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General Recommendations: 1. Children with diabetes mellitus have the same basic nutritional requirements as other children. 2. Dietary recommendations should be based on good eating habits for the whole family. Radical changes in diet involving unusual foods or eating patterns for the child with diabetes alone are not appropriate. 3. Energy requirements of children vary widely and the energy content of the diet should be based on what the child usually eats. The diet should be reviewed regularly to meet the changing needs of growth and physical exercise without obesity. 4. The insulin regimen should, as far as is possible, be chosen to fit the child's daily lifestyle and preferred eating habits. Insulin type, dose, and frequency should be reviewed with the diet as the child develops. 5. Regular distribution of meals and snacks throughout the day remains the most important way to avoid extremes of hyperglycaemia and hypoglycaemia. This distribution should be based on an exchange system, using handy measures and taking into account food and meal type, the particular insulin regimen and the child's exercise patterns and usual eating habits. Currently this exchange system is based on carbohydrate foods but in the future the energy and fat contents will need further consideration. 6. Most special 'diabetic foods' are unnecessary. Low calorie sweeteners, as used in low calorie fruit squashes and fizzy drinks, are useful. 7. Children with diabetes from specific ethnic minority groups, or on vegan diets or living in deprived circumstances require special dietary attention for their diabetes. Those with coexisting chronic disorders such as cystic fibrosis or coeliac disease, should receive dietary advice from professionals with specialist knowledge. 8. Translating the principles of diabetic dietary management into a varied diet, arranged readily by the parents and eaten by the child, is demanding. It can best be met by a skilled dietitian working in close co-operation with child, parents, diabetes specialist nurse and doctor. Infancy 9. The diet should not differ from that of infants without diabetes. Breast feeding should be encouraged or a standard infant formula-feed used. Solids may be introduced from 3-6 months, but breast milk or a modified infant formula is encouraged as part of the increasingly mixed diet to at least the end of the first year. 10. Diabetes is rare in infancy so expert advice should be sought from dietitians experienced in paediatric diabetes. Under fives: 11.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dietary recommendations for children and adolescents with diabetes: an implementation paper. British Diabetic Association's Professional Advisory Committee. 828 37

NIDDM is a heterogeneous disease and subgroups of NIDDM include MODY (Maturity Onset Diabetes of the Young), Malnutrition-related diabetes (MRDM) and Fibrocalculus pancreatic diabetes (FCPD). Endocrine cell population is relatively unchanged in NIDDM: B-cells are reduced by up to 30% and A-cells increased by 10%. Islet amyloid is found in 96% of subjects occupying up to 80% of the islet associated with a reduction in B-cells. Amyloid formation is unlikely to cause diabetes but progressive accumulation increases the severity of the disease. Islet amyloid is formed from the islet amyloid polypeptide (IAPP), a normal constituent of B-cells, co-secreted with insulin. The causal factors for IAPP fibrillogenesis are unknown but abnormal synthesis or overproduction could be involved: stimulation of B-cell secretion in NIDDM by obesity, hyperglycaemia or suphonylurea therapy may promote amyloidosis and further aggravate islet pathology. A mutation of the glucokinase gene in MODY leads to diminished B-cell secretion but not amyloid formation. Diabetes and mutations of mitochondrial DNA is associated with poorly developed islet structure. Exocrine pancreatic size is reduced and there is evidence of sub-clinical chronic pancreatitis in NIDDM. In MRDM and FCPD, chronic pancreatitis and exocrine necrosis is associated with reduced insulin secretion. Unlike cystic fibrosis where islet amyloid is present in diabetic individuals, amyloid is absent from subjects with FCPD. Pathological changes in the exocrine and endocrine pancreas in NIDDM results from and contributes to the pathophysiology of insulin secretion in NIDDM.
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PMID:Pancreatic pathology in non-insulin dependent diabetes (NIDDM). 852 18

