarchitecture damage to the trabecular bone has been demonstrated. Primary osteoporosis can be divided into "postmenopausal" or type I and "senile" or type II osteoporosis.1 Before menopause, bone loss is usually

Osteomalacia

The term osteomalacia means soft bones. It is characterized by defective calcification of osteoid that leads to a paradoxical increase in bone volume.1 This abnormality can be demonstrated on bone biopsy performed in conjunction with tetracycline labeling. It is primarily caused by vitamin D deficiency and poor calcium absorption. Osteomalacia can occur in gastrointestinal and hepatobiliary disease, with inadequate sun exposure, and disorders of vitamin D metabolism that occur in renal disease or vitamin D-dependent rickets, and vitamin D resistance. Drugs that inhibit bone mineralization can also cause osteomalacia and include anticonvulsants, fluoride, etidronate, and aluminum. Other rare causes include renal tubular acidosis, chronic hypophosphatemia, and hypophosphatasia. Although the clinical features of these disorders are similar, the biochemical defects are different and help differentiate the underlying causes of osteomalacia. The distinction between the different causes is necessary to institute therapy in a proper fashion. In children, the defect in mineralization predominantly involves the cartilage of the epiphysis, where bone growth occurs, resulting in the deformities seen with rickets.

PN-ASSOCIATED MBD

Clinical Abnormalities