Body composition in patients with primary neuromuscular disease assessed by dual energy X-ray absorptiometry (DXA) and three different bioimpedance devices.

BACKGROUND: Patients with primary neuromuscular disease have reduced muscle mass, and use of body mass index to assess nutritional status and body composition can therefore be questioned. Dual emission X-ray absorptiometry (DXA) can estimate muscle mass, but is not always readily available. Bioimpedance is a simple, portable and "easy to use" method for the assessment of body composition. OBJECTIVES: To assess muscle mass by DXA in 143 patients with primary neuromuscular disease and validate three bioimpedance devices; Impedimed SFB7, (BISIMPEDIMED), Xitron4200 (BISXITRON) and Tanita MC180MA (MFBIATANITA). METHODS: Body composition was assessed by DXA in 143, by BISIMPEDIMED in 116, by MFBIATANITA in 104 and by BISXITRON in 35 patients. RESULTS: Muscle mass assessed by DXA, and phase angle (PhA) were below reference values in all female and 96% of male patients. BISIMPEDIMED underestimated muscle mass by 6.5 ± 14.2 kg (p < 0.001), but this could be corrected after exclusion of resistance (Ri) values > 3500 Ohm (p = 0.84). MFBIATANITA overestimated muscle mass by 30.8 ± 9.1 kg (p < 0.001) with systematic bias, whereas BISXITRON was in agreement with DXA, and without systematic bias. Muscle mass was strongly correlated to PhA (rPEARSON = 0.75, p < 0.01). CONCLUSION: Patients with primary neuromuscular disease have proportionally more fat and less muscle mass than the population in general, despite normal BMI. Muscle mass can be assessed by bioimpedance in these patients, but performance and bias depends on device. Phase angle by bioimpedance correlates to muscle mass, and could therefore potentially be used a surrogate measure of muscle mass during follow up.

Increased nitric oxide in exhaled air after intake of a nitrate-rich meal.

Exhaled and nasal NO (ENO, NNO) have been suggested as markers for inflammation in lower and upper respiratory tract respectively. It is still unknown how a number of factors, apart from airway inflammation, can influence NO levels. The aim of this study was to determine the effect of a nitrate-rich meal on ENO and NNO. Sixteen healthy subjects were observed during 1 week on normal diet before a nitrate-restricted diet was introduced in the next. On day 3 of the second week they were made to ingest a nitrate rich meal. ENO, NNO, plasma nitrate and plasma L-arginine were followed before the meal and afterwards for 3 h. ENO and NNO as well as plasma nitrate and plasma L-arginine were significantly elevated after the nitrate-rich meal. The median maximal increase of ENO and NNO was 47% and 13% respectively. We found a moderate but significant correlation between the rise in plasma nitrate and ENO (r(s)=0.57, P=0.027) but none between plasma nitrate and NNO (r(s)=-0.02, P=0.95). As nitrate in the diet seems to substantially influence the levels of ENO it is important either to restrict or register the intake of nitrate-rich food prior to measuring ENO.