Metabolic bone disease and parenteral nutrition

Abstract

Metabolic bone disease (MBD) is abnormal bone metabolism and includes the common disorders of osteoporosis and osteomalacia, which can develop in patients receiving long-term parenteral nutrition (PN). Patients who require long-term PN have significant gastrointestinal failure and malabsorption, which is generally caused by severe inflammatory bowel disease, intestinal ischemia, or malignancy. The exact cause of MBD in long-term PN patients is unknown, but its origin is thought to be multifactorial, with factors including underlying disease, effect of medications used to treat this disease (eg, corticosteroids), and various components of the PN solution. Caring for patients on long-term PN requires routine assessment and monitoring for MBD. Appropriate adjustments of the PN solution can help reduce the risk for developing PN-associated MBD and in some instances improve bone mineral density. Recent developments in pharmacologic treatment for osteoporosis show promise for patients with MBD receiving PN.

Macronutrients in Parenteral Nutrition: Amino Acids

“…Intrinsic acidity of AA mixtures is often neglected [38]: metabolic acidosis (in the short term) [39,40] and metabolic bone disease (long term) [41,42] could derive from the excessive exogenous administration and/or massive endogenous production of non-volatile acids. The exogenous non-volatile acids originate from inorganic acids added to the PN mixtures to support their physical-chemical stability.…”

Parenteral Nutrition Basics for the Clinician Caring for the Adult Patient

“…Often multifactorial, this bone loss is associated with many medical conditions (diabetes mellitus, liver cirrhosis, sclerosing cholangitis, hyperthyroidism, hyperparathyroidism, pancreatic insufficiency, short bowel syndrome, Crohn's disease, and postgastrectomy syndrome) as well as immobilization. [83][84][85] Medications can also contribute to MBD, with commonly implicated ones including corticosteroids, anticonvulsants, heparin, antiretrovirals, warfarin, and overreplacement of levothyroxine. Aluminum contamination in PN and tobacco and alcohol use have also been associated with increased risk of MBD development.…”

“…Chemical markers for disease include hypercalcemia or hypocalcemia, low to normal parathyroid hormone (PTH) level, elevated urine calcium, and increased alkaline phosphatase. 84,85 Numerous elements of PN nutrient composition have been postulated to affect bone metabolism. Therefore, careful PN admixture design for the long-term PN patient is important to minimize risk.…”

“…PN Components and Factors Associated With Metabolic Bone Disease [84][85][86][87]. Ca 2+ , calcium; GFR, glomerular filtration rate; IV, intravenous; Mg 2+ , magnesium; PN, parenteral nutrition; PTH, parathyroid hormone.…”

Recent developments in aluminium contamination of products used in parenteral nutrition

“…Early papers describing the role of aluminium toxicity in patients receiving parenteral nutrition associated with abnormal bone metabolism were related to solutions containing casein hydrolysates, a precursor to today's crystalline amino acids. Parenteral nutrition solutions prepared with casein hydrolysates contained as much as 3400 mg/day of aluminium [3,52]. Popinska and colleagues [53], in 1999, revisited the problem in the era of crystalline amino acids.…”