Reducing Drug-induced Xerostomia with Sorbet

SOURCE: Crogan NL. Annals Long-Term Care 2015;23:17-21.

Xerostomia, or dry mouth, is common in senior citizens, partially because of disorders that are directly associated with xerostomia (e.g., Sjogren syndrome, HIV, hepatitis C, diabetes) and, additionally, because numerous pharmacologic treatments seniors receive produce “drying” effects: anticholinergics (e.g., antimuscarinic OAB drugs, tricyclic antidepressants), sympathomimetics (e.g., milnacipran, atomoxetine), or diuretics. Although for some geriatric patients, xerostomia is merely an irksome symptom, for others it leads to impaired nutrition as well. Pharmacologic treatments (e.g., cholinergic agonists), while having some degree of efficacy, have their own adverse-effect profile. Is there a simpler, kinder way to address the problem?

As part of a quality improvement program, Crogan performed a study in cognitively intact nursing home residents (n = 22) who scored positively on a xerostomia index and were consuming medications known to induce xerostomia. They directly measured the food intake and wasted food that had been provided in the facility dining room from these subjects, comparing results from the 7 days prior to intervention to results after 6 weeks of intervention.

The active intervention was provision of 2 ounces of sugar-free lemon-lime sorbet prior to lunch and dinner for 6 weeks. Measured outcomes included fluid intake during meals — with decreased fluid intake suggesting less dry mouth — calorie intake, and body weight.

Pre-meal sorbet was associated with a (mean) 22% increase in food intake, and 81% of participants either maintained or gained weight. Provision of pre-meal sorbet may improve nutrition among seniors treated with medications that produce xerostomia.

 

The Ongoing Search for Cognitive Impairment Biomarkers

SOURCE: Wang T, et al. J Clin Psychiatry 2015;76:135-141.

Messenger RNA (mRNA) markers are used for identification of a variety of pathologic processes, most recently malignant melanoma. Although the labels “BACE1” and “miRAN107” likely hold little meaning for most clinicians, investigators have found that diminished levels of these particular biomarkers may help identify persons with cognitive impairment, specifically in Alzheimer’s disease.

The low levels of such biomarkers in cerebrospinal fluid (CSF) as a correlate of dementia — as well as identification of their diminution being associated with tissue deposition of amyloid — strengthens the case, considering their etiologic role in dementing disorders. Because of the relative inaccessibility of CSF, however, it is fortunate that biomarker plasma levels of BACE1 and miRAN107 reflect CSF levels.

In a study of elderly patients with Alzheimer’s disease (n = 97), mild cognitive impairment (n = 116), or normal cognitive function (n = 81), investigators identified a nearly four-fold lower plasma level of BACE1 and miRAN107 in mild cognitive impairment (as well as Alzheimer’s disease) compared to healthy controls. The authors are hopeful that these biomarkers may ultimately help us identify mild cognitive impairment early, as well as discriminate Alzheimer’s disease from other forms of dementia.

 

Bipolar Disorder is Associated with New-onset CVD

SOURCE: Goldstein BI, et al. J Clin Psychiatry2015;76:163-169.

Although perhaps not widely recognized, bipolar disorder (BPD) is associated with an excessive risk of cardiovascular disease (CVD). Not only is CVD more prevalent, but it occurs as much as a decade earlier than comparators without BPD. Some of this risk is attributed to utilization of pharmacotherapies that are known to be diabetogenic (e.g., mood stabilizers), but this is insufficient to fully explain the observed increased CVD risk.

To better clarify risk of CVD in BPD patients, an analysis was performed of persons in the NESARC epidemiologic survey (National Epidemiologic Survey on Alcohol and Related Conditions). The population studied included persons with BPD (n = 1439), major depressive disorder (n = 4396), and controls (n = 26,266). The incidence of CVD was compared in two survey “waves,” the first performed in 2001-2002, and the next performed in 2004-2005.

Even within this very short window of observation, the odds ratio for new onset CVD amongst persons with BPD was over 2.5 compared to controls. In contrast, persons with Major Depressive Disorder did not have an incidence of CVD that differed meaningfully from controls.

These concerning data show a nearly 3-fold increase risk of new onset CVD in persons with BPD, despite being controlled for commonly recognized risk factors (e.g., age, smoking, HTN, obesity). Equally alarming is the observation that the mean age of CVD onset in BPD patients was 14-17 years earlier than controls! Clinicians should heighten their vigilance for addressing CVD risk factors amongst persons with BPD.