Clinical Neuroscience

[Changes of the immune functions in patients with eating disorders]

PÁLI Anikó Andrea1, PÁSZTHY Bea1

DECEMBER 20, 2008

Clinical Neuroscience - 2008;61(11-12)

[Aims - In this study we investigated whether calorie restriction or redundant food intake influences the function of regulatory T cells (Tregs), and their main regulators (dendritic cells and macrophages), or the targets of Tregs, CD4+ lymphocytes. Patients and methods - We investigated 11 white adolescents (10 girls and 1 boy) with anorexia nervosa, 12 obes adolescents and 10 healthy controlls. With flow cytometry we determined the prevalence of Tregs, myeloid and plasmacytoid dendritic cells. We applied intracellular staining to investigate TNF-alpha and IL-12 production of macrophages, moreover IL-2, IL-4, and IFN-gamma production of CD4+ cells. We also determined calcium flux kinetics upon activation in CD4+ cells. Results - We did not find any difference between obese, anorectic and control individuals in the prevalence of Tregs, dendritic cells, TNF-alpha and IL-12 positive macrophages, IL-4 and IFN-gamma positive CD4+ lymphocytes. We found that the prevalence of IL-2 positive lymphocytes after activation was lower in anorectic than in control subjects [median (range): 11.50 (7.60-15.30) vs. 13.50 (12.00-22.00), p=0.023], and in obese patients, too [12.50 (8.50-15.50) vs. 13.50 (12.00-22.00), p=0.028]. IFN-gamma/IL-4 ratio in CD4+ cells was higher in obese patients compared with control (p=0.046). The calcium flux characteristics of lymphocytes upon activation differed markedly in anorectic and healthy subjects as maximal calcium levels developed later in anorectic patients [86 (45- 232) vs. 215 (59-235) second, p<0.05]. We also tested the association between lymphocyte activation parameters and patients' clinical status, but did not find any association between the variables. Discussion - Our results suggest that the antigen presenting cell - regulatory T cell - CD4+ lymphocyte axis might be affected by calorie and nutritional disturbances, further studies are needed to elucidate the underlying processes.]

AFFILIATIONS

  1. Semmelweis Egyetem, I. Gyermekgyógyászati Klinika, Budapest

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[Pediatric intraventricular tumors present a well circumscribed group from surgical point of view. These tumors growing in the ventricular system cause hydrocephalus in most of the cases, the presenting symptoms are the signs of raised intracranial pressure. The mass lesion may remain silent for a long period, especially in infancy due to compensatory mechanisms, and the tumor might reach extreme size making the surgery a real challenge. This group has very specific postoperative problems resulting from the disturbance of CSF circulation. In this study we present the retrospective analysis of 55 patient operated for intraventricular tumor in the National Institute of Neurosurgery between 1991 and 2006. Data were analysed regarding histological type, presenting symptoms, type of surgical approach, radicalitiy of the resection and postoperative complications. In addition to our own results brief presentation of the specific histological groups is given based on the available literature.]

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[Purpose - Analysis of history of our five patients with intractable epilepsy whose illnes have begun with prolonged status epilepticus (SE) and high-grad fever of unknow cause. Methods - Retrospective study analysis of selected five intractable epileptic patients at a median age of 11.5 (8-14) years. Results - All children had normal development before epilepsy begun. Intractable SE lasted 3-10 (median seven) days by four patients and three months by one patient. The cause of illness was unknow at the beginning and the MRI were normal. Intractable epilepsy followed the SE in all cases without any latent period. Follow-up of the children was 3-15 (median 9.5) years. The seizures came continually with few-day-long breaks, antiepileptic drugs were ineffective. Semiology of seizures, EEG, and functional imaging examinations (PET, SPECT) referred to temporal and frontal lobe damages. Later on, the MR images showed hippocampal sclerosis in one patient and mild generalized brain atrophy in the others. During the years, cognitive deterioration and behavioral problems have been realized. The most severe patient developed tetraparesis, fell in vigil coma and died after five years. Conclusions - The symptoms of our patients fulfilled the criteria of devastating epileptic encephalopathy in schoolaged children.]

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[Objective and background - Severe myoclonic epilepsy in infancy (SMEI; Dravet's syndrome) is a malignant epilepsy syndrome characterized by prolonged febrile hemiconvulsions or generalized seizures starting in the first year of life. Later on myoclonic, atypical absence, and complex partial seizures appear. When one of these seizure forms is lacking the syndrome of borderline SMEI (SMEB) is defined. Psychomotor delay resulting in mental retardation is observed during the second year of life. In most patients a de novo sodium channel alfa-1 subunit (SCN1A) mutation can be identified. By reviewing the clinical, laboratory, and neuroimaging data of our SMEI patients diagnosed between 2000 and 2008, we would like to share our experiences in this rare but challenging syndrome. Our results will facilitate the earlier and better diagnosis of Hungarian children with SMEI. Patients and methods - Clinical, EEG, MRI and DNA mutation data of 20 SMEI patients treated in the Bethesda Children’s Hospital (Budapest) were reviewed. Results - The first seizure appeared at age 6.3±3.0 months. At least one of the first two seizures were complex febrile seizures in 19/20 and unilateral seizures in 12/20 children. All children except for one showed hemiconvulsions at least once; all children had seizures lasting longer than 15 minutes. Eight of twenty patients had SMEB. DNA diagnostics identified an SCN1A mutation in 17 patients (6 missense, 4 nonsense, 4 frameshift, 2 splice site, 1 deletion) while 3 children had no mutation. Conclusion - Early diagnosis of SMEI is important for the avoiding unnecessary examinations and false therapies as well as for genetic counselling. Typical symptoms of SMEI are early and prolonged febrile hemiconvulsions with neurological symptoms, mental retardation and secondary seizure types later on. The presence of an SCN1A mutation supports the diagnosis. We propose the availability of molecular diagnostics and stiripentol therapy for SMEI children in Hungary.]

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