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By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is an advisor for Endo, Kowa, Pricara, and Takeda.
Fracture Risk Stratification in Diabetics
Source: Schwartz AV, et al. Association of BMD and FRAX score with risk of fracture in older adults with type 2 diabetes. JAMA 2011;305:2184-2192.
It has recently been recognized that type 2 diabetes (DM2) increases risk for osteoporotic fracture, even though it has been demonstrated that DM2 is associated with a paradoxical increase in bone mineral density (BMD) compared to age-matched control populations. With a burgeoning prevalence of DM2 in the United States, almost 20% of the at-risk population for osteoporotic fracture has DM2, hence, clarification of risk stratification for this group is highly relevant.
The World Health Organization (WHO) and the U.S. National Osteoporosis Foundation (NOF) suggest that clinicians assess patient risk for osteoporotic fracture by means of the fracture risk algorithm (FRAX) score. FRAX, an online risk assessment tool (available free of charge at http://www.shef.ac.uk/FRAX/), allows input of patient characteristics including gender, ethnicity, body mass index, risk factors for osteoporosis, history of fracture, family history of fracture, and BMD to calculate a 10-year risk of any osteoporotic fracture as well as 10-year risk of hip fracture. Similar to the structure of the ATPIII lipid guidance, intervention is threshold-based: Anyone with a 10-year risk of hip fracture > 3%, or total fracture risk > 20%, should be considered for pharmacotherapeutics intervention.
Gathering data from three prospective observational studies (n = 9449 women, 7346 men), Schwartz et al studied the relationship between FRAX scores, BMD, and subsequent osteoporotic fractures. Of concern, for any given T-score or FRAX score, the rate of osteoporotic fractures was higher in DM2 subjects than controls. DM2 appears to be a risk factor for osteoporotic fracture, above and beyond what is predicted by BMD or FRAX.
Amantadine for Dysphagia in the Elderly
Source: Gokula M, et al. Does amantadine help elderly residents with symptomless dysphagia? Ann Long-Term Care 2011;19:37-40.
When amantadine (amtd) was an appropriate first-line treatment for influenza, clinicians gained familiarity with its use. In the last decade, influenza resistance to the adamantanes (i.e., AMTD, rimantadine) has essentially eliminated their utility. The safety profile of AMTD is excellent however, heightening interest in clinical use for other syndromes.
Dysphagia in the elderly can be problematic, potentially leading to feeding difficulties and aspiration pneumonia. Probably the two most common scenarios in which we encounter dysphagia are Parkinson's disease and post-stroke, each of which is associated with reduced levels of dopamine. Since AMTD is a dopamine agonist, there is putative rationale for its potential use in dysphagia.
Gokula et al report their clinical experiences with AMTD in elderly patients with dysphagia. Based on positive responses in two test cases, they performed an uncontrolled case series (n = 12) among dysphagia subjects in a long-term care facility using an AMTD dose of either 50 mg or 100 mg/d orally. By 4 weeks, 11 of the 12 subjects demonstrated better swallowing, decreased cough, and weight gain. Additionally, fewer episodes of aspiration were seen.
Because AMTD is generally well tolerated, inexpensive, and there is little other resource for addressing dysphagia, clinicians may wish to consider a clinical trial.
Is Homocysteine a Culprit in Aging Skin?
Source: Namazi MR, Feily A. Homocysteine may accelerate skin aging: A new chapter in the biology of skin senescence? J Am Acad Derm 2011;64: 1175-1178.
The association of homocysteine (HCST) with atherosclerosis is as strong and consistent as cholesterol, which prompted a flurry of clinical trials in the 1990s and early 2000s attempting to improve cardiovascular outcomes by lowering HCST levels (usually with pharmacologic doses of B vitamins). Unfortunately, HCST modulation did not result in cardiovascular risk reduction, to the point that interventions aimed at HCST have been largely abandoned.
HCST might, however, be a culprit in aging skin. Photoaging is attributed to up-regulation of cutaneous matrix metalloproteinases and down-regulation of collagen synthesis. Homocystinuria, an inborn error of metabolism characterized by marked elevation of HCST, is characterized by thin, transparent skin.
HCST negatively impacts the three primary structural elements of healthy skin: collagen, elastin, and proteoglycans. Not only does elevated HCST increase degradation of these components, it also inhibits their regeneration.
There have not yet been any clinical trials to examine whether HCST reduction favorably impacts skin aging.