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Severe Malnutrition (severe + malnutrition)

Distribution by Scientific Domains
Medical Sciences71%

Selected Abstracts

Liver function test abnormalities in anorexia nervosa,Cause or effect

INTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 4 2010
Vignesh Narayanan MD
Abstract Objective: Two females with severe anorexia nervosa (BMI of 10) were seen with marked abnormalities in their liver function tests before the initiation of refeeding. These paradoxically resolved with progressive refeeding and weight restoration. Method: Clinical observation during regimented medical stabilization and refeeding of two patients with severe anorexia nervosa with frequent monitoring of liver function tests. Results: Normalization of liver function tests ensued as caloric intake increased and weight gain progressed. Discussion: Although classically liver function test elevations occur during refeeding, as a manifestation of excessive calories and fat deposition in the liver, they may also be elevated due to severe malnutrition before refeeding has commenced and improved as refeeding occurs. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010 [source]

Pneumomediastinum simulating a panic attack in a patient with anorexia nervosa

INTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 1 2003
Anita Karim
Abstract Objective Pneumomediastinum is a rare complication of anorexia nervosa. Although the mechanism is unknown, severe malnutrition may affect lung mechanics by altering the connective tissue, predisposing to pneumomediastinum. Method We describe a young male with anorexia nervosa and panic disorder who presented with symptoms similar to those of a panic attack and was diagnosed with spontaneous pneumomediastinum. Results This case illustrates the importance of considering pneumomediastinum in the differential diagnosis of panic attack in patients with eating disorders. Discussion Although spontaneous pneumomediastinum has a generally benign course, it must be differentiated from the potentially life-threatening secondary pneumomediastinum due to an esophageal tear. © 2002 by Wiley Periodicals, Inc. Int J Eat Disord 33: 104,107, 2003. [source]

Critical appraisal of the management of severe malnutrition: 1.

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 10 2006
Epidemiology, treatment guidelines
Abstract: Hospital case-fatality rates for severe malnutrition in the developing world remain high, particularly in Africa where they have not changed much over recent decades. In an effort to improve case management, WHO has developed treatment guidelines. The aim of this review is to critically appraise the evidence for the guidelines and review important recent advances in the management of severe malnutrition. We conclude that not only is the evidence base deficient, but also the external generalisability of even good-quality studies is seriously compromised by the great variability in clinical practice between regions and types of health facilities in the developing world, which is much greater than between developed countries. The diagnosis of severe wasting is complicated by the dramatic change in reference standards (from CDC/WHO 1978 to CDC 2000 in EpiNut) and also by difficulties in accurate measurement of length. Although following treatment guidelines has resulted in improved outcomes, there is evidence against the statement that case-fatality rates (particularly in African hospitals) can be reduced below 5% and that higher rates are proof of poor practice, because there is wide variation in severity of illness factors. The practice of prolonged hospital treatment of severe malnutrition until wasting and/or oedema has resolved is being replaced by shorter hospital stays combined with outpatient or community follow-up because of advances in dietary management outside of hospital. [source]

Cystic fibrosis in India,

PEDIATRIC PULMONOLOGY, Issue 12 2007
S.K. Kabra
Abstract Cystic fibrosis (CF) was considered to be non-existent in Indian subcontinent. Reports in last one decade have suggested that cystic fibrosis occurs in India but its precise magnitude is not known. Studies on migrant Indian population in United States and United Kingdom estimate frequency of CF as 1:10,000 to 1:40,000. The clinical features are similar to that reported in Caucasian population. CF in Indian children is usually diagnosed late and in advanced stage. Children are more malnourished and may have clinically evident deficiency of fat soluble vitamins. The frequency of clubbing, colonization with Pseudomonas, and laboratory evidence of pseudo-Bartter syndrome is relatively more at the time of diagnosis. Diagnostic facilities in form of sweat chloride estimation and genetic studies are not available readily. Mutation profile is different. The frequency of common mutation F508del in Indian children is between 19% and 34%. Other mutations are heterogeneous. Management of CF in India is difficult due to less number of trained manpower, limited availability, and high cost of pharmacologic agents. The determinants of early death include: severe malnutrition and colonization with Pseudomonas at the time of diagnosis, more than four episodes of lower respiratory infection per year and age of onset of symptoms before 2 months of age. To conclude, CF does occur in India; however, precise magnitude of problem is not known. There is need to create awareness amongst pediatricians, developing diagnostic facilities, and management protocols based on locally available resources. Pediatr Pulmonol. 2007; 42:1087,1094. © 2007 Wiley-Liss, Inc. [source]

