Background Fetal alcohol spectrum disorders (FASD) is a group of conditions resulting from prenatal alcohol exposure (PAE). Patients with FASD experience a variety of neuropsychological symptoms resulting from central nervous system impairment. Little is known about sleep disorders associated with PAE. The objective of this study was to investigate sleep problems related to FASD. Methods Forty patients (median age 8 years (6; 11)) diagnosed with FASD and forty typically developing children (median age 10 years (8; 13)) were recruited for the 1st phase of the study. In the 1st phase, the screening of sleep problems was performed with Child Sleep Habit Questionnaire (CSHQ) filled in by a caregiver. Those of the FASD group who scored above 41 points were qualified to the 2nd phase of the study and had an in-lab attended polysomnography (PSG) performed. The measurements consisted of electroencephalogram, electrooculograms, chin and tibial electromyogram, electrocardiogram, ventilatory monitoring, breathing effort, pulse oximetry, snoring and body position. Their results were compared to PSG laboratory reference data. Results The number of participants with sleep disturbances was markedly higher in the FASD group as compared to typically developing children (55% vs. 20%). The age-adjusted odds ratio for a positive result in CSHQ was 4.31 (95% CI: 1.54–12.11; p = 0.005) for FASD patients as compared to the control group. Significant differences between the FASD as compared to the typically developing children were observed in the following subscales: sleep onset delay, night wakings, parasomnias, sleep disordered breathing, and daytime sleepiness. Children from the FASD group who underwent PSG experienced more arousals during the sleep as compared with the PSG laboratory reference data. The respiratory indices in FASD group appear higher than previously published data from typically developing children. Conclusion The results support the clinical observation that sleep disorders appear to be an important health problem in individuals with FASD. In particular distorted sleep architecture and apneic/hypopneic events need further attention.

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Congenital chloride diarrhea (CLD) is a rare, autosomal recessive disorder caused by mutations in the solute-linked carrier family 26 member 3 gene (SLC26A3) located in chromosome 7q31. The encoded protein belongs to the ion transporter family and is responsible for sodium-independent Cl À /HCO 3 À ion exchange. In this process, the exchanger protein located in the apical brush border of the intestinal epithelium in the ileum and large bowel subserves the absorption of chloride by epithelial cells and secretion of bicarbonate into the lumen of the bowel (1). Mutation disrupts this process and leads to secretory diarrhea with a high chloride content in the stool, hypochloremia, hyponatremia, and metabolic alkalosis. The first symptoms appear prenatally as polyhydramnios. Ultrasonography shows dilated intestinal loops. Premature birth is common (2). Without adequate treatment (replacement therapy with NaCl and KCl), severe electrolyte disturbances develop with episodes of dehydration. Chronic hypovolemia, followed by high aldosterone and elevated plasma renin activity, may lead to renal function impairment (2-4). Failure to thrive may occur (2).Celiac disease (CD) is characterized by immunemediated gluten intolerance resulting in enteropathy with atrophy of small bowel mucosa and impairment of food absorption. CD has a genetic background and is strongly associated with HLA DQ2, or DQ8. The prevalence of CD in Europe is estimated as 1 in 100 to 500. The most typical symptoms of its classical form in small children are chronic diarrhea and failure to thrive (5).

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