SUMMARYOBJECTIVES. Subjective sleep complaints have been reported in up to 80% of patients with end stage renal disease (ESRD). In these patients, sleep disturbances manifesting as insomnia, sleep apnea syndrome, restless leg syndrome (RLS), periodic limb movement disorder and excessive daytime sleepiness (EDS) have been frequently reported. Moreover, studies about the role of dialysis shift on sleep abnormalities, morbidity and mortality are still scarce. The aim of this study was to investigate the influence of dialysis shift on the quality of sleep and sleep abnormalities in patients with ESRD. MÉTHODS. We studied one hundred consecutive patients from a dialysis center. Quality of sleep was assessed by the Pittsburgh Sleep Quality Index and subjective EDS by the Epworth Sleepiness Scale. Restless leg syndrome was diagnosed using the four minimum criteria defined by the International Restless Legs Syndrome Study Group. Clinical and laboratory parameters were obtained by interview and chart review. Adequacy of dialysis was evaluated by the Kt/V index. RESULTS. Poor quality sleep (PSQI>6) was found in 75% of cases and was associated with RLS (p=0.004) and with snoring (p=0.016). EDS (ESS>10) was present in 28% of cases. Patients with EDS (1.33±0.29) had lower values of the Kt/v index (P=0.01) than those without EDS (1.52±0.32). RLS was present in 48% of cases. Irrespective of dialysis shift, poor quality sleep, EDS and RLS were not different among patients. CONCLUSION. Poor quality sleep, EDS and RLS were common and not related to dialysis shift.

Glutamine or alanyl-glutamine accelerated the mucosal recovery increasing mucosal tissue glutathione stores, reducing inflammatory parameters and speeding reepithelization.

A 22-year-old male was admitted to the emergency department with a sore throat, dysphagia, hemoptysis, and retrosternal pain. He had attempted suicide by ingesting 50 mL of a paraquat solution four days prior to admission and had been treated, at another facility, with gastric lavage and administration of activated charcoal. It is of note that he had attempted suicide previously, on more than one occasion.

SummaryThis research investigated the effect of glutamine (Gln) depletion on leucocyte-dependent inflammatory events. Rats were treated intraperitoneally, 16 hr prior to the peak of every parameter evaluated, with either 0Á9% NaCl, methionine-sulphoximine (MSO, an inhibitor of endogenous Gln synthesis, 25 mg/kg) or with MSO + Gln (MSO as above plus Gln 3 g/kg in three doses). MSO-induced Gln depletion increased paw oedema induced both by carrageenan (Cg) and by Clostridium difficile toxin A (TxA) (66Á2% and 45Á5%, respectively; P < 0Á05). In dextran-injected animals, oedema and myeloperoxidase (MPO) activity were not modified by Gln depletion. In Cg-treated paws, Gln depletion increased MPO activity by 44% (P < 0Á05), interleukin-1b (IL-1b) and tumour necrosis factor-a (TNF-a) concentrations by 47% and 52%, respectively (P < 0Á05), and immunostaining for TNF-a in paw tissue. In TxA-injected paws, Gln depletion increased MPO activity (46%; P < 0Á05). Gln depletion increased Cg-and TxA-induced neutrophil migration to subcutaneous air pouches by 56% and 77% (P < 0Á05), respectively, but did not affect migration induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP). Gln infusions reversed all the effects of MSO. Leucocyte counts did not differ between groups. Gln depletion potentiates acute inflammation, possibly by increasing neutrophil migration through resident cell activation and production of IL-1b and TNF-a. Gln supplementation reverses these effects and may be useful during inflammatory catabolic stress.