Introduction
Aneurysmal subarachnoid hemorrhage (SAH) survivors live with long-term residual physical and cognitive disability. We studied whether neuromuscular electrical stimulation (NMES) and ...high-protein supplementation (HPRO) in the first 2 weeks after SAH could preserve neuromotor and cognitive function as compared to standard of care (SOC) for nutrition and mobilization.
Methods
SAH subjects with a Hunt Hess (HH) grade > 1,modified Fisher score > 1 and BMI < 40 kg/m
2
were randomly assigned to SOC or NMES + HPRO. NMES was delivered to bilateral quadricep muscles daily during two 30-min sessions along with HPRO (goal:1.8 g/kg/day) between post-bleed day (PBD) 0 and 14. Primary endpoint was atrophy in the quadricep muscle as measured by the percentage difference in the cross-sectional area from baseline to PBD14 on CT scan. All subjects underwent serial assessments of physical (short performance physical battery, SPPB) cognitive (Montreal Cognitive Assessment Scale, MoCA) and global functional recovery (modified Rankin Scale, mRS) at PBD 14, 42, and 90.
Results
Twenty-five patients (SOC = 13, NMES + HPRO = 12) enrolled between December 2017 and January 2019 with no between-group differences in baseline characteristics (58 years old, 68% women, 50% HH > 3). Median duration of interventions was 12 days (range 9–14) with completion of 98% of NMES sessions and 83% of goal HPRO, and no reported serious adverse events. There was no difference in caloric intake between groups, but HPRO + NMES group received more protein (1.5 ± 0.5 g/kg/d v 0.9 ± 0.4 g/kg/d,
P
< 0.01). Muscle atrophy was less in NMES + HPRO than the SOC group (6.5 ± 4.1% vs 12.5 ± 6.4%,
P
0.01). Higher atrophy was correlated with lower daily protein intake (ρ = - 0.45,
P
= 0.03) and lower nitrogen balance (ρ = 0.47, P = 0.02); and worse 3 month SPPB (ρ = - 0.31,
P
= 0.1) and mRS (ρ = 0.4, P = 0.04). NMES + HPRO patients had a better median 25%,75 SPPB (1210, 12 v. 9 4, 12, P = 0.01) and mRS (10,2 v.21, 3,
P
= 0.04) than SOC at PBD 90.
Conclusions
NMES + HPRO appears to be feasible and safe acutely after SAH and may reduce acute quadriceps muscle wasting with a lasting benefit on recovery after SAH.
Tobacco smoking is a strong cause of lung cancer. However, because only
a small proportion of smokers develop the disease, other factors,
including genetic susceptibility, may be important in ...determining lung
cancer risk. Polymorphisms in the TP53 tumor suppressor
gene and HRAS1 proto-oncogene have been associated in
some studies with this cancer; we sought to replicate these
associations in an ethnically diverse population in Hawaii. We
conducted a population-based case-control study among 334 incident lung
cancer cases and 446 controls of Caucasian, Japanese, or Native
Hawaiian origin. In-person interviews collected detailed information on
lifestyle risk factors. DNA was extracted from peripheral blood
leukocytes, and genotyping was performed using a PCR-based assay for
the TP53 codon 72 polymorphism and Southern blot
analysis and PCR for allelic polymorphisms in the HRAS1
minisatellite. Logistic regression analyses were used to compute odds
ratios (ORs) and 95% confidence intervals (CIs) adjusting for smoking
and other risk factors. The presence of two rare HRAS1
alleles was associated with a 2.2-fold (95% CI, 1.0–5.0) increased
lung cancer risk for all ethnic groups combined. The association was
present in Native Hawaiians (OR, 5.2; 95% CI, 1.1–24.4) and was
suggested for Japanese (OR, 2.8; 95% CI, 0.6–12.5); no association
was observed in Caucasians (OR, 0.8; 95% CI, 0.2–3.6). This
association was also observed for each lung cancer cell type. The
presence of only one rare allele did not increase risk for any ethnic
group or cell type. No significant association was found between the
TP53 codon 72 polymorphism and lung cancer OR, 1.4
(95% CI, 0.8–2.4) for the Pro/Pro genotype compared
with the Arg/Arg genotype. This study suggests that
the presence of two rare HRAS1 alleles confers an
increased lung cancer risk in Native Hawaiians and Japanese but
possibly not in Caucasians. The amino acid replacement of arginine by
proline at codon 72 of TP53 appears not to be important
in determining lung cancer risk in this population.
