Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Undernutrition in older persons usually presents as weight loss and is predominantly due to protein energy wasting. The presentation of undernutrition is often subtle in older persons and there is a need to utilize screening tools and increasing physician awareness. There are multiple treatable causes of undernutrition in older persons. The major causes are anorexia, cachexia, sarcopenia, dehydration, malabsorption and hypermetabolism. This article also provides an overview of the use of nutritional supplements and an approach to managing protein energy wasting.
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PMID:Undernutrition in older adults. 2239 63

Over the last 30 years, major advances have occurred in our understanding of the disorder cystic fibrosis (CF) with the discoveries of the underlying chloride transport defect and the 'CF gene', the CF transmembrane conductance regulator gene. Equally important from a clinical and patient perspective are the improvements in median survival from less than 10 to 20 years prior to 1980, approaching 30 years during the 1980s and over 45 years more recently. Improved antibiotic regimens and lung clearance therapy contributed to the enhanced survival, but a key factor accredited as adding a further 10 years to the median survival was improving and then maintaining normal growth and nutrition. In the main, the latter were achieved by adherence to a 'high-fat high-energy' diet rather than the advocated virtually universal policy of the 'low fat', which was associated with wasting and linear growth failure. The high-fat diet in conjunction with better control of malabsorption due to microspheric pancreatic enzyme replacement therapy, attention to adequate fat-soluble vitamin supplementation and newborn screening has ensured that at least 80-90% of children with CF will achieve better health and survival through their adult years.
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PMID:Nutritional care in children with cystic fibrosis: are our patients becoming better? 2346 46

Osteomalacia is a rare disorder of bone metabolism leading to reduced bone mineralization. Underlying vitamin D deficiency and a disturbed phosphate metabolism (so-called hypophosphatemic osteomalacia) can cause the disease. Leading symptoms are dull localized or generalized bone pain, muscle weakness and cramps as well as increased incidence of falls. Rheumatic diseases, such as polymyalgia rheumatica, rheumatoid arthritis, myositis and fibromyalgia must be considered in the differential diagnosis. Alkaline phosphatase (AP) is typically elevated in osteomalacia while serum phosphate and/or 25-OH vitamin D3 levels are reduced. The diagnosis of osteomalacia can be confirmed by an iliac crest bone biopsy. Histological correlate is reduced or deficient mineralization of the newly synthesized extracellular matrix. Treatment strategies comprise supplementation of vitamin D and calcium and for patients with intestinal malabsorption syndromes vitamin D and calcium are also given parenterally. In renal phosphate wasting syndromes substitution of phosphate is the treatment of choice, except for tumor-induced osteomalacia when removal of the tumor leads to a cure in most cases.
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PMID:[Metabolic bone disease osteomalacia]. 2481 56

Malnutrition and tuberculosis are both problems mostly of the developing countries. Tuberculosis can lead to malnutrition and malnutrition may predispose to tuberculosis. Poor nutrition leads to protein-energy malnutrition and micronutrients deficiencies which lead to immunodeficiency. This secondary immunodeficiency increases the host's susceptibility to infection and hence increase the risk for developing tuberculosis. Tuberculosis itself leads to reduction in appetite, nutrient malabsorption, micronutrient malabsorption, and altered metabolism leading to wasting and poor nutritional status. Nutritional status and dietary intake and hence nutritional status of patients get improved during antituberculosis treatment.
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PMID:Significance of nutrition in pulmonary tuberculosis. 2491 51

Monoallelic desmoglein 1 mutations have been known for many years to cause striate palmoplantar keratoderma, but only recently, biallelic loss-of-function mutations were associated with a new disorder, designated as SAM syndrome (comprising severe dermatitis, multiple allergies and metabolic wasting) in two consanguineous families. We report on a new case from a third independent family with the homozygous nonsense mutation, c.2659C>T, p.R887* in exon 15 of DSG1 (desmoglein 1 gene). This mutation led to mRNA decay and loss of expression of desmoglein 1. The clinical phenotype consisted of severe palmoplantar keratoderma, dermatitis and multiple allergies. In contrast to the previous cases, malabsorption, hypoalbuminaemia, developmental delay, hypotrichosis or severe recurrent infections were not observed.
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PMID:Loss of desmoglein 1 associated with palmoplantar keratoderma, dermatitis and multiple allergies. 2504 Oct 99

Despite global efforts to reduce childhood undernutrition, current interventions have had little impact on stunting and wasting, and the mechanisms underlying growth faltering are poorly understood. There is a clear need to distinguish populations of children most likely to benefit from any given intervention and to develop tools to monitor response to therapy prior to the development of morbid sequelae. In resource-limited settings, environmental enteric dysfunction (EED) is common among children, contributing to malnutrition and increasing childhood morbidity and mortality risk. In addition to EED, early alterations in the gut microbiota can adversely affect growth through nutrient malabsorption, altered metabolism, gut inflammation, and dysregulation of the growth hormone axis. We examined the evidence linking EED and the gut microbiome to growth faltering and explored novel biomarkers to identify subgroups of children at risk of malnutrition due to underlying pathology. These and other biomarkers could be used to identify specific groups of children at risk of malnutrition and monitor response to targeted interventions.
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PMID:Biomarkers to Stratify Risk Groups among Children with Malnutrition in Resource-Limited Settings and to Monitor Response to Intervention. 2848 22

