The Impact of Agitation in Dementia on Caregivers: A Real-World Survey.

BACKGROUND: Dementia patients frequently depend on caregivers. Agitation is a common behavioral dementia symptom particularly burdensome to patients and caregivers. OBJECTIVE: To assess the association of agitation severity with non-professional caregiver hours, burden, health status, and productivity. Secondarily, to assess the association of agitation severity with these outcomes for patients receiving remote (not living with the patient) and proximate (living with the patient) caregiving. METHODS: A retrospective analysis of physician and non-professional caregiver-reported data from a US point-in-time survey. Patients were aged ≥50 years, with early cognitive impairment or dementia. Regression analyses compared outcomes by agitation severity; covariates included age, sex, and clinical characteristics. RESULTS: Data were included for 1,349 patients (non-agitated n = 656, agitated n = 693; no care n = 305, remote care n = 248, proximate care n = 691; unknown care n = 105). Greater agitation was significantly associated (p < 0.05) in all caregivers with increasing: Zarit Burden Interview (ZBI) Total Caregiver Burden, Personal Strain, Role Strain, and Guilt; Work Productivity and Activity Index (WPAI) presenteeism, overall work impairment, and total activity impairment. Higher ZBI Total Caregiver Burden, Personal Strain, and Role Strain were associated with greater agitation in proximate caregivers and higher ZBI Guilt associated with greater agitation in remote caregivers (p < 0.05). Higher WPAI presenteeism and total activity impairment were associated (p < 0.05) with greater agitation in proximate caregivers. Caregiving hours increased with increasing agitation for proximate caregiving (p = 0.001). CONCLUSION: Greater agitation severity was associated with higher caregiver burden and lower productivity, with higher indirect costs a likely outcome of agitation.

Predictors of suboptimal bowel preparation in asymptomatic patients undergoing average-risk screening colonoscopy.

AIM: To identify risk factors for a suboptimal preparation among a population undergoing screening or surveillance colonoscopy. METHODS: Retrospective review of the University of Michigan and Veteran's Administration (VA) Hospital records from 2009 to identify patients age 50 and older who underwent screening or surveillance procedure and had resection of polyps less than 1 cm in size and no more than 2 polyps. Patients with inflammatory bowel disease or a family history of colorectal cancer were excluded. Suboptimal procedures were defined as procedure preparations categorized as fair, poor or inadequate by the endoscopist. Multivariable logistic regression was used to identify predictors of suboptimal preparation. RESULTS: Of 4427 colonoscopies reviewed, 2401 met our inclusion criteria and were analyzed. Of our population, 16% had a suboptimal preparation. African Americans were 70% more likely to have a suboptimal preparation (95%CI: 1.2-2.4). Univariable analysis revealed that narcotic and tricyclic antidepressants (TCA) use, diabetes, prep type, site (VA vs non-VA), and presence of a gastroenterology (GI) fellow were associated with suboptimal prep quality. In a multivariable model controlling for gender, age, ethnicity, procedure site and presence of a GI fellow, diabetes [odds ratio (OR) = 2.3; 95%CI: 1.6-3.2], TCA use (OR = 2.5; 95%CI: 1.3-4.9), narcotic use (OR = 1.7; 95%CI: 1.2-2.5) and Miralax-Gatorade prep vs 4L polyethylene glycol 3350 (OR = 0.6; 95%CI: 0.4-0.9) were associated with a suboptimal prep quality. CONCLUSION: Diabetes, narcotics use and TCA use were identified as predictors of poor preparation in screening colonoscopies while Miralax-Gatorade preps were associated with better bowel preparation.

Characterization of dystrophic calcification induced in mice by cardiotoxin.

Dystrophic calcifications often occur after injury, infection, or onset of certain rheumatic diseases. Treatment has been limited to surgical removal following failure of medical therapy. In an attempt to establish a reproducible animal model for dystrophic calcification that permitted the screening of potential interventions, we evaluated cardiotoxin (injury)-induced calcifications in three murine strains at both the cellular and ultrastructural levels. All osteopontin null mice and tumor necrosis factor receptor null mice on a C57B6 background had calcifications at days 3 and 7 after injury compared to 75% of wild-type C57B6 mice. There was no difference in mineral content among calcifications from the three mouse strains. Osteogenesis was suggested by the expression of osteocalcin, osterix, and alkaline phosphatase in calcified murine muscle tissue. Osteoclast-like cells facilitated the removal of transient dystrophic deposits (<28 days) in all models. However, none of the models showed an association of mineral crystals with collagen, suggesting that the deposits were not bone-like. The dystrophic mechanism was validated as cell death, and mitochondrial calcifications occurred soon after skeletal muscle injury in the three murine strains.

Juvenile dermatomyositis calcifications selectively displayed markers of bone formation.

OBJECTIVE: To determine the presence of small integrin-binding ligand N-linked glycoprotein (SIBLING) and bone components in juvenile dermatomyositis (DM) pathologic calcifications. METHODS: Calcifications were removed from 4 girls with juvenile DM symptoms for mean +/- SD 36.9 +/- 48.3 months and were stained for SIBLING proteins: full-length osteopontin (OPN), bone sialoprotein (BSP), dentin matrix protein 1 (DMP1), dentin phosphoprotein (DPP), and matrix extracellular phosphoglycoprotein (MEPE); bone markers: osteocalcin (OC), core-binding factor alpha 1 (CBFalpha1), and alkaline phosphatase (AP) for osteoblasts; tartrate-resistant acid phosphatase (TRAP) for osteoclasts; and the mineral regulators osteonectin (ON) and matrix Gla protein (MGP). The deposit center, periphery, adjacent connective tissue, and vascular endothelial cells were examined. RESULTS: Alizarin red stained calcified deposits that did not localize with collagen, like bone, under polarized light. Hematoxylin and eosin stain revealed a paucity of connective tissue and absence of bone-like structures. The deposits, connective tissue, and vascular endothelial cells were positive for BSP, DPP, DMP1, and AP; MEPE was not detected. OC, ON, and MGP were present in the deposits and vascular endothelial cells; OPN and CBFalpha1 were present in deposits and connective tissue. TRAP-positive osteoclasts were localized to the calcification periphery. CONCLUSION: The disorganized juvenile DM calcifications differ in structure, composition, and protein content from bone, suggesting that they may not form through an osteogenic pathway. Osteoclasts at the deposit surface represent an attempt to initiate its resolution.