Serum ghrelin levels in children with primary protein,energy malnutrition

PEDIATRICS INTERNATIONAL, Issue 4 2008
Sevin Altinkaynak
Abstract Background: Ghrelin, an appetite-stimulating peptide, increases in cachectic conditions. It probably reflects peripheral nutritional status and influences nutrient intake and growth. The aim of the present study was to determine serum ghrelin levels in children with primary protein,energy malnutrition (PEM) and to find if any correlation exists between serum ghrelin levels and the clinical presentation of those patients. Methods: Twenty-eight children with primary PEM and 10 healthy children were included. Serum fasting ghrelin levels were measured using radioimmunoassay. Results: Mean serum ghrelin level of healthy children and those with PEM were 107.7 ± 40.1 pg/mL and 141.6 ± 123.8 pg/mL, respectively (P < 0.001). Ghrelin levels were independent of age and sex (P > 0.05). Ghrelin was negatively correlated with body mass index in healthy children (P < 0.01), but not in those with PEM (P > 0.05). Mean serum ghrelin level of children with moderate malnutrition was higher than that of children with severe malnutrition (199.2 ± 154.1 pg/mL vs 98.4 ± 74.3 pg/mL, P < 0.05). Mean serum ghrelin levels of patients with kwashiorkor, marasmic kwashiorkor, and marasmus were 127.9 ± 97.8 pg/mL, 138.7 ± 95.8 pg/mL, and 162.3 ± 185.0 pg/mL, respectively (P > 0.05). Conclusion: Serum ghrelin level is higher in patients with PEM, especially in those with marasmus, compared to healthy children. Although this observation suggests that ghrelin helps to fight malnutrition in children, it is obvious that further studies are needed to clarify the exact pathogenetic mechanism regarding this condition. [source]

Serum zinc levels in children with acute gastroenteritis

PEDIATRICS INTERNATIONAL, Issue 3 2007
AKGÜN ÖLMEZ
Abstract Background: The aim of the present study was to determine the serum zinc levels on admission and 7,10 days after clinical recovery from acute gastroenteritis of <8 days' duration. Methods: This prospective study included 82 infants aged 2,24 months who had no associated bacterial infection, chronic disease, prior antibiotic use, moderate or severe malnutrition or dysentery. Forty-one healthy children formed the control group. Results: The mean serum zinc level on admission (Zn1) was 11.85 ± 2.83 ,mol/L and at 7,10 days after recovery (Zn2) was 10.92 ± 2.17 ,mol/L; mean serum zinc level of the control group was 11.81 ± 3.45 ,mol/L. Zn2 was significantly lower than Zn1, but there was no statistical difference between the mean of the control group and Zn1 and Zn2. When dehydrated patients were excluded from the patient group, Zn1 and Zn2 did not differ. Although asymptomatic, 39% of the control group had low zinc. Serum zinc levels were not affected by sex, age, clinical characteristics of the patients or severity of gastroenteritis. Conclusion: Serum zinc levels of the patients admitted with acute gastroenteritis without any other disease and without moderate or severe malnutrition were not affected by disease state. Gastroenteritis did not further decrease serum zinc levels in patients with asymptomatic or subclinical zinc deficiency. [source]