In children with pancreatic disease, computed tomography (CT) has a primary role in the evaluation of pancreatitis, trauma, and malignancy. At CT, pancreatic abnormalities may manifest as pancreatic enlargement (tumor, acute pancreatitis), pancreatic atrophy (cystic fibrosis, chronic pancreatitis), cystic lesions (pseudocysts, congenital simple cysts, autosomal dominant polycystic kidney disease, von Hippel-Lindau disease, cystic fibrosis, cystic neoplasms), or fatty replacement (cystic fibrosis, Shwachman-Diamond syndrome, history of steroid therapy, Cushing syndrome, Johanson-Blizzard syndrome, obesity). CT is the best modality for evaluation of pancreatitis, allowing detection of pancreatic abnormalities as well as abnormal extrapancreatic fluid collections. In children who have undergone blunt abdominal trauma, CT has been shown to be the best initial imaging study, being more sensitive than ultrasound for detection of pancreatic injury. In neoplastic conditions, CT demonstrates the extent of disease, enables characterization of the tissue components of the tumor, and allows accurate posttreatment follow-up. Although the various diseases of the pancreas may have overlapping appearances at CT, the correct diagnosis can often be made on the basis of the CT findings in combination with the clinical history, laboratory data, and the patient's age.
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PMID:Pancreatic disease in children and young adults: evaluation with CT. 974 14

The mechanisms leading to hypoxemia during sleep in patients with respiratory failure remain poorly understood, with few studies providing a measure of minute ventilation (V I) during sleep. The aim of this study was to measure ventilation during sleep in patients with nocturnal desaturation secondary to different respiratory diseases. The 26 patients studied had diagnoses of chronic obstructive pulmonary disease (COPD) (n = 9), cystic fibrosis (CF) (n = 2), neuromusculoskeletal disease (n = 4), and obesity hypoventilation syndrome (OHS) (n = 11). Also reported are the results for seven normal subjects and seven patients with effectively treated obstructive sleep apnea (OSA) without desaturation during sleep. Ventilation was measured with a pneumotachograph attached to a nasal mask. In the treated patients with OSA and in the normal subjects, only minor alterations in V I were observed during sleep. In contrast, mean V I for the group with nocturnal desaturation decreased by 21% during non-rapid-eye-movement (NREM) sleep and by 39% during rapid-eye-movement (REM) sleep as compared with wakefulness. This reduction was due mainly to a decrease in tidal volume (V T). Hypoventilation was most pronounced during REM sleep, irrespective of the underlying disease. These data indicate that hypoventilation may be the major factor leading to hypoxia during sleep, and that reversal of hypoventilation during sleep should be a major therapeutic strategy for these patients.
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PMID:Breathing during sleep in patients with nocturnal desaturation. 987 27

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

Effectiveness of treatment with domiciliary nocturnal noninvasive positive pressure ventilation is analyzed in a group of patients with chronic alveolar hypoventilation of different etiologies. It was applied with two levels of pressure (BiPAP) via nasal mask. Criteria for evaluation were symptomatology and improvement in gas exchange. Data were analyzed by Student t tests. A total of 13 patients were included, mean age 55.7 range 20 to 76 years (5 male 8 female). Main diagnosis was tuberculosis in 6, four of them having had surgical procedure (thoracoplasty 2, frenicectomy 1 and neumonectomy 1), myopathy 3 (myasthenia gravis 1, muscular dystrophy 1 and diaphragmatic paralysis 1), obesity-hypoventilation syndrome 1, escoliosis 1, bronchiectasis 1 and cystic fibrosis 1. These last two patients were on waiting list for lung transplantation. At the moment of consultation, the symptoms were: dysnea 13/13 (100%), astenia 13/13 (100%), hypersomnolency 10/13 (77%), cephalea 9/13 (69%), leg edema 6/13 (46%), loss of memory 6/13 (46%). Regarding gas exchange, they showed hypoxemia and hypercapnia. Mean follow up was of 2.2 years (range 6 months to 4 years). Within the year, all 13 patients became less dyspneic. Astenia, hypersomnolency, cephalea, leg edema and memory loss disappeared. Improvement in gas exchange was: PaO2/FiO2 from 269 +/- 65.4 (basal) to 336.7 +/- 75.3 post-treatment (p = 0.0018). PaCO2 from 70.77 +/- 25.48 mmHg (basal) to 46.77 +/- 8.14 mmHg (p = 0.0013). Ventilatory support was discontinued en 5 patients: three because of pneumonia requiring intubation and conventional mechanical ventilation, two of them died and one is still with tracheostomy; One patient with bronchiectasis and one with cystic fibrosis were transplanted. The remaining eight patients are stable. In conclusion, chronic alveolar hypoventilation can be effectively treated with domiciliary nocturnal noninvasive ventilation. Long term improvement in symptomatology and arterial blood gases can be obtained without significant complications.
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PMID:[Domiciliary noninvasive positive pressure ventilation in chronic alveolar hypoventilation]. 1118 89