Cryptosporidiosis is a nationally notifiable gastrointestinal illness caused by parasitic protozoa of the genus Cryptosporidium, which can cause profuse, watery diarrhea that can last up to 2-3 weeks in immunocompetent patients and can lead to life-threatening wasting and malabsorption in immunocompromised patients. Fecal-oral transmission of Cryptosporidium oocysts, the parasite's infectious life stage, occurs via ingestion of contaminated recreational water, drinking water, or food, or following contact with infected persons or animals, particularly preweaned bovine calves (1). The typical incubation period is 2-10 days. Since 2004, the annual incidence of nationally notified cryptosporidiosis has risen approximately threefold in the United States (1). Cryptosporidium also has emerged as the leading etiology of nationally notified recreational water-associated outbreaks, particularly those associated with aquatic facilities (i.e., physical places that contain one or more aquatic venues [e.g., pools] and support infrastructure) (2). As of February 24, 2017, a total of 13 (54%) of 24 states reporting provisional data detected at least 32 aquatic facility-associated cryptosporidiosis outbreaks in 2016. In comparison, 20 such outbreaks were voluntarily reported to CDC via the National Outbreak Reporting System for 2011, 16 for 2012, 13 for 2013, and 16 for 2014. This report highlights cryptosporidiosis outbreaks associated with aquatic facilities in three states (Alabama, Arizona, and Ohio) in 2016. This report also illustrates the use of CryptoNet, the first U.S. molecularly based surveillance system for a parasitic disease, to further elucidate Cryptosporidium chains of transmission and cryptosporidiosis epidemiology. CryptoNet data can be used to optimize evidence-based prevention strategies. Not swimming when ill with diarrhea is key to preventing and controlling aquatic facility-associated cryptosporidiosis outbreaks (https://www.cdc.gov/healthywater/swimming/swimmers/steps-healthy-swimming.html).
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PMID:Using Molecular Characterization to Support Investigations of Aquatic Facility-Associated Outbreaks of Cryptosporidiosis - Alabama, Arizona, and Ohio, 2016. 2852 Jul 7

Pediatric heart failure is a complex disease occurring when cardiac output is unable to meet the metabolic demands of the body. With improved surgical interventions and medical therapies, survival rates have improved, and care has shifted from focusing on survival to optimizing quality of life and health outcomes. Based on current literature, this review addresses the nutrition needs of infants and children in heart failure and describes the pathophysiology and metabolic implications of this disease. The prevalence of wasting in pediatric heart failure has been reported to be as high as 86%, highlighting the importance of nutrition assessment through all stages of treatment to provide appropriate intake of energy, protein, and micronutrients. The etiology of malnutrition in pediatric heart failure is multifactorial and involves hypermetabolism, decreased intake, increased nutrient losses, inefficient utilization of nutrients, and malabsorption. Children in heart failure often present with tachypnea, tachycardia, fatigue, nausea, and vomiting and consequently may not be able to meet their nutrition requirements through oral intake alone. Nutrition support, including enteral nutrition and parenteral nutrition, should be considered an essential part of routine care. The involvement of multiple allied health professionals may be needed to create a feeding therapy plan to support patients and their families. With appropriate nutrition interventions, clinical outcomes and quality of life can be significantly improved.
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PMID:Optimizing Nutrition in Pediatric Heart Failure: The Crisis Is Over and Now It's Time to Feed. 2865 14

Experimental non-human primate models of obesity are induced through the introduction of atypically calorically rich diets. Studies in captive-bred macaques show the development of obesity and diabetes with similar complications to humans including eye and kidney diseases, nerve damage associated with pain and blood vessel damage. Diets differ in outcomes and here we document inflammation of the gastrointestinal tract that can be exacerbated through these dietary interventions. Following baseline physiological evaluation of body composition, Southern pigtail macaques were given a high-fat diet (HFD) for three months. This HFD consisted of lard, grains (including gluten), dairy and fructose that was otherwise omitted from a standard macaque diet (Chow). Physiological parameters were then reassessed before animals were reverted back to standard Chow for a further three months (remission). Consumption of the HFD resulted in food-mediated hypersensitivity marked by chronic weight loss, alopecia, malabsorption, protein-losing enteropathy and gross diffuse intestinal villi atrophy and lamina propria hypertrophy. Physiological changes were more highly pronounced in female macaques suggesting sex-specific differences but could be fully reversed through change of diet. Care should be taken in choosing non-human primate HFD diets for creating experimental models of obesity because they can induce severe food-driven chronic inflammation of the gastrointestinal tract that can eventuate to diet-induced chronic wasting and mortality.
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PMID:Food hypersensitivity-induced chronic gastrointestinal inflammation in a non-human primate model of diet-induced obesity. 3094 72

: Undernutrition is a major public health problem leading to 1 in 5 of all deaths in children under 5 years. Undernutrition leads to growth stunting and/or wasting and is often associated with environmental enteric dysfunction (EED). EED mechanisms leading to growth failure include intestinal hyperpermeability, villus blunting, malabsorption and gut inflammation. As non-invasive methods for investigating gut function in undernourished children are limited, pre-clinical models are relevant to elucidating the pathophysiological processes involved in undernutrition and EED, and to identifying novel therapeutic strategies. In many published models, undernutrition was induced using protein or micronutrient deficient diets, but these experimental models were not associated with EED. Enteropathy models mainly used gastrointestinal injury triggers. These models are presented in this review. We found only a few studies investigating the combination of undernutrition and enteropathy. This highlights the need for further developments to establish an experimental model reproducing the impact of undernutrition and enteropathy on growth, intestinal hyperpermeability and inflammation, that could be suitable for preclinical evaluation of innovative therapeutic intervention.
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PMID:Animal Models of Undernutrition and Enteropathy as Tools for Assessment of Nutritional Intervention. 3152 23


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