Type II odontoid fracture is a highly morbid injury among octogenarians, with 41% 1-year mortality. Our objective was to assess long-term fusion, complication, and survival rates.
Retrospective ...review of prospective trauma registry and blinded review of follow-up radiographs.
Follow-up cohort included 94 nonoperative and 17 operative patients (median, 52 and 79 months). The operative group had significantly higher rates of repeated surgery for primary treatment failure or complication (1% vs. 18%; P = 0.01) and dysphagia, aspiration events, or tracheostomy (29% vs. 78%, P = 0.002; 6% vs. 30%, P = 0.04; 1% vs. 18%, P = 0.01). Three-year all-cause mortalities were 71% and 76%, respectively (P = 0.78). No delayed myelopathy was observed. One-year postinjury radiographs were available for 13 and 6 patients in the nonoperative and operative groups (P = 0.9); bony union was observed in 3 and 5 patients (23% vs. 83%; P = 0.04). Retrolisthesis greater than 2 mm was observed in 2 and 1 patients (15% vs. 17%; P = 1.0). Two patients in the operative group underwent repeated surgery for primary treatment failure. Dysphagia was diagnosed in 3 and 5 operative patients (23% vs. 83%; P = 0.04), whereas aspiration events occurred in 0 and 3 patients (0% vs. 50%; P = 0.02). Three-year mortalities in this cohort were 38% and 67% (P = 0.35).
Radiographic union is significantly associated with operative management, but the corresponding clinical benefit is unclear. Complications were significantly more common after surgery. Long-term survival in octogenarians following type II odontoid fracture is poor, independent of management. Frequent complications without a proven survival benefit suggest that most patients are better managed conservatively.
Patients with end-stage renal failure are a high-risk group for atherosclerotic cardiovascular disease and commonly have dyslipidemia as a major factor. Dietary manipulation is the recommended first ...line of therapy for reducing lipid levels in people with normal renal function; however, complex dietary requirements of dialysis-treated patients with end-stage renal failure impose significant constraints. In this study, we evaluated the effect of trying to comply with established lipid-lowering recommendations superimposed on our normally prescribed dialysis diet over 14 weeks in stable subjects treated with either hemodialysis (HD) or chronic peritoneal dialysis (PD). Of 306 dialysis patients screened, 75 subjects were enrolled; 8 subjects did not complete the study. In the remainder, HD subjects (n equals 41) decreased saturated fat intakes by 18percnt overall and cholesterol intakes by 16percnt. This was associated with a decrease in total cholesterol levels from 232 plusmn 8 to 209 plusmn 4 mgsol dL (mean plusmn SEM; P equals 0.007) and low-density lipoprotein cholesterol levels from 147 plusmn 4 to 131 plusmn 4 mgsol dL (P equals 0.009). However, energy intakes decreased by almost 10percnt. There were no statistically significant changes in PD patients (n equals 26). Only 24.4percnt of HD (10 of 41 patients) and 15.4percnt of PD patients (4 of 26 patients) normalized their lipid levels. Considerable problems were encountered in maintaining compliance with the modified dialysis diets. This study shows that if adhered to, properly constructed dialysis diets are close to optimal lipid-lowering recommendations. Further dietary manipulation is difficult, leads to little benefit in the majority, and is accompanied by added problems of adherence. We conclude that the vast majority of dyslipidemic patients with end-stage renal failure require pharmacological therapy.
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