Steatohepatitis in children occurs in the childhood version of non-alcoholic fatty liver disease (NAFLD), as a result of hepatotoxicity and with certain genetic/metabolic diseases. Until recently, NAFLD was considered to be rare in children. It is now recognized as an important childhood liver disease, especially because childhood obesity is much more common. Children with NAFLD may present as young as 4 years old; males tend to predominate; fibrosis is often found on liver biopsy and cirrhosis has been reported. Treatment for childhood NAFLD currently consists of weight reduction plus regular aerobic exercise; vitamin E may be an effective adjunctive therapy. Drug hepatotoxicity and genetic/metabolic diseases that can cause fatty liver, such as Wilson's disease and cystic fibrosis, must be excluded since treatment is radically different. Other causes of chronic hepatitis, such as chronic viral hepatitis, must also be excluded. Multisystemic inherited diseases with hyperinsulinaemia plus insulin resistance may have NAFLD as hepatic involvement and should be identified.
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PMID:Steatohepatitis in children. 1240 43

Sleep problems are common in many pediatric medical disorders and complicate management and patient outcomes. A wide range of conditions, including asthma, cystic fibrosis, sickle cell disease, gastroesophageal reflux, neuromuscular diseases, scoliosis, craniofacial abnormalities, obesity, and chromosomal disorders, have various sleep disturbances, including sleep-disordered breathing, ventilatory dysfunction, sleep-onset and sleep maintenance problems, and circadian rhythm disturbances. Given the adverse neurocognitive and physiologic outcomes associated with a deranged night's sleep, it is important for pediatricians to be able to anticipate, recognize, and appropriately manage these problems. This article reviews the known sleep-related problems of a few relatively common pediatric disorders.
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PMID:Sleep problems in children with common medical disorders. 1500 90

The pediatric illness experience is a complex subject that requires a multidimensional, flexible, and patient-centered approach. The video intervention/prevention assessment (VIA) method, with its diverse source data and multidisciplinary analytical frameworks, generates findings that can be examined from any number of perspectives simply by asking different questions. As an exploration of human experience, VIA can be applied to various medical and psychiatric conditions. It has been used to investigate the experiences of children and adolescents who live with asthma, obesity, spina bifida, and diabetes mellitus. VIA currently is being applied to a longitudinal examination of the transition to adulthood by pediatric patients with spina bifida, cystic fibrosis, sickle cell disease, and HIV.
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PMID:Visual narratives of the pediatric illness experience: children communicating with clinicians through video. 1593 74

The human beta-2 adrenergic receptor (beta2AR) is responsible for the binding of endogenous catecholamines and their exogenously administered agonists and antagonists. Three functional polymorphisms in codons 16, 27 and 164 have been described which have clinical importance for several diseases, including asthma, hypertension, heart failure, cystic fibrosis and obesity, as well as response to beta-agonist therapy. These were evaluated in 726 individuals from 8 distinct ethnic populations (Chinese, Filipino, Southwest Asian, Saudi, Ghanaian, Kenyan, Sudanese, and European from Scotland). The results show that most haplotypes are shared among all populations, yet there are marked differences in their frequency distributions geographically. The genetic distance tree is different from standard human population distance trees, implying a different mode of evolution for this locus than that for human population gene-flow history. The multilocus frequency differences between the observed clusters of populations correspond to historical haplotype groupings that have been found to be functionally different with respect to multiple medically related phenotypes. Further studies are needed to see if functional relationships are the same across populations.
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PMID:Beta-2 adrenergic receptor genotypes and haplotypes in different ethnic groups. 1614 89


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