Vitamin B(12) and methylmalonic acid levels in patients presenting with polyneuropathy.

This study was designed to determine the prevalence of definite vitamin B(12) deficiency (defined as < or =240 pg/ml) and possible vitamin B(12) deficiency (defined as >240 pg/ml and a methylmalonic acid [MMA] level >243 nmol/L) in patients with polyneuropathy and to determine whether patients in both groups respond to vitamin B(12) repletion. We performed a retrospective cohort study of 581 patients presenting with polyneuropathy over a 2-year period; 4% had definite vitamin B(12) deficiency and 32% had possible deficiency as the sole or contributing cause for their polyneuropathy. For those who received treatment with vitamin B(12), subjective improvement was seen in 87% with definite and in 43% with possible deficiency. Possible vitamin B(12) deficiency, defined as an elevated MMA level, is a common finding in patients with polyneuropathy and treatment of these patients with vitamin B(12) may lead to clinical improvement.

Dietary treatment of gluten neuropathy.

We studied the effect of a gluten-free diet in patients with idiopathic sensorimotor axonal neuropathy and circulating antigliadin antibodies. Consecutive patients underwent baseline neurophysiological assessment and were offered a gluten-free diet. Those who went on the diet formed the intention-to-treat group and those who did not were the control group. Repeat neurophysiological assessment and subjective evaluation of neuropathy symptoms were performed at 1 year. A total of 35 patients participated in the study, with 25 patients going on the diet and 10 not doing so. There was a significant difference in the change of sural sensory action potentials (pre-defined primary endpoint), with evidence of improvement in the intention-to-treat group and deterioration in the control group. Subjective change in neuropathy symptoms also showed significant differences, with patients in the intention-to-treat group reporting improvement and those in the control group reporting deterioration. Gluten-free diet may thus be a useful therapeutic intervention for patients with gluten neuropathy.

[Contribution of nutritional support to treatment neuromuscular impairmets of critically ill patients]. / Contribución del soporte nutricional al tratamiento de las alteraciones neuro-musculares del paciente crítico.

Neuromuscular impairments occurring in the critically ill patient have been attributed to factors such as sepsis, release of inflammatory mediators, or the use of drugs unfavorably affecting neuromuscular function. The role of metabolic and nutritional factors in the development of this condition has received little attention. Currently, the use of protocols of intensive glycemia monitoring might be of great interest in preventing neuromuscular impairments in critically ill patients. The precise mechanisms of hyperglycemia involvement in this condition are still unknown, although evidence from research data is important. Cachectic myopathy (muscle atrophy) usually is the result of the obliged changes of metabolic response to stress. The effect of nutrients intake on muscle mass gaining is very limited, so that other actions aimed at more rapidly recovering lost muscle mass should be studied. Aggressive renutrition schedules should be avoided in order to prevent re-nutrition syndrome and further deterioration of muscle function. Intake of specific substrates, such as glutamine, might have a beneficial effect on recovering neuromuscular impairments in the critically ill patient. However, there are still no data to justify its use if the only purpose is to recover neuromuscular function.