Objective To assess the effectiveness and safety of melatonin in treating severe sleep problems in children with neurodevelopmental disorders.Design 12 week double masked randomised placebo controlled phase III trial.Setting 19 hospitals across England and Wales.Participants 146 children aged 3 years to 15 years 8 months were randomised. They had a range of neurological and developmental disorders and a severe sleep problem that had not responded to a standardised sleep behaviour advice booklet provided to parents four to six weeks before randomisation. A sleep problem was defined as the child not falling asleep within one hour of lights out or having less than six hours’ continuous sleep.Interventions Immediate release melatonin or matching placebo capsules administered 45 minutes before the child’s bedtime for a period of 12 weeks. All children started with a 0.5 mg capsule, which was increased through 2 mg, 6 mg, and 12 mg depending on their response to treatment.Main outcome measures Total sleep time at night after 12 weeks adjusted for baseline recorded in sleep diaries completed by the parent. Secondary outcomes included sleep onset latency, assessments of child behaviour, family functioning, and adverse events. Sleep was measured with diaries and actigraphy.Results Melatonin increased total sleep time by 22.4 minutes (95% confidence interval 0.5 to 44.3 minutes) measured by sleep diaries (n=110) and 13.3 (−15.5 to 42.2) measured by actigraphy (n=59). Melatonin reduced sleep onset latency measured by sleep diaries (−37.5 minutes, −55.3 to −19.7 minutes) and actigraphy (−45.3 minutes, −68.8 to −21.9 minutes) and was most effective for children with the longest sleep latency (P=0.009). Melatonin was associated with earlier waking times than placebo (29.9 minutes, 13.6 to 46.3 minutes). Child behaviour and family functioning outcomes showed some improvement and favoured use of melatonin. Adverse events were mild and similar between the two groups.Conclusions Children gained little additional sleep on melatonin; though they fell asleep significantly faster, waking times became earlier. Child behaviour and family functioning outcomes did not significantly improve. Melatonin was tolerable over this three month period. Comparisons with slow release melatonin preparations or melatonin analogues are required.Trial registration ISRCT No 05534585.
Migration to a different culture may affect opportunities for play and social interaction, essential for children's developing cognitive and social skills. We asked Somali migrant women about experiences of childhood (both while growing up themselves, and subsequent observations) in Somalia and the UK. In Somalia, they described a supportive, connected community and safe environment enabling children to play and learn together. In the UK, by contrast, multiple local stressors constrained children's opportunities to play and interact. Understanding and improving neighbourhood geography, as experienced and shaped by parents and children, would seem important for promoting early child development in refugee families.
A young boy presented with a rash, fever, and cervical lymphadenopathy, originally thought to be caused by tuberculosis. A lymph node biopsy showed the features of Kikuchi's disease, with necrosis and histiocytic infiltration without neutrophils. No evidence of tuberculosis was found on staining, culture, or the polymerase chain reaction. Bone marrow biopsy revealed prominent haemophagocytosis, and a diagnosis of haemophagocytic syndrome was reached. The aetiology of haemophagocytic syndrome, and its association with Kikuchi's lymphadenitis, is discussed. (J Clin Pathol 2000;53:636-638)
Cell-mediated immunity is important in maintaining the virus-host equilibrium in persistent human cytomegalovirus (HCMV) infection. The HCMV 72-kDa major immediate early 1 protein (IE1) is a target for CD8+ cytotoxic T cells in humans, as is the equivalent 89-kDa protein in mouse. Less is known about responses against this protein by CD4+ T cells, which may be important as direct effector cells or helper cells for antibody and CD8+ responses. Proliferative-T-cell responses to HCMV IE1 were studied in normal seropositive subjects. Peripheral blood mononuclear cells from 85% of seropositive subjects proliferated in response to HCMV from infected fibroblasts, and of these, 73% responded to recombinant baculovirus IEL. Responding cells were predominantly CD3+ CD4+. IEl antigen preparations, including baculovirus recombinant protein, transfected rat cell nuclei, and synthetic peptides, induced IEl-specific T-cell lines which cross-reacted between the preparations. The fine specificity of these IEl-specific T-cell lines was studied by using overlapping synthetic peptides encompassing the entire sequence of the IE1 protein. The regions of the IEl molecule recognized were identified and these varied between individuals, possibly reflecting differences in major histocompatibility complex (MHC) class II haplotype. In one subject, the peptide specificities of proliferative and MHC class I-restricted cytotoxic determinants on IE1 were spatially distinct. Thus, no single immunodominant T-cell determinant within HCMV IE1 was identified, suggesting that multiple peptides or a region of the 72-kDa TEl protein would be required to induce specific T-cell responses in humans.
Ribavirin and bronchiolitis: variation in use in the UKEDITOR,-Following a recent study demonstrating the lack of eYcacy of dexamethasone in bronchiolitis, 1 Everard has commented that there is little evidence that any specific treatment for bronchiolitis is of major clinical benefit.2 The American Academy of Pediatrics (AAP) has issued guidelines for the use of ribavirin in respiratory syncytial virus (RSV) bronchiolitis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.